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1. Miura N, Maeda Y, Kanbe T, Yazama H, Takeda Y, Sato R, Tsukamoto T, Sato E, Marumoto A, Harada T, Sano A, Kishimoto Y, Hirooka Y, Murawaki Y, Hasegawa J, Shiota G: Serum human telomerase reverse transcriptase messenger RNA as a novel tumor marker for hepatocellular carcinoma. Clin Cancer Res; 2005 May 1;11(9):3205-9
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  • In this study, we developed a quantitative detection method for serum hTERT mRNA and examined the clinical significance in HCC diagnosis.
  • We examined its sensitivity and specificity in HCC diagnosis, clinical significance in comparison with other tumor markers, and its correlations with the clinical variables by using multivariate analyses.
  • RESULTS: Serum hTERT mRNA showed higher values in patients with HCC than those with chronic liver diseases. hTERT mRNA expression was shown to be independently correlated with clinical variables such as tumor size, number, and degree of differentiation (P < 0.001, each).
  • The sensitivity/specificity of hTERT mRNA and alpha-fetoprotein (AFP) mRNA in HCC diagnosis were 88.2%/70.0% for hTERT and 71.6%/67.5% for AFP, respectively. hTERT mRNA proved to be superior to AFP mRNA, AFP, and des-gamma-carboxy prothrombin in HCC diagnosis.
  • CONCLUSIONS: The usefulness of hTERT mRNA expression in HCC diagnosis and its superiority to conventional tumor markers were shown.
  • Therefore, serum hTERT mRNA is a novel and available marker for HCC diagnosis.
  • [MeSH-major] Biomarkers, Tumor / blood. Carcinoma, Hepatocellular / diagnosis. Liver Neoplasms / diagnosis. RNA, Messenger. Telomerase / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. DNA-Binding Proteins. Female. Humans. Male. Middle Aged. Reverse Transcriptase Polymerase Chain Reaction / methods. Sensitivity and Specificity

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  • (PMID = 15867214.001).
  • [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] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / RNA, Messenger; EC 2.7.7.49 / Telomerase
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2. Gattorno M, Chicha L, Gregorio A, Ferlito F, Rossi F, Jarrossay D, Lanzavecchia A, Martini A, Manz MG: Distinct expression pattern of IFN-alpha and TNF-alpha in juvenile idiopathic arthritis synovial tissue. Rheumatology (Oxford); 2007 Apr;46(4):657-65
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  • [Title] Distinct expression pattern of IFN-alpha and TNF-alpha in juvenile idiopathic arthritis synovial tissue.
  • OBJECTIVES: Recent laboratory and clinical data suggest that two prototype autoimmune diseases, systemic lupus erythematosus and rheumatoid arthritis are mainly driven by distinct cytokines, interferon (IFN)-alpha and tumour necrosis factor (TNF)-alpha, respectively.
  • We here investigated the presence and characteristics of natural type I IFN-producing cells (IPCs), as well as IFN-alpha and TNF-alpha expression at sites of inflammation in juvenile idiopathic arthritis (JIA).
  • METHODS: Peripheral blood (PB) and synovial fluid (SF) mononuclear cells (MNCs) (n = 25 each) from JIA patients with active disease were studied.
  • IPCs and DCs were analysed for Toll-like receptor-7 and -9 mRNA expression by real-time polymerase chain reaction.
  • IFN-alpha was measured by enzyme-linked immunosorbent assay in serum, SF and in supernatants of influenza virus-infected, cultured IPCs.
  • Synovial tissues of n = 6 additional JIA patients were analysed by immunohistochemistry using mAbs against CD123, IFN-alpha, TNF-alpha, CD3, CD19 and CD138.
  • Influenza-induced, but no spontaneous IFN-alpha release was detected from SF IPCs, and serum and SF IFN-alpha levels were not elevated.
  • Nonetheless, in synovial tissue IFN-alpha producing cells accumulated at inflammatory lymph-follicular-like structures, while TNF-alpha producing cells were mostly found at the lining and sublining layers.
  • CONCLUSIONS: These data suggest that besides TNF-alpha-expressing cells, IFN-alpha-producing IPCs are involved in initiation, maintenance or regulation of the inflammatory response in JIA.
  • [MeSH-major] Arthritis, Juvenile / immunology. Autoimmune Diseases / immunology. Interferon-alpha / biosynthesis. Synovial Membrane / immunology. Tumor Necrosis Factor-alpha / biosynthesis
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Dendritic Cells / immunology. Female. Humans. Immunoenzyme Techniques. Immunophenotyping. Male. Polymerase Chain Reaction / methods. Synovial Fluid / immunology


3. Hoang LT, Lynn DJ, Henn M, Birren BW, Lennon NJ, Le PT, Duong KT, Nguyen TT, Mai LN, Farrar JJ, Hibberd ML, Simmons CP: The early whole-blood transcriptional signature of dengue virus and features associated with progression to dengue shock syndrome in Vietnamese children and young adults. J Virol; 2010 Dec;84(24):12982-94
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  • Strikingly, the only difference in the transcriptional signatures of early DSS and UC dengue cases was the greater abundance of several neutrophil-associated transcripts in patients who progressed to DSS, a finding supported by higher plasma concentrations of several canonical proteins associated with neutrophil degranulation (bactericidal/permeability-increasing protein [BPI], elastase 2 [ELA2], and defensin 1 alpha [DEF1A]).
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Disease Progression. Enzyme-Linked Immunosorbent Assay. Female. Genome, Viral / genetics. Humans. Male. Neutrophil Activation. Oligonucleotide Array Sequence Analysis. Phylogeny. Polymerase Chain Reaction. Prospective Studies. RNA, Messenger / blood. RNA, Messenger / genetics. Vietnam. Young Adult

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  • (PMID = 20943967.001).
  • [ISSN] 1098-5514
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] eng
  • [Grant] United Kingdom / Wellcome Trust / / 084368; Canada / Canadian Institutes of Health Research / / ; United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Blood Proteins; 0 / RNA, Messenger; 0 / RNA, Viral
  • [Other-IDs] NLM/ PMC3004338
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4. Paessler S, Yun NE, Judy BM, Dziuba N, Zacks MA, Grund AH, Frolov I, Campbell GA, Weaver SC, Estes DM: Alpha-beta T cells provide protection against lethal encephalitis in the murine model of VEEV infection. Virology; 2007 Oct 25;367(2):307-23
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  • [Title] Alpha-beta T cells provide protection against lethal encephalitis in the murine model of VEEV infection.
  • Wild type mice were protected against lethal VEEV challenge.
  • In contrast, alpha/beta (alphabeta) TCR-deficient mice developed lethal encephalitis following VEEV challenge, while mice deficient in gamma/delta (gammadelta) T cells were protected.
  • Surprisingly, the vaccine potency was diminished by 50% in animals lacking interferon-gamma receptor alpha chain (R1)-chain and a minority of vaccinated immunoglobulin heavy chain-deficient (microMT) mice survived challenge, which suggests that neutralizing antibody may not be absolutely required for protection.

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  • (PMID = 17610927.001).
  • [ISSN] 0042-6822
  • [Journal-full-title] Virology
  • [ISO-abbreviation] Virology
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / K08 AI059491; United States / NIAID NIH HHS / AI / U54 AI057156; United States / NIAID NIH HHS / AI / K08 AI059491-01; United States / NIAID NIH HHS / AI / AI059491-01; None / None / / U54 AI057156-05; United States / NIAID NIH HHS / AI / K08 AI059491-04; United States / NIAID NIH HHS / AI / AI059491-02; United States / NIAID NIH HHS / AI / K08 AI059491-03; United States / NIAID NIH HHS / AI / AI059491-03; United States / NIAID NIH HHS / AI / K08 AI059491-02; United States / NIAID NIH HHS / AI / U54 AI057156-05; United States / NIAID NIH HHS / AI / AI059491-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Antigen, T-Cell, alpha-beta; 0 / Vaccines, Attenuated; 0 / Viral Vaccines
  • [Other-IDs] NLM/ NIHMS32492; NLM/ PMC2067255
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5. Kim SR, Lee KS, Park HS, Park SJ, Min KH, Moon H, Puri KD, Lee YC: HIF-1α inhibition ameliorates an allergic airway disease via VEGF suppression in bronchial epithelium. Eur J Immunol; 2010 Oct;40(10):2858-69
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  • [Title] HIF-1α inhibition ameliorates an allergic airway disease via VEGF suppression in bronchial epithelium.
  • One of the HIF-1α target genes is vascular endothelial growth factor (VEGF), which is a potent stimulator of inflammation, airway remodeling, and physiologic dysregulation in allergic airway diseases.
  • Using OVA-treated mice and murine tracheal epithelial cells, the signaling networks involved in HIF-1α activation and the role of HIF-1α in the pathogenesis of allergic airway disease were investigated.
  • Our data also show that the increased numbers of inflammatory cells, increased airway hyperresponsiveness, levels of IL-4, IL-5, IL-13, and vascular permeability in the lungs after OVA inhalation were significantly reduced by 2-methoxyestradiol or a VEGF inhibitor, CBO-P11.
  • [MeSH-major] Airway Remodeling / immunology. Asthma / immunology. Hypoxia-Inducible Factor 1, alpha Subunit / antagonists & inhibitors. Hypoxia-Inducible Factor 1, alpha Subunit / immunology. Vascular Endothelial Growth Factor A / antagonists & inhibitors. Vascular Endothelial Growth Factor A / immunology
  • [MeSH-minor] Adenine / analogs & derivatives. Adenine / pharmacology. Animals. Bronchoalveolar Lavage Fluid / chemistry. Bronchoalveolar Lavage Fluid / cytology. Endothelial Growth Factors / pharmacology. Epithelial Cells. Estradiol / analogs & derivatives. Estradiol / pharmacology. Female. Histocytochemistry. Mice. Mice, Inbred C57BL. Ovalbumin / immunology. Peptides, Cyclic / pharmacology. Phosphatidylinositol 3-Kinases / antagonists & inhibitors. Phosphatidylinositol 3-Kinases / immunology. Quinazolines / pharmacology. RNA / chemistry. RNA / genetics. RNA, Small Interfering / pharmacology. Respiratory Function Tests. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction / immunology. Specific Pathogen-Free Organisms

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  • (PMID = 20827786.001).
  • [ISSN] 1521-4141
  • [Journal-full-title] European journal of immunology
  • [ISO-abbreviation] Eur. J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Endothelial Growth Factors; 0 / Hif1a protein, mouse; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / IC 87114; 0 / Peptides, Cyclic; 0 / Quinazolines; 0 / RNA, Small Interfering; 0 / Vascular Endothelial Growth Factor A; 0 / cyclo-VEGI; 4TI98Z838E / Estradiol; 63231-63-0 / RNA; 6I2QW73SR5 / 2-methoxyestradiol; 9006-59-1 / Ovalbumin; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; JAC85A2161 / Adenine
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6. Ecroyd H, Meehan S, Horwitz J, Aquilina JA, Benesch JL, Robinson CV, Macphee CE, Carver JA: Mimicking phosphorylation of alphaB-crystallin affects its chaperone activity. Biochem J; 2007 Jan 1;401(1):129-41
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  • AlphaB-crystallin is a member of the sHsp (small heat-shock protein) family that prevents misfolded target proteins from aggregating and precipitating.
  • We observed that both target protein identity and solution (buffer) conditions are critical factors in determining the relative chaperone ability of wild-type and phosphorylated alphaB-crystallins.
  • The present study provides evidence for the regulation of the chaperone activity of alphaB-crystallin by phosphorylation and indicates that this may play an important role in alleviating the pathogenic effects associated with protein conformational diseases.

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  • (PMID = 16928191.001).
  • [ISSN] 1470-8728
  • [Journal-full-title] The Biochemical journal
  • [ISO-abbreviation] Biochem. J.
  • [Language] ENG
  • [Grant] United States / NEI NIH HHS / EY / R01 EY003897; United States / NEI NIH HHS / EY / R37 EY003897; United States / NEI NIH HHS / EY / EY-3897
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Caseins; 0 / Molecular Chaperones; 0 / alpha-Crystallin B Chain; 9013-90-5 / Lactalbumin; EC 1.11.1.6 / Catalase
  • [Other-IDs] NLM/ PMC1698675
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7. Stankovic MM, Nestorovic AR, Tomovic AM, Petrovic-Stanojevic ND, Andjelic-Jelic MS, Dopudja-Pantic VB, Nagorni-Obradovic LjM, Mitic-Milikic MM, Radojkovic DP: TNF-alpha-308 promotor polymorphism in patients with chronic obstructive pulmonary disease and lung cancer. Neoplasma; 2009;56(4):348-52
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  • [Title] TNF-alpha-308 promotor polymorphism in patients with chronic obstructive pulmonary disease and lung cancer.
  • Chronic obstructive pulmonary disease (COPD) and lung cancer (LC) are a major cause of morbidity and mortality worldwide.
  • In both diseases airways inflammation plays an important role.
  • Functional promoter polymorphism, at the position -308, of tumor necrosis factor (TNF)-alpha represents attractive potential susceptibilty marker for both diseases.
  • Results of our study showed significant decrease of heterozygote for TNF-alpha-308 1/2 gene variant in COPD group in comparison to controls (p=0.043).
  • According to our results heterozygous carriers of TNF-alpha-308 1/2 polymorphism had a2.3-fold decreased risk for COPD development (OR=0.44, 95%CI=0.20-0.97).
  • In patients with lung cancer we also observed a trend of decreased distribution of TNF-alpha-308 1/2 heterozygotes, but statistical significance was not achieved.
  • To our knowledge, this is the first study implicating decreased frequency of TNF-alpha-308 1/2 gene variant in patients with COPD and LC.
  • Although these results need to be confirmed on larger cohort, they represent anew and interesting finding, not reported in other populations tested so far.
  • [MeSH-major] Lung Neoplasms / genetics. Polymorphism, Genetic / genetics. Promoter Regions, Genetic / genetics. Pulmonary Disease, Chronic Obstructive / genetics. Tumor Necrosis Factor-alpha / genetics
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / secondary. Carcinoma, Large Cell / genetics. Carcinoma, Large Cell / secondary. Case-Control Studies. Female. Humans. Male. Middle Aged. Neoplasm Staging. Polymerase Chain Reaction. Polymorphism, Restriction Fragment Length. Prognosis. Small Cell Lung Carcinoma / genetics. Small Cell Lung Carcinoma / secondary


8. Williams KL, Lich JD, Duncan JA, Reed W, Rallabhandi P, Moore C, Kurtz S, Coffield VM, Accavitti-Loper MA, Su L, Vogel SN, Braunstein M, Ting JP: The CATERPILLER protein monarch-1 is an antagonist of toll-like receptor-, tumor necrosis factor alpha-, and Mycobacterium tuberculosis-induced pro-inflammatory signals. J Biol Chem; 2005 Dec 2;280(48):39914-24
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  • [Title] The CATERPILLER protein monarch-1 is an antagonist of toll-like receptor-, tumor necrosis factor alpha-, and Mycobacterium tuberculosis-induced pro-inflammatory signals.
  • The CATERPILLER (CLR, also NOD and NLR) proteins share structural similarities with the nucleotide binding domain (NBD)-leucine-rich repeat (LRR) superfamily of plant disease-resistance (R) proteins and are emerging as important immune regulators in animals.
  • The CLR gene, Monarch-1/Pypaf7, is expressed by resting primary myeloid/monocytic cells, and its expression in these cells is reduced by Toll-like receptor (TLR) agonists tumor necrosis factor (TNF) alpha and Mycobacterium tuberculosis.
  • Monarch-1 reduces NFkappaB activation by TLR-signaling molecules MyD88, IRAK-1 (type I interleukin-1 receptor-associated protein kinase), and TRAF6 (TNF receptor (TNFR)-associated factor) as well as TNFR signaling molecules TRAF2 and RIP1 but not the downstream NFkappaB subunit p65.
  • Reducing Monarch-1 expression with small interference RNA in myeloid/monocytic cells caused a dramatic increase in NFkappaB activation and cytokine expression in response to TLR2/TLR4 agonists, TNFalpha, or M. tuberculosis infection, suggesting that Monarch-1 is a negative regulator of inflammation.

