[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 100 of about 203
1. Burleigh ME, Babaev VR, Oates JA, Harris RC, Gautam S, Riendeau D, Marnett LJ, Morrow JD, Fazio S, Linton MF: Cyclooxygenase-2 promotes early atherosclerotic lesion formation in LDL receptor-deficient mice. Circulation; 2002 Apr 16;105(15):1816-23
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Fetal liver cell transplantation was used to generate LDLR-/- mice null for expression of the COX-2 gene by macrophages.
  • CONCLUSIONS: The present studies provide strong pharmacological and genetic evidence that COX-2 promotes early atherosclerotic lesion formation in LDLR-/- mice in vivo.
  • [MeSH-minor] Animals. Blood Platelets / drug effects. Blood Platelets / metabolism. Cyclooxygenase 2. Cyclooxygenase 2 Inhibitors. Cyclooxygenase Inhibitors / pharmacology. Female. Indomethacin / pharmacology. Kinetics. Lactones / pharmacology. Lipids / blood. Liver Transplantation. Macrophages / enzymology. Male. Mice. Mice, Inbred C57BL. Mice, Knockout. Prostaglandins / urine. RNA, Messenger / biosynthesis. Sulfones. Thromboxane B2 / biosynthesis

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. INDOMETHACIN .
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11956125.001).
  • [ISSN] 1524-4539
  • [Journal-full-title] Circulation
  • [ISO-abbreviation] Circulation
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA77839; United States / NIDDK NIH HHS / DK / DK48831; United States / NIGMS NIH HHS / GM / GM42056; United States / NHLBI NIH HHS / HL / HL-53989
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclooxygenase 2 Inhibitors; 0 / Cyclooxygenase Inhibitors; 0 / Isoenzymes; 0 / Lactones; 0 / Lipids; 0 / Prostaglandins; 0 / RNA, Messenger; 0 / Receptors, LDL; 0 / Sulfones; 0QTW8Z7MCR / rofecoxib; 54397-85-2 / Thromboxane B2; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases; XXE1CET956 / Indomethacin
  •  go-up   go-down


2. Shieh JS, Kao MH, Liu CC: Genetic fuzzy modelling and control of bispectral index (BIS) for general intravenous anaesthesia. Med Eng Phys; 2006 Mar;28(2):134-48
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genetic fuzzy modelling and control of bispectral index (BIS) for general intravenous anaesthesia.
  • Based on an adaptive genetic fuzzy clustering algorithm, a derived fuzzy knowledge model is proposed for quantitatively estimating the systolic arterial pressure (SAP), heart rate (HR), and bispectral index (BIS) using 12 patients and it validates them according to pharmacological reasoning.
  • Controller performance was assessed using mean absolute error (MAE) of the BIS target, the percentage of time with acceptable BIS control (PTABC), and drug consumption (DC).
  • In contrast, there were no significant differences (P > 0.05) for these three groups in terms of drug consumption.
  • This indicates that either GPIDC or GFLC can control the BIS target set at 50 better than manual control, although the similar drug consumption is used.
  • [MeSH-major] Anesthesia, General / methods. Anesthetics, Intravenous / administration & dosage. Artificial Intelligence. Blood Pressure / drug effects. Drug Therapy, Computer-Assisted / methods. Electrocardiography / drug effects. Electroencephalography / drug effects
  • [MeSH-minor] Computer Simulation. Feedback. Female. Fuzzy Logic. Humans. Male. Models, Biological. Pattern Recognition, Automated / methods

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15961340.001).
  • [ISSN] 1350-4533
  • [Journal-full-title] Medical engineering & physics
  • [ISO-abbreviation] Med Eng Phys
  • [Language] eng
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anesthetics, Intravenous
  •  go-up   go-down


3. Shmelkov SV, Meeus S, Moussazadeh N, Kermani P, Rashbaum WK, Rabbany SY, Hanson MA, Lane WJ, St Clair R, Walsh KA, Dias S, Jacobson JT, Hempstead BL, Edelberg JM, Rafii S: Cytokine preconditioning promotes codifferentiation of human fetal liver CD133+ stem cells into angiomyogenic tissue. Circulation; 2005 Mar 8;111(9):1175-83
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytokine preconditioning promotes codifferentiation of human fetal liver CD133+ stem cells into angiomyogenic tissue.
  • BACKGROUND: CD133 (AC133) is a surface antigen that defines a broad population of stem cells, including myogenic and endothelial progenitors.
  • CD133+ cells are rare in adult tissues, and the factors that support their differentiation into mature angiomyogenic cells are not known.
  • These hurdles have hampered the use of CD133+ cells for therapeutic purposes.
  • Because human fetal liver is a rich source of CD133+ cells, we sought to identify the growth factors that promote codifferentiation of these cells into angiogenic and myogenic cells.
  • METHODS AND RESULTS: Human fetal liver CD133+ and CD133- cell subpopulations were cultured with 5'-azacytidine or vascular endothelial growth factor (VEGF165) and/or brain-derived nerve growth factor (BDNF).
  • CD133+ but not CD133- cells from human fetal liver codifferentiated into spindle-shaped cells, as well as flat adherent multinucleated cells capable of spontaneous contractions in culture.
  • The resulting spindle-shaped cells were confirmed to be endothelial cells by immunohistochemistry analysis for von Willebrand factor and by acetylated LDL uptake.
  • Multinucleated cells were characterized as striated muscles by electron microscopy and immunohistochemistry analysis for myosin heavy chain.
  • Inoculation of cells derived from CD133+ cells, but not CD133- cells, into the ear pinna of NOD/SCID mice resulted in the formation of cardiomyocytes, as identified by immunostaining with cardiac troponin-T antibody.
  • These cells generated electrical action potentials, detectable by ECG tracing.
  • CONCLUSIONS: CD133 defines a population of human fetal liver cells capable of differentiating into both angiogenic and myogenic cells.
  • Preconditioning of these CD133+ cells with VEGF165 and BDNF enhances the angiomyogenesis.
  • CD133+ fetal liver cells ultimately may be used for therapeutic angiomyogenesis.
  • [MeSH-major] Brain-Derived Neurotrophic Factor / pharmacology. Endothelial Cells / cytology. Endothelium, Vascular / cytology. Liver / cytology. Myocytes, Cardiac / cytology. Stem Cells / drug effects. Vascular Endothelial Growth Factor A / pharmacology
  • [MeSH-minor] Action Potentials. Animals. Antigens, CD / analysis. Azacitidine / pharmacology. Biomarkers. Cell Differentiation / drug effects. Cell Lineage. Cells, Cultured / cytology. Cells, Cultured / drug effects. Ear, External. Gene Expression Profiling. Glycoproteins / analysis. Humans. Lipoproteins, LDL / metabolism. Mice. Mice, Inbred NOD. Mice, SCID. Muscle Proteins / biosynthesis. Muscle Proteins / genetics. Peptides / analysis. Receptors, Immunologic / metabolism. Receptors, Scavenger. Stem Cell Transplantation. Transplantation, Heterologous. von Willebrand Factor / analysis

  • MedlinePlus Health Information. consumer health - Stem Cells.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. AZACITIDINE .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15753226.001).
  • [ISSN] 1524-4539
  • [Journal-full-title] Circulation
  • [ISO-abbreviation] Circulation
  • [Language] eng
  • [Grant] United States / NIA NIH HHS / AG / AG-19738; United States / NIA NIH HHS / AG / AG-20918; United States / NHLBI NIH HHS / HL / HL-59312; United States / NHLBI NIH HHS / HL / HL-67839; United States / NHLBI NIH HHS / HL / HL-75234; United States / NHLBI NIH HHS / HL / R01-HL-66592
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AC133 antigen; 0 / Antigens, CD; 0 / Biomarkers; 0 / Brain-Derived Neurotrophic Factor; 0 / Glycoproteins; 0 / Lipoproteins, LDL; 0 / Muscle Proteins; 0 / Peptides; 0 / Receptors, Immunologic; 0 / Receptors, Scavenger; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 0 / acetyl-LDL; 0 / von Willebrand Factor; M801H13NRU / Azacitidine
  •  go-up   go-down


Advertisement
4. Bachmann SP, Ramage G, VandeWalle K, Patterson TF, Wickes BL, López-Ribot JL: Antifungal combinations against Candida albicans biofilms in vitro. Antimicrob Agents Chemother; 2003 Nov;47(11):3657-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Candida biofilms display increased resistance to most antifungal agents.
  • We have evaluated the efficacy of combinations of fluconazole (FLC), amphotericin B, and caspofungin (CSP) against Candida albicans biofilms in vitro.
  • Indifference was observed for all the combinations of paired antifungal agents when a checkerboard titration method was used.
  • Time-kill experiments revealed an antagonistic effect of high FLC doses with CSP.

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. AMPHOTERICIN B .
  • Hazardous Substances Data Bank. CASPOFUNGIN .
  • Hazardous Substances Data Bank. FLUCONAZOLE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Methods Enzymol. 1999;310:644-56 [10547826.001]
  • [Cites] Antimicrob Agents Chemother. 2001 Apr;45(4):999-1007 [11257008.001]
  • [Cites] J Dent Res. 2001 Mar;80(3):903-8 [11379893.001]
  • [Cites] Antimicrob Agents Chemother. 2001 Sep;45(9):2475-9 [11502517.001]
  • [Cites] Am Clin Lab. 2001 Aug;20(7):42-4 [11570274.001]
  • [Cites] Antimicrob Agents Chemother. 1995 Sep;39(9):2128-31 [8540729.001]
  • [Cites] J Antimicrob Chemother. 2002 Jun;49(6):973-80 [12039889.001]
  • [Cites] Antimicrob Agents Chemother. 2002 Nov;46(11):3591-6 [12384370.001]
  • [Cites] Antimicrob Agents Chemother. 2002 Nov;46(11):3634-6 [12384379.001]
  • [Cites] Trends Microbiol. 2003 Jan;11(1):30-6 [12526852.001]
  • [Cites] Antimicrob Agents Chemother. 2002 Jun;46(6):1773-80 [12019089.001]
  • (PMID = 14576141.001).
  • [ISSN] 0066-4804
  • [Journal-full-title] Antimicrobial agents and chemotherapy
  • [ISO-abbreviation] Antimicrob. Agents Chemother.
  • [Language] ENG
  • [Grant] United States / NIDCR NIH HHS / DE / R01 DE011381; United States / NIDCR NIH HHS / DE / 5 RO1 DE11381-04
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Drug Combinations; 0 / Echinocandins; 0 / Peptides; 0 / Peptides, Cyclic; 0 / Tetrazolium Salts; 117038-70-7 / 2,3-bis(2-methoxy-4-nitro-5-sulfophenyl)-5-((phenylamino)carbonyl)-2H-tetrazolium hydroxide; 7XU7A7DROE / Amphotericin B; 8VZV102JFY / Fluconazole; F0XDI6ZL63 / caspofungin
  • [Other-IDs] NLM/ PMC253764
  •  go-up   go-down


5. Magill SS, Shields C, Sears CL, Choti M, Merz WG: Triazole cross-resistance among Candida spp.: case report, occurrence among bloodstream isolates, and implications for antifungal therapy. J Clin Microbiol; 2006 Feb;44(2):529-35
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Fluconazole (FLC) remains a first-line therapy for candidemia; and voriconazole (VRC), an expanded-spectrum triazole, was recently approved for the treatment of candidemia in nonneutropenic patients.
  • In vitro studies have suggested that VRC has potent activity against Candida spp. with reduced susceptibilities to FLC.
  • We present a case report of invasive candidiasis and candidemia due to a Candida glabrata isolate that developed resistance to all currently available triazole antifungals after a course of FLC treatment.
  • FLC MICs were determined for 125 of 153 isolates (81.7%).
  • Thirty of 125 isolates (24%) were resistant or showed reduced susceptibilites to FLC (MICs >/= 16 microg/ml).
  • These data have prompted the introduction of reflexive FLC susceptibility testing of first bloodstream Candida isolates at our institution.
  • Studies are needed to define the clinical significance of in vitro resistance to the newer antifungal agents.

  • MedlinePlus Health Information. consumer health - Yeast Infections.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. FLUCONAZOLE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Ann Surg. 2001 Apr;233(4):542-8 [11303137.001]
  • [Cites] Lancet. 2005 Oct 22-28;366(9495):1435-42 [16243088.001]
  • [Cites] Lancet Infect Dis. 2002 Feb;2(2):73-85 [11901654.001]
  • [Cites] J Clin Microbiol. 2002 Apr;40(4):1298-302 [11923348.001]
  • [Cites] Antimicrob Agents Chemother. 2002 Jun;46(6):1723-7 [12019081.001]
  • [Cites] Clin Infect Dis. 2002 Sep 1;35(5):627-30 [12173140.001]
  • [Cites] J Clin Microbiol. 2003 May;41(5):2176-9 [12734273.001]
  • [Cites] Clin Infect Dis. 2003 Sep 1;37(5):634-43 [12942393.001]
  • [Cites] Antimicrob Agents Chemother. 2003 Oct;47(10):3149-54 [14506023.001]
  • [Cites] Eur J Clin Microbiol Infect Dis. 2003 Nov;22(11):651-5 [14564539.001]
  • [Cites] Clin Infect Dis. 2004 Jan 15;38(2):161-89 [14699449.001]
  • [Cites] Surg Infect (Larchmt). 2003 Winter;4(4):345-54 [15012861.001]
  • [Cites] Diagn Microbiol Infect Dis. 2004 Mar;48(3):201-5 [15023430.001]
  • [Cites] J Clin Microbiol. 2004 Apr;42(4):1519-27 [15070998.001]
  • [Cites] Antimicrob Agents Chemother. 2004 May;48(5):1773-7 [15105134.001]
  • [Cites] J Clin Microbiol. 2004 Jul;42(7):3137-41 [15243072.001]
  • [Cites] Clin Infect Dis. 2004 Aug 1;39(3):309-17 [15306996.001]
  • [Cites] J Clin Microbiol. 1994 Jan;32(1):59-64 [7907345.001]
  • [Cites] Antimicrob Agents Chemother. 2005 Feb;49(2):767-9 [15673762.001]
  • [Cites] Antimicrob Agents Chemother. 2005 Feb;49(2):783-7 [15673768.001]
  • [Cites] J Antimicrob Chemother. 2005 Feb;55(2):194-9 [15618284.001]
  • [Cites] J Clin Microbiol. 2001 Sep;39(9):3254-9 [11526159.001]
  • (PMID = 16455909.001).
  • [ISSN] 0095-1137
  • [Journal-full-title] Journal of clinical microbiology
  • [ISO-abbreviation] J. Clin. Microbiol.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / K23 AI053601; United States / NIAID NIH HHS / AI / AI53601
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Triazoles; 8VZV102JFY / Fluconazole
  • [Other-IDs] NLM/ PMC1392670
  •  go-up   go-down


6. Bii CC, Makimura K, Abe S, Taguchi H, Mugasia OM, Revathi G, Wamae NC, Kamiya S: Antifungal drug susceptibility of Cryptococcus neoformans from clinical sources in Nairobi, Kenya. Mycoses; 2007 Jan;50(1):25-30
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Antifungal drug susceptibility of Cryptococcus neoformans from clinical sources in Nairobi, Kenya.
  • The serotypes and mating types of 80 clinical isolates of Cryptococcus neoformans from Kenya were studied and subjected to broth microdilution susceptibility testing to amphotericin B (AMP), flucytosin, fluconazole (FLC), itraconazole (ITC) and miconazole (MCZ).
  • Mating experiment confirmed all the isolates to be alpha-mating type.
  • Only 23.8% of the strains were susceptible to FLC with 65% susceptible dose-dependent (SDD) and 11.2% resistant.
  • The study reports the serotypes, mating types and highlights the existence of azoles resistance in C. neoformans in Nairobi which calls for antifungal drug resistance surveillance as prophylactic use of FLC increases because of human immunodeficiency virus/acquired immunodeficiency syndrome (HIV/AIDS) epidemic in sub-Saharan Africa.
  • [MeSH-major] Antifungal Agents / pharmacology. Cryptococcus neoformans / drug effects. Meningitis, Cryptococcal / epidemiology
  • [MeSH-minor] Azoles / pharmacology. Cerebrospinal Fluid / microbiology. Drug Resistance, Fungal. Humans. Kenya / epidemiology. Microbial Sensitivity Tests. Serotyping

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17302744.001).
  • [ISSN] 0933-7407
  • [Journal-full-title] Mycoses
  • [ISO-abbreviation] Mycoses
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Azoles
  •  go-up   go-down


7. Kacena MA, Nelson T, Clough ME, Lee SK, Lorenzo JA, Gundberg CM, Horowitz MC: Megakaryocyte-mediated inhibition of osteoclast development. Bone; 2006 Nov;39(5):991-999
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The co-culture of MK with osteoblasts (OB) resulted in increased OB proliferation in vitro, by a mechanism that required direct cell-to-cell contact.
  • Spleen or bone marrow (BM) cells from C57BL/6 mice, as a source of OC precursors, were cultured with M-CSF and RANKL to induce OC development.
  • MK were prepared by culturing fetal liver cells with thrombopoietin and separating cells into MK and non-MK populations.
  • MK were titrated into spleen cell cultures and OC were identified as tartrate-resistant acid phosphatase-positive giant cells with >3 nuclei.
  • There was a significant, P < 0.001, up to 10-fold reduction in OC formed when MK were added to the spleen cell cultures.
  • [MeSH-minor] Animals. Bone Marrow Cells / cytology. Bone Marrow Cells / drug effects. Bone Marrow Cells / metabolism. Cell Communication. Cell Proliferation. Cells, Cultured. Coculture Techniques / methods. Macrophage Colony-Stimulating Factor / pharmacology. Mice. Mice, Inbred C57BL. Mice, Knockout. Osteoblasts / cytology. Osteoblasts / metabolism. Osteoprotegerin / genetics. Osteoprotegerin / metabolism. RANK Ligand / pharmacology. Spleen / cytology. Spleen / drug effects. Spleen / metabolism. Transforming Growth Factor beta1 / metabolism

  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16782418.001).
  • [ISSN] 8756-3282
  • [Journal-full-title] Bone
  • [ISO-abbreviation] Bone
  • [Language] eng
  • [Grant] United States / NIAMS NIH HHS / AR / AR 46032; United States / NIAMS NIH HHS / AR / AR 47342
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Osteoprotegerin; 0 / RANK Ligand; 0 / Tnfsf11 protein, mouse; 0 / Transforming Growth Factor beta1; 81627-83-0 / Macrophage Colony-Stimulating Factor
  •  go-up   go-down


8. Pelletier R, Loranger L, Marcotte H, De Carolis E: Voriconazole and fluconazole susceptibility of Candida isolates. J Med Microbiol; 2002 Jun;51(6):479-83
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • An adapted NCCLS M27-A method was used to evaluate the activity of voriconazole (VRC) and fluconazole (FLC) against 295 Candida isolates collected from 189 patients (including isolates from deep sites).
  • Forty-two isolates had reduced susceptibility to FLC (MIC >8 mg/L); 83.3% of these had VRC MICs < or =2 mg/L (9 of 11 C. albicans, 18 of 19 C glabrata, 6 of 6 C. krusei, 2 of 2 C. lusitaniae and 0 of 4 C. tropicalis), including 60% of isolates collected from deep-seated infections.
  • These results suggested that in the era of azole resistance, VRC has a promising antifungal activity for serious infections with Candida spp., including most species with low susceptibility to FLC and uncommonly isolated species.
  • [MeSH-major] Antifungal Agents / pharmacology. Candida / drug effects. Candidiasis / drug therapy. Fluconazole / pharmacology. Pyrimidines / pharmacology. Triazoles / pharmacology
  • [MeSH-minor] Colony Count, Microbial. Drug Resistance, Fungal. Humans. Microbial Sensitivity Tests. Treatment Outcome. Voriconazole

  • MedlinePlus Health Information. consumer health - Yeast Infections.
  • Hazardous Substances Data Bank. FLUCONAZOLE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12018654.001).
  • [ISSN] 0022-2615
  • [Journal-full-title] Journal of medical microbiology
  • [ISO-abbreviation] J. Med. Microbiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Pyrimidines; 0 / Triazoles; 8VZV102JFY / Fluconazole; JFU09I87TR / Voriconazole
  •  go-up   go-down


9. Talbot NC, Caperna TJ, Wells KD: The PICM-19 cell line as an in vitro model of liver bile ductules: effects of cAMP inducers, biopeptides and pH. Cells Tissues Organs; 2002;171(2-3):99-116
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The PICM-19 cell line as an in vitro model of liver bile ductules: effects of cAMP inducers, biopeptides and pH.
  • The PICM-19 fetal liver cell line was isolated from the primary culture and spontaneous differentiation of pig epiblast cells, i.e. embryonic stem cells.
  • PICM-19 cells were induced to differentiate into mostly ductular formations by culturing at pH 7.6-7.8.
  • The ductules were functionally assayed by treatment with cAMP inducing agents and bioactive peptides reported to influence the secretory activity of liver bile ductules.
  • The secretory response of the cells was assessed by qualitative or quantitative measurement of the cross-sectional area of the ductal lumens and the appearance of biliary canaliculi in between PICM-19 cells that had formed monolayers instead of ducts.
  • The amounts of these proteins increased in the cultures as differentiation proceeded over time.
  • Transmission electron microscopy revealed that the ductal structures were usually sandwiched between SIM mouse, thioguanine- and ouabain-resistant (STO) feeder cells that had produced a collagen matrix.
  • Also, the ductular PICM-19 cells possessed cilia, probably occurring as a single cilium in each cell, that projected into the lumens of the ducts.
  • The results indicated that the in vitro-produced ductal structures of the PICM-19 cell line are a functional model for biliary epithelium.
  • [MeSH-major] Bile Ducts, Intrahepatic / cytology. Bile Ducts, Intrahepatic / metabolism. Cell Line. Cyclic AMP / metabolism. Liver / cytology. Peptides / pharmacology
  • [MeSH-minor] Animals. Aquaporins / metabolism. Cell Differentiation / physiology. Cholera Toxin / pharmacology. Colforsin / pharmacology. Fetus. Hydrogen-Ion Concentration. Keratin-7. Keratins / metabolism. Peptide Hormones / pharmacology. Swine. Sympathomimetics / pharmacology. Totipotent Stem Cells / cytology. Totipotent Stem Cells / metabolism. gamma-Glutamyltransferase / metabolism

  • COS Scholar Universe. author profiles.
  • Cellosaurus - a cell line knowledge resource. culture/stock collections - Cellosaurus - a cell line knowledge resource .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2002 S. Karger AG, Basel
  • (PMID = 12097833.001).
  • [ISSN] 1422-6405
  • [Journal-full-title] Cells, tissues, organs
  • [ISO-abbreviation] Cells Tissues Organs (Print)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Aquaporins; 0 / Keratin-7; 0 / Krt2-7 protein, mouse; 0 / Peptide Hormones; 0 / Peptides; 0 / Sympathomimetics; 1F7A44V6OU / Colforsin; 68238-35-7 / Keratins; 9012-63-9 / Cholera Toxin; E0399OZS9N / Cyclic AMP; EC 2.3.2.2 / gamma-Glutamyltransferase
  •  go-up   go-down


10. Schmelzer E, Reid LM: Human telomerase activity, telomerase and telomeric template expression in hepatic stem cells and in livers from fetal and postnatal donors. Eur J Gastroenterol Hepatol; 2009 Oct;21(10):1191-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Human telomerase activity, telomerase and telomeric template expression in hepatic stem cells and in livers from fetal and postnatal donors.
  • BACKGROUND: Although telomerase activity has been analyzed in various normal and malignant tissues, including liver, it is still unknown to what extent telomerase can be associated with specific maturational lineage stages.
  • METHODS: We assessed human telomerase activity, protein and gene expression for the telomerase reverse transcriptase, as well as expression of the telomeric template RNA hTER in hepatic stem cells and in various developmental stages of the liver from fetal to adult.
  • In addition, the effect of growth factors on telomerase activity was analyzed in hepatic stem cells in vitro.
  • RESULTS: Telomerase was found to be highly active in fetal liver cells and was significantly higher than in hepatic stem cells, correlating with gene and protein expression levels.
  • A short stimulation by growth factors of cultured hepatic stem cells did not increase telomerase activity.
  • CONCLUSION: Telomerase is considerably active in fetal liver and variably in postnatal livers.
  • Although telomerase protein is present at varying levels in liver cells of all donor ages, gene expression is solely associated with fetal liver cells.

  • MedlinePlus Health Information. consumer health - Stem Cells.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Br J Exp Pathol. 1977 Jun;58(3):301-10 [326290.001]
  • [Cites] J Cell Biol. 1977 Feb;72(2):441-55 [833203.001]
  • [Cites] Cell. 1985 Dec;43(2 Pt 1):405-13 [3907856.001]
  • [Cites] Cell Differ. 1988 Jun;24(1):9-24 [3409327.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 Nov 1;89(21):10114-8 [1438199.001]
  • [Cites] Science. 1994 Dec 23;266(5193):2011-5 [7605428.001]
  • [Cites] FASEB J. 1996 Sep;10(11):1249-56 [8836038.001]
  • [Cites] Gastroenterology. 1997 Feb;112(2):493-500 [9024303.001]
  • [Cites] Br J Cancer. 1997;75(4):516-22 [9052403.001]
  • [Cites] Cancer Genet Cytogenet. 1997 Jan;93(1):56-62 [9062581.001]
  • [Cites] Science. 1997 Apr 4;276(5309):60-6 [9082986.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Dec 9;94(25):13677-82 [9391085.001]
  • [Cites] Nature. 1998 Apr 9;392(6676):569-74 [9560153.001]
  • [Cites] Exp Cell Res. 1998 Jul 10;242(1):120-7 [9665809.001]
  • [Cites] Cancer Res. 1998 Sep 15;58(18):4168-72 [9751630.001]
  • [Cites] J Surg Oncol. 1998 Nov;69(3):119-24 [9846496.001]
  • [Cites] Nat Genet. 1999 Jan;21(1):115-8 [9916803.001]
  • [Cites] Am J Physiol. 1999 May;276(5 Pt 1):G1260-72 [10330018.001]
  • [Cites] Cancer Res. 1999 Aug 15;59(16):3954-60 [10463591.001]
  • [Cites] J Cell Sci. 2006 Jul 1;119(Pt 13):2797-806 [16772337.001]
  • [Cites] Stem Cells. 2006 Aug;24(8):1852-8 [16627685.001]
  • [Cites] World J Surg. 2007 May;31(5):1121-8 [17429564.001]
  • [Cites] J Exp Med. 2007 Aug 6;204(8):1973-87 [17664288.001]
  • [Cites] Hepatology. 2008 Nov;48(5):1598-607 [18972441.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Oct 24;97(22):12132-7 [11050242.001]
  • [Cites] Neoplasia. 2000 Sep-Oct;2(5):426-32 [11191109.001]
  • [Cites] Neoplasia. 2000 Sep-Oct;2(5):433-40 [11191110.001]
  • [Cites] Int J Cancer. 2001 Mar 1;91(5):644-9 [11267974.001]
  • [Cites] Hum Mol Genet. 2001 Sep 1;10(18):1945-52 [11555631.001]
  • [Cites] Exp Cell Res. 2002 Feb 15;273(2):147-56 [11822870.001]
  • [Cites] Nat Cell Biol. 2002 Sep;4(9):731-6 [12198499.001]
  • [Cites] Nat Med. 2002 Sep;8(9):934-6 [12205452.001]
  • [Cites] J Gastroenterol Hepatol. 2003 Jan;18(1):4-12 [12519217.001]
  • [Cites] J Gastroenterol Hepatol. 2003 Oct;18(10):1168-74 [12974904.001]
  • [Cites] J Cell Biol. 1968 Mar;36(3):551-65 [5645547.001]
  • [Cites] J Cell Biol. 1972 Jan;52(1):159-70 [4331297.001]
  • [Cites] J Cell Biol. 1972 Feb;52(2):261-72 [4400451.001]
  • [Cites] Virchows Arch B Cell Pathol. 1973 Nov 28;14(2):93-103 [4203888.001]
  • [Cites] Cell Tissue Kinet. 1976 Nov;9(6):517-32 [1000566.001]
  • [Cites] J Histochem Cytochem. 1978 May;26(5):409-11 [659841.001]
  • (PMID = 19240645.001).
  • [ISSN] 1473-5687
  • [Journal-full-title] European journal of gastroenterology & hepatology
  • [ISO-abbreviation] Eur J Gastroenterol Hepatol
  • [Language] ENG
  • [Grant] United States / NIAAA NIH HHS / AA / R01 AA014243; United States / NIDDK NIH HHS / DK / R01 DK052851-02; United States / NIDDK NIH HHS / DK / R01 DK52851; United States / NIDDK NIH HHS / DK / DK052851-02; United States / NIDDK NIH HHS / DK / R01 DK052851; United States / NIDDK NIH HHS / DK / R01 IP30-DK065933; United States / NIAAA NIH HHS / AA / AA014243-05; United States / NIAAA NIH HHS / AA / R01 AA014243-05
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Growth Substances; EC 2.7.7.49 / TERT protein, human; EC 2.7.7.49 / Telomerase
  • [Other-IDs] NLM/ NIHMS94551; NLM/ PMC2743773
  •  go-up   go-down


11. Gunzer M, Friedl P, Niggemann B, Bröcker EB, Kämpgen E, Zänker KS: Migration of dendritic cells within 3-D collagen lattices is dependent on tissue origin, state of maturation, and matrix structure and is maintained by proinflammatory cytokines. J Leukoc Biol; 2000 May;67(5):622-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Migration of dendritic cells within 3-D collagen lattices is dependent on tissue origin, state of maturation, and matrix structure and is maintained by proinflammatory cytokines.
  • The function of dendritic cells (DC) depends on active migration through three-dimensional (3-D) extracellular matrices.
  • We have analyzed the migration of murine DC from different tissue origins within 3-D collagen lattices through the use of time-lapse videomicroscopy and single-cell tracking.
  • Directly after incorporation, 50-90% of DC from the spleen (spDC) and Langerhans cells freshly isolated from the epidermis (fLC) displayed active motility in these matrices.
  • Whereas mature spDC showed multilateral pseudopod dynamics as well as fast and heterogeneous migration, immature fLC displayed a spherical shape with faint membrane processes and very homogenous, slow migration characteristics.
  • In the absence of external stimuli, migration of both, spDC and fLC, vanished after >36 h due to cell death.
  • Maintaining fLC viability by external granulocyte-macrophage colony-stimulating factor or tumor necrosis factor alpha prolonged migration up to 5 days.
  • During this period fLC transformed into mature cells with large dendrites, thereby developing a heterogeneous migration pattern more similar to spDC.
  • In randomly polymerized collagen matrices cell paths were without preferential orientation.
  • [MeSH-major] Collagen / physiology. Cytokines / pharmacology. Dendritic Cells / immunology. Extracellular Matrix / physiology. Langerhans Cells / immunology. Macrophages, Peritoneal / immunology
  • [MeSH-minor] Animals. Cell Line. Cell Movement / drug effects. Cell Movement / physiology. Cell Survival. Epidermis / cytology. Epidermis / immunology. Female. Granulocyte-Macrophage Colony-Stimulating Factor / pharmacology. Male. Mice. Mice, Inbred BALB C. Microscopy, Confocal. Microscopy, Video. Spleen / immunology. Tumor Necrosis Factor-alpha / pharmacology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 10811001.001).
  • [ISSN] 0741-5400
  • [Journal-full-title] Journal of leukocyte biology
  • [ISO-abbreviation] J. Leukoc. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Cytokines; 0 / Tumor Necrosis Factor-alpha; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor; 9007-34-5 / Collagen
  •  go-up   go-down


12. Horwitz BH, Mizgerd JP, Scott ML, Doerschuk CM: Mechanisms of granulocytosis in the absence of CD18. Blood; 2001 Mar 15;97(6):1578-83
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • To distinguish between these mechanisms, the hematopoietic systems of lethally irradiated wild-type (WT) mice were reconstituted with either WT fetal liver cells or CD18-deficient fetal liver cells, or an equal mixture of both types of cells.
  • Granulocytosis and splenomegaly developed in mice that received CD18-deficient fetal liver cells.
  • Splenomegaly was prevented and granulocytosis was inhibited by more than 95% in mice that had received both CD18-deficient and WT fetal liver cells, suggesting that myeloid hyperplasia was largely reactive in nature.
  • However, these animals did develop mild granulocytosis compared with mice reconstituted with WT cells alone, and a higher percentage of CD18-deficient leukocytes were neutrophils compared with the WT leukocytes.
  • These observations suggest that the granulocytosis observed in the absence of CD18 occurs through at least 2 mechanisms: one that is dramatically improved by the presence of WT cells, likely reactive in nature, and a second that is independent of the WT hematopoietic cells, involving an alteration in the lineage distribution of blood leukocytes.
  • [MeSH-major] Antigens, CD18 / pharmacology. Hematopoiesis / drug effects. Neutrophils / pathology
  • [MeSH-minor] Adoptive Transfer. Animals. Bone Marrow Cells / cytology. Bone Marrow Cells / immunology. Cell Division / drug effects. Cell Division / immunology. Cell Transplantation / rehabilitation. Disease Models, Animal. Leukocyte-Adhesion Deficiency Syndrome / etiology. Leukocyte-Adhesion Deficiency Syndrome / immunology. Leukocyte-Adhesion Deficiency Syndrome / pathology. Liver / cytology. Mice. Mice, Inbred C57BL. Whole-Body Irradiation

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11238094.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / HL48160
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD18
  •  go-up   go-down