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  • (PMID = 16203735.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] ENG
  • [Grant] United States / NIDCR NIH HHS / DE / DE16326; United States / NIAID NIH HHS / AI / R01 AI063031; United States / NIDDK NIH HHS / DK / DK38108; United States / NIAID NIH HHS / AI / L30 AI057175; United States / NIAID NIH HHS / AI / AI057175; United States / NIAID NIH HHS / AI / R01 AI080432; United States / NIAID NIH HHS / AI / AI063031; United States / NIAID NIH HHS / AI / R01 AI077454; United States / NIDDK NIH HHS / DK / P01 DK038108; United States / NIDCR NIH HHS / DE / R01 DE016326
  • [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 / AGFG1 protein, human; 0 / Adaptor Proteins, Signal Transducing; 0 / Antigens, Differentiation; 0 / Cytokines; 0 / Cytoskeletal Proteins; 0 / Intracellular Signaling Peptides and Proteins; 0 / MYD88 protein, human; 0 / Myeloid Differentiation Factor 88; 0 / NF-kappa B; 0 / NLRP12 protein, human; 0 / Nuclear Pore Complex Proteins; 0 / RELA protein, human; 0 / RNA, Small Interfering; 0 / RNA-Binding Proteins; 0 / Receptors, Immunologic; 0 / TNF Receptor-Associated Factor 2; 0 / TNF Receptor-Associated Factor 6; 0 / Toll-Like Receptors; 0 / Transcription Factor RelA; 0 / Tumor Necrosis Factor-alpha; 0 / marenostrin; 63231-63-0 / RNA; EC 1.13.12.- / Luciferases; EC 2.7.- / Protein Kinases; EC 2.7.11.1 / Interleukin-1 Receptor-Associated Kinases; EC 3.4.22.- / Caspases
  • [Other-IDs] NLM/ NIHMS684863; NLM/ PMC4422647
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9. Hernández-Pascacio J, Garza C, Banquy X, Díaz-Vergara N, Amigo A, Ramos S, Castillo R, Costas M, Piñeiro A: Cyclodextrin-based self-assembled nanotubes at the water/air interface. J Phys Chem B; 2007 Nov 8;111(44):12625-30
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  • Native alpha-cyclodextrin (alpha-CD) is found to spontaneously form films at aqueous solution/air interfaces.
  • By using isothermal titration calorimetry (ITC), Brewster angle microscopy (BAM), atomic force microscopy (AFM), and molecular dynamics (MD) simulations, it is shown that the films consist of self-assembled nanotubes whose building blocks are cyclodextrin dimers (alpha-CD2) and alpha-CD2-SDS1 complexes.

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  • (PMID = 17941668.001).
  • [ISSN] 1520-6106
  • [Journal-full-title] The journal of physical chemistry. B
  • [ISO-abbreviation] J Phys Chem B
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclodextrins; 0 / Solutions; 059QF0KO0R / Water; 368GB5141J / Sodium Dodecyl Sulfate
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10. Lee S, Kim K, Kim HA, Kim SW, Lee M: Augmentation of erythropoietin enhancer-mediated hypoxia-inducible gene expression by co-transfection of a plasmid encoding hypoxia-inducible factor 1alpha for ischemic tissue targeting gene therapy. J Drug Target; 2008 Jan;16(1):43-50
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Therapeutic angiogenesis with gene encoding vascular endothelial growth factor (VEGF) is a potential treatment for ischemic diseases.
  • [MeSH-major] Erythropoietin / physiology. Genetic Therapy / methods. Hypoxia-Inducible Factor 1, alpha Subunit / biosynthesis. Plasmids / genetics
  • [MeSH-minor] Actins / biosynthesis. Angiotensin I / biosynthesis. Cell Line. Enzyme-Linked Immunosorbent Assay. Humans. Kidney / cytology. Kidney / metabolism. Luciferases / genetics. Promoter Regions, Genetic / genetics. Reverse Transcriptase Polymerase Chain Reaction. Simian virus 40 / genetics. Transcription, Genetic / genetics. Transfection. Vascular Endothelial Growth Factor A / pharmacology

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  • (PMID = 18172819.001).
  • [ISSN] 1061-186X
  • [Journal-full-title] Journal of drug targeting
  • [ISO-abbreviation] J Drug Target
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Actins; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Vascular Endothelial Growth Factor A; 11096-26-7 / Erythropoietin; 9041-90-1 / Angiotensin I; EC 1.13.12.- / Luciferases
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11. Ichii O, Otsuka S, Sasaki N, Yabuki A, Ohta H, Takiguchi M, Hashimoto Y, Endoh D, Kon Y: Local overexpression of interleukin-1 family, member 6 relates to the development of tubulointerstitial lesions. Lab Invest; 2010 Mar;90(3):459-75
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  • Identification of factors that exacerbate a disease is important for the development of biomarkers.
  • In this study, we discovered ectopic overexpression of interleukin-1 family, member-6 (IL-1F6) in several murine renal diseases.
  • In and around these tubules, we found infiltrations of CD3-positive T-cells and nestin- or alpha-smooth-muscle actin-positive mesenchymal cells.
  • [MeSH-minor] Animals. Cells, Cultured. Female. Kidney / pathology. Kidney Function Tests. Male. Mice. Mice, Inbred C57BL. Mice, Inbred MRL lpr. Mice, Inbred NZB. Polymerase Chain Reaction. RNA, Messenger / metabolism

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  • (PMID = 20101239.001).
  • [ISSN] 1530-0307
  • [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 / Interleukin-1; 0 / RNA, Messenger; 0 / interleukin 1F6, mouse
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12. Kosloski LM, Bales IK, Allen KB, Walker BL, Borkon AM, Stuart RS, Pak AF, Wacker MJ: Purification of cardiac myocytes from human heart biopsies for gene expression analysis. Am J Physiol Heart Circ Physiol; 2009 Sep;297(3):H1163-9
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  • The collection of gene expression data from human heart biopsies is important for understanding the cellular mechanisms of arrhythmias and diseases such as cardiac hypertrophy and heart failure.
  • Many clinical and basic research laboratories conduct gene expression analysis using RNA from whole cardiac biopsies.
  • Real-time RT-PCR was performed comparing nonpurified and purified samples for the expression of troponin T (myocyte marker), vimentin (fibroblast marker), and alpha-smooth muscle actin (smooth muscle marker).
  • Troponin T expression was significantly increased, and vimentin and alpha-smooth muscle actin were significantly decreased in the purified sample (n = 8; P < 0.05).
  • [MeSH-major] Cell Separation / methods. Heart Diseases / genetics. Heart Diseases / pathology. Myocytes, Cardiac / cytology. Myocytes, Cardiac / physiology. Reverse Transcriptase Polymerase Chain Reaction / methods

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  • (PMID = 19617409.001).
  • [ISSN] 1522-1539
  • [Journal-full-title] American journal of physiology. Heart and circulatory physiology
  • [ISO-abbreviation] Am. J. Physiol. Heart Circ. Physiol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Actins; 0 / Biomarkers; 0 / Troponin T; 0 / Vimentin; 63231-63-0 / RNA
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13. Liu W, Deng J, Xu J, Wang H, Yuan M, Liu N, Jiang Y, Liu J: High-mobility group box 1 (HMGB1) downregulates cardiac transient outward potassium current (Ito) through downregulation of Kv4.2 and Kv4.3 channel transcripts and proteins. J Mol Cell Cardiol; 2010 Sep;49(3):438-48
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  • Downregulation of I(to) contributes to AP configuration alteration in myocardial infarction (MI) and numerous other heart diseases.
  • HMGB1 decreased the mRNA and protein levels of the I(to) alpha subunits Kv4.2 and Kv4.3 channels, but not the beta subunit KChIP2 and KCNE2 in NRVMs.
  • In addition to downregulating I(to), HMGB1 modestly inhibited L-type Ca(2+) current, but not I(K1).
  • [MeSH-minor] Animals. Animals, Newborn. Blotting, Western. COS Cells. Cercopithecus aethiops. Down-Regulation. Electrophysiology. RNA, Messenger / genetics. Rats. Reverse Transcriptase Polymerase Chain Reaction

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  • [Copyright] Copyright 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20483361.001).
  • [ISSN] 1095-8584
  • [Journal-full-title] Journal of molecular and cellular cardiology
  • [ISO-abbreviation] J. Mol. Cell. Cardiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / HMGB1 Protein; 0 / Hbp1 protein, rat; 0 / RNA, Messenger; 0 / Shal Potassium Channels; RWP5GA015D / Potassium
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14. Vernel-Pauillac F, Goarant C: Differential cytokine gene expression according to outcome in a hamster model of leptospirosis. PLoS Negl Trop Dis; 2010;4(1):e582
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  • METHODOLOGY/PRINCIPAL FINDINGS: Using an LD50 model of leptospirosis in hamsters, we first determined that 3 days post-infection was a time-point that allowed studying the regulation of immune gene expression and represented the onset of the clinical signs of the disease.
  • We found differential expression of both pro- and anti-inflammatory mediators, with significantly higher expression levels of tumor necrosis factor alpha, interleukin 1alpha, cyclo-oxygenase 2 and interleukin 10 genes in nonsurvivors compared to survivors.
  • [MeSH-minor] Animals. Cricetinae. Cyclooxygenase 2 / genetics. Disease Models, Animal. Gene Expression Regulation / genetics. Gene Expression Regulation / immunology. Interleukin-10 / genetics. Interleukin-1alpha / genetics. Polymerase Chain Reaction. Tumor Necrosis Factor-alpha / genetics

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  • (PMID = 20076757.001).
  • [ISSN] 1935-2735
  • [Journal-full-title] PLoS neglected tropical diseases
  • [ISO-abbreviation] PLoS Negl Trop Dis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines; 0 / Interleukin-1alpha; 0 / Tumor Necrosis Factor-alpha; 130068-27-8 / Interleukin-10; EC 1.14.99.1 / Cyclooxygenase 2
  • [Other-IDs] NLM/ PMC2797601
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15. Kim H, Yang E, Lee J, Kim SH, Shin JS, Park JY, Choi SJ, Kim SJ, Choi IH: Double-stranded RNA mediates interferon regulatory factor 3 activation and interleukin-6 production by engaging Toll-like receptor 3 in human brain astrocytes. Immunology; 2008 Aug;124(4):480-8
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  • Therefore, dsRNA-induced IL-6 production is dependent on mitogen-activated protein kinases and type I IFN production is dependent on IRF3 in brain astrocytes.
  • These results suggest that brain inflammation, which produces inflammatory cytokines and type I IFNs, may enhance TLR3 expression in astrocytes.
  • [MeSH-minor] Cells, Cultured. Dose-Response Relationship, Immunologic. Electrophoretic Mobility Shift Assay / methods. Fetus / immunology. Humans. I-kappa B Proteins / metabolism. Interferon-gamma / immunology. Mitogen-Activated Protein Kinase Kinases / immunology. NF-kappa B / metabolism. Polynucleotides / immunology. RNA, Double-Stranded / immunology. Reverse Transcriptase Polymerase Chain Reaction / methods. STAT1 Transcription Factor / metabolism. Up-Regulation / immunology

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  • (PMID = 18248388.001).
  • [ISSN] 1365-2567
  • [Journal-full-title] Immunology
  • [ISO-abbreviation] Immunology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / I-kappa B Proteins; 0 / IRF3 protein, human; 0 / Interferon Regulatory Factor-3; 0 / Interleukin-6; 0 / NF-kappa B; 0 / Polynucleotides; 0 / RNA, Double-Stranded; 0 / STAT1 Transcription Factor; 0 / STAT1 protein, human; 0 / TLR3 protein, human; 0 / Toll-Like Receptor 3; 139874-52-5 / NF-kappaB inhibitor alpha; 27380-19-4 / poly(rI).poly(dC); 82115-62-6 / Interferon-gamma; EC 2.7.12.2 / Mitogen-Activated Protein Kinase Kinases
  • [Other-IDs] NLM/ PMC2492940
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16. Iwamura C, Nakayama T: Role of alpha-galactosylceramide-activated Valpha14 natural killer T cells in the regulation of allergic diseases. Allergol Int; 2007 Mar;56(1):1-6
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  • [Title] Role of alpha-galactosylceramide-activated Valpha14 natural killer T cells in the regulation of allergic diseases.
  • Valpha14 natural killer T (NKT) cells produce large amounts of both IL-4 and IFN-gamma upon stimulation with a ligand, alpha-galactosylceramide (alpha-GalCer), and play a crucial role in various immune responses, including allergic reactions.
  • Interestingly, Valpha14 NKT cells are not essential for the induction of specific IgE response but they instead tend to induce suppression of specific IgE upon alpha-GalCer activation in vivo.
  • In an OVA-induced asthma model, alpha-GalCer administration inhibited airway inflammation and airway hyperreactivity by IFN-gamma from activated Valpha14 NKT cells, thus suggesting the negative regulation of Th2-responses by the activated Valpha14 NKT cells.

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  • (PMID = 17259803.001).
  • [ISSN] 1323-8930
  • [Journal-full-title] Allergology international : official journal of the Japanese Society of Allergology
  • [ISO-abbreviation] Allergol Int
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antigens, Differentiation, B-Lymphocyte; 0 / Galactosylceramides; 0 / Histocompatibility Antigens Class II; 0 / Receptors, Immunologic; 0 / alpha-galactosylceramide; 0 / invariant chain
  • [Number-of-references] 42
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17. Tang X, Maricic I, Purohit N, Bakamjian B, Reed-Loisel LM, Beeston T, Jensen P, Kumar V: Regulation of immunity by a novel population of Qa-1-restricted CD8alphaalpha+TCRalphabeta+ T cells. J Immunol; 2006 Dec 1;177(11):7645-55
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  • They express exclusively the CD8alphaalpha homodimer and recognize a peptide from a conserved region of the TCR Vbeta8.2 chain in the context of the Qa-1a (CD8alphaalpha Tregs).
  • They secrete type 1 cytokines but not IL-2.
  • These findings reveal an important negative feedback regulatory mechanism targeting activated T cells and have implications in the development of therapeutic strategies for autoimmune diseases and transplantation.
  • [MeSH-minor] Animals. Cell Line. Encephalomyelitis, Autoimmune, Experimental / immunology. Enzyme-Linked Immunosorbent Assay. Flow Cytometry. Lymphocyte Activation / immunology. Mice. Mice, Transgenic. Receptors, Antigen, T-Cell, alpha-beta / immunology. Receptors, Antigen, T-Cell, alpha-beta / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 17114434.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [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 / Antigens, CD8; 0 / CD8 antigen, alpha chain; 0 / Histocompatibility Antigens Class I; 0 / Q surface antigens; 0 / Receptors, Antigen, T-Cell, alpha-beta
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18. Lammers I, Buijs J, Ariese F, Gooijer C: Sensitized enantioselective laser-induced phosphorescence detection in chiral capillary electrophoresis. Anal Chem; 2010 Nov 15;82(22):9410-7
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  • Excitation was performed at 266 nm with a pulsed, small-sized, quadrupled Nd:YAG laser.

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  • (PMID = 20964317.001).
  • [ISSN] 1520-6882
  • [Journal-full-title] Analytical chemistry
  • [ISO-abbreviation] Anal. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclodextrins; 0 / Resins, Synthetic; 76-22-2 / Camphor; RAL3591W33 / camphorquinone
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19. Altavilla D, Marini H, Seminara P, Squadrito G, Minutoli L, Passaniti M, Bitto A, Calapai G, Calò M, Caputi AP, Squadrito F: Protective effects of antioxidant raxofelast in alcohol-induced liver disease in mice. Pharmacology; 2005 Apr;74(1):6-14
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  • [Title] Protective effects of antioxidant raxofelast in alcohol-induced liver disease in mice.
  • Serum alanine aminotransferase (ALT), plasma and liver triglyceride levels, hepatic malondialdehyde (MDA), reduced glutathione (GSH) concentrations, liver gene expression of Toll-like receptor-4 (TLR-4), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha) and intercellular adhesion molecule-1 (ICAM-1) were studied at the end of the study.
  • Raxofelast, an analog of vitamin E, blunted the increased hepatic nuclear factor-kappaB activity, reduced serum ALT, plasma and liver triglycerides, lowered hepatic MDA levels, prevented liver GSH depletion and decreased TLR-4, TNF-alpha, IL-6 and ICAM-1 hepatic gene expression.
  • [MeSH-major] Antioxidants / pharmacology. Benzofurans / pharmacology. Liver Diseases, Alcoholic / prevention & control. Vitamin E / analogs & derivatives
  • [MeSH-minor] Alanine Transaminase / metabolism. Animals. Female. Glutathione / metabolism. Intercellular Adhesion Molecule-1 / biosynthesis. Intercellular Adhesion Molecule-1 / genetics. Interleukin-6 / biosynthesis. Interleukin-6 / genetics. Lipid Peroxidation / drug effects. Liver / drug effects. Liver / metabolism. Liver / pathology. Liver Function Tests. Malondialdehyde / metabolism. Mice. Mice, Inbred C57BL. NF-kappa B / metabolism. Receptors, Immunologic / biosynthesis. Receptors, Immunologic / genetics. Reverse Transcriptase Polymerase Chain Reaction. Toll-Like Receptor 4. Triglycerides / metabolism. Tumor Necrosis Factor-alpha / biosynthesis. Tumor Necrosis Factor-alpha / genetics

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  • [Copyright] Copyright (c) 2005 S. Karger AG, Basel
  • (PMID = 15627848.001).
  • [ISSN] 0031-7012
  • [Journal-full-title] Pharmacology
  • [ISO-abbreviation] Pharmacology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antioxidants; 0 / Benzofurans; 0 / Interleukin-6; 0 / NF-kappa B; 0 / Receptors, Immunologic; 0 / Tlr4 protein, mouse; 0 / Toll-Like Receptor 4; 0 / Triglycerides; 0 / Tumor Necrosis Factor-alpha; 126547-89-5 / Intercellular Adhesion Molecule-1; 1406-18-4 / Vitamin E; 4Y8F71G49Q / Malondialdehyde; EC 2.6.1.2 / Alanine Transaminase; GAN16C9B8O / Glutathione; TC0T0O9VYO / Raxofelast
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20. Bartoli M, Poupiot J, Goyenvalle A, Perez N, Garcia L, Danos O, Richard I: Noninvasive monitoring of therapeutic gene transfer in animal models of muscular dystrophies. Gene Ther; 2006 Jan;13(1):20-8
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  • Muscular dystrophies are a genetically and phenotypically heterogeneous group of degenerative muscle diseases.
  • A subset of them are due to genetic deficiencies in proteins which form the dystrophin-associated complex at the membrane of the myofibers.
  • In this report, we utilized recombinant adeno-associated virus containing a U7 cassette carrying an antisense sequence aimed at inducing exon skipping of the dystrophin gene or containing the alpha-sarcoglycan gene to alleviate the dystrophic phenotype of the mdx and Sgca-null mice, respectively.
  • As these diseases are characterized by cycle of degeneration/regeneration, we postulated that a reporter gene coadministered at the time of the treatment would make it possible to follow the extent of muscle repair.
  • [MeSH-minor] Alkaline Phosphatase / analysis. Animals. Biomarkers / analysis. Dependovirus / genetics. Fluorescent Antibody Technique. Injections, Intramuscular. Male. Mice. Mice, Inbred C57BL. Mice, Inbred mdx. Mice, Knockout. Reverse Transcriptase Polymerase Chain Reaction. Sarcoglycans / genetics. Transduction, Genetic / methods

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  • (PMID = 16107863.001).
  • [ISSN] 0969-7128
  • [Journal-full-title] Gene therapy
  • [ISO-abbreviation] Gene Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Dystrophin; 0 / Oligonucleotides, Antisense; 0 / Sarcoglycans; EC 3.1.3.1 / Alkaline Phosphatase
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21. Han B, Serra P, Yamanouchi J, Amrani A, Elliott JF, Dickie P, Dilorenzo TP, Santamaria P: Developmental control of CD8 T cell-avidity maturation in autoimmune diabetes. J Clin Invest; 2005 Jul;115(7):1879-87
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  • We have carried out comprehensive studies of the diabetogenic CD8 T cell population that targets residues 206-214 of the beta cell antigen islet-specific glucose-6-phosphatase catalytic subunit-related protein (IGRP(206-214)) and undergoes avidity maturation as disease progresses.
  • However, central and peripheral tolerance selectively limit the contribution of these high-avidity T cells to the earliest stages of disease without abrogating their ability to progressively accumulate in inflamed islets and kill beta cells.
  • [MeSH-major] CD8-Positive T-Lymphocytes / immunology. Diabetes Mellitus, Type 1 / immunology
  • [MeSH-minor] Animals. Autoimmunity. Gene Rearrangement, alpha-Chain T-Cell Antigen Receptor. Glucose-6-Phosphatase / immunology. Mice. Mice, Inbred NOD. Mice, Transgenic. Peptide Fragments / immunology. Proteins / immunology. Self Tolerance


22. Kim SH, Han SY, Azam T, Yoon DY, Dinarello CA: Interleukin-32: a cytokine and inducer of TNFalpha. Immunity; 2005 Jan;22(1):131-42
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  • An IL-18 unresponsive cell was converted to a responsive cell by transfection of the IL-18 receptor beta chain, and IL-18-induced microarray revealed high expression of a cytokine-like gene.
  • Induced in human peripheral lymphocyte cells after mitogen stimulation, in human epithelial cells by IFNgamma, and in NK cells after exposure to the combination of IL-12 plus IL-18, IL-32 may play a role in inflammatory/autoimmune diseases.
  • [MeSH-major] Cytokines / genetics. Interleukins / genetics. Tumor Necrosis Factor-alpha / metabolism


23. Jiang X, Ren YP, Lv ZR: Ouabain induces cardiac remodeling in rats independent of blood pressure. Acta Pharmacol Sin; 2007 Mar;28(3):344-52
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  • After 4 and 6 weeks, echocardiography were performed, hemodynamic parameters were measured by invasive cardiac catheterization, changes in cardiac ultrastructure were analyzed using transmission electron microscopy, the collagen fraction of the left ventricle was assessed with Picrosirius red stain, and RT-PCR was applied to evaluate the mRNA level of myosin heavy chain-alpha and -beta in the left ventricle.
  • Moreover, the cardiac MHC-beta mRNA was upregulated by ouabain treatment, whereas MHC-alpha mRNA was downregulated.
  • [MeSH-minor] Animals. Echocardiography. Glyceraldehyde-3-Phosphate Dehydrogenases / biosynthesis. Glyceraldehyde-3-Phosphate Dehydrogenases / genetics. Male. Myosin Heavy Chains / biosynthesis. Myosin Heavy Chains / genetics. Rats. Rats, Sprague-Dawley. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 17302996.001).
  • [ISSN] 1671-4083
  • [Journal-full-title] Acta pharmacologica Sinica
  • [ISO-abbreviation] Acta Pharmacol. Sin.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Cardiotonic Agents; 5ACL011P69 / Ouabain; EC 1.2.1.- / Glyceraldehyde-3-Phosphate Dehydrogenases; EC 3.6.4.1 / Myosin Heavy Chains
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24. Pasquini LA, Calatayud CA, Bertone Uña AL, Millet V, Pasquini JM, Soto EF: The neurotoxic effect of cuprizone on oligodendrocytes depends on the presence of pro-inflammatory cytokines secreted by microglia. Neurochem Res; 2007 Feb;32(2):279-92
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  • In mitochondria isolated from cuprizone-treated glial cells, we observed a marked decrease in the activities of the various complexes of the respiratory chain, indicating a disruption of mitochondrial function.
  • [MeSH-major] Cell Survival / drug effects. Cuprizone / pharmacology. Interferon-gamma / secretion. Microglia / secretion. Oligodendroglia / drug effects. Tumor Necrosis Factor-alpha / secretion
  • [MeSH-minor] Animals. Cells, Cultured. Culture Media, Conditioned. Demyelinating Diseases / chemically induced. Demyelinating Diseases / prevention & control. Immunohistochemistry. Male. Mice. Minocycline / therapeutic use. Rats

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  • (PMID = 17063394.001).
  • [ISSN] 0364-3190
  • [Journal-full-title] Neurochemical research
  • [ISO-abbreviation] Neurochem. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Culture Media, Conditioned; 0 / Tumor Necrosis Factor-alpha; 5N16U7E0AO / Cuprizone; 82115-62-6 / Interferon-gamma; FYY3R43WGO / Minocycline
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25. Isaacs JD, Garden OA, Kaur G, Collinge J, Jackson GS, Altmann DM: The cellular prion protein is preferentially expressed by CD4+ CD25+ Foxp3+ regulatory T cells. Immunology; 2008 Nov;125(3):313-9
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  • Post-translational modification of the cellular prion protein (PrP(C)) is intimately associated with the pathogenesis of prion disease, yet the normal function of the protein remains unclear.
  • [MeSH-major] Forkhead Transcription Factors / analysis. Interleukin-2 Receptor alpha Subunit / analysis. PrPC Proteins / metabolism. T-Lymphocytes, Regulatory / immunology
  • [MeSH-minor] Animals. Cells, Cultured. Immune Tolerance. Mice. Mice, Inbred C57BL. Reverse Transcriptase Polymerase Chain Reaction / methods. Up-Regulation / immunology

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  • (PMID = 18462346.001).
  • [ISSN] 1365-2567
  • [Journal-full-title] Immunology
  • [ISO-abbreviation] Immunology
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MC/ U123192748; United Kingdom / Medical Research Council / / G0700153; United Kingdom / Medical Research Council / / ; United Kingdom / Medical Research Council / / MC/ U123170362; United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Forkhead Transcription Factors; 0 / Foxp3 protein, mouse; 0 / Interleukin-2 Receptor alpha Subunit; 0 / PrPC Proteins
  • [Other-IDs] NLM/ PMC2669135
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26. Giovannetti A, Pierdominici M, Esposito A, Cagliuso M, Stifano G, Giammarioli AM, Maselli A, Malorni W, Salsano F, Aiuti F: Progressive derangement of the T cell compartment in a case of Evans syndrome. Int Arch Allergy Immunol; 2008;145(3):258-67
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  • BACKGROUND: Evans syndrome (ES) is a rare disorder characterized by combined autoimmune thrombocytopenia and autoimmune hemolytic anemia.
  • Finally, restricted TCR repertoires were demonstrated by a skewed TCR beta chain variable (TCRBV) gene usage as well as oligoclonal third complementarity-determining region (CDR3) profiles.
  • A deterioration of the above-mentioned parameters and a worsening of the clinical condition were observed during the follow-up requiring more intensive treatments.
  • [MeSH-major] Anemia, Hemolytic, Autoimmune / immunology. Autoimmune Diseases / immunology. T-Lymphocyte Subsets / physiology. Thrombocytopenia / immunology
  • [MeSH-minor] Adolescent. Antigens, CD4 / analysis. Antigens, CD4 / metabolism. Apoptosis. CD4-Positive T-Lymphocytes / immunology. Cells, Cultured. Complementarity Determining Regions / analysis. Flow Cytometry. Humans. Interferon-gamma / metabolism. Interleukin-2 / metabolism. Interleukin-2 Receptor alpha Subunit / analysis. Interleukin-2 Receptor alpha Subunit / metabolism. Longitudinal Studies. Lymphocyte Activation. Male. Receptors, Antigen, T-Cell, alpha-beta / genetics. Receptors, Antigen, T-Cell, alpha-beta / immunology. Thymus Gland / immunology

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  • [Copyright] 2007 S. Karger AG, Basel
  • (PMID = 17921676.001).
  • [ISSN] 1423-0097
  • [Journal-full-title] International archives of allergy and immunology
  • [ISO-abbreviation] Int. Arch. Allergy Immunol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antigens, CD4; 0 / Complementarity Determining Regions; 0 / Interleukin-2; 0 / Interleukin-2 Receptor alpha Subunit; 0 / Receptors, Antigen, T-Cell, alpha-beta; 82115-62-6 / Interferon-gamma
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27. Tarnopolsky MA, Raha S: Mitochondrial myopathies: diagnosis, exercise intolerance, and treatment options. Med Sci Sports Exerc; 2005 Dec;37(12):2086-93
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  • [Title] Mitochondrial myopathies: diagnosis, exercise intolerance, and treatment options.
  • Mitochondrial myopathies are caused by genetic mutations that directly influence the functioning of the electron transport chain (ETC).
  • Diagnosis often requires a multifaceted approach with measurements of serum lactate and pyruvate, urine organic acids, magnetic resonance spectroscopy (MRS), muscle histology and ultrastructure, enzymology, genetic analysis, and exercise testing.
  • Treatments have included antioxidants (vitamin E, alpha lipoic acid), electron donors and acceptors (coenzyme Q10, riboflavin), alternative energy sources (creatine monohydrate), lactate reduction strategies (dichloroacetate) and exercise training.
  • Exercise is a particularly important modality in diagnosis as well as therapy (see article by Taivassalo in current issue).
  • Increased awareness of these disorders by exercise physiologists and sports medicine practitioners should lead to more accurate and more rapid diagnosis and the opportunity for therapy and genetic counseling.
  • [MeSH-major] Exercise Tolerance / physiology. Mitochondria / pathology. Mitochondrial Myopathies / diagnosis. Muscles / metabolism
  • [MeSH-minor] Antioxidants / therapeutic use. Free Radicals. Humans. Mitochondrial Diseases / physiopathology. Mutation

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  • [CommentIn] Med Sci Sports Exerc. 2005 Dec;37(12):2084-5 [16331133.001]
  • (PMID = 16331134.001).
  • [ISSN] 0195-9131
  • [Journal-full-title] Medicine and science in sports and exercise
  • [ISO-abbreviation] Med Sci Sports Exerc
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antioxidants; 0 / Free Radicals
  • [Number-of-references] 63
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28. Wagner B, Robeson J, McCracken M, Wattrang E, Antczak DF: Horse cytokine/IgG fusion proteins--mammalian expression of biologically active cytokines and a system to verify antibody specificity to equine cytokines. Vet Immunol Immunopathol; 2005 May 1;105(1-2):1-14
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  • Recombinant cytokines are valuable tools for functional studies and candidates for vaccine additives or therapeutic use in various diseases.
  • We generated a mammalian expression system for recombinant cytokines using the equine IgG1 heavy chain constant region as a tag for detection and purification of the expressed cytokine, demonstrated here using equine interferon-gamma (IFN-gamma), interleukin-2 (IL-2), interleukin-4 (IL4) and transforming growth factor-beta1 (TGF-beta1).
  • The resulting IgG1 fusion proteins were composed of the C-terminal heavy chain constant region of the IgG1 (IgGa), and the N-terminal cytokine replacing the immunoglobulin heavy chain variable domain.
  • The fusion proteins were expressed in CHO cells as dimers and their structures had similarity to that of IgG heavy chain antibodies.
  • In contrast to other tags, the IgG1 heavy chain constant region allowed the selection for clones secreting high levels of the recombinant protein by a sensitive ELISA.
  • In addition, the IgG1 heavy chain constant region facilitated identification of stable transfectants by flow cytometry and the secreted recombinant fusion protein by SDS-PAGE and Western blotting.
  • To recover the cytokine from the IgG1 fusion partner, an enterokinase cleavage site was cloned between the cytokine gene and the immunoglobulin heavy chain constant region gene.
  • The purification of the fusion protein by protein G affinity columns, the enterokinase digestion of the cytokine from the IgG1 heavy chain region after or during purification, and the biological activity of the cytokine within the fusion protein or after its isolation was demonstrated in detail for equine IFN-gamma/IgG1 by up-regulation of major histocompatibility complex (MHC) class II expression on horse lymphocytes.
  • [MeSH-minor] Animals. Antibody Specificity. Blotting, Western / veterinary. CHO Cells. Chromatography, Affinity / veterinary. Cloning, Molecular. Cricetinae. Enzyme-Linked Immunosorbent Assay / veterinary. Flow Cytometry / veterinary. Histocompatibility Antigens Class II / immunology. Immunoglobulin Heavy Chains / genetics. Interferon-gamma / biosynthesis. Interferon-gamma / genetics. Interferon-gamma / immunology. Interleukin-2 / biosynthesis. Interleukin-2 / genetics. Interleukin-2 / immunology. Interleukin-4 / biosynthesis. Interleukin-4 / genetics. Interleukin-4 / immunology. Lymphotoxin-alpha / biosynthesis. Lymphotoxin-alpha / genetics. Lymphotoxin-alpha / immunology. Transfection / veterinary