13. Lupp A, Anschütz T, Lindström-Seppä P, Müller D: Developmental changes in glutathione S-transferase isoforms expression and activity in intrasplenic fetal liver tissue transplants in rats. Exp Toxicol Pathol; 2003 Sep;55(2-3):107-19
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Developmental changes in glutathione S-transferase isoforms expression and activity in intrasplenic fetal liver tissue transplants in rats.
  • The aim of the present study was to characterise developmental changes in glutathione S-transferase (GST) isoforms expression and in glutathione conjugation capacity in intrasplenic liver tissue transplants.
  • For this purpose, syngenic fetal liver tissue suspensions were transplanted into the spleens of adult male Fischer 344 rats.
  • Three days, 1, 2, 4 weeks, 2, 4, 6 months and 1 year later, transplant-recipients and control animals were sacrificed and class alpha, mu and pi GST isoforms expression and GST activities using the substrates o-dinitrobenzene and 1-chloro-2,4-dinitrobenzene were assessed in livers and spleens.
  • Fetal livers displayed almost no class alpha and mu, but a slight class pi GST expression.
  • The same pattern was seen in 3-day-old intrasplenic liver tissue transplants.
  • From 2 months after transplantation on activities were significantly higher in transplant-containing spleens than in respective control organs with a further increase up to one year after grafting.
  • These results show that intrasplenically transplanted fetal liver cells proliferate and differentiate into mature cells displaying a GST expression pattern with respective enzyme activities similar to adult liver.
  • [MeSH-major] Fetal Tissue Transplantation / physiology. Glutathione Transferase / metabolism. Liver / enzymology. Liver Transplantation / physiology
  • [MeSH-minor] Animals. Biotransformation. Cell Differentiation. Cell Nucleus / enzymology. Cytoplasm / enzymology. Dinitrobenzenes / metabolism. Dinitrobenzenes / pharmacology. Dinitrochlorobenzene / metabolism. Dinitrochlorobenzene / pharmacology. Embryonic and Fetal Development. Hepatocytes / cytology. Hepatocytes / enzymology. Immunoenzyme Techniques. Isoenzymes / classification. Isoenzymes / metabolism. Male. Microsomes, Liver / drug effects. Microsomes, Liver / metabolism. Rats. Rats, Inbred F344. Spleen


14. Kirschner KM, Hagen P, Hussels CS, Ballmaier M, Scholz H, Dame C: The Wilms' tumor suppressor Wt1 activates transcription of the erythropoietin receptor in hematopoietic progenitor cells. FASEB J; 2008 Aug;22(8):2690-701
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The Wilms' tumor suppressor Wt1 activates transcription of the erythropoietin receptor in hematopoietic progenitor cells.
  • The Wilms' tumor protein Wt1 is required for embryonic development and has been implicated in hematologic disorders.
  • Since Wt1 deficiency may compromise the proliferation and differentiation of erythroid progenitor cells, we analyzed the possible role of the transcriptionally active Wt1 isoform, Wt1(-KTS), in regulating the expression of the erythropoietin receptor (EpoR).
  • Wt1 and EpoR were coexpressed in CD117(+) hematopoietic progenitor cells and in several hematopoietic cell lines.
  • CD117(+) cells of Wt1-deficient murine embryos (Wt1(-/-)) exhibited a significantly lower proliferation response to recombinant erythropoietin than CD117(+) cells of heterozygous (Wt1(+/-)) and wild-type littermates (Wt1(+/+)).
  • EpoR expression was significantly diminished in hematopoietic progenitors (CD117(+)) that lacked Wt1, and the erythroid colony-forming capacity was reduced by more than 50% in fetal liver cells of Wt1-deficient embryonic mice.
  • Wt1(-KTS) significantly increased endogenous EpoR transcripts in transfected cells.
  • The proximal EpoR promoter of human and mouse was stimulated more than 10-fold by Wt1(-KTS) in transiently cotransfeced K562 erythroleukemia cells.
  • [MeSH-major] Genes, Wilms Tumor. Hematopoietic Stem Cells / metabolism. Receptors, Erythropoietin / genetics
  • [MeSH-minor] Animals. Base Sequence. Binding Sites / genetics. Cell Line. DNA / genetics. DNA / metabolism. DNA Primers / genetics. Embryonic Stem Cells / metabolism. Erythropoiesis / genetics. Erythropoietin / pharmacology. Genes, Reporter. Hematopoiesis / drug effects. Hematopoiesis / genetics. Heterozygote. Humans. Mice. Mice, Knockout. Mutagenesis, Site-Directed. Promoter Regions, Genetic. Proto-Oncogene Proteins c-kit / metabolism. RNA, Messenger / genetics. RNA, Messenger / metabolism. Recombinant Proteins / genetics. Recombinant Proteins / metabolism. Transcriptional Activation. Transfection. WT1 Proteins / deficiency. WT1 Proteins / genetics. WT1 Proteins / metabolism

  • Genetic Alliance. consumer health - Wilms' tumor.
  • MedlinePlus Health Information. consumer health - Stem Cells.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18424770.001).
  • [ISSN] 1530-6860
  • [Journal-full-title] FASEB journal : official publication of the Federation of American Societies for Experimental Biology
  • [ISO-abbreviation] FASEB J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / RNA, Messenger; 0 / Receptors, Erythropoietin; 0 / Recombinant Proteins; 0 / WT1 Proteins; 11096-26-7 / Erythropoietin; 9007-49-2 / DNA; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
  •  go-up   go-down


15. Shioyama Y, Gondo Y, Nakao K, Katsuki M: Different mutation frequencies and spectra among organs by N-methyl-N-nitrosourea in rpsL (strA) transgenic mice. Jpn J Cancer Res; 2000 May;91(5):482-91
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The frequencies and spectra of N-methyl-N-nitrosourea (MNU)-induced in vivo somatic mutations were determined in rpsL (strA) transgenic mice.
  • The wild-type rpsL gene, which exhibits a streptomycin-sensitive (Sm(S)) phenotype, was used as the rescue marker gene.
  • Stable organs like the liver and brain, however, carried many fewer G:C to A:T transitions but significantly more single base deletions, of which the spectrum was very similar to that of background mutations in the rpsL transgenic mice.
  • This spectrum difference among more and less proliferating organs was confirmed by the predominant occurrence of G:C to A:T transitions in fetal liver cells exposed to transplacental MNU treatment.
  • [MeSH-major] Alkylating Agents / toxicity. Methylnitrosourea / toxicity. Mutation
  • [MeSH-minor] Age Factors. Animals. Base Sequence. Brain / drug effects. Dose-Response Relationship, Drug. Female. Frameshift Mutation. Gene Deletion. Genetic Markers. Genetic Vectors / genetics. Liver / drug effects. Lung / drug effects. Male. Mice. Mice, Transgenic. Molecular Sequence Data. Mutagenicity Tests. Mutation, Missense. Organ Specificity. Thymus Gland / drug effects

  • Hazardous Substances Data Bank. N-NITROSO-N-METHYLUREA .
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 10835492.001).
  • [ISSN] 0910-5050
  • [Journal-full-title] Japanese journal of cancer research : Gann
  • [ISO-abbreviation] Jpn. J. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] JAPAN
  • [Chemical-registry-number] 0 / Alkylating Agents; 0 / Genetic Markers; 684-93-5 / Methylnitrosourea
  •  go-up   go-down


16. Ishida K, Rodrigues JC, Ribeiro MD, Vila TV, de Souza W, Urbina JA, Nakamura CV, Rozental S: Growth inhibition and ultrastructural alterations induced by Delta24(25)-sterol methyltransferase inhibitors in Candida spp. isolates, including non-albicans organisms. BMC Microbiol; 2009;9:74
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Although Candida species are commensal microorganisms, they can cause many invasive fungal infections.
  • Reference strain C. krusei (ATCC 6258, FLC-resistant) was consistently susceptible to AZA, although not to EIL.
  • Treatment with sub-inhibitory concentrations of AZA and EIL induced several ultrastructural alterations, including changes in the cell-wall shape and thickness, a pronounced disconnection between the cell wall and cytoplasm with an electron-lucent zone between them, mitochondrial swelling, and the presence of electron-dense vacuoles.
  • Fluorescence microscopy analyses indicated an accumulation of lipid bodies and alterations in the cell cycle of the yeasts.
  • The selectivity of 24-SMTI for fungal cells versus mammalian cells was assessed by the sulforhodamine B viability assay.
  • [MeSH-major] Candida / drug effects. Enzyme Inhibitors / pharmacology. Lanosterol / analogs & derivatives. Methyltransferases / antagonists & inhibitors. Pregnanediol / analogs & derivatives
  • [MeSH-minor] Animals. Antifungal Agents / pharmacology. Cercopithecus aethiops. Drug Resistance, Fungal. Microbial Sensitivity Tests. Microscopy, Electron, Scanning. Microscopy, Electron, Transmission. Microscopy, Fluorescence. Vero Cells

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] FEMS Microbiol Lett. 2000 Feb 1;183(1):89-94 [10650207.001]
  • [Cites] J Antimicrob Chemother. 2008 Jan;61 Suppl 1:i19-30 [18063600.001]
  • [Cites] Mutagenesis. 2002 May;17(3):219-22 [11971993.001]
  • [Cites] Trends Microbiol. 2003 Jun;11(6):272-9 [12823944.001]
  • [Cites] Mem Inst Oswaldo Cruz. 2003 Apr;98(3):401-5 [12886424.001]
  • [Cites] Can J Microbiol. 2003 May;49(5):344-9 [12897828.001]
  • [Cites] Histochem Cell Biol. 2003 Aug;120(2):129-41 [12844218.001]
  • [Cites] Antimicrob Agents Chemother. 2003 Sep;47(9):2966-70 [12937003.001]
  • [Cites] Steroids. 2003 Sep;68(7-8):587-94 [12957663.001]
  • [Cites] Antimicrob Agents Chemother. 2003 Oct;47(10):3149-54 [14506023.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Nov 25;100(24):14327-32 [14623979.001]
  • [Cites] Clin Infect Dis. 2004 Jan 15;38(2):161-89 [14699449.001]
  • [Cites] Int J Antimicrob Agents. 2004 Jun;23(6):620-6 [15194134.001]
  • [Cites] Antimicrob Agents Chemother. 2004 Aug;48(8):2937-50 [15273104.001]
  • [Cites] Lipids. 1977 Aug;12(8):666-8 [331008.001]
  • [Cites] Biochemistry. 1984 Jul 31;23(16):3582-9 [6383468.001]
  • [Cites] Rev Infect Dis. 1987 Jan-Feb;9 Suppl 1:S33-42 [3027844.001]
  • [Cites] Antimicrob Agents Chemother. 1987 Jan;31(1):46-51 [3551826.001]
  • [Cites] Proc Natl Acad Sci U S A. 1987 Jun;84(12):4012-6 [2438691.001]
  • [Cites] Mol Biochem Parasitol. 1995 Jul;73(1-2):199-210 [8577328.001]
  • [Cites] Chemotherapy. 1996 Jul-Aug;42(4):294-307 [8804798.001]
  • [Cites] Antimicrob Agents Chemother. 1997 Jul;41(7):1428-32 [9210660.001]
  • [Cites] Antimicrob Agents Chemother. 1997 Aug;41(8):1840-2 [9257776.001]
  • [Cites] J Cell Biol. 1997 Nov 17;139(4):985-94 [9362516.001]
  • [Cites] J Infect Dis. 1998 Feb;177(2):425-30 [9466531.001]
  • [Cites] J Ethnopharmacol. 1999 Aug;66(2):141-50 [10433470.001]
  • [Cites] J Antimicrob Chemother. 1999 Jul;44(1):109-12 [10459817.001]
  • [Cites] J Clin Microbiol. 2005 Apr;43(4):1829-35 [15815004.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Jul 12;102(28):9878-83 [15985553.001]
  • [Cites] FEMS Microbiol Lett. 2006 Feb;255(1):33-42 [16436059.001]
  • [Cites] Proc Am Thorac Soc. 2006;3(1):35-40 [16493149.001]
  • [Cites] Int J Antimicrob Agents. 2006 May;27(5):359-66 [16647248.001]
  • [Cites] Antimicrob Agents Chemother. 2006 Aug;50(8):2595-601 [16870747.001]
  • [Cites] J Clin Microbiol. 2006 Aug;44(8):2816-23 [16891497.001]
  • [Cites] J Antimicrob Chemother. 2006 Nov;58(5):942-9 [16973655.001]
  • [Cites] Lipids. 2007 Feb;42(1):15-33 [17393207.001]
  • [Cites] J Antimicrob Chemother. 2007 Aug;60(2):424-8 [17562683.001]
  • [Cites] Protist. 2007 Oct;158(4):447-56 [17719843.001]
  • [Cites] Biochem Biophys Res Commun. 2007 Nov 16;363(2):310-6 [17870055.001]
  • [Cites] Antimicrob Agents Chemother. 2002 Feb;46(2):487-99 [11796362.001]
  • (PMID = 19379501.001).
  • [ISSN] 1471-2180
  • [Journal-full-title] BMC microbiology
  • [ISO-abbreviation] BMC Microbiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 20-piperidin-2-yl-5-pregnan-3,20-diol; 0 / Antifungal Agents; 0 / Enzyme Inhibitors; 104960-23-8 / 24,25-iminolanosterol; 1J05Z83K3M / Lanosterol; EC 2.1.1.- / Methyltransferases; EC 2.1.1.41 / delta 24-sterol methyltransferase; JR3JD1Y22C / Pregnanediol
  • [Other-IDs] NLM/ PMC2679025
  •  go-up   go-down


17. Holmes AR, Lin YH, Niimi K, Lamping E, Keniya M, Niimi M, Tanabe K, Monk BC, Cannon RD: ABC transporter Cdr1p contributes more than Cdr2p does to fluconazole efflux in fluconazole-resistant Candida albicans clinical isolates. Antimicrob Agents Chemother; 2008 Nov;52(11):3851-62
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Fluconazole (FLC) remains the antifungal drug of choice for non-life-threatening Candida infections, but drug-resistant strains have been isolated during long-term therapy with azoles.
  • Drug efflux, mediated by plasma membrane transporters, is a major resistance mechanism, and clinically significant resistance in Candida albicans is accompanied by increased transcription of the genes CDR1 and CDR2, encoding plasma membrane ABC-type transporters Cdr1p and Cdr2p.
  • We have exploited the pump-specific properties of two antibody preparations, and specific pump inhibitors, to determine the relative expression and functions of Cdr1p and Cdr2p in 18 clinical C. albicans isolates.
  • The antibodies and inhibitors were standardized using recombinant Saccharomyces cerevisiae strains that hyper-express either protein in a host strain with a reduced endogenous pump background.
  • In all 18 C. albicans strains, including 13 strains with reduced FLC susceptibilities, Cdr1p was present in greater amounts (2- to 20-fold) than Cdr2p.
  • Compounds that inhibited Cdr1p-mediated function, but had no effect on Cdr2p efflux activity, significantly decreased the resistance to FLC of seven representative C. albicans isolates, whereas three other compounds that inhibited both pumps did not cause increased chemosensitization of these strains to FLC.
  • We conclude that Cdr1p expression makes a greater functional contribution than does Cdr2p to FLC resistance in C. albicans.
  • [MeSH-major] ATP-Binding Cassette Transporters / metabolism. Antifungal Agents / pharmacokinetics. Antifungal Agents / pharmacology. Candida albicans / drug effects. Candida albicans / metabolism. Fluconazole / pharmacokinetics. Fluconazole / pharmacology. Fungal Proteins / metabolism. Membrane Transport Proteins / metabolism
  • [MeSH-minor] Antibodies, Fungal. Biological Transport, Active. Candidiasis / drug therapy. Candidiasis / microbiology. Drug Resistance, Fungal / genetics. Gene Expression. Genes, Fungal. Humans. Recombinant Proteins / genetics. Recombinant Proteins / metabolism. Saccharomyces cerevisiae / genetics. Saccharomyces cerevisiae / metabolism

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. FLUCONAZOLE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Antimicrob Agents Chemother. 2006 Apr;50(4):1148-55 [16569823.001]
  • [Cites] Biochem Biophys Res Commun. 2005 May 6;330(2):622-8 [15796929.001]
  • [Cites] Int J Med Microbiol. 2006 Oct;296(6):421-34 [16782404.001]
  • [Cites] Mol Microbiol. 2006 Oct;62(1):170-86 [16942600.001]
  • [Cites] J Immunol Methods. 2006 Aug 31;315(1-2):49-60 [16979181.001]
  • [Cites] J Pharmacol Exp Ther. 2007 Jan;320(1):81-8 [17050779.001]
  • [Cites] Biol Pharm Bull. 2007 Jan;30(1):68-73 [17202662.001]
  • [Cites] Bioorg Med Chem Lett. 2007 May 15;17(10):2802-6 [17350259.001]
  • [Cites] Nat Rev Microbiol. 2007 Jun;5(6):418-30 [17505522.001]
  • [Cites] J Proteome Res. 2007 Jun;6(6):2248-56 [17432892.001]
  • [Cites] Eukaryot Cell. 2007 Jul;6(7):1150-65 [17513564.001]
  • [Cites] PLoS Pathog. 2007 Jun;3(6):e92 [17604452.001]
  • [Cites] Microbiology. 2007 Oct;153(Pt 10):3211-7 [17906120.001]
  • [Cites] Eukaryot Cell. 2007 Oct;6(10):1889-904 [17693596.001]
  • [Cites] Eukaryot Cell. 2007 Nov;6(11):2122-38 [17905926.001]
  • [Cites] Biochem Biophys Res Commun. 2007 Dec 28;364(4):990-5 [17967417.001]
  • [Cites] ChemMedChem. 2007 Dec;2(12):1783-8 [17994597.001]
  • [Cites] Antimicrob Agents Chemother. 2000 Sep;44(9):2373-81 [10952582.001]
  • [Cites] Microbiology. 2000 Nov;146 ( Pt 11):2743-54 [11065353.001]
  • [Cites] Antimicrob Agents Chemother. 2001 Jan;45(1):52-9 [11120944.001]
  • [Cites] J Antimicrob Chemother. 2001 May;47(5):527-36 [11328762.001]
  • [Cites] Farmaco. 2001 Jan-Feb;56(1-2):81-5 [11347972.001]
  • [Cites] J Antimicrob Chemother. 2005 Oct;56(4):678-85 [16115827.001]
  • [Cites] Science. 2005 Sep 30;309(5744):2175-6 [16195450.001]
  • [Cites] Microb Drug Resist. 2005 Fall;11(3):232-8 [16201925.001]
  • [Cites] J Mol Microbiol Biotechnol. 2005;9(1):3-15 [16254441.001]
  • [Cites] Med Mycol. 2005 Nov;43(7):647-50 [16396250.001]
  • [Cites] PLoS Pathog. 2007 Nov;3(11):e164 [17983269.001]
  • [Cites] J Endod. 2008 Jan;34(1):7-10 [18155483.001]
  • [Cites] Antimicrob Agents Chemother. 2008 Feb;52(2):409-17 [18056277.001]
  • [Cites] Antimicrob Agents Chemother. 2008 Mar;52(3):1127-32 [18180354.001]
  • [Cites] Antimicrob Agents Chemother. 2008 Apr;52(4):1481-92 [18268086.001]
  • [Cites] Drug Metab Dispos. 2001 Jul;29(7):1051-6 [11408373.001]
  • [Cites] Antimicrob Agents Chemother. 2001 Oct;45(10):2676-84 [11557454.001]
  • [Cites] Antimicrob Agents Chemother. 2001 Dec;45(12):3366-74 [11709310.001]
  • [Cites] Microbiology. 2002 Apr;148(Pt 4):1061-72 [11932451.001]
  • [Cites] Antimicrob Agents Chemother. 2002 Jun;46(6):1704-13 [12019079.001]
  • [Cites] Antimicrob Agents Chemother. 2003 Apr;47(4):1220-7 [12654650.001]
  • [Cites] Antimicrob Agents Chemother. 2003 May;47(5):1543-54 [12709320.001]
  • [Cites] J Antimicrob Chemother. 2003 Jul;52(1):1 [12805255.001]
  • [Cites] Int J Antimicrob Agents. 2003 Sep;22(3):291-300 [13678837.001]
  • [Cites] Antimicrob Agents Chemother. 2004 Apr;48(4):1256-71 [15047528.001]
  • [Cites] Antimicrob Agents Chemother. 2004 Jun;48(6):2124-31 [15155210.001]
  • [Cites] Mol Genet Genomics. 2004 Jun;271(5):554-65 [15114480.001]
  • [Cites] Antimicrob Agents Chemother. 2004 Jul;48(7):2733-5 [15215138.001]
  • [Cites] Antimicrob Agents Chemother. 2004 Aug;48(8):3064-79 [15273122.001]
  • [Cites] Biochem Biophys Res Commun. 2004 Sep 17;322(2):520-5 [15325261.001]
  • [Cites] Virology. 1974 Dec;62(2):483-99 [4432376.001]
  • [Cites] J Biol Chem. 1994 Apr 29;269(17):12797-803 [8175692.001]
  • [Cites] Microbiology. 1997 Feb;143 ( Pt 2):405-16 [9043118.001]
  • [Cites] Antimicrob Agents Chemother. 1997 Jul;41(7):1482-7 [9210670.001]
  • [Cites] Antimicrob Agents Chemother. 1998 Nov;42(11):2932-7 [9797228.001]
  • [Cites] Eukaryot Cell. 2004 Dec;3(6):1639-52 [15590837.001]
  • [Cites] J Antimicrob Chemother. 2004 Dec;54(6):999-1006 [15486081.001]
  • [Cites] Antimicrob Agents Chemother. 2005 Jan;49(1):57-70 [15616276.001]
  • [Cites] Biochem Biophys Res Commun. 2005 Mar 25;328(4):1119-25 [15707993.001]
  • [Cites] Curr Drug Targets. 2006 Apr;7(4):471-81 [16611035.001]
  • (PMID = 18710914.001).
  • [ISSN] 1098-6596
  • [Journal-full-title] Antimicrobial agents and chemotherapy
  • [ISO-abbreviation] Antimicrob. Agents Chemother.
  • [Language] eng
  • [Grant] United States / NIDCR NIH HHS / DE / R01 DE016885; United States / NIDCR NIH HHS / DE / R01DE016885-01-RDC; United States / NIDCR NIH HHS / DE / R21DE015075-RDC
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ATP-Binding Cassette Transporters; 0 / Antibodies, Fungal; 0 / Antifungal Agents; 0 / CDR1 protein, Candida albicans; 0 / Fungal Proteins; 0 / Membrane Transport Proteins; 0 / Recombinant Proteins; 8VZV102JFY / Fluconazole
  • [Other-IDs] NLM/ PMC2573144
  •  go-up   go-down


18. Chamilos G, Lionakis MS, Lewis RE, Lopez-Ribot JL, Saville SP, Albert ND, Halder G, Kontoyiannis DP: Drosophila melanogaster as a facile model for large-scale studies of virulence mechanisms and antifungal drug efficacy in Candida species. J Infect Dis; 2006 Apr 1;193(7):1014-22
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Drosophila melanogaster as a facile model for large-scale studies of virulence mechanisms and antifungal drug efficacy in Candida species.
  • Furthermore, the conditional tet-NRG1 C. albicans strain displayed significantly attenuated virulence in flies fed food without doxycycline; virulence was restored to wild-type levels when the strain was injected into Tl mutant flies fed doxycycline-containing food.
  • Fluconazole (FLC) mixed into food significantly protected Tl mutant flies injected with FLC-susceptible C. albicans strains, but FLC had no activity in flies injected with FLC-resistant C. krusei strains.
  • The D. melanogaster model is a promising minihost model for large-scale studies of virulence mechanisms and antifungal drug activity in candidiasis.
  • [MeSH-major] Antifungal Agents / pharmacology. Candida / drug effects. Candida / pathogenicity. Candidiasis / microbiology. Disease Models, Animal. Drosophila melanogaster / microbiology
  • [MeSH-minor] Animals. Colony Count, Microbial. DNA-Binding Proteins / genetics. DNA-Binding Proteins / physiology. Drug Resistance, Fungal. Female. Fluconazole / administration & dosage. Fluconazole / pharmacology. Fungal Proteins / genetics. Fungal Proteins / physiology. Mutation. Repressor Proteins / genetics. Repressor Proteins / physiology. Toll-Like Receptors / genetics. Transcription Factors / genetics. Transcription Factors / physiology. Virulence / genetics. Virulence Factors / genetics

  • MedlinePlus Health Information. consumer health - Yeast Infections.
  • COS Scholar Universe. author profiles.
  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
  • FlyBase. FlyBase .
  • Hazardous Substances Data Bank. FLUCONAZOLE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [ErratumIn] J Infect Dis. 2006 Nov 1;194(9):1342
  • (PMID = 16518764.001).
  • [ISSN] 0022-1899
  • [Journal-full-title] The Journal of infectious diseases
  • [ISO-abbreviation] J. Infect. Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / CPH1 protein, Candida albicans; 0 / DNA-Binding Proteins; 0 / EFG1 protein, Candida albicans; 0 / Fungal Proteins; 0 / Repressor Proteins; 0 / Toll-Like Receptors; 0 / Transcription Factors; 0 / Virulence Factors; 8VZV102JFY / Fluconazole
  •  go-up   go-down


19. Iwahori T, Matsuura T, Maehashi H, Sugo K, Saito M, Hosokawa M, Chiba K, Masaki T, Aizaki H, Ohkawa K, Suzuki T: CYP3A4 inducible model for in vitro analysis of human drug metabolism using a bioartificial liver. Hepatology; 2003 Mar;37(3):665-73
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CYP3A4 inducible model for in vitro analysis of human drug metabolism using a bioartificial liver.
  • CYP3A is responsible for approximately 50% of the therapeutic drug-metabolizing activity in the liver.
  • The present study was undertaken to establish the CYP3A4 inducible model for analysis of human drug metabolism using a bioartificial liver composed of the functional hepatocellular carcinoma cell (HCC) line FLC-5.
  • A radial-flow bioreactor (RFB), which is a carrier-filled type bioreactor, was used for 3-dimensional perfusion culture of FLC-5 cells.
  • When testosterone, a substrate for CYP3A4, was added to the rifampicin-treated cell culture, 6 beta-hydroxy testosterone as a metabolite was formed.
  • Electrophoretic mobility shift assay (EMSA) with a CYP3A4 ER6 probe demonstrated that relatively high molecular weight complex containing pregnane X receptor (PXR)/retinoid X receptor alpha(RXR alpha), compared with that in the monolayer culture, is possibly generated in the RFB culture of FLC-5 treated with rifampicin.
  • Similarly, the assay with a probe of HNF-4 alpha-binding motif indicated the formation of a large protein complex in the RFB culture.
  • In conclusion, the bioartificial liver composed of human functional HCC cell line was useful in studying drug interactions during induction of human CYP3A4.
  • [MeSH-major] Cytochrome P-450 Enzyme System / biosynthesis. DNA-Binding Proteins. Liver / enzymology. Models, Biological. Pharmaceutical Preparations / metabolism
  • [MeSH-minor] Basic Helix-Loop-Helix Leucine Zipper Transcription Factors. Bioreactors. Carcinoma, Hepatocellular. Chromatography, High Pressure Liquid. Cytochrome P-450 CYP3A. Electrophoretic Mobility Shift Assay. Enzyme Induction. Gene Expression. Gene Expression Regulation / drug effects. Hepatocyte Nuclear Factor 4. Humans. Liver Neoplasms. Microscopy, Electron. Microsomes, Liver / enzymology. Phosphoproteins / pharmacology. Polymerase Chain Reaction. RNA, Messenger / analysis. Receptors, Cytoplasmic and Nuclear / genetics. Receptors, Steroid / genetics. Rifampin / pharmacology. Testosterone / metabolism. Transcription Factors / pharmacology. Tumor Cells, Cultured

  • MedlinePlus Health Information. consumer health - Medicines.
  • Hazardous Substances Data Bank. RIFAMPIN .
  • Hazardous Substances Data Bank. TESTOSTERONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12601364.001).
  • [ISSN] 0270-9139
  • [Journal-full-title] Hepatology (Baltimore, Md.)
  • [ISO-abbreviation] Hepatology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Leucine Zipper Transcription Factors; 0 / DNA-Binding Proteins; 0 / Hepatocyte Nuclear Factor 4; 0 / MLX protein, human; 0 / Pharmaceutical Preparations; 0 / Phosphoproteins; 0 / RNA, Messenger; 0 / Receptors, Cytoplasmic and Nuclear; 0 / Receptors, Steroid; 0 / Transcription Factors; 0 / pregnane X receptor; 3XMK78S47O / Testosterone; 9035-51-2 / Cytochrome P-450 Enzyme System; EC 1.14.13.67 / CYP3A4 protein, human; EC 1.14.14.1 / CYP3A protein, human; EC 1.14.14.1 / Cytochrome P-450 CYP3A; VJT6J7R4TR / Rifampin
  •  go-up   go-down


20. Hanada S, Kayano H, Jiang J, Kojima N, Miyajima A, Sakoda A, Sakai Y: Enhanced in vitro maturation of subcultivated fetal human hepatocytes in three dimensional culture using poly-L-lactic acid scaffolds in the presence of oncostatin M. Int J Artif Organs; 2003 Oct;26(10):943-51
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Enhanced in vitro maturation of subcultivated fetal human hepatocytes in three dimensional culture using poly-L-lactic acid scaffolds in the presence of oncostatin M.
  • Fetal human liver cell fractions, which contain large numbers of hepatocyte progenitors, have high proliferation potential in vitro.
  • To create an engineered liver tissue equivalent of a clinically significant size, however, repeated subcultivation and functional maturation are necessary in vitro.
  • A commercially available human fetal liver cell fraction that was cultivated for some time in vitro has been reported to lose liver specific functions almost completely.
  • We therefore investigated the effects of oncostatin M (OSM) and hepatocyte growth factor (HGF) in long-term three-dimensional (3D) culture using macroporous poly-L-lactic acid (PLLA) scaffolds on the restoration of such liver-specific functions of the fraction.
  • This suppression was not observed in the same types of culture of hepatocarcinoma Hep G2 cells.
  • Despite these favorable observations on the 3D culture with OSM, the final attained functional levels at the 5th week were still over ten-times lower than those of Hep G2 cells when standardized with a cellular DNA amount.
  • [MeSH-minor] Albumins / secretion. Cells, Cultured. Fetus / cytology. Hepatocyte Growth Factor. Hepatocytes. Humans. Lactic Acid. Liver / drug effects. Membranes, Artificial. Oncostatin M. Polyesters. Polymers / chemistry

  • Hazardous Substances Data Bank. LACTIC ACID .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 14636012.001).
  • [ISSN] 0391-3988
  • [Journal-full-title] The International journal of artificial organs
  • [ISO-abbreviation] Int J Artif Organs
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Albumins; 0 / Growth Inhibitors; 0 / Membranes, Artificial; 0 / OSM protein, human; 0 / Peptides; 0 / Polyesters; 0 / Polymers; 106956-32-5 / Oncostatin M; 33X04XA5AT / Lactic Acid; 459TN2L5F5 / poly(lactide); 67256-21-7 / Hepatocyte Growth Factor
  •  go-up   go-down


21. Whiteman M, Rose P, Siau JL, Cheung NS, Tan GS, Halliwell B, Armstrong JS: Hypochlorous acid-mediated mitochondrial dysfunction and apoptosis in human hepatoma HepG2 and human fetal liver cells: role of mitochondrial permeability transition. Free Radic Biol Med; 2005 Jun 15;38(12):1571-84
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hypochlorous acid-mediated mitochondrial dysfunction and apoptosis in human hepatoma HepG2 and human fetal liver cells: role of mitochondrial permeability transition.
  • Liver cirrhosis is often preceded by overt signs of hepatitis, including parenchymal cell inflammation and infiltration of polymorphonuclear (PMN) leukocytes.
  • Because the role of mitochondria in the hepatotoxicity attributed to HOCl has not been elucidated, we investigated the effects of HOCl on mitochondrial function in the human hepatoma HepG2 cell line, human fetal liver cells, and isolated rat liver mitochondria.
  • Cell death induced by HOCl exhibited several classical hallmarks of apoptosis, including annexin V labeling, caspase activation, chromatin condensation, and cell body shrinkage.
  • The induction of apoptosis by HOCl was further supported by the finding that CSA and caspase inhibitors prevented cell death.
  • For the first time, these results show that HOCl activates the MPT, which leads to the induction of apoptosis and provides a novel insight into the mechanisms of HOCl-mediated cell death at sites of chronic inflammation.
  • [MeSH-major] Apoptosis / drug effects. Hypochlorous Acid / pharmacology. Mitochondria, Liver / drug effects
  • [MeSH-minor] Animals. Bongkrekic Acid / pharmacology. Carcinoma, Hepatocellular. Caspase 3. Caspase 7. Caspases / metabolism. Cell Line. Cell Line, Tumor. Cell Survival / drug effects. Cyclosporine / pharmacology. Cytochromes c / secretion. Drug-Induced Liver Injury / etiology. Humans. Liver / cytology. Liver / drug effects. Liver / embryology. Membrane Potentials / drug effects. Mitochondrial Swelling / drug effects. Permeability / drug effects. Rats

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. CYCLOSPORIN A .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15917186.001).
  • [ISSN] 0891-5849
  • [Journal-full-title] Free radical biology & medicine
  • [ISO-abbreviation] Free Radic. Biol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 11076-19-0 / Bongkrekic Acid; 712K4CDC10 / Hypochlorous Acid; 83HN0GTJ6D / Cyclosporine; 9007-43-6 / Cytochromes c; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / CASP7 protein, human; EC 3.4.22.- / Casp3 protein, rat; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 7; EC 3.4.22.- / Caspases
  •  go-up   go-down