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  • (PMID = 15797470.001).
  • [ISSN] 0165-2427
  • [Journal-full-title] Veterinary immunology and immunopathology
  • [ISO-abbreviation] Vet. Immunol. Immunopathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Cytokines; 0 / Histocompatibility Antigens Class II; 0 / Immunoglobulin G; 0 / Immunoglobulin Heavy Chains; 0 / Interleukin-2; 0 / Lymphotoxin-alpha; 0 / Recombinant Fusion Proteins; 207137-56-2 / Interleukin-4; 82115-62-6 / Interferon-gamma
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29. Gum SI, Jo SJ, Ahn SH, Kim SG, Kim JT, Shin HM, Cho MK: The potent protective effect of wild ginseng (Panax ginseng C.A. Meyer) against benzo[alpha]pyrene-induced toxicity through metabolic regulation of CYP1A1 and GSTs. J Ethnopharmacol; 2007 Jul 25;112(3):568-76
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  • [Title] The potent protective effect of wild ginseng (Panax ginseng C.A. Meyer) against benzo[alpha]pyrene-induced toxicity through metabolic regulation of CYP1A1 and GSTs.
  • In this study, the protective effects of a water extract from the root of WG on benzo[alpha]pyrene (BP)-induced hepatotoxicity and the mechanism of these effects were investigated for the first time.
  • [MeSH-major] Cytochrome P-450 CYP1A1 / genetics. Glutathione Transferase / genetics. Liver Diseases / prevention & control. Panax / chemistry. Plant Extracts / pharmacology
  • [MeSH-minor] Administration, Oral. Alanine Transaminase / blood. Animals. Aspartate Aminotransferases / blood. Benzo(a)pyrene / administration & dosage. Benzo(a)pyrene / toxicity. Blotting, Western. Cell Line. Drug-Induced Liver Injury. Gene Expression / drug effects. Injections, Intraperitoneal. Isoenzymes / genetics. Isoenzymes / metabolism. Lipid Peroxidation / drug effects. Liver / drug effects. Liver / metabolism. Liver / pathology. Metabolic Networks and Pathways / drug effects. Plant Roots / chemistry. RNA, Messenger / genetics. RNA, Messenger / metabolism. Rats. Rats, Sprague-Dawley. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 17590295.001).
  • [ISSN] 0378-8741
  • [Journal-full-title] Journal of ethnopharmacology
  • [ISO-abbreviation] J Ethnopharmacol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Isoenzymes; 0 / Plant Extracts; 0 / RNA, Messenger; 3417WMA06D / Benzo(a)pyrene; EC 1.14.14.1 / Cytochrome P-450 CYP1A1; EC 2.5.1.18 / Glutathione Transferase; EC 2.5.1.18 / glutathione S-transferase Mu 2; EC 2.5.1.18 / glutathione S-transferase alpha; EC 2.6.1.1 / Aspartate Aminotransferases; EC 2.6.1.2 / Alanine Transaminase
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30. Mongerard-Coulanges M, Migianu-Griffoni E, Lecouvey M, Jolles B: Impact of alendronate and VEGF-antisense combined treatment on highly VEGF-expressing A431 cells. Biochem Pharmacol; 2009 May 15;77(10):1580-5
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  • Bisphosphonates, and more specially nitrogen-containing bisphosphonates, which are in current use for the treatment of bone diseases, demonstrate proapoptotic, antiproliferative, antiangiogenic and anti-invasive properties on tumor cells.
  • At 24h, the antitumor properties of alendronate were counterbalanced by a survival process, which consisted of an enhancement of VEGF expression (mRNA and protein secretion) and TGF alpha secretion.
  • The combination of such an antisense with small concentrations of alendronate (approximately 2 microM), which is of the order of clinically used concentrations, was shown to have an antiangiogenic effect as soon as 12h.
  • [MeSH-minor] Cell Line, Tumor. Cell Proliferation / drug effects. Drug Synergism. Enzyme-Linked Immunosorbent Assay. Humans. Reverse Transcriptase Polymerase Chain Reaction. Time Factors. Tumor Necrosis Factor-alpha / biosynthesis. Tumor Necrosis Factor-alpha / secretion

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  • (PMID = 19426694.001).
  • [ISSN] 1873-2968
  • [Journal-full-title] Biochemical pharmacology
  • [ISO-abbreviation] Biochem. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Oligonucleotides, Antisense; 0 / Tumor Necrosis Factor-alpha; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; X1J18R4W8P / Alendronate
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31. Ambra R, Rimbach G, de Pascual Teresa S, Fuchs D, Wenzel U, Daniel H, Virgili F: Genistein affects the expression of genes involved in blood pressure regulation and angiogenesis in primary human endothelial cells. Nutr Metab Cardiovasc Dis; 2006 Jan;16(1):35-43
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  • BACKGROUND: Several lines of evidence suggest that the dietary isoflavone genistein (Gen) has beneficial effects with regard to cardiovascular disease and in particular on aspects related to blood pressure and angiogenesis.
  • Gen significantly affected the expression of genes encoding for proteins centrally involved in the vascular tone such as endothelin-converting enzyme-1, endothelin-2, estrogen related receptor alpha and atrial natriuretic peptide receptor A precursor.
  • [MeSH-minor] Base Sequence. Blotting, Northern. Cells, Cultured. Enzyme Inhibitors / pharmacology. Humans. Lipoproteins, LDL / drug effects. Lipoproteins, LDL / metabolism. Oligonucleotide Array Sequence Analysis. Oxidation-Reduction. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16399490.001).
  • [ISSN] 0939-4753
  • [Journal-full-title] Nutrition, metabolism, and cardiovascular diseases : NMCD
  • [ISO-abbreviation] Nutr Metab Cardiovasc Dis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Lipoproteins, LDL; 0 / oxidized low density lipoprotein; DH2M523P0H / Genistein
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32. Omatsu T, Bak EJ, Ishii Y, Kyuwa S, Tohya Y, Akashi H, Yoshikawa Y: Induction and sequencing of Rousette bat interferon alpha and beta genes. Vet Immunol Immunopathol; 2008 Jul 15;124(1-2):169-76
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  • [Title] Induction and sequencing of Rousette bat interferon alpha and beta genes.
  • Bats are considered to be natural reservoirs for several viruses of clinical importance, including rabies virus, Nipah virus, and Hendra virus.
  • Type I interferons (IFNs) is an important part of the immune system in the defense against viral infection.
  • To investigate the function of type I IFNs upon viral infection in bats, the nucleic acid, and amino acid sequences of Egyptian Rousette (Rousettus aegyptiacus) IFN-alpha and -beta were characterized.
  • Sequence data indicated that bat IFN-alpha consists of 562-bp encoded 187-aa, and IFN-beta consisted of 558-bp encoded 186-aa.
  • Stimulation of bat primary kidney cells (BPKCs) and bat lung cell lines, Tb-1 Lu, with polyinosinic-polycytidylic acid (poly(I:C)) or exogenous bat type I IFNs resulted in increased type I IFNs mRNA expression in BPKCs, but not in Tb-1 Lu.
  • Characterization of the bat IFN-alpha and -beta genes allows understanding of the immune responses upon stimulation in different tissues, thus providing practical strategies for control and treatment of clinically important diseases.
  • These results are important especially for the virus infection, and suggest that future molecular studies on virus infection experiment of bats in vitro will require careful consideration of the differences of type I IFN expression patterns in different cell types.
  • [MeSH-major] Chiroptera / genetics. Chiroptera / immunology. Interferon-alpha / genetics. Interferon-beta / genetics
  • [MeSH-minor] Amino Acid Sequence. Animals. Base Sequence. Cell Line. Cloning, Molecular. DNA / chemistry. DNA / genetics. Molecular Sequence Data. Open Reading Frames. Phylogeny. Poly I-C / immunology. Polymerase Chain Reaction / veterinary

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  • (PMID = 18436311.001).
  • [ISSN] 0165-2427
  • [Journal-full-title] Veterinary immunology and immunopathology
  • [ISO-abbreviation] Vet. Immunol. Immunopathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Interferon-alpha; 24939-03-5 / Poly I-C; 77238-31-4 / Interferon-beta; 9007-49-2 / DNA
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33. Liu L, Ning X, Sun L, Shi Y, Han S, Guo C, Chen Y, Sun S, Yin F, Wu K, Fan D: Involvement of MGr1-Ag/37LRP in the vincristine-induced HIF-1 expression in gastric cancer cells. Mol Cell Biochem; 2007 Sep;303(1-2):151-60
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  • [MeSH-major] Antigens, Neoplasm / metabolism. Antineoplastic Agents, Phytogenic / pharmacology. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Stomach Neoplasms / metabolism. Vincristine / pharmacology
  • [MeSH-minor] Blotting, Western. Caspase 3 / metabolism. Cell Hypoxia. Focal Adhesion Kinase 1 / genetics. Focal Adhesion Kinase 1 / metabolism. Humans. Mitogen-Activated Protein Kinases / metabolism. Phosphatidylinositol 3-Kinases / metabolism. Proto-Oncogene Proteins c-akt / metabolism. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Small Interfering / pharmacology. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction. Transcription, Genetic. Tumor Cells, Cultured

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  • (PMID = 17476462.001).
  • [ISSN] 0300-8177
  • [Journal-full-title] Molecular and cellular biochemistry
  • [ISO-abbreviation] Mol. Cell. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Antineoplastic Agents, Phytogenic; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / MGr1-antigen, human; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 5J49Q6B70F / Vincristine; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.2 / Focal Adhesion Kinase 1; EC 2.7.10.2 / PTK2 protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; EC 3.4.22.- / Caspase 3
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34. Tilkeridis C, Bei T, Garantziotis S, Stratakis CA: Association of a COL1A1 polymorphism with lumbar disc disease in young military recruits. J Med Genet; 2005 Jul;42(7):e44
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  • [Title] Association of a COL1A1 polymorphism with lumbar disc disease in young military recruits.
  • BACKGROUND: Lumbar disc disease (LDD), one of the most common conditions for which patients seek medical care, has been associated with sequence changes of the COL genes.
  • All patients had radiological confirmation of their disease; a control group was also studied.
  • CONCLUSIONS: A previously studied sequence change of the regulatory region of the COL1A1 gene, the same as has previously been associated with low BMD in many populations and LDD in older adults, showed a strong association with LDD in young male soldiers who were recently diagnosed with this disease.
  • [MeSH-major] Collagen Type I / genetics. Intervertebral Disc / pathology. Military Personnel. Polymorphism, Genetic. Spinal Diseases / genetics
  • [MeSH-minor] Adult. Alleles. Bone Density. DNA Mutational Analysis. Genetic Predisposition to Disease. Greece. Heterozygote. Homozygote. Humans. Low Back Pain / etiology. Lumbosacral Region. Magnetic Resonance Imaging. Male

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  • (PMID = 15994869.001).
  • [ISSN] 1468-6244
  • [Journal-full-title] Journal of medical genetics
  • [ISO-abbreviation] J. Med. Genet.
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Collagen Type I; 0 / collagen type I, alpha 1 chain
  • [Other-IDs] NLM/ PMC1736100
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35. Hercus TR, Thomas D, Guthridge MA, Ekert PG, King-Scott J, Parker MW, Lopez AF: The granulocyte-macrophage colony-stimulating factor receptor: linking its structure to cell signaling and its role in disease. Blood; 2009 Aug 13;114(7):1289-98
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  • [Title] The granulocyte-macrophage colony-stimulating factor receptor: linking its structure to cell signaling and its role in disease.
  • Already 20 years have passed since the cloning of the granulocyte-macrophage colony-stimulating factor (GM-CSF) receptor alpha-chain, the first member of the GM-CSF/interleukin (IL)-3/IL-5 family of hemopoietic cytokine receptors to be molecularly characterized.
  • Unlike other hemopoietin receptors, the GM-CSF receptor has a significant nonredundant role in myeloid hematologic malignancies, macrophage-mediated acute and chronic inflammation, pulmonary homeostasis, and allergic disease.
  • The new insights in GM-CSF receptor activation have clinical significance as the structural and signaling nuances can be harnessed for the development of new treatments for malignant and inflammatory diseases.

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  • (PMID = 19436055.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI050744; United States / NIAID NIH HHS / AI / R01-AI50744-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Granulocyte-Macrophage Colony-Stimulating Factor
  • [Number-of-references] 144
  • [Other-IDs] NLM/ PMC2727416
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36. Schuh RA, Matthews CC, Fishman PS: Interaction of mitochondrial respiratory inhibitors and excitotoxins potentiates cell death in hippocampal slice cultures. J Neurosci Res; 2008 Nov 15;86(15):3306-13
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  • The broad-spectrum insecticide rotenone, an inhibitor of complex I of the mitochondrial electron transport chain (ETC), gives rise to oxidative stress and bioenergetic failure.
  • Pesticides including rotenone have been implicated in human neurodegenerative diseases, including Parkinson's disease.
  • Another intensively investigated hypothesis of neurodegenerative disease involves the toxic action of the excitatory neurotransmitter glutamate.
  • In the present study, we determined whether concomitant exposure of rotenone plus tetraethylammonium chloride (TEA) or the specific glutamate receptor agonists N-methyl-D-aspartate (NMDA) or alpha-amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid (AMPA) would cause greater cell death in organotypic hippocampal slice cultures than when given separately.

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  • (PMID = 18615648.001).
  • [ISSN] 1097-4547
  • [Journal-full-title] Journal of neuroscience research
  • [ISO-abbreviation] J. Neurosci. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Excitatory Amino Acid Agonists; 0 / Neurotoxins; 0 / Potassium Channel Blockers; 0 / Uncoupling Agents; 03L9OT429T / Rotenone; 6384-92-5 / N-Methylaspartate; 66-40-0 / Tetraethylammonium
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37. Liu YH, Zhang ZS, Zhong D, Xiao B, Liu J, Wu JB, He JD, Yang YJ, Guo WY: [Screening and preliminary analysis of colorectal carcinoma-associated antigen genes]. Nan Fang Yi Ke Da Xue Xue Bao; 2006 Feb;26(2):166-8, 173
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  • Among the 11 obtained positive clones, 3 were the same cDNA having homology with interferon-induced transmembrance protein-1 and possessing anti-proliferation effect; another 6 represented different genes, namely human BAC clone RP11-453E17 whose function have not been cleared, human cartilage-hair hypoplasia region gene responsible for cartilage-hair hypoplasia, human chromosome 5 clone CTD-2030B15 with insertion mutation, human gene similar to anti tumor necrosis factor-alpha antibody light-chain Fab fragment associated with tumor growth, mRNA of human beta-2-microglobulin in relation to tumor cell proliferation, and human aldolase A gene promoting tumor cell proliferation.