22. Minagawa K, Koyama T, Miyoshi H: Stimulating effects of fibroblast growth factors on hepatic function of fetal liver cells synergistically with oncostatin M in three-dimensional culture. J Biosci Bioeng; 2009 Mar;107(3):307-11
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Stimulating effects of fibroblast growth factors on hepatic function of fetal liver cells synergistically with oncostatin M in three-dimensional culture.
  • Fetal liver cells (FLCs) are regarded as a feasible cell source of bioartificial liver (BAL), because the FLCs have proliferating ability even in vitro.
  • However, the cellular functions of FLCs are considerably lower compared with mature hepatocytes.
  • Thus, maturation of cultured FLCs is essential for enhancing the performance of the BAL using the FLCs.
  • In the present study, the effects of fibroblast growth factors (FGF-1, FGF-2, and FGF-4) on cell growth and the liver-specific functions of mouse FLCs were investigated in the presence or absence of oncostatin M (OSM), under both three-dimensional (3-D) and monolayer culture conditions.
  • When FGF-2 was used, no stimulating effects on the albumin secretion activities of the FLCs were observed either in the 3-D or monolayer cultures, although cell growth was improved in these cultures.
  • However, in the presence of OSM, FGF-1 and FGF-4 significantly enhanced the activities of the FLCs but only in the 3-D cultures.
  • From scanning electron microscopic observation, the 3-D culture FLCs formed big cell aggregates on the surface of a porous scaffold.
  • In conclusion, it was clarified that FGF-1 and FGF-4 facilitate the maturation of 3-D culture FLCs synergistically with OSM.
  • [MeSH-major] Fetus / cytology. Fibroblast Growth Factors / pharmacology. Hepatocytes / drug effects. Liver, Artificial. Oncostatin M / pharmacology
  • [MeSH-minor] Animals. Cell Culture Techniques. Cell Proliferation / drug effects. Cells, Cultured. Drug Synergism. Mice

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19269598.001).
  • [ISSN] 1347-4421
  • [Journal-full-title] Journal of bioscience and bioengineering
  • [ISO-abbreviation] J. Biosci. Bioeng.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 106956-32-5 / Oncostatin M; 62031-54-3 / Fibroblast Growth Factors
  •  go-up   go-down


23. Cejudo MA, Gallego AG, Lacasa EC, Aller AI, Romero A, García JP, Andrés GQ, Martín-Mazuelos E: Evaluation of the VITEK 2 system to test the susceptibility of Candida spp., Trichosporon asahii and Cryptococcus neoformans to amphotericin B, flucytosine, fluconazole and voriconazole: a comparison with the M27-A3 reference method. Med Mycol; 2010 Aug;48(5):710-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We compared the susceptibilities of 302 isolates (209 Candida spp., 89 Cryptococcus neoformans and four Trichosporon asahii) against amphotericin B (AMB), flucytosine (5FC), fluconazole (FLC) and voriconazole (VRC) obtained with an automated commercial system (VITEK 2, bioMérieux, Spain) and the Clinical and Laboratory Standards Institute (CLSI M27-A3) reference broth microdilution method (BMD).
  • For Candida spp. and T. asahii, the overall MIC agreement between of the results of the VITEK 2 system and the 24/48-h BMD was: 34/62% for AMB; 96.3% at 24/48-h for 5FC; 87.8/87.3% for FLC and 95.3/92% for VRC, respectively.
  • The overall categorical agreement between both methods was: 98.5/97.6% for AMB at 24/48-h; 95.3% for 5FC at 24/48-h; 85.4/84.4% at 24/48-h for FLC; and 97.6/92.95% at 24/48-h for VRC.
  • For C. neoformans, essential agreement was good for FLC (91%) and 5FC (84.2%) but not so good for AMB (69%).
  • Excellent categorical agreement was obtained for all antifungal agents tested except for 5FC (69.7%).
  • [MeSH-major] Antifungal Agents / pharmacology. Candida / drug effects. Cryptococcus neoformans / drug effects. Mycology / methods. Trichosporon / drug effects

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20109092.001).
  • [ISSN] 1460-2709
  • [Journal-full-title] Medical mycology
  • [ISO-abbreviation] Med. Mycol.
  • [Language] eng
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antifungal Agents
  •  go-up   go-down


24. Nefedov VB, Shergina EA: [Role of bronchospasm in development of bronchial obstruction in chronic bronchitis]. Ter Arkh; 2000;72(11):57-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • MATERIALS AND METHODS: Lung capacity (LC), forced lung capacity (FLC), forced expiration volume for 1 second (FEV1), FEV1/LC%, peak volume rate (PVS), maximal volume expiration rate (MVER) at the level of 25, 50 and 75% of LC were measured in 62 patients with chronic obstructive bronchitis before and after inhalation of 1 dose of berotec and 1 dose of atrovent.
  • [MeSH-minor] Administration, Inhalation. Adolescent. Adult. Aged. Bronchoconstriction / drug effects. Bronchodilator Agents / administration & dosage. Chronic Disease. Female. Fenoterol / administration & dosage. Humans. Ipratropium / administration & dosage. Male. Middle Aged. Respiratory Function Tests. Risk Factors

  • MedlinePlus Health Information. consumer health - Acute Bronchitis.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11229314.001).
  • [ISSN] 0040-3660
  • [Journal-full-title] Terapevticheskiĭ arkhiv
  • [ISO-abbreviation] Ter. Arkh.
  • [Language] rus
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Russia
  • [Chemical-registry-number] 0 / Bronchodilator Agents; 22M9P70OQ9 / Fenoterol; GR88G0I6UL / Ipratropium
  •  go-up   go-down


25. Ehashi T, Ohshima N, Miyoshi H: Three-dimensional culture of porcine fetal liver cells for a bioartificial liver. J Biomed Mater Res A; 2006 Apr;77(1):90-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Three-dimensional culture of porcine fetal liver cells for a bioartificial liver.
  • A three-dimensional (3-D) culture experiment of porcine fetal liver cells (FLCs) was performed using a porous resin substrate, for the purpose of developing a bioartificial liver.
  • To promote cell growth and maturation, human oncostatin M (OSM), the human leukemia inhibitory factor (LIF), or cortisol was added to the cultures, and the effect of each agent on cell proliferation and liver-specific cellular functions was investigated.
  • The cell numbers in both the monolayer and 3-D cultures increased gradually with time, irrespective of the supplementation of the stimulating agents.
  • In the monolayer culture, the albumin secretion of FLCs decreased rapidly, and scarce activity was detected from 2 weeks onward under all culture conditions tested.
  • In the 3-D cultures, neither human OSM nor human LIF had any definite effect on the albumin secretion of FLCs.
  • However, in the cultures with cortisol, albumin secretion was maintained for a considerably long period.
  • These findings suggest that a bioartificial liver can be developed by culturing porcine FLCs with cortisol as the stimulant.
  • [MeSH-major] Cell Culture Techniques / methods. Hepatocytes / metabolism. Liver, Artificial
  • [MeSH-minor] Animals. Cells, Cultured. Culture Media / chemistry. Cytokines / metabolism. Fetus / cytology. Growth Inhibitors / metabolism. Humans. Hydrocortisone / metabolism. Interleukin-6 / metabolism. Leukemia Inhibitory Factor. Microscopy, Electron, Scanning. Oncostatin M. Swine. Urea / metabolism. alpha-Fetoproteins / genetics. alpha-Fetoproteins / metabolism

  • Hazardous Substances Data Bank. HYDROCORTISONE .
  • Hazardous Substances Data Bank. UREA .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2005 Wiley Periodicals, Inc.
  • (PMID = 16355413.001).
  • [ISSN] 1549-3296
  • [Journal-full-title] Journal of biomedical materials research. Part A
  • [ISO-abbreviation] J Biomed Mater Res A
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Culture Media; 0 / Cytokines; 0 / Growth Inhibitors; 0 / Interleukin-6; 0 / LIF protein, human; 0 / Leukemia Inhibitory Factor; 0 / OSM protein, human; 0 / alpha-Fetoproteins; 106956-32-5 / Oncostatin M; 8W8T17847W / Urea; WI4X0X7BPJ / Hydrocortisone
  •  go-up   go-down


26. Lewis ID, Verfaillie CM: Multi-lineage expansion potential of primitive hematopoietic progenitors: superiority of umbilical cord blood compared to mobilized peripheral blood. Exp Hematol; 2000 Sep;28(9):1087-95
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVE: The majority of studies assessing ex-vivo expansion of primitive hematopoietic cells only address production of myeloid progeny whereas it may be more appropriate to maintain or expand progenitors that retain capacity for multilineage differentiation.
  • In this study, we assessed the capacity of the murine fetal liver cell line AFT024 to expand primitive myeloid progenitors (LTC-IC) and lymphoid progenitors (NK-IC) from umbilical cord blood (CB) and mobilized peripheral blood (PB) CD34(+)lin(-)38(-) cells.
  • METHODS: Sorted cells were established in expansion cultures in direct contact with the feeder or in a transwell above the feeder (noncontact culture) and various combinations of Flt-3L (FL), stem cell factor, interleukin 7, thrombopoietin (Tpo), and macrophage inflammatory protein-1alpha added.
  • CONCLUSIONS: These results demonstrate that AFT024 can expand primitive hematopoietic progenitors from CB and PB and expanded cells retain the capacity for myeloid and lymphoid differentiation.
  • Elucidation of specific factors necessary for ex-vivo expansion will contribute to the development of a clinically applicable system.
  • [MeSH-major] Cell Lineage / physiology. Stem Cells / cytology
  • [MeSH-minor] Animals. Antigens, CD34 / blood. Cell Division / drug effects. Cell Line. Coculture Techniques. Cytokines / pharmacology. Fetal Blood / cytology. Hematopoiesis / drug effects. Hematopoietic Stem Cell Mobilization. Humans. Killer Cells, Natural / cytology. Killer Cells, Natural / physiology. Mice. Time Factors

  • MedlinePlus Health Information. consumer health - Stem Cells.
  • COS Scholar Universe. author profiles.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11008022.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01-CA-6549; United States / NHLBI NIH HHS / HL / R01-HL-54039
  • [Publication-type] Comparative Study; Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] NETHERLANDS
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Cytokines
  •  go-up   go-down


27. Sobue S, Sekiguchi K, Nabeshima T: Intracutaneous distributions of fluconazole, itraconazole, and griseofulvin in Guinea pigs and binding to human stratum corneum. Antimicrob Agents Chemother; 2004 Jan;48(1):216-23
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We have compared the distribution of fluconazole (FLC) with that of itraconazole (ITC) and griseofulvin (GRF) in the abdominal skin tissues after a single oral dose was administered to guinea pigs.
  • The FLC concentrations in the stratum corneum reached a peak at 2 h after administration and were similar to those of ITC and higher than those of GRF in spite of the administration of a lower dose.
  • GRF was eliminated from the stratum corneum faster than FLC and ITC.
  • The FLC concentrations were also remarkably higher than those of ITC and GRF in the epidermis-cutis but lower in the subcutaneous fatty tissue.
  • The distribution characteristics of each drug result from differences in their physicochemical properties.
  • Following the administration of multiple doses, the FLC concentrations in the stratum corneum were highest in the abdominal skin tissues; those at 24 h after each administration increased gradually and were maintained at a level more than 10 times higher than that of the plasma concentrations.
  • The FLC concentrations in the planta pedis stratum corneum and in the nail showed good dose proportionality and obvious accumulation and were 60 and 40 times as high as that in plasma on day 14.
  • The extent of binding of FLC to human corneous keratin in vitro was about 10%, which is lower than those of ITC (94 to 97%) and GRF (36 to 38%).
  • FLC, unlike ITC, therefore, is presumed to exist in the stratum corneum at high concentrations in an active nonbinding form.
  • These excellent intracutaneous pharmacokinetic properties of FLC probably account in large part for the in vivo efficacy of FLC.
  • [MeSH-major] Antifungal Agents / pharmacokinetics. Fluconazole / pharmacokinetics. Griseofulvin / pharmacokinetics. Itraconazole / pharmacokinetics. Skin / metabolism
  • [MeSH-minor] Administration, Topical. Animals. Area Under Curve. Guinea Pigs. Half-Life. Humans. In Vitro Techniques. Keratins / metabolism. Nails / metabolism

  • Hazardous Substances Data Bank. GRISEOFULVIN .
  • Hazardous Substances Data Bank. Itraconazole .
  • Hazardous Substances Data Bank. FLUCONAZOLE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Clin Microbiol. 2000 Jan;38(1):341-4 [10618112.001]
  • [Cites] J Antibiot (Tokyo). 2000 Feb;53(2):207-10 [10805585.001]
  • [Cites] Antimicrob Agents Chemother. 2001 May;45(5):1493-9 [11302816.001]
  • [Cites] J Infect Chemother. 2000 Mar;6(1):41-4 [11810530.001]
  • [Cites] Microbiol Immunol. 2002;46(7):425-32 [12222928.001]
  • [Cites] Antimicrob Agents Chemother. 1991 May;35(5):846-50 [1854166.001]
  • [Cites] Jpn J Antibiot. 1991 May;44(5):552-61 [1880935.001]
  • [Cites] Clin Exp Dermatol. 1993 Mar;18(2):102-6 [8481982.001]
  • [Cites] Mycoses. 1994 Mar-Apr;37(3-4):127-30 [7845418.001]
  • [Cites] Mycoses. 1994 Nov-Dec;37(11-12):447-9 [7659135.001]
  • [Cites] Acta Derm Venereol. 1995 Sep;75(5):361-3 [8615052.001]
  • [Cites] Mycoses. 1998 Mar-Apr;41(3-4):153-62 [9670768.001]
  • [Cites] Antimicrob Agents Chemother. 2002 Dec;46(12):3797-801 [12435679.001]
  • [Cites] Arch Dermatol. 1972 Sep;106(3):344-8 [5055093.001]
  • [Cites] J Chromatogr. 1978 Aug 1;155(1):206-8 [681488.001]
  • [Cites] Antimicrob Agents Chemother. 1985 May;27(5):832-5 [2990328.001]
  • [Cites] Antimicrob Agents Chemother. 1985 Dec;28(6):815-8 [3002246.001]
  • [Cites] Antimicrob Agents Chemother. 1985 Nov;28(5):648-53 [3004323.001]
  • [Cites] J Chromatogr. 1987 Jan 23;413:332-7 [3031106.001]
  • [Cites] J Am Acad Dermatol. 1988 Feb;18(2 Pt 1):263-8 [2831254.001]
  • [Cites] Jpn J Antibiot. 1989 Jan;42(1):1-16 [2540356.001]
  • [Cites] Rev Infect Dis. 1990 Mar-Apr;12 Suppl 3:S318-26 [2184510.001]
  • [Cites] Clin Ther. 1990 May-Jun;12(3):206-15 [2379224.001]
  • (PMID = 14693542.001).
  • [ISSN] 0066-4804
  • [Journal-full-title] Antimicrobial agents and chemotherapy
  • [ISO-abbreviation] Antimicrob. Agents Chemother.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antifungal Agents; 304NUG5GF4 / Itraconazole; 32HRV3E3D5 / Griseofulvin; 68238-35-7 / Keratins; 8VZV102JFY / Fluconazole
  • [Other-IDs] NLM/ PMC310182
  •  go-up   go-down


28. Miersch J, Grancharov K, Pajpanova T, Tabakova S, Stoev S, Krauss GJ, Golovinsky E: Synthesis and biological activity of canavanine hydrazide derivatives. Amino Acids; 2000;18(1):41-59
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Synthesis and biological activity of canavanine hydrazide derivatives.
  • The canavanine derivatives L-canavanine hydrazide (CH), L-canavanine-bis-(2-chloroethyl)hydrazide (CBCH) and L-canavanine phenylhydrazide (CPH) were synthesized and evaluated for biological activity in microorganisms, plants and tumor cells using canavanine as a positive control. (1) In microbial systems, the compounds exerted activity, as assessed in 14 bacterial strains.
  • The effect of canavanine was easily removed by equimolar concentrations of arginine or ornithine, while the effect of CBCH or CPH was abolished by 10-fold excess of arginine or 10- to 100-fold excess of ornithine. (2) In plants, the activity of CH and CBCH were relatively low, whereas the inhibitory potential of CPH was comparable or even superior to that of canavanine, resulting at 1 mM concentration in a nearly complete block of tomato cell growth, and reducing by up to 80% the length of radicles of cress, amaranth, cabbage and pumpkin. (3) In pumpkin seeds, CPH or canavanine induced the synthesis of four small heat shock proteins of hsp-17 family in the pH range of 6 to 7.5.
  • The proteins exhibited in both cases a similar profile, but differed in the timing of their expression and/or accumulation.
  • With canavanine, the highest hsp-17 expression was found after 48 h of drug treatment, while with CPH this maximum was shifted to 24 h. (4) CPH proved to be highly cytotoxic against Friend leukemia cells in culture, exceeding by one order of magnitude the cytotoxicity of canavanine.
  • [MeSH-minor] Animals. Anti-Bacterial Agents / metabolism. Bacteria / drug effects. Cell Division / drug effects. Cells, Cultured. Dose-Response Relationship, Drug. Electrophoresis, Gel, Two-Dimensional. Friend murine leukemia virus / metabolism. Hydrogen-Ion Concentration. Inhibitory Concentration 50. Leukemia, Experimental / metabolism. Lycopersicon esculentum / drug effects. Mice. Plants / drug effects. Time Factors. Tumor Cells, Cultured

  • Hazardous Substances Data Bank. (L)-CANAVANINE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 10794131.001).
  • [ISSN] 0939-4451
  • [Journal-full-title] Amino acids
  • [ISO-abbreviation] Amino Acids
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] AUSTRIA
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Hydrazines; 0 / canavanine phenylhydrazide; 0 / canavanine-bis-(2-chloroethyl)hydrazide; 3HZV514J4B / Canavanine
  •  go-up   go-down


29. Passegué E, Jochum W, Schorpp-Kistner M, Möhle-Steinlein U, Wagner EF: Chronic myeloid leukemia with increased granulocyte progenitors in mice lacking junB expression in the myeloid lineage. Cell; 2001 Jan 12;104(1):21-32
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chronic myeloid leukemia with increased granulocyte progenitors in mice lacking junB expression in the myeloid lineage.
  • Transgenic mice specifically lacking JunB expression in the myeloid lineage (junB(-/-)Ubi-junB mice) develop a transplantable myeloproliferative disease eventually progressing to blast crisis, which resembles human chronic myeloid leukemia.
  • Similarly, mice reconstituted with ES cell-derived junB-/- fetal liver cells also develop a myeloproliferative disease.
  • In both cases, the absence of JunB expression results in increased numbers of granulocyte progenitors, which display enhanced GM-CSF-mediated proliferation and extended survival, associated with changes in the expression levels of the GM-CSFalpha receptor, the anti-apoptotic proteins Bcl2 and Bclx, and the cell cycle regulators p16(INK4a) and c-Jun.
  • Importantly, ectopic expression of JunB fully reverts the immature and hyperproliferative phenotype of JunB-deficient myeloid cells.
  • These results identify JunB as a key transcriptional regulator of myelopoiesis and a potential tumor suppressor gene.
  • [MeSH-major] Granulocytes / cytology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / physiopathology. Proto-Oncogene Proteins c-jun / genetics. Stem Cells / cytology
  • [MeSH-minor] Animals. Cell Differentiation / immunology. Cell Division / drug effects. Cell Division / immunology. Cell Lineage / immunology. Gene Expression / immunology. Granulocyte-Macrophage Colony-Stimulating Factor / pharmacology. In Vitro Techniques. Leukopoiesis / immunology. Mice. Mice, Knockout. Phenotype. Transgenes / immunology


30. Gutierrez-Galhardo MC, Zancopé-Oliveira RM, Monzón A, Rodriguez-Tudela JL, Cuenca-Estrella M: Antifungal susceptibility profile in vitro of Sporothrix schenckii in two growth phases and by two methods: microdilution and E-test. Mycoses; 2010 May;53(3):227-31
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Fluconazole (FLC) and voriconazole (VRC) were inactive in vitro against both phases.
  • The E-test technique was also performed with 41 representative isolates for AMB, FLC, ITC and VRC.
  • Average agreement rates between yeast phase microdilution results and E-test results were high for AMB (77.5%) and FLC (87.8%), but low for ITC and VRC with rates of 56.4% and 54.5%, respectively.
  • AFST-EUCAST is not the most recommended test to perform drug susceptibility testing of S. schenckii in clinical laboratories, and E-test could be an alternative methodology for this purpose, mainly when the activity in vitro of antifungal agents of AMB and FLC are evaluated.
  • [MeSH-major] Antifungal Agents / pharmacology. Sporothrix / drug effects
  • [MeSH-minor] Humans. Microbial Sensitivity Tests / methods. Mycelium / drug effects. Sporotrichosis / microbiology. Yeasts / drug effects


31. Tsao S, Rahkhoodaee F, Raymond M: Relative contributions of the Candida albicans ABC transporters Cdr1p and Cdr2p to clinical azole resistance. Antimicrob Agents Chemother; 2009 Apr;53(4):1344-52
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Candida albicans frequently develops resistance to treatment with azole drugs due to the acquisition of gain-of-function mutations in the transcription factor Tac1p.
  • We found that deleting CDR1 had a major effect, reducing resistance to fluconazole (FLC), ketoconazole (KTC), and itraconazole (ITC) by 6-, 4-, and 8-fold, respectively.
  • Deleting CDR2 had a much weaker effect, reducing FLC or KTC resistance by 1.5-fold, and had no effect on ITC resistance.
  • [MeSH-major] ATP-Binding Cassette Transporters / physiology. Antifungal Agents / pharmacology. Azoles / pharmacology. Candida albicans / drug effects. Fungal Proteins / physiology. Membrane Transport Proteins / physiology
  • [MeSH-minor] Drug Resistance, Fungal. Fluconazole / pharmacology. Itraconazole / pharmacology. Ketoconazole / pharmacology. Microbial Sensitivity Tests. Rhodamines / pharmacology

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. KETOCONAZOLE .
  • Hazardous Substances Data Bank. Itraconazole .
  • Hazardous Substances Data Bank. FLUCONAZOLE .
  • Hazardous Substances Data Bank. RHODAMINE 6G .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • Saccharomyces Genome Database. Saccharomyces Genome Database .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] FEMS Microbiol Lett. 2000 Apr 1;185(1):59-63 [10731607.001]
  • [Cites] Curr Opin Hematol. 2008 May;15(3):191-5 [18391783.001]
  • [Cites] J Antimicrob Chemother. 2001 May;47(5):527-36 [11328762.001]
  • [Cites] Yeast. 2002 Mar 15;19(4):303-18 [11870854.001]
  • [Cites] Mol Microbiol. 2002 Mar;43(5):1197-214 [11918807.001]
  • [Cites] Antimicrob Agents Chemother. 2003 May;47(5):1543-54 [12709320.001]
  • [Cites] Trends Microbiol. 2003 Jun;11(6):272-9 [12823944.001]
  • [Cites] Int J Antimicrob Agents. 2003 Sep;22(3):291-300 [13678837.001]
  • [Cites] Eukaryot Cell. 2003 Dec;2(6):1361-75 [14665469.001]
  • [Cites] FEMS Yeast Res. 2004 Oct;5(1):63-72 [15381123.001]
  • [Cites] Gene. 2004 Oct 27;341:119-27 [15474295.001]
  • [Cites] Mol Gen Genet. 1984;198(2):179-82 [6394964.001]
  • [Cites] J Biol Chem. 1994 Jan 21;269(3):2206-14 [8294477.001]
  • [Cites] Curr Genet. 1995 Mar;27(4):320-9 [7614555.001]
  • [Cites] Antimicrob Agents Chemother. 1995 Nov;39(11):2378-86 [8585712.001]
  • [Cites] Antimicrob Agents Chemother. 1996 Oct;40(10):2300-5 [8891134.001]
  • [Cites] Microbiology. 1997 Feb;143 ( Pt 2):405-16 [9043118.001]
  • [Cites] Clin Microbiol Rev. 1998 Apr;11(2):382-402 [9564569.001]
  • [Cites] J Biol Chem. 1998 May 15;273(20):12612-22 [9575223.001]
  • [Cites] Methods Enzymol. 1998;292:130-62 [9711551.001]
  • [Cites] J Biol Chem. 1999 Jan 22;274(4):1934-41 [9890948.001]
  • [Cites] FEMS Microbiol Lett. 1999 Apr 15;173(2):475-81 [10227177.001]
  • [Cites] Biochemistry. 1999 May 25;38(21):6887-96 [10346910.001]
  • [Cites] J Antimicrob Chemother. 1999 Jul;44(1):27-31 [10459807.001]
  • [Cites] Eukaryot Cell. 2004 Dec;3(6):1639-52 [15590837.001]
  • [Cites] J Antimicrob Chemother. 2004 Dec;54(6):999-1006 [15486081.001]
  • [Cites] Biochemistry. 2005 May 3;44(17):6650-61 [15850398.001]
  • [Cites] Med Mycol. 2005 Jun;43(4):285-318 [16110776.001]
  • [Cites] Arch Med Res. 2005 Nov-Dec;36(6):660-71 [16216647.001]
  • [Cites] Microbiology. 2006 May;152(Pt 5):1559-73 [16622073.001]
  • [Cites] Genetics. 2006 Apr;172(4):2139-56 [16452151.001]
  • [Cites] Biochem Soc Trans. 2006 Jun;34(Pt 3):359-62 [16709161.001]
  • [Cites] Mol Microbiol. 2006 Jun;60(6):1546-62 [16796687.001]
  • [Cites] Mycopathologia. 2007 Jul;164(1):1-17 [17574539.001]
  • [Cites] Eukaryot Cell. 2007 Jul;6(7):1150-65 [17513564.001]
  • [Cites] Mol Microbiol. 2007 Oct;66(2):440-52 [17897373.001]
  • [Cites] Eukaryot Cell. 2007 Oct;6(10):1889-904 [17693596.001]
  • [Cites] Biochemistry. 2007 Oct 30;46(43):12081-90 [17924650.001]
  • [Cites] Eukaryot Cell. 2007 Nov;6(11):2122-38 [17905926.001]
  • [Cites] PLoS Pathog. 2007 Nov;3(11):e164 [17983269.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Apr 1;105(13):5069-74 [18356296.001]
  • [Cites] Trends Plant Sci. 2008 Apr;13(4):151-9 [18299247.001]
  • [Cites] Eukaryot Cell. 2008 Jul;7(7):1180-90 [18487346.001]
  • [Cites] Mol Microbiol. 2000 May;36(4):856-65 [10844673.001]
  • (PMID = 19223631.001).
  • [ISSN] 1098-6596
  • [Journal-full-title] Antimicrobial agents and chemotherapy
  • [ISO-abbreviation] Antimicrob. Agents Chemother.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ATP-Binding Cassette Transporters; 0 / Antifungal Agents; 0 / Azoles; 0 / CDR1 protein, Candida albicans; 0 / Fungal Proteins; 0 / Membrane Transport Proteins; 0 / Rhodamines; 037VRW83CF / rhodamine 6G; 304NUG5GF4 / Itraconazole; 8VZV102JFY / Fluconazole; R9400W927I / Ketoconazole
  • [Other-IDs] NLM/ PMC2663127
  •  go-up   go-down


32. Miceli MH, Bernardo SM, Lee SA: In vitro analyses of the combination of high-dose doxycycline and antifungal agents against Candida albicans biofilms. Int J Antimicrob Agents; 2009 Oct;34(4):326-32
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] In vitro analyses of the combination of high-dose doxycycline and antifungal agents against Candida albicans biofilms.
  • The potential of antifungal agents used as antimicrobial lock therapy (ALT) for the conservative management of catheter-related candidemia has not been fully defined.
  • We sought to determine the antifungal effect of high-dose doxycycline (DOX), alone or in combination with standard concentrations of amphotericin B (AMB), caspofungin (CAS) or fluconazole (FLC), against biofilms formed by Candida albicans in vitro.
  • Regardless of the concentration tested, FLC alone showed minimal activity (mean 22.9% reduction) against the C. albicans biofilm.
  • When DOX 2048 microg/mL was used in combination with FLC, antifungal activity also increased up to 85%, suggesting an additive effect.
  • DOX 128 microg/mL in combination with FLC demonstrated synergy (mean 58.3% reduction).
  • Maximal efficacy against the biofilm was observed with CAS at 8-0.25 microg/mL compared with FLC and AMB alone.
  • These findings suggest that a high-dose DOX-based ALT strategy in combination with traditional antifungal agents may be useful for the treatment of C. albicans biofilms.
  • [MeSH-major] Antifungal Agents / pharmacology. Biofilms / drug effects. Candida albicans / drug effects. Doxycycline / pharmacology
  • [MeSH-minor] Amphotericin B / pharmacology. Dose-Response Relationship, Drug. Drug Interactions. Drug Therapy, Combination. Echinocandins / pharmacology. Fluconazole / pharmacology. Humans. Microbial Sensitivity Tests

  • Hazardous Substances Data Bank. AMPHOTERICIN B .
  • Hazardous Substances Data Bank. CASPOFUNGIN .
  • Hazardous Substances Data Bank. DOXYCYCLINE .
  • Hazardous Substances Data Bank. FLUCONAZOLE .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19515537.001).
  • [ISSN] 1872-7913
  • [Journal-full-title] International journal of antimicrobial agents
  • [ISO-abbreviation] Int. J. Antimicrob. Agents
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / T32 AI007538
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Echinocandins; 7XU7A7DROE / Amphotericin B; 8VZV102JFY / Fluconazole; F0XDI6ZL63 / caspofungin; N12000U13O / Doxycycline
  •  go-up   go-down


33. Moon J, Suh SS, Lee H, Choi KR, Hong CB, Paek NC, Kim SG, Lee I: The SOC1 MADS-box gene integrates vernalization and gibberellin signals for flowering in Arabidopsis. Plant J; 2003 Sep;35(5):613-23
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In addition, we show that vernalization-induced repression of FLOWERING LOCUS C (FLC), an upstream negative regulator of SOC1, is not sufficient to activate SOC1; positive factors are also required.
  • In contrast to SOC1, the GA pathway does not regulate expression of other flowering integrators FLC and FT.
  • [MeSH-major] Arabidopsis / genetics. Arabidopsis Proteins / genetics. Flowers / genetics. Gibberellins / pharmacology. MADS Domain Proteins / genetics. Signal Transduction / genetics
  • [MeSH-minor] Gene Expression Regulation, Developmental / drug effects. Gene Expression Regulation, Plant / drug effects. Mutation. Photoperiod

  • The Arabidopsis Information Resource. Linked Gene Data (subscription/membership/fee required).
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [ErratumIn] Plant J. 2004 Feb;37(3):459
  • (PMID = 12940954.001).
  • [ISSN] 0960-7412
  • [Journal-full-title] The Plant journal : for cell and molecular biology
  • [ISO-abbreviation] Plant J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AGL20 protein, Arabidopsis; 0 / Arabidopsis Proteins; 0 / FLF protein, Arabidopsis; 0 / FT protein, Arabidopsis; 0 / Gibberellins; 0 / MADS Domain Proteins
  •  go-up   go-down


34. Kantarcioğlu AS, Boekhout T, Yücel A, Altas K: Susceptibility testing of Cryptococcus diffluens against amphotericin B, flucytosine, fluconazole, itraconazole, voriconazole and posaconazole. Med Mycol; 2009 Mar;47(2):169-76
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We evaluated the application of the Clinical Laboratory Standards Institute (CLSI, formerly NCCLS) macro- and microbroth dilution methods and the E-test agar diffusion method to determine the in vitro susceptibilities of known strains of C. diffluens against amphotericin B (AMB), flucytosine (5-FC), fluconazole (FLC), itraconazole (ITC) and the novel triazoles, voriconazole (VRC) and posaconazole (PSC).
  • Seven strains were found to be resistant in vitro to AMB (MICs >/=2 microg/ml), five were resistant to 5-FC (MICs of >/=32 microg/ml), four were resistant to FLC (MICs of FLC >/=32 microg/ml) and nine were resistant to ITC (MICs of ITC >1 microg/ml).
  • A clinical isolate showing phenotypic switching exhibited elevated MICs to both agents, i.e., VRC (>16 microg/ml) and PSC (>8 microg/ml).
  • [MeSH-major] Amphotericin B / pharmacology. Antifungal Agents / pharmacology. Azoles / pharmacology. Cryptococcus / drug effects. Flucytosine / pharmacology
  • [MeSH-minor] Culture Media. Drug Resistance, Fungal. Fluconazole / pharmacology. Humans. Itraconazole / pharmacology. Microbial Sensitivity Tests / methods. Microbial Sensitivity Tests / standards. Pyrimidines / pharmacology. Triazoles / pharmacology. Voriconazole

  • Hazardous Substances Data Bank. AMPHOTERICIN B .
  • Hazardous Substances Data Bank. FLUCYTOSINE .
  • Hazardous Substances Data Bank. Itraconazole .
  • Hazardous Substances Data Bank. FLUCONAZOLE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18654925.001).
  • [ISSN] 1369-3786
  • [Journal-full-title] Medical mycology
  • [ISO-abbreviation] Med. Mycol.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Azoles; 0 / Culture Media; 0 / Pyrimidines; 0 / Triazoles; 304NUG5GF4 / Itraconazole; 6TK1G07BHZ / posaconazole; 7XU7A7DROE / Amphotericin B; 8VZV102JFY / Fluconazole; D83282DT06 / Flucytosine; JFU09I87TR / Voriconazole
  •  go-up   go-down


35. Li Y, Brazzell J, Herrera A, Walcheck B: ADAM17 deficiency by mature neutrophils has differential effects on L-selectin shedding. Blood; 2006 Oct 1;108(7):2275-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Tumor necrosis factor-alpha-converting enzyme (TACE, or ADAM17) is a sheddase of L-selectin; however, Adam17 gene targeting (ADAM17(DeltaZn/DeltaZn)) in mice is perinatal lethal and its role in L-selectin shedding by mature neutrophils has not been determined.
  • This was addressed here by using radiation-chimeric mice reconstituted with ADAM17(DeltaZn/DeltaZn) fetal liver cells.
  • In addition, the absence of functional ADAM17 resulted in significantly increased levels of L-selectin surface expression by peripheral-blood leukocytes, indicating the sheddase also plays a role in the constitutive cleavage of L-selectin.
  • Interestingly, not all manners of L-selectin turnover required ADAM17.
  • Plasma L-selectin levels were similar between ADAM17(DeltaZn/DeltaZn)-chimeric and control mice, as was the shedding of L-selectin by neutrophils undergoing spontaneous apoptosis.
  • The latter process, however, was diminished by a metalloprotease inhibitor, indicating the role of a sheddase other than ADAM17.

  • COS Scholar Universe. author profiles.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Leukoc Biol. 2000 Mar;67(3):415-22 [10733103.001]
  • [Cites] Nature. 1997 Feb 20;385(6618):729-33 [9034190.001]
  • [Cites] Antisense Nucleic Acid Drug Dev. 2001 Apr;11(2):107-16 [11334139.001]
  • [Cites] Clin Exp Pharmacol Physiol. 2001 May-Jun;28(5-6):376-80 [11380509.001]
  • [Cites] J Biol Chem. 2001 Aug 17;276(33):30631-40 [11375402.001]
  • [Cites] Resuscitation. 2002 Feb;52(2):127-41 [11841880.001]
  • [Cites] Blood. 2002 Jun 1;99(11):4063-9 [12010808.001]
  • [Cites] J Immunol. 2002 Aug 15;169(4):2034-43 [12165530.001]
  • [Cites] Intensive Care Med. 2002 Nov;28(11):1613-8 [12415449.001]
  • [Cites] Chem Rev. 2002 Dec;102(12):4627-38 [12475204.001]
  • [Cites] J Leukoc Biol. 2003 Apr;73(4):464-71 [12660221.001]
  • [Cites] J Exp Med. 2003 May 19;197(10):1355-63 [12756271.001]
  • [Cites] J Leukoc Biol. 2003 Sep;74(3):389-94 [12949242.001]
  • [Cites] J Biol Chem. 2003 Sep 26;278(39):37459-64 [12878595.001]
  • [Cites] J Exp Med. 2003 Nov 3;198(9):1323-35 [14597735.001]
  • [Cites] Immunity. 2003 Nov;19(5):713-24 [14614858.001]
  • [Cites] Cell Mol Life Sci. 2003 Nov;60(11):2402-8 [14625685.001]
  • [Cites] Acta Haematol. 2004;111(1-2):56-66 [14646345.001]
  • [Cites] J Immunol. 1989 Nov 15;143(10):3318-24 [2553811.001]
  • [Cites] J Biol Chem. 1990 May 15;265(14):7760-7 [1692315.001]
  • [Cites] J Immunol Methods. 1992 Nov 25;156(1):115-23 [1385536.001]
  • [Cites] J Cell Biol. 1994 Apr;125(2):461-70 [7512970.001]
  • [Cites] Nature. 1997 Feb 20;385(6618):733-6 [9034191.001]
  • [Cites] J Immunol. 1997 May 1;158(9):4365-72 [9127000.001]
  • [Cites] J Immunol. 1997 Jul 15;159(2):952-63 [9218616.001]
  • [Cites] J Biol Chem. 1997 Sep 26;272(39):24588-93 [9305925.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Mar 31;95(7):3408-12 [9520379.001]
  • [Cites] Science. 1998 Nov 13;282(5392):1281-4 [9812885.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Mar 30;96(7):3922-7 [10097139.001]
  • [Cites] J Biol Chem. 2006 Feb 10;281(6):3157-64 [16332693.001]
  • [Cites] Eur J Immunol. 2006 Apr;36(4):968-76 [16541467.001]
  • [Cites] Science. 1989 Sep 15;245(4923):1238-41 [2551036.001]
  • [Cites] Lancet. 1994 Jul 23;344(8917):215-9 [7518025.001]
  • [Cites] Blood. 1994 Aug 15;84(4):1249-56 [7519478.001]
  • [Cites] J Exp Med. 1994 Nov 1;180(5):1785-92 [7525838.001]
  • [Cites] Agents Actions Suppl. 1995;47:121-34 [7540352.001]
  • [Cites] Nature. 1996 Apr 25;380(6576):720-3 [8614468.001]
  • [Cites] J Biol Chem. 1996 Mar 22;271(12):7019-24 [8636132.001]
  • [Cites] J Clin Invest. 1996 Sep 1;98(5):1081-7 [8787668.001]
  • [Cites] Arch Surg. 1996 Nov;131(11):1141-6; discussion 1147 [8911253.001]
  • [Cites] FEBS Lett. 1997 Jan 6;400(3):333-5 [9009225.001]
  • [Cites] Eur J Biochem. 2000 May;267(9):2624-31 [10785383.001]
  • (PMID = 16735599.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / HL61613
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 126880-86-2 / L-Selectin; EC 3.4.24.- / ADAM Proteins; EC 3.4.24.- / tumor necrosis factor-alpha convertase
  • [Other-IDs] NLM/ PMC1895557
  •  go-up   go-down


36. Sharma M, Manoharlal R, Negi AS, Prasad R: Synergistic anticandidal activity of pure polyphenol curcumin I in combination with azoles and polyenes generates reactive oxygen species leading to apoptosis. FEMS Yeast Res; 2010 Aug 1;10(5):570-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • For this, pure polyphenol CUR-I was tested for synergy with five azole and two polyene drugs - fluconazole (FLC), miconazole, ketoconazole (KTC), itraconazole (ITR), voriconazole (VRC), nystatin (NYS) and amphotericin B (AMB) - against 21 clinical isolates of Candida albicans with reduced antifungal sensitivity, as well as a drug-sensitive laboratory strain.
  • Notably, there was a 10-35-fold drop in the MIC(80) values of the drugs when CUR-I was used in combination with azoles and polyenes, with fractional inhibitory concentration index (FICI) values ranging between 0.09 and 0.5.
  • Interestingly, the synergistic effect of CUR-I with FLC and AMB was associated with the accumulation of reactive oxygen species, which could be reversed by the addition of an antioxidant such as ascorbic acid.
  • Furthermore, the combination of CUR-I and FLC/AMB triggered apoptosis that could also be reversed by ascorbic acid.
  • [MeSH-major] Apoptosis. Azoles / pharmacology. Candida albicans / drug effects. Curcumin / pharmacology. Flavonoids / pharmacology. Phenols / pharmacology. Polyenes / pharmacology. Reactive Oxygen Species / metabolism
  • [MeSH-minor] Antifungal Agents / pharmacology. Antioxidants / pharmacology. Ascorbic Acid / pharmacology. Candidiasis / microbiology. Drug Synergism. Humans. Microbial Sensitivity Tests. Microbial Viability / drug effects. Polyphenols

  • Hazardous Substances Data Bank. Sodium ascorbate .
  • Hazardous Substances Data Bank. CURCUMIN .
  • Hazardous Substances Data Bank. L-Ascorbic Acid .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20528949.001).
  • [ISSN] 1567-1364
  • [Journal-full-title] FEMS yeast research
  • [ISO-abbreviation] FEMS Yeast Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Antioxidants; 0 / Azoles; 0 / Flavonoids; 0 / Phenols; 0 / Polyenes; 0 / Polyphenols; 0 / Reactive Oxygen Species; IT942ZTH98 / Curcumin; PQ6CK8PD0R / Ascorbic Acid
  •  go-up   go-down


37. Campbell KJ, Bath ML, Turner ML, Vandenberg CJ, Bouillet P, Metcalf D, Scott CL, Cory S: Elevated Mcl-1 perturbs lymphopoiesis, promotes transformation of hematopoietic stem/progenitor cells, and enhances drug resistance. Blood; 2010 Oct 28;116(17):3197-207
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Elevated Mcl-1 perturbs lymphopoiesis, promotes transformation of hematopoietic stem/progenitor cells, and enhances drug resistance.
  • Their lymphoid and myeloid cells displayed increased resistance to a variety of cytotoxic agents.
  • Myelopoiesis was relatively normal, but lymphopoiesis was clearly perturbed, with excess mature B and T cells accumulating.
  • Rather than the follicular lymphomas typical of vavP-BCL-2 mice, aging vavP-Mcl-1 mice were primarily susceptible to lymphomas having the phenotype of a stem/progenitor cell (11 of 30 tumors) or pre-B cell (12 of 30 tumors).
  • Most vavP-Mcl-1/ Eμ-Myc mice died around birth, and transplantation of blood from bitransgenic E18 embryos into unirradiated mice resulted in stem/progenitor cell tumors.
  • Furthermore, lethally irradiated mice transplanted with E13 fetal liver cells from Mcl-1/Myc bitransgenic mice uniformly died of stem/progenitor cell tumors.
  • Collectively, these results demonstrate that Mcl-1 overexpression renders hematopoietic cells refractory to many cytotoxic insults, perturbs lymphopoiesis and promotes malignant transformation of hematopoietic stem and progenitor cells.

  • MedlinePlus Health Information. consumer health - Lymphoma.
  • MedlinePlus Health Information. consumer health - Stem Cells.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Genes Dev. 1999 Oct 15;13(20):2658-69 [10541552.001]
  • [Cites] Blood. 2007 Jun 1;109(11):4907-13 [17317859.001]
  • [Cites] Science. 1999 Nov 26;286(5445):1735-8 [10576740.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Dec 21;96(26):14943-8 [10611317.001]
  • [Cites] Genes Dev. 2000 Jan 1;14(1):23-7 [10640272.001]
  • [Cites] Blood. 2008 Nov 1;112(9):3807-17 [18599795.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Nov 18;105(46):17961-6 [19004807.001]
  • [Cites] Blood. 2009 Mar 19;113(12):2805-15 [19064728.001]
  • [Cites] J Biol Chem. 2009 Jul 3;284(27):18311-22 [19351886.001]
  • [Cites] J Cell Biol. 2009 Nov 2;187(3):429-42 [19948485.001]
  • [Cites] Blood. 2010 Feb 4;115(5):1018-25 [19965632.001]
  • [Cites] Nature. 2010 Feb 18;463(7283):899-905 [20164920.001]
  • [Cites] Blood. 2010 Sep 2;116(9):1433-42 [20525924.001]
  • [Cites] Blood. 2001 Jun 15;97(12):3902-9 [11389033.001]
  • [Cites] Dev Cell. 2001 Nov;1(5):645-53 [11709185.001]
  • [Cites] Blood. 2002 Mar 15;99(6):1885-93 [11877256.001]
  • [Cites] J Exp Med. 2003 Oct 6;198(7):1119-26 [14517273.001]
  • [Cites] Nature. 2003 Dec 11;426(6967):671-6 [14668867.001]
  • [Cites] J Biol Chem. 2007 Aug 17;282(33):23919-36 [17561513.001]
  • [Cites] Oncol Rep. 2008 Apr;19(4):933-7 [18357378.001]
  • [Cites] J Immunol. 2008 Jul 1;181(1):374-82 [18566403.001]
  • [Cites] J Immunol. 2008 Jul 1;181(1):521-8 [18566418.001]
  • [Cites] J Mol Biol. 2008 Jul 25;380(5):958-71 [18589438.001]
  • [Cites] J Cell Biol. 2004 Jan 5;164(1):89-96 [14709542.001]
  • [Cites] Blood. 2004 Mar 15;103(6):2276-83 [14630790.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Apr 20;101(16):6164-9 [15079075.001]
  • [Cites] J Immunol. 2004 Jun 1;172(11):6684-91 [15153484.001]
  • [Cites] Nature. 1990 Nov 22;348(6299):331-3 [2250704.001]
  • [Cites] Mol Cell Biol. 1991 Feb;11(2):1176-9 [1990273.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Apr 15;90(8):3516-20 [7682708.001]
  • [Cites] J Cell Biol. 1995 Mar;128(6):1173-84 [7896880.001]
  • [Cites] Leuk Res. 1996 Feb;20(2):101-7 [8628007.001]
  • [Cites] EMBO J. 1996 Dec 16;15(24):6979-90 [9003774.001]
  • [Cites] J Immunol. 1997 Sep 1;159(5):2301-11 [9278319.001]
  • [Cites] EMBO J. 1997 Aug 1;16(15):4628-38 [9303307.001]
  • [Cites] Blood. 1998 Jan 15;91(2):419-30 [9427694.001]
  • [Cites] Blood. 1998 Feb 1;91(3):991-1000 [9446661.001]
  • [Cites] Blood. 1998 May 1;91(9):3379-89 [9558396.001]
  • [Cites] Blood. 1998 Nov 1;92(9):3226-39 [9787159.001]
  • [Cites] Blood. 1999 Sep 15;94(6):1855-63 [10477714.001]
  • [Cites] Mol Cell. 2005 Feb 4;17(3):393-403 [15694340.001]
  • [Cites] Science. 2005 Feb 18;307(5712):1101-4 [15718471.001]
  • [Cites] Mol Cell. 2005 Feb 18;17(4):525-35 [15721256.001]
  • [Cites] Genes Dev. 2005 Jun 1;19(11):1294-305 [15901672.001]
  • [Cites] Blood. 2007 Feb 15;109(4):1620-6 [17062731.001]
  • [Cites] Science. 2007 Feb 9;315(5813):856-9 [17289999.001]
  • [Cites] Cell. 2007 Mar 23;128(6):1173-86 [17382885.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Apr 10;104(15):6217-22 [17389404.001]
  • [Cites] Genes Dev. 1999 Oct 15;13(20):2670-7 [10541553.001]
  • (PMID = 20631380.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA043540; United States / NCI NIH HHS / CA / R01 CA043540-22; United States / NCI NIH HHS / CA / CA43540
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Apoptosis Regulatory Proteins; 0 / Bcl-2-like protein 11; 0 / Mcl1 protein, mouse; 0 / Membrane Proteins; 0 / Myc protein, mouse; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Proto-Oncogene Proteins c-myc; 8N3DW7272P / Cyclophosphamide
  • [Other-IDs] NLM/ PMC2995351
  •  go-up   go-down


38. Anderson JB, Sirjusingh C, Syed N, Lafayette S: Gene expression and evolution of antifungal drug resistance. Antimicrob Agents Chemother; 2009 May;53(5):1931-6
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gene expression and evolution of antifungal drug resistance.
  • In this study, we asked whether any changes in gene expression are required for the evolution of a drug-resistant phenotype in populations.
  • We examined the changes in gene expression resulting from the evolution of resistance in experimental populations of the yeast Saccharomyces cerevisiae with two antifungal drugs, fluconazole (FLC) in a previous study and amphotericin B (AmB) in this study, in which five populations were subjected to increasing concentrations of AmB, from 0.25 to 128 microg/ml in twofold increments.
  • Six genes, YGR035C, YOR1, ICT1, GRE2, PDR16, and YPLO88W, were consistently overexpressed with resistance to AmB reported here and with resistance to FLC involving a mechanism of increased efflux reported previously.
  • We then asked if the deletion of these genes impaired the ability of populations to evolve resistance to FLC over 108 generations of asexual reproduction in 32 and 128 microg/ml FLC, the same conditions under which FLC-resistant types evolved originally.
  • For each of three deletion strains, YOR1, ICT1, and PDR16 strains, extinctions occurred in one of two replicate populations growing in 128 microg/ml FLC.
  • Each of these three deletion strains was mixed 1:1 with a marked version of the wild type to measure the relative ability of the deletion strain to adapt over 108 generations.
  • In these assays, only the PDR16 deletion strain consistently became extinct both at 32 and at 128 microg/ml FLC.
  • The deletion of PDR16 reduces the capacity of a population to evolve to resistance to FLC.
  • [MeSH-major] Antifungal Agents / pharmacology. Drug Resistance, Fungal. Evolution, Molecular. Gene Expression Profiling. Gene Expression Regulation, Fungal. Saccharomyces cerevisiae / drug effects
  • [MeSH-minor] Amphotericin B / pharmacology. Fluconazole / pharmacology. Molecular Sequence Data. Oligonucleotide Array Sequence Analysis. Saccharomyces cerevisiae Proteins / genetics. Saccharomyces cerevisiae Proteins / metabolism

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. AMPHOTERICIN B .
  • Hazardous Substances Data Bank. FLUCONAZOLE .
  • Saccharomyces Genome Database. Saccharomyces Genome Database .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Biochim Biophys Acta. 2008 Jan;1778(1):68-78 [17950691.001]
  • [Cites] Nature. 2007 May 31;447(7144):585-8 [17538619.001]
  • [Cites] J Biol Chem. 2008 Apr 11;283(15):9768-75 [18252723.001]
  • [Cites] FEBS Lett. 2000 Mar 24;470(2):156-60 [10734226.001]
  • [Cites] Nat Genet. 2000 Jul;25(3):333-7 [10888885.001]
  • [Cites] Mol Microbiol. 2001 Jun;40(5):1067-83 [11401713.001]
  • [Cites] Trends Mol Med. 2002 Feb;8(2):76-81 [11815273.001]
  • [Cites] Lancet Infect Dis. 2002 Feb;2(2):73-85 [11901654.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Jul 9;99(14):9284-9 [12089321.001]
  • [Cites] Curr Opin Microbiol. 2002 Aug;5(4):379-85 [12160856.001]
  • [Cites] Genetics. 2003 Apr;163(4):1287-98 [12702675.001]
  • [Cites] Yeast. 2003 Apr 30;20(6):545-54 [12722185.001]
  • [Cites] J Biol Chem. 2003 Dec 26;278(52):52641-50 [14512416.001]
  • [Cites] J Biol Chem. 1998 May 15;273(20):12612-22 [9575223.001]
  • [Cites] J Biol Chem. 1999 Jan 22;274(4):1934-41 [9890948.001]
  • [Cites] Genetics. 2004 Dec;168(4):1915-23 [15371350.001]
  • [Cites] Nat Rev Microbiol. 2005 Jul;3(7):547-56 [15953931.001]
  • [Cites] Science. 2005 Sep 30;309(5744):2185-9 [16195452.001]
  • [Cites] Eukaryot Cell. 2006 Aug;5(8):1243-51 [16896209.001]
  • [Cites] Nat Rev Microbiol. 2008 Mar;6(3):187-98 [18246082.001]
  • (PMID = 19273689.001).
  • [ISSN] 1098-6596
  • [Journal-full-title] Antimicrobial agents and chemotherapy
  • [ISO-abbreviation] Antimicrob. Agents Chemother.
  • [Language] eng
  • [Databank-accession-numbers] GEO/ GSE12055
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Saccharomyces cerevisiae Proteins; 7XU7A7DROE / Amphotericin B; 8VZV102JFY / Fluconazole
  • [Other-IDs] NLM/ PMC2681570
  •  go-up   go-down


39. Krzyściak P, Macura AB: Drug susceptibility of 64 strains of Rhodotorula sp. Wiad Parazytol; 2010;56(2):167-70
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Drug susceptibility of 64 strains of Rhodotorula sp.
  • Knowledge about the susceptibility of Rhodotorula strains to the common antifungal drugs is essential for the treatment of such new infections.
  • The 68 isolates identified as: Rhodotorula mucilaginosa (47 strains; 69%), R. minuta (14; 21%) and R. glutinis (7; 10%) obtained from various sources (feces, skin and nails, vagina and hospital environment) were tested for susceptibility to 5-fluorocytosine (5FC), amphotericin B (AMB), fluconazole (FLC) and itraconazole (ITR).
  • For ITR, the R. minuta isolates had the lowest MICs within a range 0.125-0.25 mg/l and for FLC all isolates affected within the range 2-64 mg/l.
  • The majority of R. mucilaginosa isolates (82.2%) had MICs in the range 64-128 mg/l for FLC and 95.6% of isolates had MICs above or equal to 2 mg/1 for ITR.
  • [MeSH-major] Antifungal Agents / pharmacology. Rhodotorula / classification. Rhodotorula / drug effects

  • Hazardous Substances Data Bank. AMPHOTERICIN B .
  • Hazardous Substances Data Bank. FLUCYTOSINE .
  • Hazardous Substances Data Bank. Itraconazole .
  • Hazardous Substances Data Bank. FLUCONAZOLE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20707302.001).
  • [ISSN] 0043-5163
  • [Journal-full-title] Wiadomości parazytologiczne
  • [ISO-abbreviation] Wiad Parazytol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Antifungal Agents; 304NUG5GF4 / Itraconazole; 7XU7A7DROE / Amphotericin B; 8VZV102JFY / Fluconazole; D83282DT06 / Flucytosine
  •  go-up   go-down


40. Radosevic N, Winterstein D, Keller JR, Neubauer H, Pfeffer K, Linnekin D: JAK2 contributes to the intrinsic capacity of primary hematopoietic cells to respond to stem cell factor. Exp Hematol; 2004 Feb;32(2):149-56
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] JAK2 contributes to the intrinsic capacity of primary hematopoietic cells to respond to stem cell factor.
  • OBJECTIVE: Stem cell factor (SCF) is the ligand for the receptor tyrosine kinase (RTK) Kit.
  • Here we use a genetic approach to determine the direct role of JAK2 in SCF-mediated growth and differentiation of primary hematopoietic cells.
  • MATERIALS AND METHODS: Fetal liver cells were isolated from JAK2-deficient murine embryos at day 12 of development.
  • SCF-induced growth and differentiation of this unfractionated population of cells were determined by 3H-thymidine incorporation in bulk cultures, single-cell colony assays, and cytochemistry.
  • In addition, Kit+ cells were isolated from fetal liver by fluorescence-activated cell sorting (FACS) and assessed for growth using 3H-thymidine and colony assays.
  • RESULTS: SCF-induced growth of unfractionated JAK2-deficient fetal liver cells was reduced by 70% compared to cells from wild-type fetal liver in single-cell assays.
  • This was of particular note because there were three-fold more Kit+ cells in JAK2-deficient fetal liver.
  • Reductions in SCF-induced growth were not observed in bulk cultures of JAK2-deficient fetal liver, suggesting that additional factors cooperate with SCF to overcome the absence of JAK2 in this heterogeneous population of cells.
  • SCF-induced 3H-thymidine incorporation of FACS-purified Kit+ fetal liver deficient for JAK2 was impaired by approximately 50%, whereas colony formation in methylcellulose was reduced 95%.
  • JAK2 also was required for differentiation of this purified population of progenitors into mast cells.
  • CONCLUSION: JAK2 contributes to the intrinsic capacity of fetal liver hematopoietic progenitor cells to proliferate and differentiate in response to SCF.
  • [MeSH-major] Hematopoietic Stem Cells / drug effects. Protein-Tyrosine Kinases / physiology. Proto-Oncogene Proteins. Stem Cell Factor / pharmacology
  • [MeSH-minor] Animals. Cell Differentiation / drug effects. Cell Division / drug effects. Hepatocytes / cytology. Janus Kinase 2. Mast Cells / cytology. Mice

  • MedlinePlus Health Information. consumer health - Stem Cells.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15102475.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CO / N01-CO-12400
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins; 0 / Stem Cell Factor; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Jak2 protein, mouse; EC 2.7.10.2 / Janus Kinase 2
  •  go-up   go-down


41. Maruyama M, Matsunaga T, Harada E, Ohmori S: Comparison of basal gene expression and induction of CYP3As in HepG2 and human fetal liver cells. Biol Pharm Bull; 2007 Nov;30(11):2091-7
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Comparison of basal gene expression and induction of CYP3As in HepG2 and human fetal liver cells.
  • Human fetal liver (HFL) cell culture was initiated from a pool of six normal human liver tissues.
  • The proliferation and viability of HFL cells were evaluated using 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide assay, and the cells increased by more than 100-fold by culture for 15 d.
  • The levels of expression of albumin (ALB), hepatocyte nuclear factor 4alpha, hepatocyte growth factor, CYP3A4, CYP3A5, and CYP3A7 mRNAs in HFL cells increased with culture period, while that of alpha-fetoprotein (AFP) mRNA decreased gradually.
  • In HepG2 cells, however, the expression levels of ALB and AFP mRNAs were not changed, and the levels of expression of CYP3A4, CYP3A5, and CYP3A7 mRNAs decreased gradually.
  • The mRNA expression of major CYP isoforms including CYP3As, i.e., CYP1A2, CYP2A6, CYP2B6, CYP2C (2C9 and 2C19), CYP2D6, and CYP2E1, could be detected in HepG2 cells.
  • With the exception of CYP1A2, all of the CYP mRNAs expressed in HepG2 cells were detected in HFL cells.
  • In HFL cells, CYP3A4 and CYP3A7 mRNA expression levels were markedly up-regulated by dexamethasone (DEX), but not by rifampicin (RIF).
  • On the other hand, CYP3A4, CYP3A5, and CYP3A7 mRNA expression levels in HepG2 cells were increased from 2- to 3-fold by treatment with DEX and RIF.
  • Pregnane X receptor mRNA was expressed in HepG2 cells, but not HFL cells.
  • These results indicate that the character of HFL cells with regard to CYP expression was different from that of HepG2 cells.
  • [MeSH-major] Carcinoma, Hepatocellular / enzymology. Cytochrome P-450 Enzyme System / biosynthesis. Hepatocytes / enzymology. Liver Neoplasms / enzymology
  • [MeSH-minor] Aryl Hydrocarbon Hydroxylases. Cell Line, Tumor. Cytochrome P-450 CYP3A. Dexamethasone / pharmacology. Enzyme Induction / drug effects. Fetus. Formazans / metabolism. Gene Expression Regulation, Enzymologic / drug effects. Humans. Isoenzymes / biosynthesis. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Tetrazolium Salts / metabolism. Time Factors

  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • Hazardous Substances Data Bank. DEXAMETHASONE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17978482.001).
  • [ISSN] 0918-6158
  • [Journal-full-title] Biological & pharmaceutical bulletin
  • [ISO-abbreviation] Biol. Pharm. Bull.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Formazans; 0 / Isoenzymes; 0 / RNA, Messenger; 0 / Tetrazolium Salts; 23305-68-2 / MTT formazan; 7S5I7G3JQL / Dexamethasone; 9035-51-2 / Cytochrome P-450 Enzyme System; EC 1.14.14.1 / Aryl Hydrocarbon Hydroxylases; EC 1.14.14.1 / CYP3A protein, human; EC 1.14.14.1 / CYP3A5 protein, human; EC 1.14.14.1 / CYP3A7 protein, human; EC 1.14.14.1 / Cytochrome P-450 CYP3A
  •  go-up   go-down


42. Majcherczyk PA, Moreillon P, Decosterd LA, Sanglard D, Bille J, Glauser MP, Marchetti O: Single-step extraction of fluconazole from plasma by ultra-filtration for the measurement of its free concentration by high performance liquid chromatography. J Pharm Biomed Anal; 2002 May 15;28(3-4):645-51
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • This technique requires careful sample preparation.
  • This constraint makes it difficult to determine drug levels when blood sample volumes are limited.
  • However, drugs with low plasma-protein binding can be reliably extracted from plasma by ultra-filtration with a minimal loss due to the protein-bound fraction.
  • This study validated a single-step ultra-filtration method for extracting fluconazole (FLC), a first-line antifungal agent with a weak plasma-protein binding, from plasma to determine its concentration by HPLC.
  • Spiked FLC standards and unknowns were prepared in human and rat plasma.
  • Samples (240 microl) were transferred into disposable microtube filtration units containing cellulose or polysulfone filters with a 5 kDa cut-off.
  • After centrifugation for 60 min at 15000g, FLC concentrations were measured by direct injection of the filtrate into the HPLC.
  • Using cellulose filters, low molecular weight proteins were eluted early in the chromatogram and well separated from FLC that eluted at 8.40 min as a sharp single peak.
  • In contrast, with polysulfone filters several additional peaks interfering with the FLC peak were observed.
  • Moreover, the FLC recovery using cellulose filters compared to polysulfone filters was higher and had a better reproducibility.
  • Standard curves with a quadratic regression coefficient > or = 0.9999 were obtained in the concentration range of 0.195-100 mgl(-1).
  • Furthermore, no analytical interference was observed with commonly used antibiotics, antifungals, antivirals and immunosuppressive agents.
  • Ultra-filtration of plasma with cellulose filters permits the extraction of FLC from small volumes (240 microl).
  • The determination of FLC concentrations by HPLC after this single-step procedure is selective, precise and accurate.
  • [MeSH-major] Antifungal Agents / blood. Fluconazole / blood
  • [MeSH-minor] Animals. Cellulose. Chromatography, High Pressure Liquid. Humans. Polymers. Rats. Reference Standards. Reproducibility of Results. Sulfones. Ultrafiltration

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. FLUCONAZOLE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12008144.001).
  • [ISSN] 0731-7085
  • [Journal-full-title] Journal of pharmaceutical and biomedical analysis
  • [ISO-abbreviation] J Pharm Biomed Anal
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Polymers; 0 / Sulfones; 25135-51-7 / polysulfone P 1700; 8VZV102JFY / Fluconazole; 9004-34-6 / Cellulose
  •  go-up   go-down


43. Chan W, Naghdy F: Prognosis of body fluid level by fuzzy logic technique. Methods Inf Med; 2001 Mar;40(1):52-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Surgical fluid replacement is a critical issue in medicine as the fluid volume excess or deficit can both complicate the patient's condition.
  • The development of a decision support system (DSS) to assist the anaesthetist in estimating the required fluid infusion rate for a particular patient has been the focus of this research paper.
  • The DSS is developed based on Fuzzy Logic Control (FLC) technique which is ideal for developing input/output models in an unstructured and/or complex environment.
  • The DSS employs a Multi Rule Base (MRB) learning scheme to adapt its model according to the significant variation in the physiological parameters of a patient.
  • [MeSH-major] Diagnosis, Computer-Assisted. Fluid Therapy / methods. Fuzzy Logic. Intraoperative Care. Water-Electrolyte Imbalance / diagnosis

  • MedlinePlus Health Information. consumer health - Fluid and Electrolyte Balance.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11310160.001).
  • [ISSN] 0026-1270
  • [Journal-full-title] Methods of information in medicine
  • [ISO-abbreviation] Methods Inf Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  •  go-up   go-down


44. Mukhopadhyay K, Kohli A, Prasad R: Drug susceptibilities of yeast cells are affected by membrane lipid composition. Antimicrob Agents Chemother; 2002 Dec;46(12):3695-705
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Drug susceptibilities of yeast cells are affected by membrane lipid composition.
  • In the present study we have exploited isogenic erg mutants of Saccharomyces cerevisiae to examine the contribution of an altered lipid environment on drug susceptibilities of yeast cells.
  • It is observed that erg mutants, which possess high levels of membrane fluidity, were hypersensitive to the drugs tested, i.e., cycloheximide (CYH), o-phenanthroline, sulfomethuron methyl, 4-nitroquinoline oxide, and methotrexate.
  • Most of the erg mutants except mutant erg4 were, however, resistant to fluconazole (FLC).
  • By using the fluorophore rhodamine-6G and radiolabeled FLC to monitor the passive diffusion, it was observed that erg mutant cells elicited enhanced diffusion.
  • The addition of a membrane fluidizer, benzyl alcohol (BA), to S. cerevisiae wild-type cells led to enhanced membrane fluidity.
  • However, a 10 to 12% increase in BA-induced membrane fluidity did not alter the drug susceptibilities of the S. cerevisiae wild-type cells.
  • In order to ascertain the functioning of drug extrusion pumps encoding the genes CDR1 (ATP-binding cassette family) and CaMDR1 (MFS family) of Candida albicans in a different lipid environment, they were independently expressed in an S. cerevisiae erg mutant background.
  • While the fold change in drug resistance mediated by CaMDR1 remained the same or increased in erg mutants, susceptibility to FLC and CYH mediated by CDR1 was increased (decrease in fold resistance).
  • Our results demonstrate that between the two drug extrusion pumps, Cdr1p appeared to be more adversely affected by the fluctuations in the membrane lipid environment (particularly to ergosterol).
  • Taken together it appears that multidrug resistance in yeast is closely linked to the status of membrane lipids, wherein the overall drug susceptibility phenotype of a cell appears to be an interplay among drug diffusion, extrusion pumps, and the membrane lipid environment.
  • [MeSH-minor] Candida albicans / drug effects. Candida albicans / genetics. Drug Resistance, Multiple / genetics