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  • (PMID = 16503520.001).
  • [ISSN] 1673-4254
  • [Journal-full-title] Nan fang yi ke da xue xue bao = Journal of Southern Medical University
  • [ISO-abbreviation] Nan Fang Yi Ke Da Xue Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / DNA, Complementary; 0 / Peptide Library; 0 / TRAPPC10 protein, human; 0 / Vesicular Transport Proteins
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38. Salter-Cid LM, Wang E, O'Rourke AM, Miller A, Gao H, Huang L, Garcia A, Linnik MD: Anti-inflammatory effects of inhibiting the amine oxidase activity of semicarbazide-sensitive amine oxidase. J Pharmacol Exp Ther; 2005 Nov;315(2):553-62
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  • LJP 1207 also reduced serum levels of tumor necrosis factor-alpha and interleukin 6 in lipopolysaccharide (LPS)-challenged mice and prolonged survival post-LPS-induced endotoxemia.
  • Overall, the data suggest that small molecule SSAO/VAP-1 inhibitors may provide clinical benefit in the treatment of acute and chronic inflammatory diseases.
  • [MeSH-minor] Animals. Carrageenan. Cell Adhesion / drug effects. Cloning, Molecular. Colitis / chemically induced. Colitis / drug therapy. Cyclooxygenase 2 / genetics. Cyclooxygenase 2 / metabolism. Cytokines / metabolism. Edema / chemically induced. Edema / drug therapy. Endothelial Cells / drug effects. Endotoxemia / chemically induced. Endotoxemia / drug therapy. Female. Inflammation / drug therapy. Inflammation / pathology. Male. Mice. Mice, Inbred Strains. Oxazolone. Rats. Rats, Sprague-Dawley. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16081681.001).
  • [ISSN] 0022-3565
  • [Journal-full-title] The Journal of pharmacology and experimental therapeutics
  • [ISO-abbreviation] J. Pharmacol. Exp. Ther.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Cytokines; 0 / Hydrazines; 0 / Monoamine Oxidase Inhibitors; 0 / N'-(2-phenylallyl)hydrazine; 15646-46-5 / Oxazolone; 9000-07-1 / Carrageenan; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.4.3.21 / Amine Oxidase (Copper-Containing)
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39. Shaikh M, Mohanty J, Bhasikuttan AC, Pal H: Tuning dual emission behavior of p-dialkylaminobenzonitriles by supramolecular interactions with cyclodextrin hosts. Photochem Photobiol Sci; 2008 Aug;7(8):979-85
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  • Ground state absorption and steady-state and time-resolved fluorescence measurements have been carried out to understand the host-guest interactions of p-diethylaminobenzonitrile (DEABN) and p-dimethylaminobenzonitrile (DMABN) dyes with alpha-cyclodextrin (alpha-CD) and beta-cyclodextrin (beta-CD) hosts.
  • DEABN and DMABN dyes show both locally excited (LE) state and intramolecular charge transfer (ICT) state emissions in solution.
  • The LE and ICT emissions of the dyes are seen to get modulated in the presence of alpha-CD and beta-CD hosts.
  • The results indicate that the dyes form 1 : 1 inclusion complexes with both the hosts.
  • Comparing the binding constants and the fluorescence characteristics of different dye x CD systems it is inferred that DEABN adopts a completely different orientation on complexation with alpha-CD than in the other cases of dye.CD systems.
  • It is indicated that while in all other cases of dye x CD systems the N,N-dialkyl group of the dyes enters the host cavity leaving the C[triple bond, length as m-dash]N group projected out into the water phase, the DEABN dye enters the alpha-CD cavity (smallest CD) with its C[triple bond, length as m-dash]N group entering the host cavity.
  • The differences in the orientation of the dye in the host cavities is understood to be determined by the requirement of maximum van der Waals contact of the encapsulated dye with the host cavity for maximum stability of the complex and the relative sizes of the substituents of the dye compared to the host cavities.

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  • (PMID = 18688506.001).
  • [ISSN] 1474-905X
  • [Journal-full-title] Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology
  • [ISO-abbreviation] Photochem. Photobiol. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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40. Sierra S, Lara-Villoslada F, Comalada M, Olivares M, Xaus J: Dietary fish oil n-3 fatty acids increase regulatory cytokine production and exert anti-inflammatory effects in two murine models of inflammation. Lipids; 2006 Dec;41(12):1115-25
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  • The higher incidence of inflammatory diseases in Western countries might be related, in part, to a high consumption of saturated fatty acids and n-6 polyunsaturated fatty acids (PUFA) and an insufficient intake of n-3 fatty acids.
  • Balb/C mice were fed for 3 wk either n-6 or n-3 PUFA-fortified diets.
  • Reduction in weight, edema, thickness, leukocyte infiltration, and enhancement of antioxidant defenses in the inflamed ears of mice from both models along with the prevention of delayed-type hypersensitivity induced in atopic dermatitis proved n-3 PUFA efficacy.
  • [MeSH-minor] Animals. Anti-Inflammatory Agents / administration & dosage. Anti-Inflammatory Agents / pharmacology. Cell Proliferation / drug effects. Cells, Cultured. Dermatitis / prevention & control. Eicosanoids / metabolism. Enzyme-Linked Immunosorbent Assay. Gene Expression / drug effects. Lipids / blood. Lymphocytes / cytology. Lymphocytes / drug effects. Lymphocytes / metabolism. Macrophages / drug effects. Macrophages / metabolism. Male. Mice. Mice, Inbred BALB C. PPAR alpha / genetics. PPAR gamma / genetics. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 17269557.001).
  • [ISSN] 0024-4201
  • [Journal-full-title] Lipids
  • [ISO-abbreviation] Lipids
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Cytokines; 0 / Eicosanoids; 0 / Fatty Acids, Omega-3; 0 / Fish Oils; 0 / Lipids; 0 / PPAR alpha; 0 / PPAR gamma; 0 / RNA, Messenger
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41. Collado-Romero M, Arce C, Ramírez-Boo M, Carvajal A, Garrido JJ: Quantitative analysis of the immune response upon Salmonella typhimurium infection along the porcine intestinal gut. Vet Res; 2010 Mar-Apr;41(2):23
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  • [Title] Quantitative analysis of the immune response upon Salmonella typhimurium infection along the porcine intestinal gut.
  • Salmonella enterica serovar Typhimurium causes enteric disease and compromises food safety.
  • In pigs, the molecular response of the intestine to S. typhimurium has been traditionally characterized by in vitro models that do not reflect the actual immunological competence of the intestinal mucosa.
  • In this work, we performed an oral S. typhimurium infection study to obtain insight into the in vitro response in three different sections (jejunum, ileum and colon) of the porcine intestine.
  • For this, samples from one-month-old infected piglets were collected during a time course comprising 1, 2, and 6 days post inoculation to evaluate the intestinal response by quantifying the mRNA expression of gene coding for 28 innate immune system molecules using quantitative real-time PCR assays.
  • In addition, samples from non-infected control animals were also employed to establish differences in the steady state gene expression between intestinal sections.
  • Changes in gene expression occurred in the three different parts of the intestine and during the course of the S. typhimurium infection.
  • Moreover, the high variation observed in expression patterns of genes coding for inflammatory mediators could indicate that each intestinal section responds differently to the infection.
  • In conclusion, our results reveal regional differences in gene expression profiles along the porcine intestinal gut as well as regional differences in the inflammatory response to S. typhimurium infection.
  • Taken together, these data should provide a basis for a complete understanding of the porcine intestinal response to bacterial infection.
  • [MeSH-major] Intestinal Mucosa / immunology. Salmonella Infections, Animal / immunology. Salmonella typhimurium / immunology. Swine Diseases / immunology
  • [MeSH-minor] Animals. Caspase 1 / genetics. Caspase 1 / metabolism. Female. Gene Expression Profiling. Gene Expression Regulation. Interleukin-8 / blood. Interleukin-8 / metabolism. Male. Myeloid Differentiation Factor 88 / genetics. Myeloid Differentiation Factor 88 / metabolism. NF-kappa B / genetics. NF-kappa B / metabolism. Polymerase Chain Reaction / veterinary. RNA, Messenger / genetics. RNA, Messenger / metabolism. Swine. Tumor Necrosis Factor-alpha / blood. Tumor Necrosis Factor-alpha / metabolism

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  • [Copyright] INRA, EDP Sciences, 2010
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  • (PMID = 19941811.001).
  • [ISSN] 0928-4249
  • [Journal-full-title] Veterinary research
  • [ISO-abbreviation] Vet. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Interleukin-8; 0 / Myeloid Differentiation Factor 88; 0 / NF-kappa B; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; EC 3.4.22.36 / Caspase 1
  • [Other-IDs] NLM/ PMC2820228
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42. Zimman A, Chen SS, Komisopoulou E, Titz B, Martínez-Pinna R, Kafi A, Berliner JA, Graeber TG: Activation of aortic endothelial cells by oxidized phospholipids: a phosphoproteomic analysis. J Proteome Res; 2010 Jun 4;9(6):2812-24
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  • Previous studies have shown that oxidized products of the phospholipid PAPC (Ox-PAPC) are strong activators of aortic endothelial cells and play an important role in atherosclerosis and other inflammatory diseases.

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  • (PMID = 20307106.001).
  • [ISSN] 1535-3907
  • [Journal-full-title] Journal of proteome research
  • [ISO-abbreviation] J. Proteome Res.
  • [Language] ENG
  • [Grant] United States / NHGRI NIH HHS / HG / K22 HG002807-05; United States / NHGRI NIH HHS / HG / HG002807; United States / NHLBI NIH HHS / HL / HL030568; United States / NHGRI NIH HHS / HG / K22 HG002807; United States / NHLBI NIH HHS / HL / HL030568-150006; United States / NCI NIH HHS / CA / T32 CA009056; None / None / / K22 HG002807-05; United States / NHLBI NIH HHS / HL / P01 HL030568; United States / NHLBI NIH HHS / HL / P01 HL030568-150006
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Myosin Light Chains; 0 / Peptide Fragments; 0 / Phosphatidylcholines; 0 / Phosphoproteins; 0 / Proteome; 0 / myosin light chain 2; 0 / oxidized-L-alpha-1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphorylcholine; EC 2.7.10.1 / Receptor, TIE-1; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 3.6.1.- / Cardiac Myosins
  • [Other-IDs] NLM/ NIHMS193036; NLM/ PMC2922471
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43. Ergang P, Leden P, Bryndová J, Zbánková S, Miksík I, Kment M, Pácha J: Glucocorticoid availability in colonic inflammation of rat. Dig Dis Sci; 2008 Aug;53(8):2160-7
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  • Recent in vitro studies have shown the involvement of pro-inflammatory cytokines in the regulation of the local metabolism of glucocorticoids via 11beta-hydroxysteroid dehydrogenase type 1 and type 2 (11HSD1 and 11HSD2).
  • We have therefore examined the changes in the local metabolism of glucocorticoids during colonic inflammation induced by TNBS and the consequences of corticosterone metabolism inhibition by carbenoxolone on 11HSD1, 11HSD2, cyclooxygenase 2 (COX-2), mucin 2 (MUC-2), tumor necrosis factor alpha (TNF-alpha), and interleukin 1beta (IL-1beta).
  • The metabolism of glucocorticoids was measured in tissue slices in vitro and their 11HSD1, 11HSD2, COX-2, MUC-2, TNF-alpha, and IL-1beta mRNA abundances by quantitative reverse transcription-polymerase chain reaction.
  • In contrast to the local metabolism of glucocorticoids, carbenoxolone neither potentiates nor diminishes gene expression for COX-2, TNF-alpha, and IL-1beta, despite the fact that budesonide down-regulated all of them.
  • However, these changes in the local metabolism of glucocorticoids do not modulate the expression of COX-2, TNF-alpha, and IL-1beta in inflamed tissue.
  • [MeSH-minor] 11-beta-Hydroxysteroid Dehydrogenase Type 1 / genetics. 11-beta-Hydroxysteroid Dehydrogenase Type 1 / metabolism. 11-beta-Hydroxysteroid Dehydrogenase Type 2 / genetics. 11-beta-Hydroxysteroid Dehydrogenase Type 2 / metabolism. Animals. Budesonide / pharmacology. Carbenoxolone / pharmacology. Cyclooxygenase 2 / genetics. Cyclooxygenase 2 / metabolism. Disease Models, Animal. Hormone Antagonists / pharmacology. Interleukin-1beta / genetics. Interleukin-1beta / metabolism. Male. Mifepristone / pharmacology. Mucin-2. Mucins / genetics. Mucins / metabolism. Peroxidase / metabolism. RNA, Messenger / metabolism. Rats. Rats, Wistar. Reverse Transcriptase Polymerase Chain Reaction. Trinitrobenzenesulfonic Acid. Tumor Necrosis Factor-alpha / genetics. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 18095161.001).
  • [ISSN] 0163-2116
  • [Journal-full-title] Digestive diseases and sciences
  • [ISO-abbreviation] Dig. Dis. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glucocorticoids; 0 / Hormone Antagonists; 0 / Interleukin-1beta; 0 / Muc2 protein, rat; 0 / Mucin-2; 0 / Mucins; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 320T6RNW1F / Mifepristone; 51333-22-3 / Budesonide; 8T3HQG2ZC4 / Trinitrobenzenesulfonic Acid; EC 1.1.1.146 / 11-beta-Hydroxysteroid Dehydrogenase Type 1; EC 1.1.1.146 / 11-beta-Hydroxysteroid Dehydrogenase Type 2; EC 1.11.1.7 / Peroxidase; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / Ptgs2 protein, rat; MM6384NG73 / Carbenoxolone; W980KJ009P / Corticosterone
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44. Zhu ZX, Xu YJ, Zou H, Zhang ZX, Ni W, Chen SX: [Pulmonary vascular remodeling and protein kinase C-alpha expression in chronic smoke exposure and/or hypoxia rats]. Zhonghua Jie He He Hu Xi Za Zhi; 2005 Dec;28(12):825-9
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  • [Title] [Pulmonary vascular remodeling and protein kinase C-alpha expression in chronic smoke exposure and/or hypoxia rats].
  • OBJECTIVE: To investigate pulmonary vascular remodeling and protein kinase C-alpha (PKC-alpha) expression in chronic smoke exposure and/or hypoxia rats.
  • To evaluate vascular remodeling, alpha-smooth muscle actin (alpha-SM-actin) staining and count of the percentage of muscularized small pulmonary arteries which was determined by morphometric analysis of histological sections were used.
  • Reverse transcription-polymerase chain reaction (RT-PCR), immunofluorescence staining and Western blot analysis were used for the detection of PKC-alpha mRNA and protein expression in pulmonary arteries.
  • In S(4W), S(8W), H(4W), H(8W), SH(4W) and SH(8W) group, RVHI (0.258 +/- 0.024, 0.394 +/- 0.021, 0.374 +/- 0.020, 0.414 +/- 0.019, 0.434 +/- 0.023, 0.442 +/- 0.020, respectively), the percentage of muscularized arteries [(33.5 +/- 6.8)%, (41.1 +/- 9.8)%, (35.9 +/- 6.6)%, (46.0 +/- 6.3)%, (42.9 +/- 6.5)%, (50.2 +/- 9.9)%, respectively] and alpha-SM-actin expression (53 +/- 15, 75 +/- 14, 56 +/- 11, 82 +/- 17, 83 +/- 17, 98 +/- 16, respectively) were increased significantly (all P < 0.01).
  • The expressions of PKC-alpha mRNA and protein were higher than those of C group (all P < 0.01).
  • [MeSH-major] Anoxia. Environmental Exposure. Muscle, Smooth, Vascular / metabolism. Protein Kinase C-alpha / metabolism. Smoke / adverse effects