  • Hazardous Substances Data Bank. ERGOSTEROL .
  • Saccharomyces Genome Database. Saccharomyces Genome Database .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] FEBS Lett. 2000 Mar 17;470(1):83-7 [10722850.001]
  • [Cites] J Biol Chem. 2001 Jun 29;276(26):23674-80 [11323424.001]
  • [Cites] Lancet Infect Dis. 2002 Feb;2(2):73-85 [11901654.001]
  • [Cites] FEBS Lett. 2002 Jun 19;521(1-3):57-61 [12067726.001]
  • [Cites] Adv Microb Physiol. 2002;46:155-201 [12073653.001]
  • [Cites] J Biol Chem. 2002 Jul 19;277(29):26177-84 [12006573.001]
  • [Cites] Antimicrob Agents Chemother. 2002 Aug;46(8):2477-81 [12121921.001]
  • [Cites] J Gen Microbiol. 1986 Sep;132(9):2421-31 [3540203.001]
  • [Cites] Crit Rev Microbiol. 1987;15(1):111-5 [3319418.001]
  • [Cites] Genetics. 1990 May;125(1):13-20 [2160400.001]
  • [Cites] Mol Gen Genet. 1991 Jun;227(2):318-29 [2062311.001]
  • [Cites] J Biol Chem. 1992 Dec 15;267(35):24995-5002 [1360981.001]
  • [Cites] Biochem Soc Trans. 1993 Nov;21(4):1039-47 [8131894.001]
  • [Cites] Lipids. 1995 Mar;30(3):221-6 [7791529.001]
  • [Cites] Curr Genet. 1995 Mar;27(4):320-9 [7614555.001]
  • [Cites] J Biol Chem. 1996 Feb 2;271(5):2634-40 [8576233.001]
  • [Cites] Lancet. 1996 Nov 30;348(9040):1523-4 [8942815.001]
  • [Cites] Antimicrob Agents Chemother. 1997 Jan;41(1):196-9 [8980781.001]
  • [Cites] Yeast. 2001 Sep 15;18(12):1117-29 [11536334.001]
  • [Cites] J Biosci. 2001 Sep;26(3):333-9 [11568478.001]
  • [Cites] Antimicrob Agents Chemother. 2001 Dec;45(12):3366-74 [11709310.001]
  • [Cites] Yeast. 2002 Mar 15;19(4):303-18 [11870854.001]
  • [Cites] Antimicrob Agents Chemother. 2002 Apr;46(4):1046-52 [11897588.001]
  • [Cites] Eur J Biochem. 2000 Jan;267(2):277-94 [10632698.001]
  • [Cites] J Biol Chem. 1997 Jan 10;272(2):1026-31 [8995398.001]
  • [Cites] FEBS Lett. 1997 Jan 2;400(1):80-2 [9000517.001]
  • [Cites] J Cell Biol. 1997 Jul 28;138(2):255-70 [9230069.001]
  • [Cites] Antimicrob Agents Chemother. 1997 Oct;41(10):2229-37 [9333053.001]
  • [Cites] Biochem Soc Trans. 1997 Aug;25(3):1088-96 [9388605.001]
  • [Cites] Mol Biol Cell. 1998 Feb;9(2):523-43 [9450972.001]
  • [Cites] Clin Microbiol Rev. 1998 Apr;11(2):382-402 [9564569.001]
  • [Cites] J Biol Chem. 1998 May 15;273(20):12612-22 [9575223.001]
  • [Cites] Antimicrob Agents Chemother. 1998 May;42(5):1160-7 [9593144.001]
  • [Cites] Curr Genet. 1998 Sep;34(3):192-9 [9745021.001]
  • [Cites] J Bacteriol. 1999 Jan;181(1):231-40 [9864335.001]
  • [Cites] J Biol Chem. 1999 Jan 22;274(4):1934-41 [9890948.001]
  • [Cites] Med Mycol. 1998;36 Suppl 1:68-78 [9988494.001]
  • [Cites] Yeast. 1999 Jan 30;15(2):111-21 [10029989.001]
  • [Cites] Microbiology. 1999 Apr;145 ( Pt 4):809-18 [10220160.001]
  • [Cites] FEMS Microbiol Lett. 1999 Apr 15;173(2):475-81 [10227177.001]
  • [Cites] J Bacteriol. 1999 Jul;181(13):4041-9 [10383973.001]
  • [Cites] Antimicrob Agents Chemother. 1999 Jul;43(7):1621-30 [10390213.001]
  • [Cites] Antimicrob Agents Chemother. 1999 Jul;43(7):1725-8 [10390230.001]
  • [Cites] Gene. 1999 Aug 5;236(1):43-51 [10433965.001]
  • [Cites] J Clin Microbiol. 1999 Oct;37(10):3332-7 [10488201.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Mar 28;97(7):3254-9 [10716729.001]
  • [Cites] Biochemistry. 2000 Jul 4;39(26):7651-61 [10869171.001]
  • [Cites] J Antimicrob Chemother. 2000 Aug;46(2):191-7 [10933640.001]
  • [Cites] J Antimicrob Chemother. 2000 Aug;46(2):199-203 [10933641.001]
  • [Cites] FEMS Microbiol Lett. 2000 Apr 1;185(1):59-63 [10731607.001]
  • (PMID = 12435664.001).
  • [ISSN] 0066-4804
  • [Journal-full-title] Antimicrobial agents and chemotherapy
  • [ISO-abbreviation] Antimicrob. Agents Chemother.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Membrane Lipids; Z30RAY509F / Ergosterol
  • [Other-IDs] NLM/ PMC132749
  •  go-up   go-down


45. Gate L, Couvreur P, Nguyen-Ba G, Tapiero H: N-methylation of anthracyclines modulates their cytotoxicity and pharmacokinetic in wild type and multidrug resistant cells. Biomed Pharmacother; 2003 Sep;57(7):301-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] N-methylation of anthracyclines modulates their cytotoxicity and pharmacokinetic in wild type and multidrug resistant cells.
  • Anthracyclines are the most commonly used classes of anticancer agents in chemotherapy.
  • This pump, which is responsible for the multidrug resistance (MDR) phenotype, decreases the toxicity of a wide range of unrelated anticancer drugs by increasing their cellular efflux.
  • Here, we used three new anthracyclines that shared the same chromophore but differed by the degree of N-methylation of their sugar moiety.
  • In sensitive cells (FLC), reduced cytotoxicity was related to the level of N-methylation; whereas in resistant cells (DOX-RFLC(1) and DOX-RFLC(2)) overexpressing different levels of P-gp, increased N-methylation enhanced anthracycline cytotoxicity.
  • Decreased resistance in DOX-RFLCs was associated with an increased drug accumulation due to a reduced cellular efflux.
  • These results suggest that N-methylation of anthracyclines circumvents resistance by diminishing drug transport by P-gp in MDR-positive cells.
  • These observations could be the consequence of the steric hindrance created by the methyl group(s) which may impair the interaction between the positively charged amino group and the active site of P-gp.
  • [MeSH-major] Anthracyclines / chemistry. Anthracyclines / pharmacokinetics. Antineoplastic Agents / chemistry. Antineoplastic Agents / pharmacokinetics. Leukemia, Erythroblastic, Acute / metabolism
  • [MeSH-minor] Animals. Biological Transport. Cell Division / drug effects. Cell Survival / drug effects. Drug Resistance, Multiple. Drug Resistance, Neoplasm. Methylation. Mice. Multidrug Resistance-Associated Proteins / biosynthesis. P-Glycoprotein / biosynthesis. Structure-Activity Relationship. Tumor Cells, Cultured

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 14499178.001).
  • [ISSN] 0753-3322
  • [Journal-full-title] Biomedicine & pharmacotherapy = Biomédecine & pharmacothérapie
  • [ISO-abbreviation] Biomed. Pharmacother.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Anthracyclines; 0 / Antineoplastic Agents; 0 / Multidrug Resistance-Associated Proteins; 0 / P-Glycoprotein
  •  go-up   go-down


46. Kawano Y, Nakama T, Hata H, Kimura E, Maruyoshi N, Uchino M, Mitsuya H: Successful treatment with rituximab and thalidomide of POEMS syndrome associated with Waldenstrom macroglobulinemia. J Neurol Sci; 2010 Oct 15;297(1-2):101-4
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • A POEMS syndrome is a rare disorder characterized by polyneuropathy, organomegaly, endocrinopathy, monoclonal gammopathy and skin abnormalities including hyperpigmentation and hypertrichosis.
  • Here we report a 55-year-old female case of a POEMS syndrome associated with Waldenstrom macroglobulinemia.
  • The patient had bed-bound polyneuropathy, splenomegaly, IgM-λ type monoclonal (M) protein, elevated λ-type free light chain (FLC), infiltration of CD20-positive lymphoplasmacytic cells in bone marrow, edema and hypertrichosis, and was diagnosed to have an 'atypical' POEMS syndrome associated with macroglobulinemia.
  • [MeSH-major] Antibodies, Monoclonal, Murine-Derived / therapeutic use. Immunologic Factors / therapeutic use. POEMS Syndrome / drug therapy. Thalidomide / therapeutic use. Waldenstrom Macroglobulinemia / drug therapy
  • [MeSH-minor] Female. Humans. Lymphocytes / drug effects. Middle Aged. Neural Conduction / drug effects. Rituximab

  • Genetic Alliance. consumer health - POEMS syndrome.
  • Genetic Alliance. consumer health - Waldenstrom macroglobulinemia.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. RITUXIMAB .
  • Hazardous Substances Data Bank. THALIDOMIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2010 Elsevier B.V. All rights reserved.
  • (PMID = 20673674.001).
  • [ISSN] 1878-5883
  • [Journal-full-title] Journal of the neurological sciences
  • [ISO-abbreviation] J. Neurol. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Immunologic Factors; 4F4X42SYQ6 / Rituximab; 4Z8R6ORS6L / Thalidomide
  •  go-up   go-down


47. Kosaka N, Sugiura K, Yamamoto Y, Yoshioka Y, Miyazaki H, Komatsu N, Ochiya T, Kato T: Identification of erythropoietin-induced microRNAs in haematopoietic cells during erythroid differentiation. Br J Haematol; 2008 Jun;142(2):293-300
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of erythropoietin-induced microRNAs in haematopoietic cells during erythroid differentiation.
  • It has not yet been clearly elucidated whether miRNAs participate in haematopoietic processes such as cell differentiation, apoptosis and maintenance of adequate levels of circulating blood cells.
  • A human miRNA microarray was used to analyze miRNA expression in the erythropoietin-dependent cell line UT-7/EPO compared to other factor-dependent UT-7 cell lines.
  • Among 324 human miRNAs, MIRN188, MIRN362 and MIRN210 levels were significantly elevated in UT-7/EPO cells, and stimulation with EPO in UT-7 cells increased the level of these three miRNAs.
  • Notably, knockdown of MIRN210 in UT-7/EPO cells led to apoptosis.
  • In mouse fetal liver cells, MIRN210 expression was twofold higher in TER-119-positive cells than in TER-119-negative cells.
  • [MeSH-major] Erythrocytes / cytology. Erythropoiesis / drug effects. Erythropoietin / pharmacology. MicroRNAs / analysis
  • [MeSH-minor] Animals. Apoptosis / drug effects. Apoptosis / genetics. Cell Line / metabolism. Gene Expression Regulation / drug effects. Humans. Mice. Microarray Analysis. RNA, Messenger / metabolism

  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18492109.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MicroRNAs; 0 / RNA, Messenger; 11096-26-7 / Erythropoietin
  •  go-up   go-down


48. Spreghini E, Maida CM, Tomassetti S, Orlando F, Giannini D, Milici ME, Scalise G, Barchiesi F: Posaconazole against Candida glabrata isolates with various susceptibilities to fluconazole. Antimicrob Agents Chemother; 2008 Jun;52(6):1929-33
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We investigated the in vitro activities of posaconazole (POS), fluconazole (FLC), amphotericin B (AMB), and caspofungin (CAS) against four clinical isolates of Candida glabrata with various susceptibilities to FLC (FLC MICs ranging from 1.0 to >64 microg/ml).
  • When FLC MICs increased, so did POS MICs, although we did not observe any isolate with a POS MIC greater than 0.5 mug/ml.
  • Time-kill experiments showed that POS, FLC, and CAS were fungistatic against all isolates, while AMB at eight times the MIC was fungicidal against three out of four isolates of C. glabrata tested.
  • Then, we investigated the activity of POS in an experimental model of disseminated candidiasis using three different isolates of C. glabrata: one susceptible to FLC (S; FLC MICs ranging from 1.0 to 4.0 microg/ml; POS MIC of < or =0.03 microg/ml), one susceptible in a dose-dependent manner (SDD; FLC MICs ranging from 32 to 64 microg/ml; POS MICs ranging from 0.125 to 0.25 microg/ml), and another one resistant to FLC (R; FLC MIC of >64 microg/ml; POS MIC of 0.5 microg/ml).
  • FLC significantly reduced the kidney burden of mice infected with the S strain (P = 0.0070) but not of those infected with the S-DD and R strains.
  • Additionally, the new triazole may be a therapeutic option in those cases where an FLC-resistant isolate is found to retain a relatively low POS MIC.
  • [MeSH-major] Antifungal Agents / pharmacology. Antifungal Agents / therapeutic use. Candida glabrata / drug effects. Candidiasis / drug therapy. Drug Resistance, Fungal. Fluconazole / pharmacology. Triazoles / pharmacology. Triazoles / therapeutic use
  • [MeSH-minor] Animals. Humans. Kidney / microbiology. Male. Mice. Microbial Sensitivity Tests. Treatment Outcome


49. Shieh JS, Fan SZ, Chang LW, Liu CC: Hierarchical rule-based monitoring and fuzzy logic control for neuromuscular block. J Clin Monit Comput; 2000;16(8):583-92
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Therefore, this study examined the application of a simple technique (i.e., fuzzy logic) to an almost ideal muscle relaxant (i.e., rocuronium) at general anaesthesia in order to control the system more easily, efficiently, intelligently and safely during an operation.
  • RESULTS: The system achieved stable control of muscle relaxation with a mean T1% error of -0.19 (SD 0.66) % accommodating a range in mean infusion rate (MIR) of 0.21-0.49 mg x kg(-1) x h(-1).
  • The controller activity of these two drugs showed no significant difference (p > 0.5).
  • [MeSH-major] Androstanols / administration & dosage. Electromyography. Fuzzy Logic. Monitoring, Intraoperative. Neuromuscular Blockade. Neuromuscular Nondepolarizing Agents / administration & dosage

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Br J Anaesth. 1995 Jul;75(1):1-2 [7669446.001]
  • [Cites] Br J Anaesth. 1997 Apr;78(4):412-5 [9135363.001]
  • [Cites] Eur J Clin Pharmacol. 1991;40(3):293-6 [2060567.001]
  • [Cites] Int J Clin Monit Comput. 1996 Nov;13(4):243-52 [9080245.001]
  • [Cites] Anaesthesia. 1987 Nov;42(11):1212-7 [3434744.001]
  • [Cites] Med Biol Eng Comput. 1997 Sep;35(5):498-503 [9374054.001]
  • [Cites] Anesthesiology. 1989 Mar;70(3):386-94 [2564261.001]
  • [Cites] Br J Anaesth. 1986 Oct;58(10):1100-3 [2876720.001]
  • [Cites] Br J Anaesth. 1989 Jul;63(1):31-5 [2548549.001]
  • [Cites] Eur J Anaesthesiol. 1987 Jan;4(1):9-15 [3582378.001]
  • [Cites] Br J Anaesth. 1994 Jun;72(6):686-7 [7912949.001]
  • [Cites] Anaesthesia. 1987 Oct;42(10):1085-91 [3688392.001]
  • [Cites] Anesthesiology. 1991 Aug;75(2):191-6 [1859007.001]
  • [Cites] Br J Anaesth. 1988 Dec;61(6):685-92 [3207541.001]
  • [Cites] Br J Anaesth. 1996 Mar;76(3):396-400 [8785140.001]
  • [Cites] Eur J Anaesthesiol. 1984 Dec;1(4):353-9 [6152617.001]
  • [Cites] J Biomed Eng. 1986 Jan;8(1):72-5 [3512915.001]
  • [Cites] Anesthesiology. 1991 Feb;74(2):258-63 [1990902.001]
  • (PMID = 12580234.001).
  • [ISSN] 1387-1307
  • [Journal-full-title] Journal of clinical monitoring and computing
  • [ISO-abbreviation] J Clin Monit Comput
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Androstanols; 0 / Neuromuscular Nondepolarizing Agents; WRE554RFEZ / rocuronium
  •  go-up   go-down


50. Comenzo RL: Systemic immunoglobulin light-chain amyloidosis. Clin Lymphoma Myeloma; 2006 Nov;7(3):182-5
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Systemic immunoglobulin light-chain amyloidosis, usually caused by free light chains (FLCs) made by clonal plasma cells, is the most frequent type.
  • Rarely, a patient with a tissue diagnosis of amyloidosis might have a monoclonal gammopathy and a hereditary protein.
  • In systemic immunoglobulin light-chain amyloidosis, circulating clonal light chains can be measured with the FLC assay and provide a target for therapy aimed at eliminating the underlying plasma cell disorder while supporting the patient.
  • Elimination of the pathologic FLC can lead to resorption of amyloid deposits and improvement in organ function.
  • Monthly oral melphalan and dexamethasone for 1 year is effective therapy for patients not eligible for autologous stem cell transplantation (SCT) but carries a risk of myelodysplasia.
  • For patients with limited organ involvement, SCT is an effective approach and, when followed after SCT by adjuvant thalidomide and dexamethasone for persistent plasma cell disease, achieves a high 1-year hematologic response rate.
  • New agents, such as bortezomib and lenalidomide, have shown promising activity, and novel monoclonal antibody approaches are also under active investigation.
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Congo Red / pharmacology. Disease Progression. Humans. Microscopy, Electron. Paraproteinemias / therapy. Prealbumin / genetics. Stem Cell Transplantation. Time Factors

  • Genetic Alliance. consumer health - Amyloidosis.
  • MedlinePlus Health Information. consumer health - Amyloidosis.
  • Hazardous Substances Data Bank. C.I. DIRECT RED 28 .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17229332.001).
  • [ISSN] 1557-9190
  • [Journal-full-title] Clinical lymphoma & myeloma
  • [ISO-abbreviation] Clin Lymphoma Myeloma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Immunoglobulin Light Chains; 0 / Prealbumin; 3U05FHG59S / Congo Red
  • [Number-of-references] 29
  •  go-up   go-down


51. Barchiesi F, Spreghini E, Baldassarri I, Marigliano A, Arzeni D, Giannini D, Scalise G: Sequential therapy with caspofungin and fluconazole for Candida albicans infection. Antimicrob Agents Chemother; 2004 Oct;48(10):4056-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • A sequential therapy of caspofungin (CAS) and fluconazole (FLC) administration for treatment of Candida albicans infection was investigated.
  • Treatment with CAS followed by FLC was as effective as CAS treatment given alone for the same duration.
  • Our data suggest that switching from CAS to FLC is a potentially explorable therapeutic option for treatment of systemic candidiasis.
  • [MeSH-major] Antifungal Agents / therapeutic use. Candidiasis / drug therapy. Fluconazole / therapeutic use. Peptides, Cyclic / therapeutic use
  • [MeSH-minor] Animals. Candida albicans / drug effects. Colony Count, Microbial. Drug Therapy, Combination. Echinocandins. Humans. Kidney / microbiology. Male. Mice

  • MedlinePlus Health Information. consumer health - Yeast Infections.
  • Hazardous Substances Data Bank. CASPOFUNGIN .
  • Hazardous Substances Data Bank. FLUCONAZOLE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Antimicrob Agents Chemother. 2002 Jan;46(1):245-7 [11751145.001]
  • [Cites] J Clin Microbiol. 2002 Jun;40(6):2228-30 [12037093.001]
  • [Cites] Antimicrob Agents Chemother. 2002 Aug;46(8):2564-8 [12121933.001]
  • [Cites] Antimicrob Agents Chemother. 2002 Sep;46(9):3039-41 [12183266.001]
  • [Cites] N Engl J Med. 2002 Dec 19;347(25):2020-9 [12490683.001]
  • [Cites] Antimicrob Agents Chemother. 2003 Mar;47(3):1068-71 [12604543.001]
  • [Cites] Diagn Microbiol Infect Dis. 1999 Sep;35(1):19-25 [10529877.001]
  • [Cites] Drug Resist Updat. 2003 Oct;6(5):257-69 [14643296.001]
  • [Cites] N Engl J Med. 1994 Jan 27;330(4):263-72 [8272088.001]
  • [Cites] Antimicrob Agents Chemother. 1997 Jul;41(7):1612-4 [9210698.001]
  • [Cites] Antimicrob Agents Chemother. 1997 Nov;41(11):2326-32 [9371328.001]
  • [Cites] Eur J Clin Microbiol Infect Dis. 1999 Apr;18(4):302-4 [10385023.001]
  • [Cites] Antimicrob Agents Chemother. 2003 Jul;47(7):2373-5 [12821503.001]
  • (PMID = 15388480.001).
  • [ISSN] 0066-4804
  • [Journal-full-title] Antimicrobial agents and chemotherapy
  • [ISO-abbreviation] Antimicrob. Agents Chemother.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Echinocandins; 0 / Peptides, Cyclic; 8VZV102JFY / Fluconazole; F0XDI6ZL63 / caspofungin
  • [Other-IDs] NLM/ PMC521911
  •  go-up   go-down


52. Marchetti O, Majcherczyk PA, Glauser MP, Bille J, Moreillon P, Sanglard D: Sensitive bioassay for determination of fluconazole concentrations in plasma using a Candida albicans mutant hypersusceptible to azoles. Antimicrob Agents Chemother; 2001 Mar;45(3):696-700
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The antifungal agent fluconazole (FLC) is widely used in clinical practice.
  • Monitoring FLC levels is useful in complicated clinical settings and in experimental infection models.
  • A bioassay using Candida pseudotropicalis, a simple and cost-effective method, is validated only for FLC levels ranging from 5 to 40 mg/liter.
  • A new bioassay in RPMI agar containing methylene blue was developed using C. albicans DSY1024, a mutant rendered hypersusceptible to FLC constructed by the deletion of the multidrug efflux transporter genes CDR1, CDR2, CaMDR1, and FLU1.
  • Reproducible standard curves were obtained with FLC concentrations in plasma ranging from 1 to 100 mg/liter (quadratic regression coefficient > 0.997).
  • The absolute sensitivity was 0.026 microg of FLC.
  • FLC levels measured by bioassay and by high-performance liquid chromatography (HPLC) performed with 62 plasma samples from humans and rats showed a strong correlation (coefficients, 0.979 and 0.995, respectively; percent deviations of bioassay from HPLC values, 0.44% +/- 15.31% and 2.66% +/- 7.54%, respectively).
  • It allows nonspecialized laboratories to determine FLC levels in plasma to within the clinically relevant concentration range and represents a useful tool for experimental treatment models.
  • [MeSH-major] Antifungal Agents / blood. Candida albicans / drug effects. Fluconazole / blood
  • [MeSH-minor] Animals. Azoles / blood. Azoles / pharmacology. Biological Assay. Chromatography, High Pressure Liquid. Colony Count, Microbial. Female. Humans. Microbial Sensitivity Tests. Models, Animal. Rats. Rats, Wistar

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. FLUCONAZOLE .
  • StrainInfo. culture/stock collections - online strain list (subscription/membership/fee required).
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Microbiology. 2000 Nov;146 ( Pt 11):2743-54 [11065353.001]
  • [Cites] Antimicrob Agents Chemother. 1998 Jun;42(6):1512-4 [9624506.001]
  • [Cites] J Clin Microbiol. 1986 Oct;24(4):600-6 [3771749.001]
  • [Cites] Drugs. 1990 Jun;39(6):877-916 [2196167.001]
  • [Cites] Antimicrob Agents Chemother. 1991 May;35(5):846-50 [1854166.001]
  • [Cites] Eur J Drug Metab Pharmacokinet. 1991 Oct-Dec;16(4):249-55 [1823867.001]
  • [Cites] Antimicrob Agents Chemother. 1993 Nov;37(11):2449-53 [8285632.001]
  • [Cites] J Infect Dis. 1995 Aug;172(2):599-602 [7622915.001]
  • [Cites] Antimicrob Agents Chemother. 1995 Oct;39(10):2197-200 [8619566.001]
  • [Cites] Zentralbl Bakteriol. 1996 Apr;283(4):492-6 [8737947.001]
  • [Cites] Antimicrob Agents Chemother. 1996 Oct;40(10):2300-5 [8891134.001]
  • [Cites] J Clin Microbiol. 1996 Mar;34(3):489-95 [8904400.001]
  • [Cites] Clin Infect Dis. 1997 Feb;24(2):235-47 [9114154.001]
  • [Cites] Antimicrob Agents Chemother. 1998 Jan;42(1):129-34 [9449272.001]
  • [Cites] Clin Infect Dis. 1998 Jan;26(1):1-10; quiz 11-2 [9455502.001]
  • [Cites] Antimicrob Agents Chemother. 1985 Nov;28(5):648-53 [3004323.001]
  • (PMID = 11181345.001).
  • [ISSN] 0066-4804
  • [Journal-full-title] Antimicrobial agents and chemotherapy
  • [ISO-abbreviation] Antimicrob. Agents Chemother.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Azoles; 8VZV102JFY / Fluconazole
  • [Other-IDs] NLM/ PMC90358
  •  go-up   go-down


53. Kasamatsu T, Mizobe K, Sutter EE: Muscimol and baclofen differentially suppress retinotopic and nonretinotopic responses in visual cortex. Vis Neurosci; 2005 Nov-Dec;22(6):839-58
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • This study relates to local field potentials and single-unit responses in cat visual cortex elicited by contrast reversal of bar gratings that were presented in single, double, or multiple discrete patch (es) of the visual field.
  • An analysis identified two distinct components of local field potentials: a fast local component (FLC) and a slow distributed component (SDC).
  • The FLC is thought to be a primarily postsynaptic response, as judged by its relatively short latency.
  • It is directly generated by thalamocortical volleys following retinotopic stimulation of receptive fields of a small cluster of single cells, combined with responses to recurrent excitation and inhibition derived from the cells under study and immediately neighboring cells.
  • We compared the suppressive effects of a GABA(A)-receptor agonist, muscimol, on the FLC and SDC with those of a GABA(B)-receptor agonist, baclofen, and found that muscimol more strongly suppressed the FLC than the SDC, and that the reverse was the case for baclofen.
  • The differential suppression of the FLC and SDC found in the present study is consistent with the notion that intracortical electrical signals related to the FLC terminate on the somata and proximal/basal dendrites, while those related to the SDC terminate on distal dendrites.
  • [MeSH-major] Baclofen / pharmacology. GABA Agonists / pharmacology. Muscimol / pharmacology. Retina / drug effects. Visual Cortex / physiology
  • [MeSH-minor] Animals. Cats. Data Interpretation, Statistical. Electrophysiology. Evoked Potentials, Visual / drug effects. Evoked Potentials, Visual / physiology. Microinjections. Photic Stimulation. Receptors, GABA-A / drug effects. Receptors, GABA-B / drug effects

  • Hazardous Substances Data Bank. MUSCIMOL .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16469192.001).
  • [ISSN] 0952-5238
  • [Journal-full-title] Visual neuroscience
  • [ISO-abbreviation] Vis. Neurosci.
  • [Language] eng
  • [Grant] United States / NEI NIH HHS / EY / EY-012413; United States / NEI NIH HHS / EY / EY-06861; United States / NEI NIH HHS / EY / EY-06883
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / GABA Agonists; 0 / Receptors, GABA-A; 0 / Receptors, GABA-B; 2763-96-4 / Muscimol; H789N3FKE8 / Baclofen
  •  go-up   go-down


54. Sahin F, Kannangai R, Adegbola O, Wang J, Su G, Torbenson M: mTOR and P70 S6 kinase expression in primary liver neoplasms. Clin Cancer Res; 2004 Dec 15;10(24):8421-5
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] mTOR and P70 S6 kinase expression in primary liver neoplasms.
  • The role of mTOR and S6K in hepatocellular carcinoma has not been investigated, but this pathway is of particular interest because an effective inhibitor, rapamycin, is available.
  • This study was undertaken to determine the prevalence and clinicopathological correlates of mTOR pathway activation in hepatocellular carcinoma and to determine whether rapamycin inhibits the pathway in cell culture.
  • EXPERIMENTAL DESIGN: Total and phosphorylated mTOR and S6K protein expression were studied by immunohistochemistry in hepatocellular carcinomas (n = 73), fibrolamellar carcinomas (n = 13), and hepatic adenomas (n = 15).
  • Results were correlated with tumor growth pattern as defined by the WHO (trabecular, pseudoglandular/acinar, compact, and scirrhous), tumor size, Ki-67 proliferation index, and the modified Edmondson nuclear grade, which has a scale of 1 to 4.
  • HepG2 and Hep3B cell lines were treated with rapamycin to see the effect on proliferation and S6K phosphorylation.
  • RESULTS: Increased expression of total mTOR was seen in 5% of hepatocellular carcinoma, whereas overexpression of phospho-mTOR was evident in 15% of hepatocellular carcinoma.
  • Total S6K overexpression was positively correlated with tumor nuclear grade, inversely with tumor size, and was unassociated with the proliferation index or WHO growth pattern.
  • Rapamycin treatment of HepG2 and Hep3B cell lines markedly inhibited cell proliferation and reduced S6K phosphorylation in both cell lines.
  • CONCLUSIONS: The mTOR pathway is activated in a subset of hepatocellular carcinoma.
  • Rapamycin can inhibit proliferation of neoplastic hepatocytes in cell culture.
  • [MeSH-major] Liver Neoplasms / metabolism. Protein Kinases / metabolism. Ribosomal Protein S6 Kinases, 70-kDa / metabolism
  • [MeSH-minor] Adenoma / metabolism. Adenoma / pathology. Antibiotics, Antineoplastic / pharmacology. Carcinoma, Hepatocellular / metabolism. Carcinoma, Hepatocellular / pathology. Cell Proliferation / drug effects. Female. Genetic Heterogeneity. Hepatitis / metabolism. Hepatitis / pathology. Humans. Immunoenzyme Techniques. Ki-67 Antigen / metabolism. Male. Middle Aged. Phosphorylation / drug effects. Sirolimus / pharmacology. TOR Serine-Threonine Kinases. Tumor Cells, Cultured / drug effects

  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • Hazardous Substances Data Bank. SIROLIMUS .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15623621.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Ki-67 Antigen; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.11.1 / Ribosomal Protein S6 Kinases, 70-kDa; W36ZG6FT64 / Sirolimus
  •  go-up   go-down


55. Florent M, Noël T, Ruprich-Robert G, Da Silva B, Fitton-Ouhabi V, Chastin C, Papon N, Chapeland-Leclerc F: Nonsense and missense mutations in FCY2 and FCY1 genes are responsible for flucytosine resistance and flucytosine-fluconazole cross-resistance in clinical isolates of Candida lusitaniae. Antimicrob Agents Chemother; 2009 Jul;53(7):2982-90
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The aim of this work was to elucidate the molecular mechanisms of flucytosine (5FC) resistance and 5FC/fluconazole (FLC) cross-resistance in 11 genetically and epidemiologically unrelated clinical isolates of Candida lusitaniae.
  • We first showed that the levels of transcription of the FCY2 gene encoding purine-cytosine permease (PCP) in the isolates were similar to that in the wild-type strain, 6936.
  • Nucleotide sequencing of the FCY2 alleles revealed that 5FC and 5FC/FLC resistance could be correlated with a cytosine-to-thymine substitution at nucleotide 505 in the fcy2 genes of seven clinical isolates, resulting in a nonsense mutation and in a putative nonfunctional truncated PCP of 168 amino acids.
  • Reintroducing a FCY2 wild-type allele at the fcy2 locus of a ura3 auxotrophic strain derived from the clinical isolate CL38 fcy2(C505T) restored levels of susceptibility to antifungals comparable to those of the wild-type strains.
  • Introducing this mutated allele into a 5FC- and 5FC/FLC-resistant fcy1Delta strain failed to restore antifungal susceptibility, while susceptibility was obtained by introducing a wild-type FCY1 allele.
  • We thus found a correlation between the fcy1 T26C mutation and both 5FC and 5FC/FLC resistances.
  • We demonstrated that only two genetic events occurred in 11 unrelated clinical isolates of C. lusitaniae to support 5FC and 5FC/FLC resistance: either the nonsense mutation C505T in the fcy2 gene or the missense mutation T26C in the fcy1 gene.
  • [MeSH-major] Antifungal Agents / pharmacology. Candidiasis / microbiology. Codon, Nonsense / genetics. Fluconazole / pharmacology. Flucytosine / pharmacology. Mutation, Missense / genetics
  • [MeSH-minor] Blotting, Northern. Blotting, Southern. Candida / drug effects. Candida / genetics. Drug Resistance, Fungal / genetics. Fungal Proteins / genetics. Fungal Proteins / physiology. Humans. Microbial Sensitivity Tests. Polymerase Chain Reaction

  • MedlinePlus Health Information. consumer health - Yeast Infections.
  • Hazardous Substances Data Bank. FLUCYTOSINE .
  • Hazardous Substances Data Bank. FLUCONAZOLE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Eur J Clin Microbiol Infect Dis. 2000 May;19(5):393-5 [10898145.001]
  • [Cites] Eukaryot Cell. 2007 Oct;6(10):1782-94 [17660361.001]
  • [Cites] Clin Infect Dis. 2001 Jan 15;32(2):186-90 [11170906.001]
  • [Cites] J Clin Microbiol. 2001 Nov;39(11):3906-14 [11682506.001]
  • [Cites] Lancet Infect Dis. 2002 Feb;2(2):73-85 [11901654.001]
  • [Cites] Drugs. 2002;62(7):1025-40 [11985489.001]
  • [Cites] Clin Infect Dis. 2003 Jan 15;36(2):e14-8 [12522762.001]
  • [Cites] Antimicrob Agents Chemother. 2003 Apr;47(4):1275-84 [12654658.001]
  • [Cites] J Biol Chem. 2003 May 23;278(21):19111-7 [12637534.001]
  • [Cites] Structure. 2003 Aug;11(8):961-72 [12906827.001]
  • [Cites] Diagn Microbiol Infect Dis. 2003 Sep;47(1):331-9 [12967746.001]
  • [Cites] Antimicrob Agents Chemother. 2004 Jan;48(1):262-6 [14693548.001]
  • [Cites] Mol Biol Cell. 2004 Feb;15(2):883-95 [14657252.001]
  • [Cites] Yeast. 2004 Jan 30;21(2):95-106 [14755635.001]
  • [Cites] Antimicrob Agents Chemother. 2004 Jun;48(6):2223-7 [15155225.001]
  • [Cites] Antimicrob Agents Chemother. 2004 Nov;48(11):4377-86 [15504867.001]
  • [Cites] J Clin Microbiol. 1983 Aug;18(2):443-4 [6619295.001]
  • [Cites] J Clin Microbiol. 1987 Apr;25(4):675-9 [3033016.001]
  • [Cites] Crit Rev Microbiol. 1987;15(1):45-56 [3319420.001]
  • [Cites] Nucleic Acids Res. 1994 Nov 11;22(22):4673-80 [7984417.001]
  • [Cites] Diagn Microbiol Infect Dis. 1994 Nov;20(3):127-33 [7874879.001]
  • [Cites] Antimicrob Agents Chemother. 1997 Jul;41(7):1537-40 [9210680.001]
  • [Cites] Nucleic Acids Res. 1997 Sep 1;25(17):3389-402 [9254694.001]
  • [Cites] J Bacteriol. 1999 Mar;181(6):1793-800 [10074071.001]
  • [Cites] Eur J Biochem. 1999 Feb;260(1):22-30 [10091580.001]
  • [Cites] Eur J Biochem. 1999 Jul;263(1):57-64 [10429187.001]
  • [Cites] Antimicrob Agents Chemother. 2005 Aug;49(8):3101-8 [16048910.001]
  • [Cites] J Clin Microbiol. 2005 Aug;43(8):4026-36 [16081946.001]
  • [Cites] J Clin Microbiol. 2005 Nov;43(11):5593-600 [16272492.001]
  • [Cites] Antimicrob Agents Chemother. 2007 Jan;51(1):369-71 [17060521.001]
  • [Cites] J Antimicrob Chemother. 2000 Aug;46(2):171-9 [10933638.001]
  • (PMID = 19414575.001).
  • [ISSN] 1098-6596
  • [Journal-full-title] Antimicrobial agents and chemotherapy
  • [ISO-abbreviation] Antimicrob. Agents Chemother.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Codon, Nonsense; 0 / Fungal Proteins; 8VZV102JFY / Fluconazole; D83282DT06 / Flucytosine
  • [Other-IDs] NLM/ PMC2704628
  •  go-up   go-down


56. Murata H, Tsuji S, Tsujii M, Sakaguchi Y, Fu HY, Kawano S, Hori M: Promoter hypermethylation silences cyclooxygenase-2 (Cox-2) and regulates growth of human hepatocellular carcinoma cells. Lab Invest; 2004 Aug;84(8):1050-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Promoter hypermethylation silences cyclooxygenase-2 (Cox-2) and regulates growth of human hepatocellular carcinoma cells.
  • Epidemiologically, chemopreventive effects of COX-2 inhibitors have been proven on numerous cancers, but not on hepatocellular carcinoma (HCC).
  • Although the antiapoptotic feature of COX-2 generally supports cancer cell growth, previous reports have shown that COX-2 expression, upregulated in early HCC, is downregulated in advanced HCC.
  • We examined the methylation status of the Cox-2 promoter in six human HCC cell lines (Hep3B, HepG2, SK-Hep1, HuH7, PLC, and FLC-7 cells) using methylation-specific PCR.
  • The promoter was remarkably hypermethylated in Hep3B and FLC-7 cells and moderately in HepG2 and SK-Hep1 cells, but not in HuH7 and PLC cells.
  • In Hep3B cells, coincubation with 5-aza-2'-deoxycytidine, a demethylator, demethylated the promoter and upregulated COX-2 expression as well as prostaglandin E2 production dose dependently.
  • On the other hand, no such effects were observed in HuH7 cells.
  • Additionally, the methylator suppressed growth of Hep3B cells dose dependently, accompanied by cyclin D1 downregulation, and the growth suppression was abrogated by potent COX-2 inhibition with a COX-2 selective inhibitor celecoxib, but these responses were not found in HuH7 cells.
  • These results indicated that cell growth was largely retarded by Cox-2 upregulation via promoter demethylation, rather than the potentially reactivated genes concurrently demethylated by 5-aza-2'-deoxycytidine.
  • In conclusion, promoter hypermethylation transcriptionally silences Cox-2 in HCC cells.
  • Epigenetic alteration of Cox-2, at least in part, modulates the growth of HCC cells.
  • [MeSH-major] Azacitidine / analogs & derivatives. Carcinoma, Hepatocellular / enzymology. Carcinoma, Hepatocellular / genetics. Gene Silencing. Isoenzymes / genetics. Liver Neoplasms / enzymology. Liver Neoplasms / genetics. Promoter Regions, Genetic. Prostaglandin-Endoperoxide Synthases / genetics
  • [MeSH-minor] Base Sequence. Cell Division / drug effects. Cell Line, Tumor. Cell Survival / drug effects. Cyclooxygenase 2. DNA Methylation. DNA, Neoplasm / chemistry. DNA, Neoplasm / genetics. DNA, Neoplasm / metabolism. Dinoprostone / biosynthesis. Humans. Membrane Proteins

  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • Hazardous Substances Data Bank. AZACITIDINE .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15156159.001).
  • [ISSN] 0023-6837
  • [Journal-full-title] Laboratory investigation; a journal of technical methods and pathology
  • [ISO-abbreviation] Lab. Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Isoenzymes; 0 / Membrane Proteins; 776B62CQ27 / decitabine; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases; K7Q1JQR04M / Dinoprostone; M801H13NRU / Azacitidine
  •  go-up   go-down


57. Metwally L, Hogg G, Coyle PV, Hay RJ, Hedderwick S, McCloskey B, O'Neill HJ, Ong GM, Thompson G, Webb CH, McMullan R: Rapid differentiation between fluconazole-sensitive and -resistant species of Candida directly from positive blood-culture bottles by real-time PCR. J Med Microbiol; 2007 Jul;56(Pt 7):964-70
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In view of both the delay in obtaining identification by conventional methods following blood-culture positivity in patients with candidaemia and the close relationship between species and fluconazole (FLC) susceptibility, early speciation of positive blood cultures has the potential to influence therapeutic decisions.
  • The aim was to develop a rapid test to differentiate FLC-resistant from FLC-sensitive Candida species.
  • Three TaqMan-based real-time PCR assays were developed to identify up to six Candida species directly from BacT/Alert blood-culture bottles that showed yeast cells on Gram staining at the time of initial positivity.
  • The first four of these (the characteristically FLC-sensitive group) were identified in a single reaction tube using one fluorescent TaqMan probe targeting 18S rRNA sequences conserved in the four species.
  • The FLC-resistant species C. krusei and C. glabrata were detected in two further reactions, each with species-specific probes.
  • The reported assay significantly reduces the time required to identify the presence of C. glabrata and C. krusei in comparison with a conventional phenotypic method, from approximately 72 to <3 h, and consequently allows optimization of the antifungal regimen at an earlier stage.
  • [MeSH-major] Antifungal Agents / pharmacology. Blood / microbiology. Candida / drug effects. Culture Media. Drug Resistance, Fungal. Fluconazole / pharmacology. Polymerase Chain Reaction / methods
  • [MeSH-minor] Candida albicans / classification. Candida albicans / drug effects. Candida albicans / genetics. DNA, Fungal / analysis. DNA, Fungal / isolation & purification. Fungemia / microbiology. Humans. Microbial Sensitivity Tests. Microbiological Techniques. Mycological Typing Techniques. Phenotype. Sensitivity and Specificity. Time Factors

  • MedlinePlus Health Information. consumer health - Blood.
  • Hazardous Substances Data Bank. FLUCONAZOLE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17577063.001).
  • [ISSN] 0022-2615
  • [Journal-full-title] Journal of medical microbiology
  • [ISO-abbreviation] J. Med. Microbiol.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Culture Media; 0 / DNA, Fungal; 8VZV102JFY / Fluconazole
  •  go-up   go-down


58. Ghannoum MA, Kuhn DM: Voriconazole -- better chances for patients with invasive mycoses. Eur J Med Res; 2002 May 31;7(5):242-56
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The past two decades have witnessed an increase in serious fungal infections, without corresponding growth in available antifungal agents.
  • Voriconazole has in vitro activity against yeasts and yeast-like fungi similar, or superior to, fluconazole (FLC), itraconazole (ITC) and amphotericin B (AMB).
  • The drug possesses potent fungicidal activity against moulds including Aspergillus, Scedosporium, and Fusarium.
  • [MeSH-major] Antifungal Agents / therapeutic use. Mycoses / drug therapy. Pyrimidines / therapeutic use. Triazoles / therapeutic use
  • [MeSH-minor] Candida / drug effects. Candida / metabolism. Candida / ultrastructure. Candidiasis / drug therapy. Drug Interactions. Drug Resistance, Fungal. Drug Tolerance. Humans. Safety. Voriconazole

  • MedlinePlus Health Information. consumer health - Fungal Infections.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12069915.001).
  • [ISSN] 0949-2321
  • [Journal-full-title] European journal of medical research
  • [ISO-abbreviation] Eur. J. Med. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Pyrimidines; 0 / Triazoles; JFU09I87TR / Voriconazole
  • [Number-of-references] 111
  •  go-up   go-down


59. Suzuki Inoue K, Inoue O, Ozaki Y: [Identification of the novel platelet activation receptor CLEC-2 and Its pathological and physiological roles]. Rinsho Byori; 2010 Dec;58(12):1193-202
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Podoplanin is expressed on the surface of tumor cells and facilitates tumor metastasis by inducing platelet aggregation.
  • We showed that an antibody that blocked the binding between CLEC-2 and podoplanin inhibited tumor metastasis using an experimental lung metastasis model in mice.
  • Podoplanin is also expressed in lymphatic endothelial cells, but the physiological role of the interaction between CLEC-2 and podoplanin in lymphatic endothelial cells has not been elucidated.
  • Moreover, through the transplantation of fetal liver cells from CLEC-2 +/+ or CLEC-2-/- embryos, we were able to demonstrate that CLEC-2 is involved in thrombus stabilization in vitro and in vivo, possibly through homophilic interactions without any apparent increase in the bleeding tendency.
  • These findings revealed that CLEC-2 plays a crucial role in not only tumor metastasis, but also in lymphangiogenesis and thrombus stabilization.
  • We propose that CLEC-2 could be an ideal novel target protein for an anti-platelet drug, which inhibits pathological thrombus formation but not physiological hemostasis, as well as a novel target protein for an anti-metastatic drug.
  • [MeSH-major] Lectins, C-Type / isolation & purification. Lectins, C-Type / physiology. Membrane Glycoproteins / isolation & purification. Membrane Glycoproteins / physiology. Platelet Activation
  • [MeSH-minor] Animals. Antineoplastic Agents. Drug Design. Humans. Ligands. Lymphangiogenesis. Mice. Molecular Targeted Therapy. Neoplasm Metastasis. Neovascularization, Physiologic. Platelet Aggregation. Platelet Aggregation Inhibitors. Thrombosis / etiology

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 21348239.001).
  • [ISSN] 0047-1860
  • [Journal-full-title] Rinsho byori. The Japanese journal of clinical pathology
  • [ISO-abbreviation] Rinsho Byori
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CLEC2B protein, human; 0 / Lectins, C-Type; 0 / Ligands; 0 / Membrane Glycoproteins; 0 / PDPN protein, human; 0 / Platelet Aggregation Inhibitors
  •  go-up   go-down


60. Monk BC, Niimi K, Lin S, Knight A, Kardos TB, Cannon RD, Parshot R, King A, Lun D, Harding DR: Surface-active fungicidal D-peptide inhibitors of the plasma membrane proton pump that block azole resistance. Antimicrob Agents Chemother; 2005 Jan;49(1):57-70
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The C-terminal motif concentrated the library members at the fungal cell surface.
  • Optimization of BM0 led to the construction of BM2 (D-NH(2)-RRRFWWFRRR-CONH(2)), which had broad-spectrum fungicidal activity against S. cerevisiae, Candida species, and Cryptococcus neoformans; bound strongly to the surfaces of fungal cells; inhibited the physiological activity of Pma1p; and appeared to target Pma1p, with 50% inhibitory concentrations in the range of 0.5 to 2.5 microM.
  • At sub-MICs (<5 microM), BM2 chemosensitized to fluconazole (FLC) S. cerevisiae strains functionally hyperexpressing fungal lanosterol 14alpha-demethylase and resistance-conferring transporters of azole drugs.
  • BM2 chemosensitized to FLC some FLC-resistant clinical isolates of C. albicans and C. dubliniensis and chemosensitized to itraconazole clinical isolates of C. krusei that are intrinsically resistant to FLC.
  • The growth-inhibitory concentrations of BM2 did not cause fungal cell permeabilization, significant hemolysis of red blood cells, or the death of cultured HEp-2 epithelial cells.
  • BM2 represents a novel class of broad-spectrum, surface-active, Pma1p-targeting fungicides which increases the potencies of azole drugs and circumvents azole resistance.

  • COS Scholar Universe. author profiles.
  • Faculty of 1000. commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine. (subscription/membership/fee required).
  • Saccharomyces Genome Database. Saccharomyces Genome Database .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Proc Natl Acad Sci U S A. 2000 Aug 1;97(16):8856-61 [10922046.001]
  • [Cites] Clin Microbiol Rev. 1998 Apr;11(2):382-402 [9564569.001]
  • [Cites] Trends Microbiol. 2000 Sep;8(9):402-10 [10989307.001]
  • [Cites] Biochim Biophys Acta. 1998 Jul 17;1372(2):261-71 [9675306.001]
  • [Cites] Antimicrob Agents Chemother. 1999 Jan;43(1):1-11 [9869556.001]
  • [Cites] Antimicrob Agents Chemother. 1999 May;43(5):1267-9 [10223949.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Mar 28;97(7):3254-9 [10716729.001]
  • [Cites] Antimicrob Agents Chemother. 2000 Dec;44(12):3306-9 [11083632.001]
  • [Cites] J Pept Res. 2000 Nov;56(5):318-25 [11095185.001]
  • [Cites] Peptides. 2001 Oct;22(10):1669-74 [11587795.001]
  • [Cites] Antimicrob Agents Chemother. 2001 Dec;45(12):3366-74 [11709310.001]
  • [Cites] J Am Chem Soc. 2002 Apr 3;124(13):3284-91 [11916412.001]
  • [Cites] Appl Environ Microbiol. 2002 May;68(5):2453-60 [11976121.001]
  • [Cites] Bioorg Med Chem Lett. 2002 Jun 3;12(11):1473-6 [12031322.001]
  • [Cites] J Pept Sci. 2002 Aug;8(8):431-7 [12212806.001]
  • [Cites] Science. 2002 Sep 6;297(5587):1692-6 [12169656.001]
  • [Cites] J Biol Chem. 2002 Nov 29;277(48):46809-21 [12244114.001]
  • [Cites] J Chromatogr B Analyt Technol Biomed Life Sci. 2002 Dec 25;782(1-2):245-52 [12458010.001]
  • [Cites] Pharmacol Rev. 2003 Mar;55(1):27-55 [12615953.001]
  • [Cites] Antimicrob Agents Chemother. 2003 Apr;47(4):1213-9 [12654649.001]
  • [Cites] J Biol Chem. 2003 Aug 1;278(31):28553-61 [12761219.001]
  • [Cites] Antimicrob Agents Chemother. 2004 Apr;48(4):1256-71 [15047528.001]
  • [Cites] Nature. 1986 Feb 20-26;319(6055):689-93 [3005867.001]
  • [Cites] FEBS Lett. 1987 Nov 16;224(1):193-7 [2960559.001]
  • [Cites] Eur J Biochem. 1989 Dec 22;186(3):501-7 [2532597.001]
  • [Cites] J Biol Chem. 1991 Sep 25;266(27):18097-103 [1833392.001]
  • [Cites] J Bacteriol. 1991 Nov;173(21):6826-36 [1834633.001]
  • [Cites] Nature. 1991 Nov 7;354(6348):84-6 [1719428.001]
  • [Cites] Biotechniques. 1992 Dec;13(6):901-5 [1476743.001]
  • [Cites] J Biol Chem. 1993 Jun 5;268(16):11792-7 [8505307.001]
  • [Cites] J Bacteriol. 1993 Sep;175(17):5566-74 [8366041.001]
  • [Cites] Crit Rev Microbiol. 1994;20(3):209-23 [7802957.001]
  • [Cites] Biochim Biophys Acta. 1995 Oct 4;1239(1):81-90 [7548148.001]
  • [Cites] Methods Enzymol. 1996;267:220-34 [8743319.001]
  • [Cites] Antimicrob Agents Chemother. 1996 Nov;40(11):2443-6 [8913443.001]
  • [Cites] Biochim Biophys Acta. 1996 Oct 23;1284(2):181-90 [8914582.001]
  • [Cites] Antimicrob Agents Chemother. 1996 Dec;40(12):2835-41 [9124851.001]
  • [Cites] Biochim Biophys Acta. 1997 Jun 12;1326(2):249-56 [9218555.001]
  • [Cites] Biochem J. 1997 Aug 15;326 ( Pt 1):39-45 [9337848.001]
  • [Cites] Trends Biotechnol. 1998 Feb;16(2):82-8 [9487736.001]
  • [Cites] Annu Rev Biophys Biomol Struct. 2000;29:291-325 [10940251.001]
  • (PMID = 15616276.001).
  • [ISSN] 0066-4804
  • [Journal-full-title] Antimicrobial agents and chemotherapy
  • [ISO-abbreviation] Antimicrob. Agents Chemother.
  • [Language] ENG
  • [Grant] United States / NIDCR NIH HHS / DE / R21DE15075
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Azoles; 0 / Oligopeptides; 0 / Peptide Library; 0 / Saccharomyces cerevisiae Proteins; 0 / arginyl-arginyl-arginyl-phenylalanyl-tryptophyl-tryptophyl-phenylalanyl-arginyl-aginyl-argininamide; EC 3.6.1.- / PMA1 protein, S cerevisiae; EC 3.6.3.14 / Proton-Translocating ATPases
  • [Other-IDs] NLM/ PMC538910
  •  go-up   go-down


61. Gerdolle DA, Mortier E, Droz D: Microleakage and polymerization shrinkage of various polymer restorative materials. J Dent Child (Chic); 2008 May-Aug;75(2):125-33
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The cavities were restored with 4 different materials: a packable resin composite (Filtek P60), a compomer (Compoglass F), an ormocer (Admira) and their associated bonding agents (Scotchbond 1, Excite, and Admira Bond, respectively), and a resin-modified glass ionomer (Fuji II LC).
  • Dye penetration was evaluated for all materials, which were analyzed using a multivariate model (alpha=0.05): influence of microleakage score, margin location (enamel/cementum), and preparation location (buccal/lingual).
  • RESULTS: Regarding polymerization shrinkage, the P60 demonstrated the lowest value, followed by ADM and COF, whereas FLC presented the highest shrinkage-strain (P<.0001).
  • The preparation location had no significant effect on dye penetration (P=.86).
  • [MeSH-minor] Ceramics / chemistry. Coloring Agents. Compomers / chemistry. Composite Resins / chemistry. Dental Cavity Preparation / classification. Dental Cementum / pathology. Dental Enamel / pathology. Dental Marginal Adaptation. Dental Restoration, Permanent / classification. Dentin-Bonding Agents / chemistry. Glass Ionomer Cements / chemistry. Humans. Materials Testing. Methacrylates / chemistry. Methylene Blue. Organically Modified Ceramics. Polymers / chemistry. Resin Cements / chemistry. Silanes / chemistry. Siloxanes / chemistry. Surface Properties. Time Factors. Tooth Cervix / pathology

  • Hazardous Substances Data Bank. METHYLENE BLUE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18647507.001).
  • [ISSN] 1935-5068
  • [Journal-full-title] Journal of dentistry for children (Chicago, Ill.)
  • [ISO-abbreviation] J Dent Child (Chic)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Coloring Agents; 0 / Compoglass; 0 / Compomers; 0 / Composite Resins; 0 / Dental Materials; 0 / Dentin-Bonding Agents; 0 / Excite cement; 0 / Filtek P60 Composite Resin; 0 / Fuji II LC cement; 0 / Glass Ionomer Cements; 0 / Methacrylates; 0 / Organically Modified Ceramics; 0 / Polymers; 0 / Resin Cements; 0 / Resins, Synthetic; 0 / Silanes; 0 / Siloxanes; 0 / admira; 0 / admira bond; 90881-69-9 / Scotchbond; T42P99266K / Methylene Blue
  •  go-up   go-down


62. Whiteman M, Spencer JP, Szeto HH, Armstrong JS: Do mitochondriotropic antioxidants prevent chlorinative stress-induced mitochondrial and cellular injury? Antioxid Redox Signal; 2008 Mar;10(3):641-50
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Since mitochondria are key mediators of apoptosis and necrosis, we hypothesized that mitochondriotropic antioxidants could limit HOCl-mediated intracellular oxidative injury to human fetal liver cells, preserve mitochondrial function, and prevent cell death.
  • In this current study, we show that recently developed mitochondria-targeted antioxidants (MitoQ and SS31) significantly protected against HOCl-induced mitochondrial damage and cell death at concentrations >or=25 nM.
  • Our study highlights the potential application of mitochondria-specific targeted antioxidants for the prevention of cellular dysfunction and cell death under conditions of chlorinative stress, as occurs during chronic inflammation.
  • [MeSH-major] Antioxidants / pharmacology. Hypochlorous Acid / toxicity. Mitochondria / drug effects
  • [MeSH-minor] Humans. Membrane Potentials / drug effects. Superoxides / metabolism

  • MedlinePlus Health Information. consumer health - Antioxidants.
  • COS Scholar Universe. author profiles.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18052717.001).
  • [ISSN] 1523-0864
  • [Journal-full-title] Antioxidants & redox signaling
  • [ISO-abbreviation] Antioxid. Redox Signal.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antioxidants; 11062-77-4 / Superoxides; 712K4CDC10 / Hypochlorous Acid
  •  go-up   go-down


63. Zhang J, Lodish HF: Identification of K-ras as the major regulator for cytokine-dependent Akt activation in erythroid progenitors in vivo. Proc Natl Acad Sci U S A; 2005 Oct 11;102(41):14605-10
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Despite intensive investigation, controversial results have been obtained concerning the precise signaling pathway(s) regulated by K-ras in different cell types.
  • We show that in primary fetal liver erythroid progenitors, erythropoietin activates all three Ras isoforms, but preferentially N- and K-ras.
  • In K-ras(-/-) fetal liver cells (FLC), erythropoietin- or stem cell factor-dependent Akt activation is greatly reduced, whereas other pathways including Stat5 and p44/p42 MAP kinase are activated normally.
  • We find that freshly isolated K-ras(-/-) FLC show an approximately 7-fold increase of apoptosis and delayed erythroid differentiation, but only at the stage of erythroid progenitors and very early erythroblasts.
  • Furthermore, we show that partial pharmacologic inhibition of the phosphatidylinositol 3-kinase/Akt pathway in wild-type erythroid progenitors leads to a delay in erythroid differentiation similar to that observed in K-ras(-/-) FLC.

  • COS Scholar Universe. author profiles.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cell. 1995 Oct 6;83(1):59-67 [7553874.001]
  • [Cites] Mol Cell Biol. 2000 Apr;20(7):2475-87 [10713171.001]
  • [Cites] EMBO J. 1996 Dec 2;15(23):6541-51 [8978681.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Mar 4;94(5):1806-10 [9050860.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Apr 1;94(7):3016-21 [9096338.001]
  • [Cites] Curr Biol. 1997 Apr 1;7(4):261-9 [9094314.001]
  • [Cites] Eur J Biochem. 1997 Jun 15;246(3):633-7 [9219519.001]
  • [Cites] Science. 1997 Jul 25;277(5325):567-70 [9228007.001]
  • [Cites] Oncogene. 1997 Sep 4;15(10):1151-9 [9294608.001]
  • [Cites] Hematol Oncol Clin North Am. 2000 Jun;14(3):517-35 [10909038.001]
  • [Cites] J Biol Chem. 2000 Aug 4;275(31):23559-68 [10801808.001]
  • [Cites] Mol Cell. 2000 Oct;6(4):909-19 [11090628.001]
  • [Cites] Mol Cell Biol. 2001 Mar;21(5):1444-52 [11238881.001]
  • [Cites] EMBO J. 2001 Oct 15;20(20):5666-77 [11598010.001]
  • [Cites] J Biol Chem. 2002 Jan 4;277(1):272-8 [11689566.001]
  • [Cites] EMBO J. 2002 Mar 1;21(5):1021-30 [11867530.001]
  • [Cites] Nat Cell Biol. 2002 May;4(5):343-50 [11988737.001]
  • [Cites] Cancer Cell. 2003 Aug;4(2):111-20 [12957286.001]
  • [Cites] Blood. 2003 Dec 1;102(12):3938-46 [12907435.001]
  • [Cites] Mol Cell Biol. 2003 Dec;23(24):9245-50 [14645534.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Jan 13;101(2):597-602 [14699048.001]
  • [Cites] J Clin Invest. 2004 Feb;113(4):528-38 [14966562.001]
  • [Cites] Cancer Cell. 2004 Apr;5(4):375-87 [15093544.001]
  • [Cites] Annu Rev Biochem. 1987;56:779-827 [3304147.001]
  • [Cites] EMBO J. 1988 Apr;7(4):1003-11 [2456920.001]
  • [Cites] Genes Dev. 1989 Jun;3(6):816-26 [2473008.001]
  • [Cites] Nucleic Acids Res. 1991 Aug 11;19(15):4293 [1870982.001]
  • [Cites] J Biol Chem. 1993 May 5;268(13):9157-60 [8486615.001]
  • [Cites] Blood. 1993 Jun 15;81(12):3204-10 [7685197.001]
  • [Cites] J Biol Chem. 1994 Nov 25;269(47):29962-9 [7961995.001]
  • [Cites] Mol Cell Biol. 1995 Feb;15(2):593-600 [7529871.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Feb 28;92(5):1709-13 [7878045.001]
  • [Cites] Genes Dev. 1997 Oct 1;11(19):2468-81 [9334313.001]
  • [Cites] J Biol Chem. 1997 Oct 17;272(42):26173-8 [9334184.001]
  • [Cites] Science. 1998 Jan 30;279(5351):710-4 [9445477.001]
  • [Cites] Oncogene. 1998 Mar;16(11):1417-28 [9525741.001]
  • [Cites] J Biol Chem. 1998 Sep 11;273(37):24052-6 [9727023.001]
  • [Cites] Blood. 1999 Jun 1;93(11):3893-9 [10339498.001]
  • [Cites] Cell. 1999 Jul 9;98(1):69-80 [10412982.001]
  • [Cites] Science. 2005 Feb 18;307(5712):1098-101 [15718470.001]
  • [Cites] Blood. 2005 May 1;105(9):3538-41 [15644420.001]
  • [Cites] J Biol Chem. 1995 Oct 6;270(40):23402-8 [7559499.001]
  • (PMID = 16203968.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / P01 HL032262; United States / NHLBI NIH HHS / HL / P01 HL 32262
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chromones; 0 / Cytokines; 0 / Morpholines; 154447-36-6 / 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.6.5.2 / ras Proteins
  • [Other-IDs] NLM/ PMC1253609
  •  go-up   go-down


64. Zhang S, Yang C, Peng J, Sun S, Wang X: GASA5, a regulator of flowering time and stem growth in Arabidopsis thaliana. Plant Mol Biol; 2009 Apr;69(6):745-59
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Phenotypic analysis showed that a GASA5 null mutant (gasa5-1) flowered earlier than wild type with a faster stem growth rate under both long-day (LD) and short-day (SD) photoperiods.
  • In contrast, transgenic plants overexpressing GASA5 demonstrated delayed flowering, with a slower stem growth rate compared to wild-type plants.
  • Further transcript profiling analysis suggested that GASA5 delayed flowering by enhancing FLOWERING LOCUS C (FLC) expression and repressing the expression of key flowering-time genes, FLOWERING LOCUS T (FT) and LEAFY (LFY).
  • [MeSH-major] Arabidopsis / genetics. Arabidopsis Proteins / genetics. Flowers / genetics. Plant Stems / genetics
  • [MeSH-minor] Gene Expression Profiling. Gene Expression Regulation, Developmental / drug effects. Gene Expression Regulation, Plant / drug effects. Gibberellins / pharmacology. Glucuronidase / genetics. Glucuronidase / metabolism. Green Fluorescent Proteins / genetics. Green Fluorescent Proteins / metabolism. Mutation. Plant Growth Regulators / pharmacology. Plants, Genetically Modified. Recombinant Fusion Proteins / genetics. Recombinant Fusion Proteins / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Time Factors

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • The Arabidopsis Information Resource. Linked Gene Data (subscription/membership/fee required).
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Plant Physiol. 2006 Oct;142(2):509-25 [16920880.001]
  • [Cites] Plant Physiol. 2001 Jul;126(3):1085-91 [11457959.001]
  • [Cites] Curr Opin Plant Biol. 2007 Oct;10(5):461-5 [17900970.001]
  • [Cites] Plant Cell. 2008 Sep;20(9):2447-59 [18827182.001]
  • [Cites] Genetics. 2001 Oct;159(2):777-85 [11606552.001]
  • [Cites] Plant J. 2006 Dec;48(5):796-805 [17076804.001]
  • [Cites] Plant J. 2002 Dec;32(6):935-47 [12492836.001]
  • [Cites] Plant Cell. 2002 Dec;14(12):3191-200 [12468736.001]
  • [Cites] J Exp Bot. 2006;57(10):2401-11 [16804055.001]
  • [Cites] Plant J. 2004 Jan;37(2):229-38 [14690507.001]
  • [Cites] Plant Cell. 1999 Jun;11(6):1093-104 [10368180.001]
  • [Cites] Nature. 2000 Apr 20;404(6780):889-92 [10786797.001]
  • [Cites] Plant Mol Biol. 1996 Dec;32(6):1067-74 [9002605.001]
  • [Cites] Plant Cell. 2001 Feb;13(2):303-18 [11226187.001]
  • [Cites] Plant J. 1998 Dec;16(6):735-43 [10069079.001]
  • [Cites] Plant J. 2005 Oct;44(1):88-99 [16167898.001]
  • [Cites] Mol Gen Genet. 1991 Sep;229(1):57-66 [1896021.001]
  • [Cites] Plant Physiol. 2002 Mar;128(3):951-61 [11891250.001]
  • [Cites] Plant Cell. 2002 May;14 (5):969-77 [12034890.001]
  • [Cites] Plant Cell. 2002;14 Suppl:S111-30 [12045273.001]
  • [Cites] Plant Mol Biol. 1995 Feb;27(4):743-52 [7727751.001]
  • [Cites] Plant Cell. 1998 Feb;10(2):155-69 [9490740.001]
  • [Cites] Genes Dev. 2000 Sep 15;14(18):2366-76 [10995392.001]
  • [Cites] Plant Cell. 2007 Oct;19(10):3037-57 [17933900.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Apr 13;96(8):4698-703 [10200325.001]
  • [Cites] Plant Cell. 1998 May;10(5):791-800 [9596637.001]
  • [Cites] Genes Genet Syst. 2006 Jun;81(3):171-80 [16905871.001]
  • [Cites] Plant Cell. 2001 Jul;13(7):1555-66 [11449051.001]
  • [Cites] Plant J. 1992 Mar;2(2):153-9 [1302047.001]
  • [Cites] Plant Physiol. 2001 Dec;127(4):1682-93 [11743113.001]
  • [Cites] Plant Cell. 2008 Sep;20(9):2437-46 [18827181.001]
  • [Cites] Plant Cell. 1993 Aug;5(8):887-96 [8400871.001]
  • [Cites] Plant Physiol. 2000 Sep;124(1):31-8 [10982419.001]
  • [Cites] Cell. 1995 Mar 24;80(6):847-57 [7697715.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Aug 24;101(34):12759-64 [15310842.001]
  • [Cites] Plant Cell. 1999 May;11(5):949-56 [10330478.001]
  • [Cites] Plant Cell. 2007 Apr;19(4):1192-208 [17449805.001]
  • [Cites] Plant Physiol. 2004 Jun;135(2):1008-19 [15173565.001]
  • [Cites] Genes Dev. 2006 Apr 1;20(7):898-912 [16600915.001]
  • [Cites] Plant Mol Biol. 2001 Sep;47(1-2):197-206 [11554472.001]
  • [Cites] Int J Dev Biol. 2005;49(5-6):585-93 [16096967.001]
  • [Cites] Science. 2000 Jun 2;288(5471):1613-6 [10834834.001]
  • [Cites] Plant Mol Biol. 1985 Mar;5(2):69-76 [24306565.001]
  • [Cites] Trends Plant Sci. 2003 Oct;8(10):492-7 [14557046.001]
  • [Cites] Science. 1999 Dec 3;286(5446):1960-2 [10583960.001]
  • [Cites] Plant Cell. 2006 Sep;18(9):2172-81 [16920780.001]
  • [Cites] Development. 2004 Mar;131(5):1055-64 [14973286.001]
  • [Cites] Plant J. 2007 Jul;51(2):262-80 [17565583.001]
  • [Cites] Plant Mol Biol. 1998 Apr;36(6):871-83 [9520278.001]
  • [Cites] Science. 1999 Dec 3;286(5446):1962-5 [10583961.001]
  • [Cites] Plant Cell. 2004;16 Suppl:S18-31 [15037730.001]
  • [Cites] Genetics. 2001 Oct;159(2):767-76 [11606551.001]
  • [Cites] Plant Mol Biol. 2003 Sep;53(1-2):247-59 [14756321.001]
  • [Cites] Science. 2003 Mar 21;299(5614):1853-4 [12649470.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 May 18;101(20):7827-32 [15128937.001]
  • [Cites] Development. 1997 Oct;124(19):3835-44 [9367439.001]
  • [Cites] Nature. 2005 Sep 29;437(7059):693-8 [16193045.001]
  • [Cites] Plant Cell. 2004 Mar;16(3):731-40 [14973162.001]
  • [Cites] Genetics. 1997 Jul;146(3):1087-99 [9215910.001]
  • [Cites] Plant Cell Physiol. 2007 Mar;48(3):471-83 [17284469.001]
  • [Cites] Plant Cell. 2006 Feb;18(2):278-82 [16452510.001]
  • [Cites] Plant Physiol. 2004 Jun;135(2):668-76 [15208413.001]
  • [Cites] Plant Physiol. 1997 Aug;114(4):1471-6 [9276956.001]
  • [Cites] Genes Dev. 1997 Dec 1;11(23):3194-205 [9389651.001]
  • [Cites] Mol Plant Microbe Interact. 1999 Jan;12(1):16-23 [9885189.001]
  • (PMID = 19190987.001).
  • [ISSN] 0167-4412
  • [Journal-full-title] Plant molecular biology
  • [ISO-abbreviation] Plant Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Arabidopsis Proteins; 0 / GASA5 protein, Arabidopsis; 0 / Gibberellins; 0 / Plant Growth Regulators; 0 / Recombinant Fusion Proteins; 147336-22-9 / Green Fluorescent Proteins; EC 3.2.1.31 / Glucuronidase
  •  go-up   go-down