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  • (PMID = 16409783.001).
  • [ISSN] 1001-0939
  • [Journal-full-title] Zhonghua jie he he hu xi za zhi = Zhonghua jiehe he huxi zazhi = Chinese journal of tuberculosis and respiratory diseases
  • [ISO-abbreviation] Zhonghua Jie He He Hu Xi Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Smoke; EC 2.7.11.13 / Protein Kinase C-alpha
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45. Gomes MA, Rodrigues FH, Afonso-Cardoso SR, Buso AM, Silva AG, Favoreto S Jr, Souza MA: Levels of immunoglobulin A1 and messenger RNA for interferon gamma and tumor necrosis factor alpha in total saliva from patients with diabetes mellitus type 2 with chronic periodontal disease. J Periodontal Res; 2006 Jun;41(3):177-83
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  • [Title] Levels of immunoglobulin A1 and messenger RNA for interferon gamma and tumor necrosis factor alpha in total saliva from patients with diabetes mellitus type 2 with chronic periodontal disease.
  • BACKGROUND: Diabetes mellitus and periodontal disease have high incidence in the general population and are associated with various degrees of dysfunction in the immune system.
  • It has been shown that diabetic patients with severe periodontal disease have more complications of diabetes and less effective metabolic control compared with diabetic patients with healthy gingiva.
  • Patients with diabetes and severe periodontal disease present higher levels of serous immunoglobulin A (IgA).
  • OBJECTIVE: In this study we tested the hypothesis that type 2 diabetic patients with chronic moderate periodontal disease have differences in salivary IgA1 titers and cytokine expression when compared with the chronic severe periodontal disease cases.
  • METHODS: We utilized a jacalin-IgA capture assay to determine the IgA1 titers in total saliva and reverse transcriptase-polymerase chain reaction to detect mRNA for interferon gamma (IFN-gamma) and tumor necrosis factor alpha (TNF-alpha) in total saliva samples of 13 patients with chronic moderate periodontal disease and 10 with chronic severe periodontal disease.
  • RESULTS AND CONCLUSIONS: We observed a predominance of IgA1 titers of 64 (45.5%) in saliva samples from chronic severe periodontal disease patients and titers averaging 512 (30.8%) in chronic moderate periodontal disease patients.
  • We detected mRNA for IFN-gamma in six out of 10 chronic severe periodontal disease subjects and in two out of 13 chronic moderate periodontal disease patients.
  • TNF-alpha expression was similar in both groups.
  • Our data suggest that higher levels of IgA1 may exert partial protection of the periodontal tissue in chronic moderate periodontal disease diabetic patients when compared to severe periodontal disease.
  • Despite the small number of patients, IFN-gamma expression had a trend association with severity of periodontitis and TNF-alpha gene expression did not correlate with severity of periodontal disease.
  • [MeSH-major] Diabetes Mellitus, Type 2 / immunology. Immunoglobulin A / analysis. Interferon-gamma / analysis. Periodontal Diseases / immunology. RNA, Messenger / analysis. Saliva / immunology. Tumor Necrosis Factor-alpha / analysis
  • [MeSH-minor] Artocarpus. Chronic Disease. Female. Humans. Male. Middle Aged. Plant Lectins. Reverse Transcriptase Polymerase Chain Reaction. Salivary Proteins and Peptides / analysis

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  • (PMID = 16677285.001).
  • [ISSN] 0022-3484
  • [Journal-full-title] Journal of periodontal research
  • [ISO-abbreviation] J. Periodont. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Immunoglobulin A; 0 / Plant Lectins; 0 / RNA, Messenger; 0 / Salivary Proteins and Peptides; 0 / Tumor Necrosis Factor-alpha; 0 / jacalin; 82115-62-6 / Interferon-gamma
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46. Xiaomin L, Fenglin C, Jianmin H, Yuzhi S, Binsheng G, Yingmei Z: Correlation between genetic polymorphism of cytokine genes, plasma protein levels and bronchial asthma in the Han people in northern China. J Asthma; 2008 Sep;45(7):583-9
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  • The polymorphism-based genotypes were identified by the sequence-specific primer-polymerase chain reaction.
  • In this network, IL-6 and TNF-alpha, were found with a high degree (D = 343 and 235, respectively) and IL-1beta with a moderate degree of connection (D = 155).
  • During the analysis of correlation between genetic polymorphism and a complex disease, the effects of environmental factors should be taken into account.
  • The information at the protein level should be fully developed and the bioinformatics techniques can be used for the comprehensive analysis, to have a deep understanding of molecular mechanisms of incidence and development of diseases.
  • [MeSH-minor] Adolescent. Adult. Aged. Case-Control Studies. China / epidemiology. Enzyme-Linked Immunosorbent Assay. Female. Gene Expression. Genetic Predisposition to Disease. Humans. Incidence. Male. Middle Aged. Polymerase Chain Reaction

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  • (PMID = 18773331.001).
  • [ISSN] 1532-4303
  • [Journal-full-title] The Journal of asthma : official journal of the Association for the Care of Asthma
  • [ISO-abbreviation] J Asthma
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Blood Proteins; 0 / Cytokines
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47. Murakami M, Ohta T, Ito S: Interleukin-1beta enhances the action of bradykinin in rat myenteric neurons through up-regulation of glial B1 receptor expression. Neuroscience; 2008 Jan 2;151(1):222-31
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  • Interleukin (IL)-1beta and tumor necrosis factor alpha (TNFalpha) are released under pathological conditions in the gastrointestinal tract such as inflammatory bowel diseases (IBD).
  • In both cell types, the [Ca(2+)]i responses to BK were abolished by D-Arg(0)[Hyp(3), Thi(5), D-Tic(7), Oic(8)]-BK (HOE140), a B2R antagonist, but not affected by des-Arg(9)-HOE140, a B1R antagonist.
  • Only in glial cells did the B1R agonists des-Arg(9)-BK and BK fragment 1-8 evoke a [Ca(2+)]i rise in a dose-dependent manner.
  • The alteration of phenotypes of glial cells may be the cause of the changes in neural function in the enteric nervous system in IBD.
  • [MeSH-minor] Animals. Calcium / metabolism. Calcium / physiology. Cells, Cultured. Cytokines / biosynthesis. Dinoprostone / metabolism. Dinoprostone / physiology. Enteric Nervous System / drug effects. Female. Immunohistochemistry. Male. Neuroglia / drug effects. Neuroglia / metabolism. Rats. Rats, Wistar. Receptor Cross-Talk / drug effects. Receptor, Bradykinin B1 / biosynthesis. Receptor, Bradykinin B1 / drug effects. Reverse Transcriptase Polymerase Chain Reaction. Tumor Necrosis Factor-alpha / pharmacology. Up-Regulation / drug effects

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  • (PMID = 18053651.001).
  • [ISSN] 0306-4522
  • [Journal-full-title] Neuroscience
  • [ISO-abbreviation] Neuroscience
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines; 0 / Interleukin-1beta; 0 / Receptor, Bradykinin B1; 0 / Tumor Necrosis Factor-alpha; K7Q1JQR04M / Dinoprostone; S8TIM42R2W / Bradykinin; SY7Q814VUP / Calcium
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48. Gary-Bobo M, Elachouri G, Gallas JF, Janiak P, Marini P, Ravinet-Trillou C, Chabbert M, Cruccioli N, Pfersdorff C, Roque C, Arnone M, Croci T, Soubrié P, Oury-Donat F, Maffrand JP, Scatton B, Lacheretz F, Le Fur G, Herbert JM, Bensaid M: Rimonabant reduces obesity-associated hepatic steatosis and features of metabolic syndrome in obese Zucker fa/fa rats. Hepatology; 2007 Jul;46(1):122-9
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  • This study investigated the effects of rimonabant (SR141716), an antagonist of the cannabinoid receptor type 1 (CB1), on obesity-associated hepatic steatosis and related features of metabolic syndrome: inflammation (elevated plasma levels of tumor necrosis factor alpha [TNFalpha]), dyslipidemia, and reduced plasma levels of adiponectin.
  • These results demonstrate that rimonabant plays a hepatoprotective role and suggest that this CB1 receptor antagonist potentially has clinical applications in the treatment of obesity-associated liver diseases and related features of metabolic syndrome.
  • [MeSH-minor] Animals. Cannabinoid Receptor Antagonists. Inflammation / prevention & control. Liver / drug effects. Liver / pathology. Male. RNA / genetics. RNA / isolation & purification. Rats. Rats, Zucker. Reverse Transcriptase Polymerase Chain Reaction. Tumor Necrosis Factor-alpha / blood


49. Zhang W, Sharma R, Ju ST, He XS, Tao Y, Tsuneyama K, Tian Z, Lian ZX, Fu SM, Gershwin ME: Deficiency in regulatory T cells results in development of antimitochondrial antibodies and autoimmune cholangitis. Hepatology; 2009 Feb;49(2):545-52
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  • There have been several descriptions of mouse models that manifest select immunological and clinical features of autoimmune cholangitis with similarities to primary biliary cirrhosis in humans.
  • Some of these models require immunization with complete Freund's adjuvant, whereas others suggest that a decreased frequency of T regulatory cells (Tregs) facilitates spontaneous disease.
  • Furthermore, mice have moderate to severe lymphocytic infiltrates surrounding portal areas with evidence of biliary duct damage, and dramatic elevation of cytokines in serum and messenger RNAs encoding cytokines in liver tissue, including tumor necrosis factor alpha, interferon-gamma, interleukin (IL)-6, IL-12, and IL-23.

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  • (PMID = 19065675.001).
  • [ISSN] 1527-3350
  • [Journal-full-title] Hepatology (Baltimore, Md.)
  • [ISO-abbreviation] Hepatology
  • [Language] ENG
  • [Grant] United States / NIAMS NIH HHS / AR / P50 AR045222; United States / NIDDK NIH HHS / DK / DK074768; United States / NIAMS NIH HHS / AR / AR051203; United States / NIDDK NIH HHS / DK / DK039588-21; United States / NIDDK NIH HHS / DK / R21 DK077961; United States / NIAMS NIH HHS / AR / AR047988; United States / NIDDK NIH HHS / DK / R01 DK074768; United States / NIDDK NIH HHS / DK / DK39588; United States / NIAMS NIH HHS / AR / R01 AR051203; United States / NIDDK NIH HHS / DK / R37 DK039588-21; United States / NIDCR NIH HHS / DE / DE017579; United States / NIAMS NIH HHS / AR / AR049449; United States / NIAMS NIH HHS / AR / R01 AR049449; United States / NIDDK NIH HHS / DK / R37 DK039588; United States / NIAMS NIH HHS / AR / R01 AR047988; United States / NIDDK NIH HHS / DK / R01 DK039588; United States / NIAMS NIH HHS / AR / AR045222; United States / NIDDK NIH HHS / DK / DK077961
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines
  • [Other-IDs] NLM/ NIHMS77273; NLM/ PMC2635418
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50. Sakamoto A, Chen M, Nakamura T, Xie T, Karsenty G, Weinstein LS: Deficiency of the G-protein alpha-subunit G(s)alpha in osteoblasts leads to differential effects on trabecular and cortical bone. J Biol Chem; 2005 Jun 3;280(22):21369-75
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  • [Title] Deficiency of the G-protein alpha-subunit G(s)alpha in osteoblasts leads to differential effects on trabecular and cortical bone.
  • The G-protein alpha-subunit G(s)alpha is required for the intracellular cAMP responses to hormones and other agonists.
  • G(s)alpha is known to mediate the cAMP response to parathyroid hormone and other hormones and cytokines in bone and cartilage.
  • To analyze the in vivo role of G(s)alpha signaling in osteoblasts, we developed mice with osteoblast/osteocyte-specific G(s)alpha deficiency (BGsKO) by mating G(s)alpha-floxed mice with collagen Ialpha1 promoter-Cre recombinase transgenic mice.
  • Overall, our findings have similarities to parathyroid hormone null mice and confirm that the differential effects of parathyroid hormone on trabecular and cortical bone are primarily mediated via G(s)alpha in osteoblasts.
  • Osteoblast-specific G(s)alpha deficiency leads to reduced bone turnover.
  • [MeSH-major] Bone and Bones / metabolism. GTP-Binding Protein alpha Subunits, Gs / chemistry. Osteoblasts / metabolism
  • [MeSH-minor] Acid Phosphatase / pharmacology. Alkaline Phosphatase / metabolism. Animals. Bone Marrow Cells / metabolism. Carrier Proteins / metabolism. Cartilage / metabolism. Cell Differentiation. Chondrocytes / metabolism. Collagen Type I / metabolism. Cyclic AMP / metabolism. Cytokines / metabolism. DNA Primers / chemistry. Gene Expression Regulation. Isoenzymes / pharmacology. Membrane Glycoproteins / metabolism. Mice. Mice, Knockout. Mice, Transgenic. Models, Biological. Models, Genetic. Osteocalcin / metabolism. Osteopontin. Phenotype. Polymerase Chain Reaction. Promoter Regions, Genetic. RANK Ligand. Receptor Activator of Nuclear Factor-kappa B. Reverse Transcriptase Polymerase Chain Reaction. Sialoglycoproteins / metabolism. Signal Transduction. Skull / metabolism. Time Factors


51. Ramasawmy R, Cunha-Neto E, Faé KC, Müller NG, Cavalcanti VL, Drigo SA, Ianni B, Mady C, Kalil J, Goldberg AC: BAT1, a putative anti-inflammatory gene, is associated with chronic Chagas cardiomyopathy. J Infect Dis; 2006 May 15;193(10):1394-9
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  • Heart-infiltrating lymphocytes from patients with CCC also express proinflammatory cytokines (tumor necrosis factor- alpha and interferon- gamma ) that are detectable in biopsy samples and surgical heart-tissue samples.
  • METHODS: We assessed, by polymerase chain reaction restriction fragment-length polymorphism analysis, BAT1 variants in the promoter region at positions -22C/G and -348C/T in 154 patients with CCC and in 76 T. cruzi-infected but asymptomatic (ASY) patients.
  • [MeSH-major] Chagas Cardiomyopathy / genetics. Genetic Predisposition to Disease. RNA Helicases / genetics
  • [MeSH-minor] Brazil. Chronic Disease. DEAD-box RNA Helicases. DNA / analysis. Female. Humans. Male. Middle Aged. Polymerase Chain Reaction. Polymorphism, Genetic. Polymorphism, Restriction Fragment Length. Promoter Regions, Genetic / genetics

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  • (PMID = 16619187.001).
  • [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] 9007-49-2 / DNA; EC 3.6.1.- / DDX39B protein, human; EC 3.6.4.13 / DEAD-box RNA Helicases; EC 3.6.4.13 / RNA Helicases
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52. Giamarellos-Bourboulis EJ, Mouktaroudi M, Bodar E, van der Ven J, Kullberg BJ, Netea MG, van der Meer JW: Crystals of monosodium urate monohydrate enhance lipopolysaccharide-induced release of interleukin 1 beta by mononuclear cells through a caspase 1-mediated process. Ann Rheum Dis; 2009 Feb;68(2):273-8
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  • Production of tumour necrosis factor alpha (TNFalpha), interleukin (IL)1 beta and IL6, as well as the intracellular concentrations of proIL1 beta were measured by ELISA. mRNA transcripts of TNFalpha and IL1 beta were assessed by real-time PCR.
  • [MeSH-minor] Adult. Carrier Proteins / genetics. Cells, Cultured. Crystallization. Cytokines / biosynthesis. Dose-Response Relationship, Immunologic. Female. Gene Expression Regulation / immunology. Humans. Inflammation Mediators / metabolism. Male. Mutation. Polymerase Chain Reaction / methods. RNA, Messenger / genetics. Young Adult

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  • (PMID = 18390571.001).
  • [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 / Carrier Proteins; 0 / Cytokines; 0 / Inflammation Mediators; 0 / Interleukin-1beta; 0 / Lipopolysaccharides; 0 / NLRP3 protein, human; 0 / RNA, Messenger; 268B43MJ25 / Uric Acid; EC 3.4.22.36 / Caspase 1
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53. Tripputi P, Bianchi S, Fedele L: A possible mechanism for non-replication of allelic association between a single nucleotide polymorphism of the human beta T-cell receptor and autoimmune diseases. Int J Immunogenet; 2008 Apr;35(2):141-4
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  • [Title] A possible mechanism for non-replication of allelic association between a single nucleotide polymorphism of the human beta T-cell receptor and autoimmune diseases.
  • Gene polymorphisms, in particular single nucleotide polymorphisms (SNPs), have been associated to multifactorial diseases such as cancer, inflammation and autoimmunity.
  • Indeed for some autoimmune diseases, it has been possible to identify critical residues that play a major role in susceptibility to diseases.
  • The association of a common T/C polymorphism in the promoter region of the beta 2 constant chain of the T-cell receptor with autoimmune diseases, such as insulin-dependent diabetes, autoimmune hepatitis, IgA nephropathy, membranous nephropathy, Graves' disease and Hashimoto's thyroiditis, was described in the 1990 s.
  • This finding led us to make an allele frequency study of this single nucleotide polymorphism between sexes in a new series of patients.
  • If the higher frequency of CC homozygous genotype (that is associated with an increased risk of autoimmune diseases) in females would be confirmed in normal population, this could be an explanation of the controversial results obtained by association studies made between this SNP and autoimmune diseases.
  • [MeSH-major] Alleles. Autoimmune Diseases / genetics. Gene Frequency / genetics. Polymorphism, Single Nucleotide. Receptors, Antigen, T-Cell, alpha-beta / genetics