65. Jin J, Guo N, Zhang J, Ding Y, Tang X, Liang J, Li L, Deng X, Yu L: The synergy of honokiol and fluconazole against clinical isolates of azole-resistant Candida albicans. Lett Appl Microbiol; 2010 Sep;51(3):351-7
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • AIMS: To evaluate the interaction of fluconazole (FLC) and honokiol (HNK) in vitro and vivo against azole-resistant (azole-R) clinical isolates of Candida albicans.
  • METHODS AND RESULTS: A checkerboard microdilution method was used to study the in vitro interaction of FLC and HNK in 24 azole-R clinical isolates of C. albicans.
  • In vivo antifungal activity was performed to further analyse the interaction between FLC and HNK.
  • In the in vitro study, synergism was observed in all 24 FLC-resistant strains tested as determined by fractional inhibitory concentration index (FICI), and in 22 strains by Delta E models.
  • These positive interactions were also confirmed by using the time-killing test for the selected strain C. albicans YL371, which shows strong susceptible to the combination of HNK and FLC.
  • In the in vivo study, the mice with candidiasis were treated successfully by a combination therapy of HNK with FLC, the results showed a decrease of the colony forming unit in infected and treated animals compared to the controls, at the conditions of the treatment used in this study.
  • CONCLUSIONS: Synergistic activity of HNK and FLC against clinical isolates of FLC-resistant C. albicans was observed in vitro and in vivo.
  • SIGNIFICANCE AND IMPACT OF THE STUDY: This report might provide a potential therapeutic method to overcome the problem of drug-resistance in C. albicans.
  • [MeSH-major] Antifungal Agents / pharmacology. Biphenyl Compounds / pharmacology. Candida albicans / drug effects. Drug Resistance, Fungal. Fluconazole / pharmacology. Lignans / pharmacology
  • [MeSH-minor] Animals. Candidiasis / drug therapy. Candidiasis / microbiology. Colony Count, Microbial. Drug Synergism. Humans. Mice. Microbial Sensitivity Tests. Microbial Viability / drug effects. Treatment Outcome

  • Hazardous Substances Data Bank. FLUCONAZOLE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20681969.001).
  • [ISSN] 1472-765X
  • [Journal-full-title] Letters in applied microbiology
  • [ISO-abbreviation] Lett. Appl. Microbiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Biphenyl Compounds; 0 / Lignans; 11513CCO0N / honokiol; 8VZV102JFY / Fluconazole
  •  go-up   go-down


66. Kurt IH, Yavuzer K, Batur MK: Short-term effect of levosimendan on free light chain kappa and lambda levels in patients with decompensated chronic heart failure. Heart Vessels; 2010 Sep;25(5):392-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • To investigate the effects of levosimendan, a positive inotropic agent, on the new heart failure markers immunoglobulin free light chains kappa and lambda (FLC-kappa and FLC-lambda) in decompensated chronic heart failure (HF), 59 patients with New York Heart Association (NYHA) class III-IV HF were enrolled.
  • Serum FLC-kappa and FLC-lambda, brain natriuretic peptide (BNP), and ejection fraction (EF) were measured before treatment and on the 5th day of treatment initiation.
  • FLC-kappa (P < 0.05) and FLC-lambda (P < 0.05) were significantly decreased in the levosimendan group compared to baseline, but no difference in either marker in the standard treatment group was observed.
  • Pre- and post-treatment FLC-kappa/FLC-lambda ratios in both groups were similar, whereas FLC-kappa and FLC-lambda levels and the FLC-kappa/FLC-lambda ratio showed no significant correlation with NYHA class, brain natriuretic peptide (BNP) and ejection fraction (EF) levels; and BNP and EF changes after the treatment.
  • In conclusion, levosimendan caused short-term hemodynamic and symptomatic improvements, with a more pronounced decrease in FLC levels in patients with advanced decompensated HF.
  • [MeSH-major] Cardiotonic Agents / therapeutic use. Heart Failure / drug therapy. Hydrazones / therapeutic use. Immunoglobulin kappa-Chains / blood. Immunoglobulin lambda-Chains / blood. Pyridazines / therapeutic use
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biomarkers / blood. Chronic Disease. Down-Regulation. Female. Humans. Male. Middle Aged. Natriuretic Peptide, Brain / blood. Severity of Illness Index. Stroke Volume / drug effects. Time Factors. Treatment Outcome. Turkey

  • MedlinePlus Health Information. consumer health - Heart Failure.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Eur J Heart Fail. 2005 Aug;7(5):882-7 [15921958.001]
  • [Cites] Am J Cardiol. 1983 Nov 1;52(8):1072-8 [6356861.001]
  • [Cites] J Clin Invest. 1993 Jun;91(6):2727-33 [8390488.001]
  • [Cites] Clin Cardiol. 1999 Dec;22(12):811-3 [10626084.001]
  • [Cites] Leukemia. 2009 Feb;23(2):215-24 [19020545.001]
  • [Cites] Circulation. 1994 Oct;90(4):2051-5 [7923693.001]
  • [Cites] J Exp Med. 2002 Feb 4;195(3):375-81 [11828013.001]
  • [Cites] Am J Cardiol. 2005 Aug 1;96(3):423-6 [16054474.001]
  • [Cites] Circulation. 2003 Mar 25;107(11):1486-91 [12654604.001]
  • [Cites] N Engl J Med. 1990 Jul 26;323(4):236-41 [2195340.001]
  • [Cites] J Clin Chem Clin Biochem. 1989 Aug;27(8):519-23 [2509630.001]
  • [Cites] Circulation. 1997 Sep 2;96(5):1501-6 [9315538.001]
  • [Cites] J Am Soc Echocardiogr. 2005 Dec;18(12 ):1440-63 [16376782.001]
  • [Cites] J Pharmacol Exp Ther. 2007 Oct;323(1):31-8 [17620456.001]
  • [Cites] Heart Vessels. 2009 Jan;24(1):16-21 [19165563.001]
  • [Cites] Am J Cardiol. 2008 Jan 15;101(2):231-7 [18178412.001]
  • [Cites] Circulation. 2002 Sep 24;106(12 Suppl 1):I284-9 [12354747.001]
  • [Cites] Lancet. 2002 Jul 20;360(9328):196-202 [12133653.001]
  • [Cites] J Mol Cell Cardiol. 1985 Jun;17(6):603-17 [2991541.001]
  • [Cites] J Am Coll Cardiol. 1999 Apr;33(5):1400-7 [10193745.001]
  • [Cites] Eur J Heart Fail. 2001 Aug;3(4):415-21 [11511426.001]
  • [Cites] Eur J Heart Fail. 2005 Dec;7(7):1156-63 [16084762.001]
  • [Cites] Eur Heart J. 2006 Aug;27(16):1908-20 [16682381.001]
  • [Cites] Curr Med Chem Cardiovasc Hematol Agents. 2005 Jul;3(3):243-7 [15974888.001]
  • [Cites] Am J Physiol Renal Physiol. 2006 Jun;290(6):F1453-62 [16418300.001]
  • [Cites] J Cardiovasc Pharmacol. 1995;26 Suppl 1:S10-9 [8907127.001]
  • [Cites] JAMA. 2007 May 2;297(17):1883-91 [17473298.001]
  • [Cites] Am J Clin Pathol. 2003 Feb;119(2):274-8 [12579999.001]
  • [Cites] Am J Cardiol. 2006 Jul 1;98(1):102-6 [16784930.001]
  • [Cites] Atherosclerosis. 2007 Dec;195(2):e210-5 [17707851.001]
  • [Cites] Eur J Pharmacol. 2006 Mar 8;533(1-3):319-26 [16455071.001]
  • [Cites] Int J Cardiol. 2010 Feb 18;139(1):75-9 [18973957.001]
  • [Cites] J Autoimmun. 1990 Apr;3(2):187-200 [2187452.001]
  • [Cites] Jpn Circ J. 1987 Jun;51(6):665-75 [3669276.001]
  • [Cites] Cardiovasc Drugs Ther. 2003 Mar;17(2):111-3 [14562823.001]
  • [Cites] Heart Vessels. 2009 Jan;24(1):22-6 [19165564.001]
  • [Cites] Circulation. 2000 Feb 1;101(4):385-91 [10653829.001]
  • (PMID = 20676961.001).
  • [ISSN] 1615-2573
  • [Journal-full-title] Heart and vessels
  • [ISO-abbreviation] Heart Vessels
  • [Language] eng
  • [Publication-type] Journal Article; Randomized Controlled Trial
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Cardiotonic Agents; 0 / Hydrazones; 0 / Immunoglobulin kappa-Chains; 0 / Immunoglobulin lambda-Chains; 0 / Pyridazines; 114471-18-0 / Natriuretic Peptide, Brain; 349552KRHK / simendan
  •  go-up   go-down


67. Goncharova R, Zabrejko S, Dalivelya O, Kuzhir T: Anticlastogenicity of two derivatives of 1,4-dihydroisonicotinic acid in mouse micronucleus test. Mutat Res; 2001 Sep 20;496(1-2):129-35
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Effects of two derivatives of 1,4-dihydroisonicotinic acid (1,4-DHINA) against the monofunctional alkylating agent ethyl methanesulfonate (EMS) were studied in the micronucleus test in (CBA x C57Bl/6(j)) mice.
  • The frequencies of micronucleated (MN) polychromatic erythrocytes (PCEs) in mouse bone marrow and foetal liver were analysed 6, 12, 18, 24, 30, 36, 48 or 24, 48 and 72 h after the mutagen injection.
  • Simultaneously with maternal bone marrow, foetal liver cells were analysed for MNs in the transplacental test.
  • Results presented indicate a peak of EMS-induced micronucleated cells in mouse bone marrow 24 or 36 h and in foetal liver 24h after animal treatment.
  • [MeSH-major] Antimutagenic Agents / pharmacology. DNA Damage / drug effects. Isonicotinic Acids / pharmacology. Micronucleus Tests
  • [MeSH-minor] Animals. Bone Marrow Cells / cytology. Bone Marrow Cells / drug effects. Dose-Response Relationship, Drug. Embryonic and Fetal Development / drug effects. Erythrocytes / cytology. Erythrocytes / drug effects. Ethyl Methanesulfonate / toxicity. Female. Liver / cytology. Liver / drug effects. Liver / embryology. Male. Maternal Exposure / adverse effects. Maternal-Fetal Exchange. Mice. Mice, Inbred C57BL. Mice, Inbred CBA. Mutagens / toxicity. Pregnancy

  • Hazardous Substances Data Bank. ETHYL METHANESULFONATE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11551488.001).
  • [ISSN] 0027-5107
  • [Journal-full-title] Mutation research
  • [ISO-abbreviation] Mutat. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antimutagenic Agents; 0 / Isonicotinic Acids; 0 / Mutagens; 9H154DI0UP / Ethyl Methanesulfonate
  •  go-up   go-down


68. Terrier B, Sène D, Saadoun D, Ghillani-Dalbin P, Thibault V, Delluc A, Piette JC, Cacoub P: Serum-free light chain assessment in hepatitis C virus-related lymphoproliferative disorders. Ann Rheum Dis; 2009 Jan;68(1):89-93
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVE: To evaluate the relevance of serum-free light chain (FLC) assessment in hepatitis C virus (HCV)-related lymphoproliferative disorders, including mixed cryoglobulinemia (MC) and B cell non-Hodgkin lymphoma (B-NHL).
  • Clinical and biological data were recorded at the time of the initial evaluation and at the end of follow-up.
  • Serum FLC quantitation was carried out using a serum FLC assay.
  • RESULTS: The mean (SD) serum kappa FLC level was higher in patients with asymptomatic MC (27.9 (8.6) mg/litre), MC vasculitis (36.7 (46.2) mg/litre) and B-NHL (51.3 (78.3) mg/litre) than without MC (21.7 (17.6) mg/litre) (p = 0.047, 0.025 and 0.045, respectively).
  • The mean serum FLC ratio was higher in patients with MC vasculitis (2.08 (2.33)) and B-NHL (3.14 (3.49)) than in patients without MC (1.03 (0.26)) (p = 0.008).
  • The rate of abnormal serum FLC ratio (>1.65) correlated with the severity of HCV-related B cell disorder: 0/17 (0%) without MC, 0/7 (0%) asymptomatic MC, 6/26 (23%) MC vasculitis without B-NHL and 4/9 (44%) B-NHL (p = 0.002).
  • Serum kappa FLC levels and the serum FLC ratio correlated with the cryoglobulin level (r = 0.32, p<0.001 and r = 0.25, p = 0.002, respectively) and the severity of the B cell disorder (r = 0.26, p = 0.045 and r = 0.41, p = 0.001, respectively).
  • Among patients with an abnormal serum FLC ratio at baseline, the FLC ratio correlated with the virological response to HCV treatment.
  • CONCLUSIONS: In patients infected with HCV, an abnormal serum FLC ratio appears to be a very interesting marker, as it is consistently associated with the presence of MC vasculitis and/or B-NHL.
  • After antiviral therapy, the serum FLC ratio could be used as a surrogate marker of the control of the HCV-related lymphoproliferation.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antiviral Agents / therapeutic use. Biomarkers / blood. Cryoglobulinemia / drug therapy. Cryoglobulinemia / immunology. Cryoglobulinemia / virology. Female. Humans. Lymphoma, B-Cell / drug therapy. Lymphoma, B-Cell / immunology. Lymphoma, B-Cell / virology. Male. Middle Aged. Prospective Studies. Treatment Outcome

  • Genetic Alliance. consumer health - Hepatitis.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18375535.001).
  • [ISSN] 1468-2060
  • [Journal-full-title] Annals of the rheumatic diseases
  • [ISO-abbreviation] Ann. Rheum. Dis.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antiviral Agents; 0 / Biomarkers; 0 / Immunoglobulin Light Chains
  •  go-up   go-down


69. Angiolella L, Stringaro AR, De Bernardis F, Posteraro B, Bonito M, Toccacieli L, Torosantucci A, Colone M, Sanguinetti M, Cassone A, Palamara AT: Increase of virulence and its phenotypic traits in drug-resistant strains of Candida albicans. Antimicrob Agents Chemother; 2008 Mar;52(3):927-36
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Increase of virulence and its phenotypic traits in drug-resistant strains of Candida albicans.
  • There is concern about the rise of antifungal drug resistance, but little is known about comparative biological properties and pathogenicity of drug-resistant strains.
  • We generated fluconazole (FLC; CO23 RFLC)- or micafungin (FK; CO23 RFK)-resistant strains of Candida albicans by treating a FLC- and FK-susceptible strain of this fungus (CO23 S) with stepwise-increasing concentrations of either drug.
  • Molecular analyses showed that CO23 RFLC had acquired markedly increased expression of the drug-resistance efflux pump encoded by the MDR1 gene, whereas CO23 RFK had a homozygous mutation in the FSK1 gene.
  • These genetic modifications did not alter to any extent the growth capacity of the drug-resistant strains in vitro, either at 28 degrees C or at 37 degrees C, but markedly increased their experimental pathogenicity in a systemic mouse infection model, as assessed by the overall mortality and target organ invasion.
  • The increased pathogenicity of drug-resistant strains for systemic infection was associated with a number of biochemical and physiological changes, including (i) marked cellular alterations associated with a different expression and content of major cell wall polysaccharides, (ii) more rapid and extensive hypha formation in both liquid and solid media, and (iii) increased adherence to plastic and a propensity for biofilm formation.
  • Overall, our data demonstrate that experimentally induced resistance to antifungal drugs, irrespective of drug family, can substantially divert C. albicans biology, affecting in particular biological properties of potential relevance for deep-seated candidiasis.
  • [MeSH-major] Antifungal Agents / pharmacology. Candida albicans / drug effects. Candida albicans / pathogenicity. Candidiasis / microbiology. Drug Resistance, Fungal. Host-Pathogen Interactions
  • [MeSH-minor] Animals. Biofilms / growth & development. Candidiasis, Vulvovaginal / microbiology. Cell Adhesion. Echinocandins / pharmacology. Female. Fluconazole / pharmacology. Fungal Proteins / genetics. Fungal Proteins / metabolism. Humans. Lipopeptides. Lipoproteins / pharmacology. Male. Mice. Mice, Inbred BALB C. Microscopy, Electron, Scanning. Phenotype. Rats. Rats, Wistar. Virulence


70. Sionov E, Lee H, Chang YC, Kwon-Chung KJ: Cryptococcus neoformans overcomes stress of azole drugs by formation of disomy in specific multiple chromosomes. PLoS Pathog; 2010 Apr 01;6(4):e1000848
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cryptococcus neoformans overcomes stress of azole drugs by formation of disomy in specific multiple chromosomes.
  • Fluconazole (FLC), a triazole, is widely used for the maintenance therapy of cryptococcosis.
  • Heteroresistance to FLC, an adaptive mode of azole resistance, was associated with FLC therapy failure cases but the mechanism underlying the resistance was unknown.
  • We used comparative genome hybridization and quantitative real-time PCR in order to show that C. neoformans adapts to high concentrations of FLC by duplication of multiple chromosomes.
  • Formation of disomic chromosomes in response to FLC stress was observed in both serotype A and D strains.
  • Strains that adapted to FLC concentrations higher than their minimal inhibitory concentration (MIC) contained disomies of chromosome 1 and stepwise exposure to even higher drug concentrations induced additional duplications of several other specific chromosomes.
  • The number of disomic chromosomes in each resistant strain directly correlated with the concentration of FLC tolerated by each strain.
  • Upon removal of the drug pressure, strains that had adapted to high concentrations of FLC returned to their original level of susceptibility by initially losing the extra copy of chromosome 1 followed by loss of the extra copies of the remaining disomic chromosomes.
  • The duplication of chromosome 1 was closely associated with two of its resident genes: ERG11, the target of FLC and AFR1, the major transporter of azoles in C. neoformans.
  • This adaptive mechanism in C. neoformans may play an important role in FLC therapy failure of cryptococcosis leading to relapse during azole maintenance therapy.

  • Faculty of 1000. commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine. (subscription/membership/fee required).
  • Hazardous Substances Data Bank. FLUCONAZOLE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Nat Rev Genet. 2005 Jun;6(6):451-64 [15883588.001]
  • [Cites] J Cell Physiol Suppl. 1958 Dec;52(Supp 1):1-27; discussion 27-34 [13641342.001]
  • [Cites] Science. 2005 Sep 30;309(5744):2185-9 [16195452.001]
  • [Cites] Antimicrob Agents Chemother. 2006 Mar;50(3):1100-3 [16495279.001]
  • [Cites] Antimicrob Agents Chemother. 2006 Apr;50(4):1384-92 [16569856.001]
  • [Cites] Science. 2006 Jul 21;313(5785):367-70 [16857942.001]
  • [Cites] Mol Biol Evol. 2006 Oct;23(10):1879-90 [16870684.001]
  • [Cites] Clin Infect Dis. 2006 Oct 15;43(8):1069-73 [16983622.001]
  • [Cites] Eukaryot Cell. 2006 Dec;5(12):2184-8 [17056742.001]
  • [Cites] Eukaryot Cell. 2007 Jul;6(7):1150-65 [17513564.001]
  • [Cites] Mol Microbiol. 2007 Aug;65(4):1018-33 [17645443.001]
  • [Cites] Science. 2007 Aug 17;317(5840):916-24 [17702937.001]
  • [Cites] Nature. 2007 Sep 6;449(7158):54-61 [17805289.001]
  • [Cites] Eukaryot Cell. 2007 Oct;6(10):1889-904 [17693596.001]
  • [Cites] Mol Microbiol. 2008 Apr;68(1):186-201 [18312269.001]
  • [Cites] Semin Respir Crit Care Med. 2008 Apr;29(2):198-210 [18366001.001]
  • [Cites] Mol Microbiol. 2008 May;68(3):624-41 [18363649.001]
  • [Cites] Eukaryot Cell. 2008 May;7(5):747-64 [18375617.001]
  • [Cites] Cell. 2008 Nov 28;135(5):879-93 [19041751.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Feb 24;106(8):2688-93 [19204294.001]
  • [Cites] Antimicrob Agents Chemother. 2009 Jul;53(7):2804-15 [19414582.001]
  • [Cites] FEMS Microbiol Lett. 2009 Jun;296(2):257-65 [19486162.001]
  • [Cites] Nature. 2009 Jul 9;460(7252):278-82 [19506557.001]
  • [Cites] Microbiology. 1999 Oct;145 ( Pt 10):2701-13 [10537192.001]
  • [Cites] Antimicrob Agents Chemother. 1999 Nov;43(11):2798-800 [10543768.001]
  • [Cites] AIDS. 2001 Nov 23;15(17):2344-5 [11698718.001]
  • [Cites] Trends Mol Med. 2002 Feb;8(2):76-81 [11815273.001]
  • [Cites] Lancet Infect Dis. 2002 Feb;2(2):73-85 [11901654.001]
  • [Cites] Antimicrob Agents Chemother. 2002 Jun;46(6):1704-13 [12019079.001]
  • [Cites] Annu Rev Microbiol. 2002;56:139-65 [12142485.001]
  • [Cites] Infect Dis Clin North Am. 2002 Dec;16(4):837-74, v-vi [12512184.001]
  • [Cites] J Clin Microbiol. 2003 Jan;41(1):267-72 [12517859.001]
  • [Cites] Mol Microbiol. 2003 Jan;47(2):357-71 [12519188.001]
  • [Cites] Antimicrob Agents Chemother. 2004 May;48(5):1773-7 [15105134.001]
  • [Cites] Antimicrob Agents Chemother. 2004 May;48(5):1788-96 [15105136.001]
  • [Cites] Exp Cell Res. 2004 Oct 15;300(1):109-20 [15383319.001]
  • [Cites] Genetics. 1976 Apr;82(4):605-27 [773747.001]
  • [Cites] Genetics. 1978 Dec;90(4):735-60 [744475.001]
  • [Cites] Mol Cell Biol. 1994 Jul;14(7):4912-9 [8007987.001]
  • [Cites] Curr Genet. 1994 Jul;26(1):54-61 [7954897.001]
  • [Cites] Clin Infect Dis. 1994 Nov;19(5):975-6 [7893896.001]
  • [Cites] Microbiol Rev. 1995 Dec;59(4):686-98 [8531892.001]
  • [Cites] Int J STD AIDS. 1995 Sep-Oct;6(5):353-5 [8547418.001]
  • [Cites] Clin Infect Dis. 1996 Dec;23(6):1337-8 [8953097.001]
  • [Cites] Antimicrob Agents Chemother. 1997 Apr;41(4):748-51 [9087482.001]
  • [Cites] Clin Infect Dis. 1998 Jan;26(1):186-7 [9455533.001]
  • [Cites] Antimicrob Agents Chemother. 1999 Aug;43(8):1856-61 [10428902.001]
  • [Cites] Med Mycol. 2005 Jun;43(4):285-318 [16110776.001]
  • (PMID = 20368972.001).
  • [ISSN] 1553-7374
  • [Journal-full-title] PLoS pathogens
  • [ISO-abbreviation] PLoS Pathog.
  • [Language] ENG
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Azoles; 8VZV102JFY / Fluconazole
  • [Other-IDs] NLM/ PMC2848560
  •  go-up   go-down


71. Min CK, Lee MJ, Eom KS, Lee S, Lee JW, Min WS, Kim CC, Kim M, Lim J, Kim Y, Han K: Bortezomib in combination with conventional chemotherapeutic agents for multiple myeloma compared with bortezomib alone. Jpn J Clin Oncol; 2007 Dec;37(12):961-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bortezomib in combination with conventional chemotherapeutic agents for multiple myeloma compared with bortezomib alone.
  • BACKGROUND: Recent studies have demonstrated synergy between bortezomib and a number of conventional cytotoxic agents.
  • This study examined whether or not the speed of the response, progression and safety from a combination treatment of bortezomib with common chemotherapeutic drugs is superior to bortezomib monotherapy.
  • Thirty-two patients were treated with bortezomib alone and 25 were treated with chemotherapeutic agents that were given in combination with bortezomib.
  • The monoclonal immunoglobulin (mIg) or free light chain (FLC) concentrations were determined in the sera before and after two cycles of bortezomib treatment.
  • RESULTS: Thirty-one of the 57 patients (54.4%) attained an early objective response (EOR) after the second bortezomib treatment, defined as a >/=50% decrease in the serum mIg or FLC concentration.
  • Improvements in the response were observed when common chemotherapeutic agents were added to bortezomib monotherapy.
  • In patients who received bortezomib combined with chemotherapeutic agents, 19 out of 25 patients (76%) showed an EOR, whereas 12 out of 32 patients (37.5%) given bortezomib monotherapy achieved an EOR after the second cycle of bortezomib treatment (P = 0.004); the median decrease from the baseline in the paraprotein level was 74.6 +/- 5.9 and 39.7 +/- 4.2%, respectively (P = 0.003).
  • CONCLUSIONS: Bortezomib in combination with common chemotherapeutic agents is more active in the treatment of relapsed, refractory MM than with bortezomib alone.
  • However, more effective post-bortezomib treatment is needed to reduce the rate of disease progression particularly in patients with high tumor burden.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Boronic Acids / therapeutic use. Multiple Myeloma / drug therapy. Pyrazines / therapeutic use

  • Genetic Alliance. consumer health - Multiple myeloma.
  • MedlinePlus Health Information. consumer health - Multiple Myeloma.
  • Hazardous Substances Data Bank. BORTEZOMIB .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18156171.001).
  • [ISSN] 1465-3621
  • [Journal-full-title] Japanese journal of clinical oncology
  • [ISO-abbreviation] Jpn. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Controlled Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Boronic Acids; 0 / Immunoglobulin Light Chains; 0 / Pyrazines; 69G8BD63PP / Bortezomib; EC 1.1.- / Lactate Dehydrogenases; EC 3.1.3.1 / Alkaline Phosphatase
  •  go-up   go-down


72. Otto KG, Broudy VC, Lin NL, Parganas E, Luthi JN, Drachman JG, Ihle JN, Blau CA: Membrane localization is not required for Mpl function in normal hematopoietic cells. Blood; 2001 Oct 1;98(7):2077-83
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Membrane localization is not required for Mpl function in normal hematopoietic cells.
  • Cellular trafficking of growth factor receptors, including cross-talk among receptors at the cell surface, may be important for signal transduction in normal hematopoietic cells.
  • To test this idea, the signaling domain of Mpl (the thrombopoietin receptor) was targeted to the plasma membrane, or to the cytoplasm of murine marrow cells, and the ability of the cells to proliferate and differentiate in response to Mpl dimerized at the plasma membrane or free in the cytoplasm was assessed.
  • Constructs encoding the signaling domain of Mpl linked to an FK506 binding protein domain (to permit dimerization by the membrane-permeable ligand AP20187) with or without a myristylation sequence (to target the receptor to the plasma membrane) and a hemagglutinin epitope tag were generated and introduced into murine marrow cells using a murine stem cell virus (MSCV)-based retroviral vector.
  • Both populations of transduced marrow cells proliferated in Iscoves modified Dulbecco medium-10% FCS-100 nM AP20187 without exogenous growth factors for more than 100 days and achieved greater than a 10(7)-fold expansion of cells by day 50 (n = 4 transductions).
  • Activation of Mpl either at the plasma membrane or in the cytoplasm allowed for the terminal maturation of transduced progenitor cells.
  • Introduction of membrane-targeted or cytoplasmic Mpl into fetal liver cells from homozygous JAK2 knock-out mice or wild-type littermates demonstrated that both forms of Mpl require JAK2 for signaling.
  • These data show that the activation of Mpl independent of its normal plasma membrane location can support production of the full range of normal hematopoietic progenitor cells in vitro.
  • [MeSH-major] Cell Membrane / metabolism. Hematopoietic Stem Cells / drug effects. Milk Proteins. Neoplasm Proteins. Proto-Oncogene Proteins / physiology. Receptors, Cytokine
  • [MeSH-minor] Animals. Bone Marrow Cells / cytology. Bone Marrow Cells / drug effects. Cell Differentiation / drug effects. Cell Division / drug effects. Cell Line. Cytoplasm / chemistry. DNA-Binding Proteins / pharmacology. DNA-Binding Proteins / physiology. Dimerization. Janus Kinase 2. Mice. Microscopy, Fluorescence. Protein Transport. Protein-Tyrosine Kinases / pharmacology. Protein-Tyrosine Kinases / physiology. Receptors, Thrombopoietin. STAT5 Transcription Factor. Signal Transduction. Trans-Activators / pharmacology. Trans-Activators / physiology

  • MedlinePlus Health Information. consumer health - Stem Cells.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11567993.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK49855; United States / NIDDK NIH HHS / DK / P01DK47754; United States / NHLBI NIH HHS / HL / P01HL53750; United States / NIDDK NIH HHS / DK / R01DK52997; United States / NIDDK NIH HHS / DK / R01DK57525
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Milk Proteins; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins; 0 / Receptors, Cytokine; 0 / Receptors, Thrombopoietin; 0 / STAT5 Transcription Factor; 0 / Trans-Activators; 143641-95-6 / MPL protein, human; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Jak2 protein, mouse; EC 2.7.10.2 / Janus Kinase 2
  •  go-up   go-down


73. Burkill GJ, Mannion EM, Healy JC: Technical report: lymph node enhancement at MRI with MnDPDP in primary hepatic carcinoma. Clin Radiol; 2001 Jan;56(1):67-71
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Technical report: lymph node enhancement at MRI with MnDPDP in primary hepatic carcinoma.
  • AIMS: To report two cases of lymph node enhancement in primary hepatic carcinoma following the administration of Mangafodipir trisodium (MnDPDP, Teslascan(R), Nycomed Amersham U.K.
  • ), an hepatocyte specific magnetic resonance imaging (MRI) contrast agent.
  • To review our experience with this contrast agent and the literature to establish if such enhancement occurs in normal lymph nodes or has been previously described in hepatocellular carcinoma (HCC) or other lesions.
  • These two cases had hepatocellular carcinoma and fibrolamellar hepatocellular carcinoma, respectively, confirmed on liver biopsy.
  • Although histological confirmation of the lymph nodes was not obtained, the authors propose that the lymph node enhancement was due to functioning hepatocytes in lymph node metastases from the patients' histologically confirmed hepatocellular carcinomas.
  • [MeSH-major] Carcinoma, Hepatocellular / secondary. Contrast Media. Edetic Acid / analogs & derivatives. Liver Neoplasms / diagnosis. Lymphatic Metastasis / diagnosis. Pyridoxal Phosphate / analogs & derivatives

  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • Hazardous Substances Data Bank. Disodium EDTA .
  • Hazardous Substances Data Bank. ETHYLENEDIAMINE TETRAACETIC ACID .
  • Hazardous Substances Data Bank. DISODIUM CALCIUM EDTA .
  • Hazardous Substances Data Bank. MANGANESE, ELEMENTAL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2001 The Royal College of Radiologists.
  • (PMID = 11162701.001).
  • [ISSN] 0009-9260
  • [Journal-full-title] Clinical radiology
  • [ISO-abbreviation] Clin Radiol
  • [Language] eng
  • [Publication-type] Case Reports; Technical Report
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Contrast Media; 42Z2K6ZL8P / Manganese; 5V5IOJ8338 / Pyridoxal Phosphate; 9G34HU7RV0 / Edetic Acid; P28BIW0UTB / N,N'-bis(pyridoxal-5-phosphate)ethylenediamine-N,N'-diacetic acid
  •  go-up   go-down


74. Salama SM, Atwal H, Gandhi A, Simon J, Poglod M, Montaseri H, Khan JK, Furukawa T, Saito H, Nishida K, Higashitani F, Uji T, Unemi N, Daneshtalab M, Micetich RG: In vitro and in vivo activities of syn2836, syn2869, syn2903, and syn2921: new series of triazole antifungal agents. Antimicrob Agents Chemother; 2001 Sep;45(9):2420-6
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] In vitro and in vivo activities of syn2836, syn2869, syn2903, and syn2921: new series of triazole antifungal agents.
  • The in vitro and in vivo activities of four azole compounds belonging to a new series of 2(2,4-difluorophenyl)-3-(4-substituted piperazin-1-yl)-1-(1,2,4-triazol-1-yl) butanol antifungal agents is described.
  • The in vitro activities of Syn2869, Syn2836, Syn2903, and Syn2921 against a panel of over 240 recently collected clinical isolates of yeast and molds were determined, and the results were compared with those obtained with fluconazole (FLC), itraconazole (ITC), and amphotericin B (AMB).
  • All compounds were also active against FLC-resistant Candida albicans and other Candida sp. strains.
  • Moreover, MIC(90)s for strains of Cryptococcus neoformans, Aspergillus spp., Trichophyton spp., and Microsporum spp. were also low and ranged from <0.048 to 0.39 microg/ml.
  • The results for Syn2903 were similar to those for FLC, while the other compounds were slightly less effective but had ranges of activities similar to the range of activity of ITC.
  • It was concluded from the data generated for this new series of azole compounds in the studies described above that further pharmacokinetic and toxicologic evaluations are warranted prior to selection of a candidate compound for preclinical testing.
  • [MeSH-major] Antifungal Agents / therapeutic use. Aspergillosis / drug therapy. Candidiasis / drug therapy
  • [MeSH-minor] Animals. Aspergillus / drug effects. Candida albicans / drug effects. Disease Models, Animal. Mice. Microbial Sensitivity Tests. Piperazines / pharmacology. Piperazines / therapeutic use. Treatment Outcome. Triazoles / pharmacology. Triazoles / therapeutic use

  • MedlinePlus Health Information. consumer health - Aspergillosis.
  • MedlinePlus Health Information. consumer health - Yeast Infections.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Antimicrob Agents Chemother. 2000 Apr;44(4):910-5 [10722490.001]
  • [Cites] Antimicrob Agents Chemother. 1985 Nov;28(5):648-53 [3004323.001]
  • [Cites] Ann Intern Med. 1987 Feb;106(2):209-16 [3541723.001]
  • [Cites] J Heart Transplant. 1988 Sep-Oct;7(5):390-4 [3058911.001]
  • [Cites] Eur J Clin Microbiol Infect Dis. 1989 May;8(5):402-12 [2546775.001]
  • [Cites] Antimicrob Agents Chemother. 1997 Mar;41(3):617-23 [9056003.001]
  • [Cites] Am J Med. 1994 Aug;97(2):135-44 [8059779.001]
  • [Cites] Antimicrob Agents Chemother. 1995 Aug;39(8):1696-9 [7486903.001]
  • [Cites] Clin Infect Dis. 1995 Oct;21(4):897-904 [8645837.001]
  • [Cites] Antimicrob Agents Chemother. 1997 Jan;41(1):196-9 [8980781.001]
  • [Cites] Eur J Clin Microbiol Infect Dis. 1992 Apr;11(4):287-91 [1396747.001]
  • (PMID = 11502508.001).
  • [ISSN] 0066-4804
  • [Journal-full-title] Antimicrobial agents and chemotherapy
  • [ISO-abbreviation] Antimicrob. Agents Chemother.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Piperazines; 0 / SYN 2836; 0 / Syn 2869; 0 / Syn2903; 0 / Syn2921; 0 / Triazoles
  • [Other-IDs] NLM/ PMC90671
  •  go-up   go-down


75. He Z, Zhang H, Zhang X, Xie D, Chen Y, Wangensteen KJ, Ekker SC, Firpo M, Liu C, Xiang D, Zi X, Hui L, Yang G, Ding X, Hu Y, Wang X: Liver xeno-repopulation with human hepatocytes in Fah-/-Rag2-/- mice after pharmacological immunosuppression. Am J Pathol; 2010 Sep;177(3):1311-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Liver xeno-repopulation with human hepatocytes in Fah-/-Rag2-/- mice after pharmacological immunosuppression.
  • Functional human hepatocytes xeno-engrafted in mouse liver can be used as a model system to study hepatitis virus infection and vaccine efficacy.
  • Significant liver xeno-repopulation has been reported in two kinds of genetically modified mice that have both immune deficiency and liver injury-induced donor hepatocyte selection: the uPA/SCID mice and Fah(-/-) Rag2(-/-)Il2rg(-/-) mice.
  • Improving the transplantation protocol for liver xeno-repopulation from human hepatocytes will increase the model efficiency and application.
  • In this study, we successfully apply immunosuppressive drug treatments of anti-asialo GM1 and FK506 in Fah(-/-)Rag2(-/-) mice, resulting in significant liver xeno-repopulation from human hepatocytes and human fetal liver cells.
  • When infected with hepatitis B virus (HBV) sera, Fah(-/-)Rag2(-/-) mice with liver xeno-repopulation from human hepatocytes accumulate significant levels of HBV DNA and HBV proteins.
  • Our new protocol for humanized liver could be applied in the study of human hepatitis virus infection in vivo, as well as the pharmacokinetics and efficacy of potential vaccines.