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  • (PMID = 18279372.001).
  • [ISSN] 1744-313X
  • [Journal-full-title] International journal of immunogenetics
  • [ISO-abbreviation] Int. J. Immunogenet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Receptors, Antigen, T-Cell, alpha-beta
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54. Pettersson-Kastberg J, Aits S, Gustafsson L, Mossberg A, Storm P, Trulsson M, Persson F, Mok KH, Svanborg C: Can misfolded proteins be beneficial? The HAMLET case. Ann Med; 2009;41(3):162-76
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  • Amyloid-forming proteins are one example, in which conformational change may lead to fibril formation and, in many cases, neurodegenerative disease.
  • We have proposed that partial unfolding provides a mechanism to generate new and useful functional variants from a given polypeptide chain.
  • Here we present HAMLET (Human Alpha-lactalbumin Made LEthal to Tumor cells) as an example where partial unfolding and the incorporation of cofactor create a complex with new, beneficial properties.
  • Native alpha-lactalbumin functions as a substrate specifier in lactose synthesis, but when partially unfolded the protein binds oleic acid and forms the tumoricidal HAMLET complex.
  • [MeSH-minor] Amyloid / chemistry. Amyloid / metabolism. Animals. Antimicrobial Cationic Peptides / chemistry. Antimicrobial Cationic Peptides / metabolism. Antineoplastic Agents / chemistry. Antineoplastic Agents / therapeutic use. Calcium / metabolism. Cell Death / drug effects. Humans. Models, Molecular. Neoplasms / drug therapy. Neoplasms / metabolism. Neoplasms / pathology. Neurodegenerative Diseases / metabolism. Neurodegenerative Diseases / pathology. Prions / chemistry. Prions / metabolism. Protein Binding. Protein Conformation

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  • (PMID = 18985467.001).
  • [ISSN] 1365-2060
  • [Journal-full-title] Annals of medicine
  • [ISO-abbreviation] Ann. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Sweden
  • [Chemical-registry-number] 0 / Amyloid; 0 / Antimicrobial Cationic Peptides; 0 / Antineoplastic Agents; 0 / HAMLET complex, human; 0 / Oleic Acids; 0 / Prions; 9013-90-5 / Lactalbumin; SY7Q814VUP / Calcium
  • [Number-of-references] 106
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55. Nishida H, Ichikawa H, Konishi T: Shengmai-san enhances antioxidant potential in C2C12 myoblasts through the induction of intracellular glutathione peroxidase. J Pharmacol Sci; 2007 Dec;105(4):342-52
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  • Because of its antioxidative property, SMS might be useful not only for the oxidative damage associated diseases but also for the transplantation of myoblasts into muscular dystrophy patients.
  • [MeSH-minor] Acetylcysteine / pharmacology. Animals. Apoptosis / drug effects. Cell Line. Cell Survival / drug effects. Dose-Response Relationship, Drug. Drug Combinations. Drug Synergism. Enzyme-Linked Immunosorbent Assay. Glutathione / metabolism. Hydrogen Peroxide / pharmacology. Immunoblotting. Immunohistochemistry. In Situ Nick-End Labeling. Intracellular Fluid / drug effects. Intracellular Fluid / enzymology. Protein Carbonylation / drug effects. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Time Factors. alpha-Tocopherol / pharmacology

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  • (PMID = 18057775.001).
  • [ISSN] 1347-8613
  • [Journal-full-title] Journal of pharmacological sciences
  • [ISO-abbreviation] J. Pharmacol. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antioxidants; 0 / Drug Combinations; 0 / Drugs, Chinese Herbal; 0 / RNA, Messenger; 0 / fructus schizandrae, radix ginseng, radix ophiopogonis drug combination; BBX060AN9V / Hydrogen Peroxide; EC 1.11.1.9 / Glutathione Peroxidase; GAN16C9B8O / Glutathione; H4N855PNZ1 / alpha-Tocopherol; WYQ7N0BPYC / Acetylcysteine
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56. Hu XD, Yang Y, Zhong XG, Zhang XH, Zhang YN, Zheng ZP, Zhou Y, Tang W, Yang YF, Hu LH, Zuo JP: Anti-inflammatory effects of Z23 on LPS-induced inflammatory responses in RAW264.7 macrophages. J Ethnopharmacol; 2008 Dec 8;120(3):447-51
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  • RESULTS: Z23 significantly decreased the production of PGE2, NO, tumour necrosis factor alpha (TNFalpha) and IL6 production.
  • ) Merr and indicated that Z23 has the potential for treatment of various inflammatory diseases where the overproduction of NO, PGE2 and inflammatory cytokines has been shown to play a role, e.g. rheumatoid arthritis.
  • [MeSH-major] Amides / pharmacology. Annonaceae / chemistry. Anti-Inflammatory Agents / pharmacology. Interleukin-6 / metabolism. Nitric Oxide / metabolism. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Animals. Cell Line. Cyclooxygenase 2 / genetics. Cyclooxygenase 2 / metabolism. Cytokines / metabolism. Dinoprostone / metabolism. Gene Expression. Herbal Medicine. Lipopolysaccharides. Macrophages / drug effects. Macrophages / metabolism. Medicine, Chinese Traditional. Mice. Nitric Oxide Synthase / genetics. Nitric Oxide Synthase / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 18952160.001).
  • [ISSN] 0378-8741
  • [Journal-full-title] Journal of ethnopharmacology
  • [ISO-abbreviation] J Ethnopharmacol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / 7'-(3',4'-dihydroxyphenyl)-N-((4-methoxyphenyl)ethyl)propenamide; 0 / Amides; 0 / Anti-Inflammatory Agents; 0 / Cytokines; 0 / Interleukin-6; 0 / Lipopolysaccharides; 0 / Tumor Necrosis Factor-alpha; 31C4KY9ESH / Nitric Oxide; EC 1.14.13.39 / Nitric Oxide Synthase; EC 1.14.99.1 / Cyclooxygenase 2; K7Q1JQR04M / Dinoprostone
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57. Lau AC, Duong TT, Ito S, Yeung RS: Intravenous immunoglobulin and salicylate differentially modulate pathogenic processes leading to vascular damage in a model of Kawasaki disease. Arthritis Rheum; 2009 Jul;60(7):2131-41
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  • [Title] Intravenous immunoglobulin and salicylate differentially modulate pathogenic processes leading to vascular damage in a model of Kawasaki disease.
  • OBJECTIVE: Kawasaki disease (KD) is a multisystem vasculitis affecting children and is characterized by immune activation in the acute stage of disease.
  • KD is the leading cause of acquired heart disease among children in North America.
  • The aim of this study was to examine the effect of IVIG and salicylate at each stage of disease development.
  • METHODS: Using a murine model of KD, we established and validated several in vitro techniques to reflect 3 key steps involved in disease pathogenesis, as follows: thymidine incorporation to evaluate T cell activation, enzyme-linked immunosorbent assay to measure tumor necrosis factor alpha (TNFalpha) production, and real-time polymerase chain reaction to examine TNFalpha-mediated expression of matrix metalloproteinase 9 (MMP-9).
  • [MeSH-major] Immunoglobulins, Intravenous / therapeutic use. Immunologic Factors / therapeutic use. Mucocutaneous Lymph Node Syndrome / complications. Mucocutaneous Lymph Node Syndrome / drug therapy. Salicylates / therapeutic use. Vascular Diseases / etiology
  • [MeSH-minor] Animals. Cell Proliferation. Cells, Cultured. Disease Models, Animal. Dose-Response Relationship, Drug. Matrix Metalloproteinase 9 / metabolism. Mice. Mice, Inbred C57BL. Mice, Knockout. NF-kappa B / metabolism. Receptors, Tumor Necrosis Factor, Type I / metabolism. T-Lymphocytes / metabolism. T-Lymphocytes / pathology. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 19565485.001).
  • [ISSN] 0004-3591
  • [Journal-full-title] Arthritis and rheumatism
  • [ISO-abbreviation] Arthritis Rheum.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunoglobulins, Intravenous; 0 / Immunologic Factors; 0 / NF-kappa B; 0 / Receptors, Tumor Necrosis Factor, Type I; 0 / Salicylates; 0 / Tumor Necrosis Factor-alpha; EC 3.4.24.35 / Matrix Metalloproteinase 9
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58. Momeni P, Cairns NJ, Perry RH, Bigio EH, Gearing M, Singleton AB, Hardy J: Mutation analysis of patients with neuronal intermediate filament inclusion disease (NIFID). Neurobiol Aging; 2006 May;27(5):778.e1-778.e6
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  • [Title] Mutation analysis of patients with neuronal intermediate filament inclusion disease (NIFID).
  • Abnormal neuronal aggregates of alpha-internexin and the three neurofilament (NF) subunits, NFL, NFM, and NFH have recently been identified as the signature lesions of neuronal intermediate filament (IF) inclusion disease (NIFID), a novel neurological disease of early onset with a variable clinical phenotype including frontotemporal dementia, pyramidal and extrapyramidal signs.
  • In other neurodegenerative diseases in which protein aggregates contribute to disease pathogenesis, mutations in the encoding protein cause the hereditary variant of the disease.
  • To determine the molecular genetic contribution to this disease we performed a mutation analysis of all type IV neuronal IF, SOD1 and NUDEL genes in cases of NIFID and unaffected control cases.
  • [MeSH-major] Inclusion Bodies / genetics. Neurodegenerative Diseases / genetics. Neurofilament Proteins / genetics
  • [MeSH-minor] Adult. Amino Acid Substitution. Case-Control Studies. Cloning, Molecular. DNA / biosynthesis. DNA / genetics. DNA Primers. Exons / genetics. Female. Gene Deletion. Gene Frequency. Great Britain / epidemiology. Humans. Intermediate Filament Proteins / genetics. Male. Middle Aged. Mutation. Reverse Transcriptase Polymerase Chain Reaction. Risk. Superoxide Dismutase / genetics. United States / epidemiology

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  • (PMID = 16005115.001).
  • [ISSN] 1558-1497
  • [Journal-full-title] Neurobiology of aging
  • [ISO-abbreviation] Neurobiol. Aging
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Intermediate Filament Proteins; 0 / Neurofilament Proteins; 0 / alpha-internexin; 9007-49-2 / DNA; EC 1.15.1.- / superoxide dismutase 1; EC 1.15.1.1 / Superoxide Dismutase
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59. Bhavsar MD, Amiji MM: Oral IL-10 gene delivery in a microsphere-based formulation for local transfection and therapeutic efficacy in inflammatory bowel disease. Gene Ther; 2008 Sep;15(17):1200-9
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  • [Title] Oral IL-10 gene delivery in a microsphere-based formulation for local transfection and therapeutic efficacy in inflammatory bowel disease.
  • The objective of this study was to examine the potential of oral interleukin-10 (IL-10) gene therapy for the treatment of inflammatory bowel disease (IBD).
  • Nanoparticles-in-microsphere oral system (NiMOS) was formulated with murine IL-10-expressing plasmid DNA in type-B gelatin nanoparticles, which were further encapsulated in poly(epsilon-caprolactone) microsphere matrix.
  • Upon oral administration in an acute colitis model, IL-10 expression in the large intestine was measured by quantitative real-time PCR and ELISA.
  • The locally expressed IL-10 was able to suppress the levels of proinflammatory cytokines, such as IFN-gamma, TNF-alpha, IL-1alpha, IL-1beta and IL-12, as well as certain chemokines.
  • The therapeutic benefits of transfected IL-10 were further demonstrated by an increase in body weight, favorable clinical activity score, restoration in colon length and weight, and suppression of inflammatory response as assessed by tissue histological analysis and myeloperoxidase activity.
  • [MeSH-major] Genetic Therapy / methods. Inflammatory Bowel Diseases / therapy. Interleukin-10 / genetics. Transfection / methods
  • [MeSH-minor] Administration, Oral. Animals. Biomarkers / analysis. Chemistry, Pharmaceutical. Colon / immunology. Colon / pathology. Enzyme-Linked Immunosorbent Assay. Female. Gelatin. Gene Expression. Intestinal Mucosa / immunology. Intestinal Mucosa / pathology. Mice. Mice, Inbred BALB C. Microscopy, Electron, Scanning. Microspheres. Models, Animal. Nanoparticles. Peroxidase / analysis. Reverse Transcriptase Polymerase Chain Reaction. Transgenes. Trinitrobenzenesulfonic Acid

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  • (PMID = 18418416.001).
  • [ISSN] 1476-5462
  • [Journal-full-title] Gene therapy
  • [ISO-abbreviation] Gene Ther.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers; 130068-27-8 / Interleukin-10; 8T3HQG2ZC4 / Trinitrobenzenesulfonic Acid; 9000-70-8 / Gelatin; EC 1.11.1.7 / Peroxidase
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60. di Meglio P, Ianaro A, Ghosh S: Amelioration of acute inflammation by systemic administration of a cell-permeable peptide inhibitor of NF-kappaB activation. Arthritis Rheum; 2005 Mar;52(3):951-8
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  • The expression levels of NF-kappaB-regulated cyclooxygenase 2 (COX-2) protein and tumor necrosis factor alpha (TNFalpha) messenger RNA (mRNA) were evaluated by immunoblot analysis and polymerase chain reaction amplification of reverse-transcribed mRNA, respectively.
  • CONCLUSION: These studies further establish NF-kappaB as a target for antiinflammatory therapy and provide support for the use of the NBD peptide as a possible therapeutic agent for inflammatory diseases.

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  • (PMID = 15751079.001).
  • [ISSN] 0004-3591
  • [Journal-full-title] Arthritis and rheumatism
  • [ISO-abbreviation] Arthritis Rheum.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R37 AI033443; United States / NHLBI NIH HHS / HV / N01-HV-28186; United States / NIAID NIH HHS / AI / R37-AI-33443
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / NBD peptide, mouse; 0 / NF-kappa B; 0 / Peptides; 0 / Polysaccharides; 0 / Tumor Necrosis Factor-alpha; 9000-07-1 / Carrageenan; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases
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61. Nunes JS, Lawhon SD, Rossetti CA, Khare S, Figueiredo JF, Gull T, Burghardt RC, Bäumler AJ, Tsolis RM, Andrews-Polymenis HL, Adams LG: Morphologic and cytokine profile characterization of Salmonella enterica serovar typhimurium infection in calves with bovine leukocyte adhesion deficiency. Vet Pathol; 2010 Mar;47(2):322-33
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  • [Title] Morphologic and cytokine profile characterization of Salmonella enterica serovar typhimurium infection in calves with bovine leukocyte adhesion deficiency.
  • Morphologic studies revealed that infection of CD18- calves with S Typhimurium resulted in no significant tissue infiltration by neutrophils, less tissue damage, reduced luminal fluid accumulation, and increased bacterial invasion, when compared with CD18+ calves.
  • Study of cytokine gene expression by quantitative real-time polymerase chain reaction revealed that early stages of acute infection (4-8 hours postinfection) were associated with increased interleukin 8 gene expression in the absence of tissue influx of neutrophils in CD18- calves, whereas later stages of infection (12 hours postinfection) were associated with increased expression of growth-related oncogene alpha in the presence of neutrophil influx in CD18+ calves.
  • In contrast, the proinflammatory cytokines interleukin 1beta and tumor necrosis factor alpha were poorly correlated with the presence or absence of tissue neutrophils.

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  • (PMID = 20118318.001).
  • [ISSN] 1544-2217
  • [Journal-full-title] Veterinary pathology
  • [ISO-abbreviation] Vet. Pathol.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI044170-01A1; United States / NIAID NIH HHS / AI / R01 AI076246; United States / NIAID NIH HHS / AI / R01 AI044170; United States / NIAID NIH HHS / AI / AI044170-01A1; United States / PHS HHS / / 1 RO1 A144170-01A1
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD18; 0 / CXCL1 protein, Bos taurus; 0 / Chemokine CXCL1; 0 / Interleukin-1beta; 0 / Interleukin-8; 0 / Tumor Necrosis Factor-alpha; 63231-63-0 / RNA
  • [Other-IDs] NLM/ NIHMS165622; NLM/ PMC2848297
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62. Okabayashi K, Kano R, Watanabe T, Hasegawa A: Serotypes and mating types of clinical isolates from feline cryptococcosis in Japan. J Vet Med Sci; 2006 Jan;68(1):91-4
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  • [Title] Serotypes and mating types of clinical isolates from feline cryptococcosis in Japan.
  • Most isolates of Cryptococcus neoformans (teleomorph: Filobasidiella neoformans) from human patients and from environmental materials in Japan have been identified as serotype A mating type a by the seroagglutination test and mating experiments.
  • A PCR method using the mating type alpha allele-specific primer of the STE12 gene and the serotype- and mating type-specific primers of the STE20 gene for identification of C. neoformans has been developed.
  • Using the PCR method, conserved strains and clinical isolates from feline cryptococcosis were examined for serotype and the mating type.
  • The results showed that all clinical isolates examined were identified as serotype A, MATalpha, indicating that feline cryptococcsis cases in Japan are caused by C. neoformans serotype A, MATalpha, as is the case in humans.