  • COS Scholar Universe. author profiles.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Science. 2004 Apr 2;304(5667):104-7 [15064419.001]
  • [Cites] Mol Immunol. 2003 Jul;39(17-18):1073-7 [12835079.001]
  • [Cites] Genes Dev. 1993 Dec;7(12A):2298-307 [8253378.001]
  • [Cites] Science. 1994 Feb 25;263(5150):1149-52 [8108734.001]
  • [Cites] Nat Genet. 1995 Aug;10(4):453-60 [7545495.001]
  • [Cites] Am J Pathol. 1997 Nov;151(5):1273-80 [9358753.001]
  • [Cites] J Immunol. 1998 Feb 1;160(3):1098-105 [9570522.001]
  • [Cites] Hepatology. 2005 Apr;41(4):847-56 [15791625.001]
  • [Cites] Hepatology. 2005 Jul;42(1):130-9 [15895427.001]
  • [Cites] Gastroenterology. 2006 Feb;130(2):507-20; quiz 590 [16472603.001]
  • [Cites] Nat Rev Immunol. 2007 Feb;7(2):118-30 [17259968.001]
  • [Cites] Mol Ther. 2007 Jul;15(7):1280-7 [17440442.001]
  • [Cites] Immunobiology. 2007;212(7):567-76 [17678714.001]
  • [Cites] Nat Biotechnol. 2007 Aug;25(8):903-10 [17664939.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Dec 18;104(51):20507-11 [18077355.001]
  • [Cites] Gastroenterology. 2008 Mar;134(3):823-32 [18262526.001]
  • [Cites] Hepatology. 2008 Jun;47(6):1846-55 [18452146.001]
  • [Cites] Hepatology. 2008 Oct;48(4):1079-86 [18697217.001]
  • [Cites] Xenotransplantation. 2008 Jul-Aug;15(4):235-45 [18957046.001]
  • [Cites] Gastroenterology. 2009 Feb;136(2):652-62.e3 [19041311.001]
  • [Cites] Neurol Res. 2009 Dec;31(10):1060-7 [19138474.001]
  • [Cites] Am J Pathol. 2001 Oct;159(4):1323-34 [11583960.001]
  • [Cites] Hepatology. 2001 Apr;33(4):981-8 [11283864.001]
  • [Cites] Eur J Pharmacol. 2001 May 4;419(1):99-105 [11348636.001]
  • [Cites] Nat Med. 2001 Aug;7(8):927-33 [11479625.001]
  • [Cites] Am J Pathol. 2002 Aug;161(2):565-74 [12163381.001]
  • [Cites] Hepatology. 2002 Sep;36(3):555-61 [12198647.001]
  • [Cites] Am J Respir Crit Care Med. 2003 Jun 15;167(12):1641-9 [12626348.001]
  • [Cites] Am J Pathol. 2004 Sep;165(3):901-12 [15331414.001]
  • (PMID = 20651238.001).
  • [ISSN] 1525-2191
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R21 DK074561; United States / NIAID NIH HHS / AI / AI065565; United States / NIAID NIH HHS / AI / R03 AI065565; United States / NIDDK NIH HHS / DK / DK074561; United States / NIDA NIH HHS / DA / R01 DA014546
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2928964
  •  go-up   go-down


76. Donovan S, See W, Bonifas J, Stokoe D, Shannon KM: Hyperactivation of protein kinase B and ERK have discrete effects on survival, proliferation, and cytokine expression in Nf1-deficient myeloid cells. Cancer Cell; 2002 Dec;2(6):507-14
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hyperactivation of protein kinase B and ERK have discrete effects on survival, proliferation, and cytokine expression in Nf1-deficient myeloid cells.
  • The Nf1 tumor suppressor encodes a GTPase-activating protein for Ras.
  • Previous work has implicated hyperactive Ras in the aberrant growth of Nf1-deficient cells; however, there are limited data on which effectors modulate specific phenotypes.
  • To address this, we generated myeloid cell lines by infecting fetal liver cells with a retrovirus encoding a truncated allele of c-Myb.
  • Granulocyte-macrophage colony stimulating factor (GM-CSF) promoted the survival of wild-type Myb cells in a dose-dependent manner.
  • By contrast, Nf1-deficient myeloid cells deprived of growth factors, were resistant to apoptosis due to hyperactivation of the phosphoinositide-3-OH kinase/protein kinase B cascade.
  • Nf1(-/-) cells also demonstrated growth factor-independent proliferation and upregulation of GM-CSF mRNA production that were dependent upon Raf/MEK/ERK signaling.
  • These data link specific Ras effectors with discrete cellular phenotypes in Nf1-deficient cells.
  • [MeSH-major] Genes, ras / physiology. Mitogen-Activated Protein Kinases / metabolism. Neurofibromin 1 / deficiency. Proto-Oncogene Proteins / metabolism
  • [MeSH-minor] Animals. Apoptosis. Cell Division / drug effects. Cells, Cultured. Dose-Response Relationship, Drug. Enzyme Inhibitors / pharmacology. Fetus. Genes, myb. Granulocyte-Macrophage Colony-Stimulating Factor / biosynthesis. Granulocyte-Macrophage Colony-Stimulating Factor / pharmacology. Hepatocytes / drug effects. Hepatocytes / pathology. Hepatocytes / physiology. Myeloid Cells / physiology. Protein-Serine-Threonine Kinases / antagonists & inhibitors. Protein-Serine-Threonine Kinases / metabolism. Proto-Oncogene Proteins c-akt. RNA, Messenger / analysis. Signal Transduction. Transfection

  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12498719.001).
  • [ISSN] 1535-6108
  • [Journal-full-title] Cancer cell
  • [ISO-abbreviation] Cancer Cell
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA72614; United States / NCI NIH HHS / CA / CA84221
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Neurofibromin 1; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.24 / Mitogen-Activated Protein Kinases
  •  go-up   go-down


77. Riswoko A, Aoki Y, Hirose T, Nohira H: Optical resolution of 5-alkyl-delta-valerolactones and synthesis of optically active 5-fluoroalkanols. Enantiomer; 2002 Jan-Feb;7(1):33-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Optical resolutions of 5-alkyl-delta-valerolactones were carried out by derivatization to the diastereomeric amides, in which (R)-(+)-1-(1-naphthyl)ethylamine or (S)-(-)-1-phenylethylamine were used as resolving agents.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12043944.001).
  • [ISSN] 1024-2430
  • [Journal-full-title] Enantiomer
  • [ISO-abbreviation] Enantiomer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  •  go-up   go-down


78. Matsunaga T, Toba M, Teramoto T, Mizuya M, Aikawa K, Ohmori S: Formation of large vacuoles induced by cooperative effects of oncostatin M and dexamethasone in human fetal liver cells. Med Mol Morphol; 2008 Mar;41(1):53-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Formation of large vacuoles induced by cooperative effects of oncostatin M and dexamethasone in human fetal liver cells.
  • The morphology of human fetal liver cells treated with both oncostatin M and dexamethasone was strikingly different from those of cells treated with either oncostatin M or dexamethasone alone.
  • The size of the vacuoles varied among individual cells, ranging from 0.05 to 20 mum depending on the cell.
  • Electron microscopy indicated that swollen large vacuoles in the human fetal liver cells were generally electron lucent.
  • Electron microscopic analysis indicated direct fusion among the vacuoles formed in the cytoplasm of human fetal liver cells.
  • To our knowledge, this is the first report of large swollen vacuoles formed in cells by the cooperative effects of oncostatin M and dexamethasone.
  • [MeSH-major] Dexamethasone / pharmacology. Hepatocytes / drug effects. Oncostatin M / pharmacology. Vacuoles / drug effects
  • [MeSH-minor] Cell Differentiation / drug effects. Cells, Cultured. Drug Synergism. Fetus / cytology. Humans. Microscopy, Electron, Transmission

  • Hazardous Substances Data Bank. DEXAMETHASONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Hepatology. 2004 Mar;39(3):635-44 [14999682.001]
  • [Cites] Cell Signal. 2007 May;19(5):1034-43 [17210246.001]
  • [Cites] J Immunol. 2006 Dec 15;177(12):8740-7 [17142776.001]
  • [Cites] Nat Genet. 2003 Mar;33(3):375-81 [12598897.001]
  • [Cites] Biochem Soc Trans. 2001 Aug;29(Pt 4):476-80 [11498012.001]
  • [Cites] Am J Pathol. 2007 Sep;171(3):872-81 [17640959.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Jun 22;96(13):7265-70 [10377403.001]
  • [Cites] EMBO J. 1999 Apr 15;18(8):2127-36 [10205167.001]
  • [Cites] Rev Physiol Biochem Pharmacol. 2003;149:39-52 [12811586.001]
  • [Cites] J Exp Med. 1994 May 1;179(5):1653-58 [8163943.001]
  • [Cites] Hepatology. 2003 Nov;38(5):1095-106 [14578848.001]
  • [Cites] J Immunol. 2004 Jun 15;172(12):7254-62 [15187100.001]
  • [Cites] Toxicon. 2001 Nov;39(11):1757-67 [11595638.001]
  • [Cites] Biol Pharm Bull. 2007 Nov;30(11):2091-7 [17978482.001]
  • [Cites] Mol Biol Cell. 2004 Jul;15(7):3132-45 [15121881.001]
  • [Cites] J Cell Sci. 2006 Apr 1;119(Pt 7):1219-32 [16522686.001]
  • [Cites] J Cell Sci. 2000 May;113 ( Pt 9):1515-24 [10751143.001]
  • [Cites] J Cell Biol. 1981 Sep;90(3):656-64 [7287819.001]
  • [Cites] Microbes Infect. 2003 Jul;5(8):715-21 [12814772.001]
  • [Cites] Cytokine Growth Factor Rev. 2000 Sep;11(3):177-83 [10817961.001]
  • [Cites] Semin Liver Dis. 2007 May;27(2):214-26 [17520519.001]
  • [Cites] Nat Clin Pract Gastroenterol Hepatol. 2007 Jan;4(1):24-34 [17203086.001]
  • [Cites] Life Sci. 1999;65(20):2019-30 [10579456.001]
  • [Cites] J Cell Sci. 1996 Apr;109 ( Pt 4):749-62 [8718666.001]
  • [Cites] J Natl Cancer Inst. 2002 Nov 20;94(22):1680-7 [12441323.001]
  • [Cites] J Cell Sci. 2002 Nov 1;115(Pt 21):4117-31 [12356916.001]
  • [Cites] J Biol Chem. 1995 Jul 28;270(30):17771-7 [7629077.001]
  • (PMID = 18470681.001).
  • [ISSN] 1860-1480
  • [Journal-full-title] Medical molecular morphology
  • [ISO-abbreviation] Med Mol Morphol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 106956-32-5 / Oncostatin M; 7S5I7G3JQL / Dexamethasone
  •  go-up   go-down


79. Yan L, Zhang JD, Cao YB, Gao PH, Jiang YY: Proteomic analysis reveals a metabolism shift in a laboratory fluconazole-resistant Candida albicans strain. J Proteome Res; 2007 Jun;6(6):2248-56
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Multifactorial and multistep alterations are involved in acquired fluconazole (FLC) resistance in Candida albicans.
  • In this study, a FLC-resistant C. albicans strain was obtained by serial cultures of a FLC-susceptible C. albicans strain in incrementally increasing concentrations of FLC.
  • The comparative proteomic study, confirmed by real-time RT-PCR, was performed with the susceptible parental strain and the resistant daughter strain to identify proteins altered during the development of FLC resistance.
  • Our analysis of the differentially expressed proteins identified 22 different proteins, most of which were related to energy metabolisms (e.g., Pgk1, Fba1, and Adh1), and some of which have been previously identified as being involved in FLC resistance in C. albicans (e.g., Ald5, Cdc19, and Gap1).
  • Functional analysis revealed lower intracellular ATP level and mitochondrial membrane potential, less endogenous reactive oxygen species generation in response to antifungal agents, and identical susceptibility to exogenous hydrogen peroxide, heat, and hyperosmotic shock in the resistant strain compared with the susceptible strain.
  • Our results suggest that a metabolism shift might contribute to FLC resistance in C. albicans.
  • [MeSH-major] Antifungal Agents / pharmacology. Candida albicans / drug effects. Drug Resistance, Fungal. Fluconazole / pharmacology. Fungal Proteins / analysis. Proteomics

  • Hazardous Substances Data Bank. FLUCONAZOLE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17432892.001).
  • [ISSN] 1535-3893
  • [Journal-full-title] Journal of proteome research
  • [ISO-abbreviation] J. Proteome Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Fungal Proteins; 0 / Reactive Oxygen Species; 8L70Q75FXE / Adenosine Triphosphate; 8VZV102JFY / Fluconazole
  •  go-up   go-down


80. Gao H, Lukin K, Ramírez J, Fields S, Lopez D, Hagman J: Opposing effects of SWI/SNF and Mi-2/NuRD chromatin remodeling complexes on epigenetic reprogramming by EBF and Pax5. Proc Natl Acad Sci U S A; 2009 Jul 7;106(27):11258-63
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Accessibility of these genes requires their modification by chromatin remodeling complexes (CRCs), which are recruited to promoters by sequence-specific DNA-binding proteins.
  • Early B-cell factor (EBF), which is crucial for B-cell lineage specification, reprograms mb-1 (Ig-alpha) promoters by increasing chromatin accessibility and initiating the loss of DNA methylation.
  • Fusion of EBF and Pax5 with the ligand-binding domain of ERalpha allowed for 4-hydroxytamoxifen-dependent, synergistic activation of mb-1 transcription in plasmacytoma cells.
  • In EBF- or EBF/Pax5-deficient fetal liver cells, both EBF and Pax5 were required for efficient demethylation of mb-1 promoters.
  • Together, our data suggest that Mi-2/NuRD is important for the maintenance of hypermethylated chromatin in B cells.
  • We conclude that SWI/SNF and Mi-2/NuRD function in opposition to enable or limit the reprogramming of genes by EBF and Pax5 during B-cell development.

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. TAMOXIFEN .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Mol Immunol. 1999 Oct-Nov;36(15-16):1067-77 [10698309.001]
  • [Cites] Cell. 2008 Dec 26;135(7):1201-12 [19109892.001]
  • [Cites] Cell. 2000 Nov 10;103(4):667-78 [11106736.001]
  • [Cites] Curr Biol. 2001 Mar 6;11(5):R185-97 [11267889.001]
  • [Cites] Mol Cell Biol. 2001 Oct;21(20):6782-95 [11564863.001]
  • [Cites] Mol Cell. 2002 Feb;9(2):279-89 [11864602.001]
  • [Cites] Nature. 2002 Jul 11;418(6894):195-9 [12110891.001]
  • [Cites] EMBO J. 2002 Aug 1;21(15):4094-103 [12145209.001]
  • [Cites] Mol Cell Biol. 2002 Dec;22(24):8539-51 [12446773.001]
  • [Cites] Mol Cell Biol. 2003 Mar;23(6):1946-60 [12612069.001]
  • [Cites] Mol Cell Biol. 2003 Jun;23(11):3837-46 [12748286.001]
  • [Cites] Mol Cell Biol. 2003 Oct;23(19):6944-57 [12972612.001]
  • [Cites] J Exp Med. 2003 Dec 15;198(12):1937-49 [14676303.001]
  • [Cites] Immunity. 2004 Mar;20(3):349-60 [15030778.001]
  • [Cites] Immunity. 2004 Jun;20(6):719-33 [15189737.001]
  • [Cites] J Exp Med. 2004 Jun 21;199(12):1689-700 [15210745.001]
  • [Cites] Cell. 2004 Oct 1;119(1):75-86 [15454082.001]
  • [Cites] Nat Immunol. 2004 Oct;5(10):1069-77 [15361869.001]
  • [Cites] Dev Cell. 2004 Oct;7(4):607-17 [15469848.001]
  • [Cites] Mol Cell Biol. 1991 Nov;11(11):5756-66 [1922076.001]
  • [Cites] Mol Cell Biol. 1992 Jun;12(6):2662-72 [1375324.001]
  • [Cites] Cell. 1994 Dec 2;79(5):901-12 [8001127.001]
  • [Cites] Nature. 1995 Jul 20;376(6537):263-7 [7542362.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Jul 18;92(15):6991-5 [7624356.001]
  • [Cites] J Exp Med. 1996 Nov 1;184(5):1631-8 [8920853.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Apr 28;95(9):4947-52 [9560208.001]
  • [Cites] Cell. 1998 Oct 16;95(2):279-89 [9790534.001]
  • [Cites] Nature. 1998 Oct 29;395(6705):917-21 [9804427.001]
  • [Cites] Mol Cell. 1998 Dec;2(6):851-61 [9885572.001]
  • [Cites] Genes Dev. 1999 Aug 1;13(15):1924-35 [10444591.001]
  • [Cites] Trends Immunol. 2005 Sep;26(9):455-61 [16027038.001]
  • [Cites] Genes Dev. 2006 Feb 1;20(3):282-96 [16452502.001]
  • [Cites] Immunity. 2007 Jun;26(6):715-25 [17582344.001]
  • [Cites] Nat Immunol. 2007 Aug;8(8):809-16 [17589511.001]
  • [Cites] Immunity. 2007 Nov;27(5):723-34 [17980631.001]
  • [Cites] Mol Immunol. 2008 Aug;45(14):3786-96 [18606452.001]
  • [Cites] J Immunol. 2008 Sep 1;181(5):3364-72 [18714008.001]
  • [Cites] Blood. 2008 Sep 1;112(5):1673-82 [18552207.001]
  • [Cites] Trends Genet. 2000 Aug;16(8):351-6 [10904264.001]
  • (PMID = 19549820.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI54661; United States / NIAID NIH HHS / AI / R01 AI056322; United States / NIAID NIH HHS / AI / T32 AI007405; United States / NIAID NIH HHS / AI / T32-AI007405; United States / NCI NIH HHS / CA / P30 CA046934; United States / NIAID NIH HHS / AI / R01 AI054661; United States / NIAID NIH HHS / AI / R01 AI56322; United States / NIAID NIH HHS / AI / P01 AI22295; United States / NIAID NIH HHS / AI / P01 AI022295
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Autoantigens; 0 / B-Cell-Specific Activator Protein; 0 / CHD4 protein, human; 0 / Chromosomal Proteins, Non-Histone; 0 / Ebf1 protein, mouse; 0 / PAX5 protein, human; 0 / Pax5 protein, mouse; 0 / SWI-SNF-B chromatin-remodeling complex; 0 / Trans-Activators; 0 / Transcription Factors; 094ZI81Y45 / Tamoxifen; 17197F0KYM / afimoxifene; EC 3.5.1.98 / Histone Deacetylases; EC 3.5.1.98 / Mi-2 Nucleosome Remodeling and Deacetylase Complex; EC 3.6.4.- / DNA Helicases
  • [Other-IDs] NLM/ PMC2708696
  •  go-up   go-down


81. Mullan RH, McCormick J, Connolly M, Bresnihan B, Veale DJ, Fearon U: A role for the high-density lipoprotein receptor SR-B1 in synovial inflammation via serum amyloid-A. Am J Pathol; 2010 Apr;176(4):1999-2008
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Here we report alternative signaling through the high-density lipoprotein receptor scavenger receptor-class B type 1 (SR-B1).
  • Quantitative expression/localization of SR-B1 in RA SM, RA fibroblast-like cells (FLCs), and microvascular endothelial cells (ECs) was assessed by Western blotting and immunohistology/fluorescence.
  • A-SAA-mediated effects were examined using a specific antibody against SR-B1 or amphipathic alpha-Helical Peptides (the SR-B1 antagonists L-37pA and D-37pA), in RA FLCs and ECs.
  • Differential SR-B1 expression in RA FLC lines (n = 5) and ECs correlated closely with A-SAA, but not tumor necrosis factor alpha-induced intercellular adhesion molecule-1 upregulation.
  • A-SAA-induced interleukin-6 and -8 production was inhibited in the presence of anti-SR-B1 in human microvascular endothelial cells and RA FLCs.
  • Moreover, D-37pA and L-37pA inhibited A-SAA-induced vascular cell adhesion molecule-1 and intercellular adhesion molecule expression from ECs in a dose-dependent manner.
  • As SR-B1 is expressed in RA synovial tissue and mediates A-SAA-induced pro-inflammatory pathways, a better understanding of A-SAA-mediated inflammatory pathways may lead to novel treatment strategies for RA.
  • [MeSH-minor] Arthroscopy / methods. Biopsy. Dose-Response Relationship, Drug. Endothelium, Vascular / cytology. Humans. Interleukin-6 / metabolism. Interleukin-8 / metabolism. Peptides / chemistry. Phenotype

  • MedlinePlus Health Information. consumer health - Rheumatoid Arthritis.
  • COS Scholar Universe. author profiles.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Perinatol. 2007 May;27(5):297-302 [17344924.001]
  • [Cites] Ann Rheum Dis. 2007 Dec;66(12):1656-60 [17604286.001]
  • [Cites] J Rheumatol. 2008 May;35(5):752-6 [18322992.001]
  • [Cites] J Immunol. 2008 Jul 1;181(1):22-6 [18566366.001]
  • [Cites] Dev Comp Immunol. 2003 Feb;27(2):105-10 [12543124.001]
  • [Cites] Amyloid. 2002 Dec;9(4):237-41 [12557751.001]
  • [Cites] Blood. 2003 Feb 15;101(4):1572-81 [12393391.001]
  • [Cites] J Rheumatol. 2003 Feb;30(2):260-8 [12563678.001]
  • [Cites] J Lipid Res. 2003 Apr;44(4):828-36 [12562845.001]
  • [Cites] Am J Pathol. 2003 May;162(5):1549-57 [12707039.001]
  • [Cites] Arthritis Res Ther. 2003;5(2):94-103 [12718749.001]
  • [Cites] Ann Rheum Dis. 2003 Jul;62(7):635-8 [12810425.001]
  • [Cites] Mediators Inflamm. 2003 Jun;12(3):173-8 [12857601.001]
  • [Cites] Biochem Soc Symp. 2003;(70):125-33 [14587288.001]
  • [Cites] Biochem Biophys Res Commun. 2004 Feb 6;314(2):363-9 [14733913.001]
  • [Cites] Immunol Lett. 2004 Jan 30;91(1):33-7 [14757367.001]
  • [Cites] J Lipid Res. 2004 Feb;45(2):317-25 [14595002.001]
  • [Cites] Circulation. 2004 Feb 17;109(6):726-32 [14970107.001]
  • [Cites] Int J Immunopathol Pharmacol. 2004 May-Aug;17(2):145-56 [15171815.001]
  • [Cites] Matrix Biol. 2004 Apr;23(1):35-46 [15172036.001]
  • [Cites] Arthritis Rheum. 2004 Jun;50(6):1761-9 [15188351.001]
  • [Cites] Arthritis Rheum. 2004 Jun;50(6):1788-99 [15188355.001]
  • [Cites] J Biol Chem. 2004 Aug 20;279(34):36072-82 [15199068.001]
  • [Cites] Curr Opin Hematol. 2000 Jan;7(1):64-9 [10608507.001]
  • [Cites] J Rheumatol. 2000 Jan;27(1):58-63 [10648018.001]
  • [Cites] Scand J Immunol. 2000 Feb;51(2):141-6 [10652160.001]
  • [Cites] J Am Coll Cardiol. 2000 Feb;35(2):358-62 [10676681.001]
  • [Cites] Biochem Biophys Res Commun. 2000 Feb 16;268(2):405-8 [10679217.001]
  • [Cites] J Leukoc Biol. 2000 Mar;67(3):381-6 [10733099.001]
  • [Cites] Ann Rheum Dis. 2000 Nov;59 Suppl 1:i65-71 [11053092.001]
  • [Cites] J Exp Zool. 2000 Dec 15;288(4):335-44 [11144282.001]
  • [Cites] J Immunol. 2001 Feb 15;166(4):2801-7 [11160347.001]
  • [Cites] Blood. 2001 Apr 15;97(8):2381-9 [11290601.001]
  • [Cites] Atherosclerosis. 2002 Feb;160(2):471-6 [11849673.001]
  • [Cites] Ann N Y Acad Sci. 1982;389:39-48 [7046585.001]
  • [Cites] J Biol Chem. 1982 Sep 10;257(17):10518-22 [6809750.001]
  • [Cites] Scand J Immunol. 1984 Mar;19(3):193-8 [6200925.001]
  • [Cites] Proc Natl Acad Sci U S A. 1987 Jul;84(14):4796-800 [3474626.001]
  • [Cites] Arthritis Rheum. 1988 Mar;31(3):315-24 [3358796.001]
  • [Cites] J Trauma. 1989 Jan;29(1):71-4 [2463372.001]
  • [Cites] Ann Rheum Dis. 1990 Jun;49 Suppl 1:480-6 [2197999.001]
  • [Cites] Genomics. 1994 Jan 15;19(2):228-35 [8188253.001]
  • [Cites] J Exp Med. 1994 Jul 1;180(1):203-9 [7516407.001]
  • [Cites] Clin Biochem. 1994 Dec;27(6):469-73 [7535207.001]
  • [Cites] J Immunol. 1995 Aug 1;155(3):1184-90 [7636186.001]
  • [Cites] J Immunol. 1996 Feb 1;156(3):1189-95 [8557997.001]
  • [Cites] Eur J Clin Invest. 1996 Jun;26(6):427-35 [8817153.001]
  • [Cites] Vet Pathol. 1996 Jul;33(4):428-30 [8817841.001]
  • [Cites] Hepatogastroenterology. 1997 Jan-Feb;44(13):90-107 [9058126.001]
  • [Cites] J Biol Chem. 1997 May 16;272(20):13242-9 [9148942.001]
  • [Cites] Biochim Biophys Acta. 1997 Apr 25;1339(1):143-54 [9165109.001]
  • [Cites] Mol Biol Cell. 1997 Mar;8(3):501-15 [9188101.001]
  • [Cites] Am J Physiol. 1997 Jul;273(1 Pt 1):C179-87 [9252455.001]
  • [Cites] Arterioscler Thromb Vasc Biol. 1997 Nov;17(11):2341-9 [9409200.001]
  • [Cites] Lab Invest. 1998 May;78(5):535-9 [9605178.001]
  • [Cites] Scand J Immunol. 1998 Oct;48(4):410-8 [9790312.001]
  • [Cites] Arthritis Rheum. 1998 Dec;41(12):2196-204 [9870876.001]
  • [Cites] J Biol Chem. 2005 Mar 4;280(9):8031-40 [15576377.001]
  • [Cites] Arthritis Rheum. 2005 Jul;52(7):1999-2002 [15986342.001]
  • [Cites] Arterioscler Thromb Vasc Biol. 2005 Aug;25(8):1711-7 [15961705.001]
  • [Cites] J Biol Chem. 2005 Oct 28;280(43):35890-5 [16120612.001]
  • [Cites] Arthritis Rheum. 2006 Jan;54(1):105-14 [16385502.001]
  • [Cites] Arthritis Rheum. 2006 Jun;54(6):1795-804 [16729282.001]
  • [Cites] FASEB J. 2006 Jul;20(9):1540-2 [16754744.001]
  • [Cites] PLoS Med. 2006 Jun;3(6):e287 [16737350.001]
  • [Cites] Int J Obes (Lond). 2006 Dec;30(12):1714-20 [16652132.001]
  • [Cites] Ann Surg Oncol. 2007 Jan;14(1):84-93 [17063306.001]
  • [Cites] Curr Opin Rheumatol. 2007 May;19(3):246-51 [17414950.001]
  • (PMID = 20304957.001).
  • [ISSN] 1525-2191
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD36; 0 / Interleukin-6; 0 / Interleukin-8; 0 / Peptides; 0 / Serum Amyloid A Protein
  • [Other-IDs] NLM/ PMC2843487
  •  go-up   go-down


82. Ramani R, Chaturvedi V: Antifungal susceptibility profiles of Coccidioides immitis and Coccidioides posadasii from endemic and non-endemic areas. Mycopathologia; 2007 Jun;163(6):315-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The causal agents are Coccidioides immitis and C. posadasii.
  • Results indicated that geometric mean MICs of amphotericin B (AMB, 0.06 microg/ml), fluconazole (FLC, 8.0 microg/ml), itraconazole (ITC, 0.07 microg/ml), ketoconazole (KTC, 0.04 microg/ml), voriconazole (VRC, 0.04 microg/ml), posaconazole (PSC, 0.17 microg/ml) and caspofungin (CSP, 0.15 microg/ml) were in susceptible range as per breakpoints published for pathogenic Candida species.
  • However, geometric MFC for FLC was relatively higher (52.4 microg/ml).
  • In conclusion, current methods for antifungal susceptibility testing yield reproducible profiles for Coccidioides species, which appear to be highly susceptible to most antifungal agents.
  • [MeSH-major] Antifungal Agents / pharmacology. Coccidioides / drug effects. Coccidioidomycosis / epidemiology. Endemic Diseases
  • [MeSH-minor] Humans. Microbial Sensitivity Tests / methods. New York / epidemiology. Reagent Kits, Diagnostic. Reference Standards

  • MedlinePlus Health Information. consumer health - Valley Fever.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Clin Microbiol. 2000 Sep;38(9):3457-9 [10970403.001]
  • [Cites] Diagn Microbiol Infect Dis. 2006 Sep;56(1):53-5 [16650953.001]
  • [Cites] J Infect Dis. 2005 Jun 1;191(11):1981-7 [15871133.001]
  • [Cites] Antimicrob Agents Chemother. 2002 May;46(5):1352-6 [11959568.001]
  • [Cites] Emerg Infect Dis. 2000 Jan-Feb;6(1):25-9 [10653565.001]
  • [Cites] Med Mycol. 2005 May;43(3):281-4 [16010855.001]
  • [Cites] Mycopathologia. 1999;145(3):121-6 [10685446.001]
  • [Cites] Curr Opin Infect Dis. 2001 Dec;14(6):693-6 [11964886.001]
  • [Cites] South Med J. 2005 Sep;98(9):930-2 [16217988.001]
  • [Cites] Antimicrob Agents Chemother. 2001 Jun;45(6):1854-9 [11353637.001]
  • [Cites] Mycologia. 2002 Jan-Feb;94(1):73-84 [21156479.001]
  • [Cites] J Urban Health. 2005 Jun;82(2):339-45 [15890762.001]
  • [Cites] J Appl Microbiol. 2001 Oct;91(4):602-5 [11576294.001]
  • [Cites] Ann Intern Med. 2000 Nov 7;133(9):676-86 [11074900.001]
  • [Cites] Clin Infect Dis. 2005 Jun 15;40(12):1770-6 [15909265.001]
  • [Cites] Mycopathologia. 2006 Jan;161(1):21-6 [16389480.001]
  • [Cites] Antimicrob Agents Chemother. 2000 Jun;44(6):1734-6 [10817743.001]
  • [Cites] Mycopathologia. 2001;149(2):57-61 [11270394.001]
  • [Cites] South Med J. 2005 Nov;98(11):1139-41 [16351037.001]
  • (PMID = 17484074.001).
  • [ISSN] 0301-486X
  • [Journal-full-title] Mycopathologia
  • [ISO-abbreviation] Mycopathologia
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Reagent Kits, Diagnostic
  •  go-up   go-down


83. Quindós G, Carrillo-Muñoz AJ, Arévalo MP, Salgado J, Alonso-Vargas R, Rodrigo JM, Ruesga MT, Valverde A, Pemán J, Cantón E, Martín-Mazuelos E, Pontón J: In vitro susceptibility of Candida dubliniensis to current and new antifungal agents. Chemotherapy; 2000 Nov-Dec;46(6):395-401
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] In vitro susceptibility of Candida dubliniensis to current and new antifungal agents