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  • (PMID = 16462126.001).
  • [ISSN] 0916-7250
  • [Journal-full-title] The Journal of veterinary medical science
  • [ISO-abbreviation] J. Vet. Med. Sci.
  • [Language] ENG
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / DNA Primers
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63. Ferrarezi MC, Cardoso TC, Dutra IS: Genotyping of Clostridium perfringens isolated from calves with neonatal diarrhea. Anaerobe; 2008 Dec;14(6):328-31
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  • Clostridium perfringens is a widespread enteropathogen, and is responsible for many animal diseases such as bovine neonatal diarrhea.
  • Multiple isolates from primary isolation plates were subjected to simultaneous genotyping by multiplex PCR, with primers amplifying fragments of alpha (cpa), beta (cpb), epsilon (etx), iota (itxA), enterotoxin (cpe) and beta2 (cpb2) toxin-encoding genes.
  • Fourteen isolate mixtures from animals with diarrhea had only cpa (type A), one had cpa and cpb2 (type A beta2 positive), one with cpa, itxA, and cpb2 (type E, beta2 positive), and one with cpa, etx, itxA, and cpb2 toxin producing strains.
  • Among 17 isolate mixtures from healthy calves, 10 were exclusively type A, one was type A cpb2 positive, two were type E, three were type E cpb2 positive, and one was types D and E cpb2 positive.
  • There was no correlation between isolation of a given toxin type and the presence of diarrhea.
  • [MeSH-major] Cattle Diseases / microbiology. Clostridium perfringens / classification. Clostridium perfringens / genetics. Diarrhea / veterinary
  • [MeSH-minor] Animals. Animals, Newborn. Bacterial Toxins / genetics. Cattle. DNA, Bacterial / genetics. Female. Genotype. Male. Polymerase Chain Reaction / methods

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  • (PMID = 19114113.001).
  • [ISSN] 1095-8274
  • [Journal-full-title] Anaerobe
  • [ISO-abbreviation] Anaerobe
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Bacterial Toxins; 0 / DNA, Bacterial
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64. Ko H, Das A, Carter RL, Fricks IP, Zhou Y, Ivanov AA, Melman A, Joshi BV, Kovác P, Hajduch J, Kirk KL, Harden TK, Jacobson KA: Molecular recognition in the P2Y(14) receptor: Probing the structurally permissive terminal sugar moiety of uridine-5'-diphosphoglucose. Bioorg Med Chem; 2009 Jul 15;17(14):5298-311
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  • For example, the carboxylate group of uridine-5'-diphosphoglucuronic acid proved to be suitable for flexible substitution by chain extension through an amide linkage.
  • Functionalized congeners containing terminal 2-acylaminoethylamides prepared by this strategy retained P2Y(14) activity, and molecular modeling predicted close proximity of this chain to the second extracellular loop of the receptor.
  • The beta-glucoside was twofold less potent than the native alpha-isomer, but methylene replacement of the 1''-oxygen abolished activity.

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  • (PMID = 19502066.001).
  • [ISSN] 1464-3391
  • [Journal-full-title] Bioorganic & medicinal chemistry
  • [ISO-abbreviation] Bioorg. Med. Chem.
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM038213; United States / Intramural NIH HHS / / Z01 DK031116-20; United States / Intramural NIH HHS / / Z99 DK999999; United States / NIGMS NIH HHS / GM / GM38213
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / P2Y14 receptor, human; 0 / Purinergic P2 Receptor Agonists; 0 / Receptors, Purinergic P2; 0 / Uracil Nucleotides; EC 3.1.4.- / Type C Phospholipases; V50K1D7P4Y / Uridine Diphosphate Glucose
  • [Other-IDs] NLM/ NIHMS130149; NLM/ PMC2760346
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65. Shen CL, Chen WH, Zou SX: In vitro and in vivo effects of hydrolysates from conglycinin on intestinal microbial community of mice after Escherichia coli infection. J Appl Microbiol; 2007 Jan;102(1):283-9
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  • [Title] In vitro and in vivo effects of hydrolysates from conglycinin on intestinal microbial community of mice after Escherichia coli infection.
  • AIMS: To detect the effect of pepsin-hydrolysate conglycinin (PTC) on the growth of Escherichia coli O(138)in vitro, and investigate the effect of PTC on intestinal microbial community of mice after E. coli infection.
  • The mice activities were monitored and polymerase chain reaction-denaturing gradient gel electrophoresis was used to analyse the microbial community in mice faeces.
  • There was high similarity of intestinal microbial community in mice between PTC and normal groups.
  • SIGNIFICANCE AND IMPACT OF THE STUDY: This study demonstrated the antibacterial activity of PTC against E. coli and its ability to maintain healthy intestinal microbial community in mice even after they were infected with E. coli.
  • This observation is significant in the application of PTC to prevent gastrointestinal diseases caused by E. coli and unbalanced intestinal microflora.
  • [MeSH-minor] Animals. Antigens, Plant. Electrophoresis, Polyacrylamide Gel / methods. Feces / microbiology. Hydrolysis. Intestines / microbiology. Male. Mice. Pepsin A / metabolism. Polymerase Chain Reaction / methods. Seed Storage Proteins. Soybeans / chemistry

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  • (PMID = 17184345.001).
  • [ISSN] 1364-5072
  • [Journal-full-title] Journal of applied microbiology
  • [ISO-abbreviation] J. Appl. Microbiol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Antigens, Plant; 0 / Globulins; 0 / Seed Storage Proteins; 0 / Soybean Proteins; 0 / alpha-conglycinin, Glycine max; 0 / beta-conglycinin protein, Glycine max; EC 3.4.23.1 / Pepsin A
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66. Gloerich J, Ijlst L, Wanders RJ, Ferdinandusse S: Bezafibrate induces FALDH in human fibroblasts; implications for Sjögren-Larsson syndrome. Mol Genet Metab; 2006 Sep-Oct;89(1-2):111-5
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  • In animal studies, the expression of the murine ortholog of FALDH, has been shown to be under the control of peroxisome proliferator-activated receptor alpha (PPARalpha).

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  • (PMID = 16837225.001).
  • [ISSN] 1096-7192
  • [Journal-full-title] Molecular genetics and metabolism
  • [ISO-abbreviation] Mol. Genet. Metab.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hypolipidemic Agents; 0 / Peroxisome Proliferator-Activated Receptors; EC 1.2.- / Aldehyde Oxidoreductases; EC 1.2.1.48 / long-chain-aldehyde dehydrogenase; Y9449Q51XH / Bezafibrate
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67. Malik ZA, Hailpern SM, Burk RD: Predictors of seropositivity to human papillomavirus type 53: one of the most prevalent high risk-related cervical human papillomaviruses. Viral Immunol; 2008 Sep;21(3):371-7
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  • [Title] Predictors of seropositivity to human papillomavirus type 53: one of the most prevalent high risk-related cervical human papillomaviruses.
  • HPV53, part of the alpha 6 species group along with HPV types 30, 56, and 66, is one of the most prevalent high risk-related HPV types, yet little is known about the molecular basis of its benign behavior.
  • In conclusion, host serological responses to HPV53 VLPs are strongly type-specific, and subjects' risk for HPV53 seropositivity is independently associated with sexual behavior and OCP use.
  • [MeSH-minor] Adolescent. Adult. Contraception. Female. Humans. Immunoglobulin G / blood. Polymerase Chain Reaction. Prevalence. Risk Factors. Sexual Behavior. Sexual Partners. United States / epidemiology. Vaginal Smears

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  • (PMID = 18681800.001).
  • [ISSN] 1557-8976
  • [Journal-full-title] Viral immunology
  • [ISO-abbreviation] Viral Immunol.
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI031055
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Viral; 0 / Immunoglobulin G
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68. Andersson D, Kotarsky K, Wu J, Agace W, Duan RD: Expression of alkaline sphingomyelinase in yeast cells and anti-inflammatory effects of the expressed enzyme in a rat colitis model. Dig Dis Sci; 2009 Jul;54(7):1440-8
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  • Alkaline sphingomyelinase (Alk-SMase) is a key enzyme in the intestinal tract for digestion of dietary sphingomyelin (SM), which generates lipid messengers with cell-cycle regulating effects.
  • We found a tendency for decreased tumor necrosis factor (TNF)-alpha expression in the Alk-SMase-treated group.
  • This study, for the first time, provides a method to produce the enzyme and shows the potential applicability of the enzyme in the treatment of inflammatory bowel diseases.
  • [MeSH-minor] Administration, Rectal. Animals. Colon / pathology. Dextran Sulfate / adverse effects. Disease Models, Animal. Female. Inflammation / prevention & control. Intestinal Mucosa / drug effects. Intestinal Mucosa / pathology. Pichia / cytology. Pilot Projects. Polymerase Chain Reaction. Rats. Rats, Sprague-Dawley. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 18989780.001).
  • [ISSN] 1573-2568
  • [Journal-full-title] Digestive diseases and sciences
  • [ISO-abbreviation] Dig. Dis. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Tumor Necrosis Factor-alpha; 9042-14-2 / Dextran Sulfate; EC 3.1.4.12 / Sphingomyelin Phosphodiesterase; EC 3.1.4.12 / intestinal alkaline sphingomyelinase, human
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69. Tuin A, Huizinga-Van der Vlag A, van Loenen-Weemaes AM, Meijer DK, Poelstra K: On the role and fate of LPS-dephosphorylating activity in the rat liver. Am J Physiol Gastrointest Liver Physiol; 2006 Feb;290(2):G377-85
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  • Gut-derived lipopolysaccharide (LPS) plays a role in the pathogenesis of liver diseases like fibrosis.
  • The enzyme alkaline phosphatase (AP) is present in, among others, the intestinal wall and liver and has been previously shown to dephosphorylate LPS.
  • Furthermore, in vitro and in vivo studies showed that exogenous intestinal AP quickly bound to the asialoglycoprotein receptor on hepatocytes.
  • This intestinal isoform significantly attenuated LPS-induced hepatic tumor necrosis factor-alpha and nitric oxide (nitrite and nitrate) responses in vitro.
  • This study shows that LPS enhances AP expression in hepatocytes and that intestinal AP is rapidly taken up by these same cells, leading to an attenuation of LPS-induced responses in vivo.
  • [MeSH-minor] Animals. Antigens, CD14 / metabolism. Collagen Type III / metabolism. Enterocytes / enzymology. Gluconeogenesis / drug effects. Hepatocytes / enzymology. Hepatocytes / metabolism. Hepatocytes / ultrastructure. Immunohistochemistry. In Vitro Techniques. Kidney / enzymology. Kidney / metabolism. Kidney / ultrastructure. Liver Cirrhosis / metabolism. Liver Cirrhosis / pathology. Male. Nitric Oxide / metabolism. Phosphorylation. RNA / biosynthesis. Rats. Rats, Wistar. Reverse Transcriptase Polymerase Chain Reaction. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 16223948.001).
  • [ISSN] 0193-1857
  • [Journal-full-title] American journal of physiology. Gastrointestinal and liver physiology
  • [ISO-abbreviation] Am. J. Physiol. Gastrointest. Liver Physiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD14; 0 / Collagen Type III; 0 / Lipopolysaccharides; 0 / Tumor Necrosis Factor-alpha; 31C4KY9ESH / Nitric Oxide; 63231-63-0 / RNA; EC 3.1.3.1 / Alkaline Phosphatase
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70. Attanasio F, Cataldo S, Fisichella S, Nicoletti S, Nicoletti VG, Pignataro B, Savarino A, Rizzarelli E: Protective effects of L- and D-carnosine on alpha-crystallin amyloid fibril formation: implications for cataract disease. Biochemistry; 2009 Jul 14;48(27):6522-31
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  • [Title] Protective effects of L- and D-carnosine on alpha-crystallin amyloid fibril formation: implications for cataract disease.
  • Mildly denaturing conditions induce bovine alpha-crystallin, the major structural lens protein, to self-assemble into fibrillar structures in vitro.
  • The natural dipeptide l-carnosine has been shown to have potential protective and therapeutic significance in many diseases.
  • Here we report the inhibitory effect induced by the peptide (l- and d-enantiomeric form) on alpha-crystallin fibrillation and the almost complete restoration of the chaperone activity lost after denaturant and/or heat stress.
  • Scanning force microscopy (SFM), thioflavin T, and a turbidimetry assay have been used to determine the morphology of alpha-crystallin aggregates in the presence and absence of carnosine.
  • DSC and a near-UV CD assay evidenced that the structural precursors of amyloid fibrils are polypeptide chain segments that lack stable structural elements.
  • Moreover, we have found a disassembling effect of carnosine on alpha-crystallin amyloid fibrils.
  • [MeSH-major] Amyloid / chemistry. Carnosine / chemistry. Cataract / metabolism. alpha-Crystallins / chemistry

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  • (PMID = 19441807.001).
  • [ISSN] 1520-4995
  • [Journal-full-title] Biochemistry
  • [ISO-abbreviation] Biochemistry
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amyloid; 0 / Molecular Chaperones; 0 / alpha-Crystallins; 8HO6PVN24W / Carnosine
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71. Javor J, Bucova M, Ferencik S, Grosse-Wilde H, Buc M: Single nucleotide polymorphisms of cytokine genes in the healthy Slovak population. Int J Immunogenet; 2007 Aug;34(4):273-80
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  • Several cytokine gene polymorphisms have been identified to play a role in susceptibility to various diseases, including autoimmune, infectious, allergic or cardiovascular diseases.
  • A polymerase chain reaction with sequence-specific primers was used to genotype polymorphisms within genes encoding IL-1alpha, IL-1beta, IL-1R, IL-1RA, IL-4Ralpha, IL-12, IFN-gamma, TGF-beta, TNF-alpha, IL-2, IL-4, IL-6 and IL-10 in a sample of 140 unrelated Slovak subjects.
  • The obtained data represent a basis for further studies on association of cytokine gene polymorphisms with some diseases.

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  • (PMID = 17627763.001).
  • [ISSN] 1744-3121
  • [Journal-full-title] International journal of immunogenetics
  • [ISO-abbreviation] Int. J. Immunogenet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines
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72. Kim N, Cho SI, Yim JY, Kim JM, Lee DH, Park JH, Kim JS, Jung HC, Song IS: The effects of genetic polymorphisms of IL-1 and TNF-A on Helicobacter pylori-induced gastroduodenal diseases in Korea. Helicobacter; 2006 Apr;11(2):105-12
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  • [Title] The effects of genetic polymorphisms of IL-1 and TNF-A on Helicobacter pylori-induced gastroduodenal diseases in Korea.
  • OBJECTIVE: To evaluate whether or not genetic polymorphism of IL-1B, IL-1RN, and TNF-Alpha is an important factor in the different expression of gastroduodenal diseases after Helicobacter pylori infection.
  • METHODS: This study consisted of 1360 subjects: control, gastric cancer (GC, intestinal type, and diffuse type), benign gastric ulcer (BGU), duodenal ulcer, and first-degree gastric cancer relative (GCR).
  • IL-1Beta-511 and TNF-A-308 biallelic polymorphism were genotyped by 5' nuclease polymerase chain reaction (PCR) assays, and PCR-restriction fragment length polymorphism (PCR-RFLP).
  • There was no significance in the polymorphism of TNF-Alpha-308 regardless of H. pylori-induced gastroduodenal diseases.
  • CONCLUSIONS: The IL-1Beta-511 T-carrier polymorphism has a negative effect on the development of H. pylori-positive BGU, and high frequency of IL-1RN 2/2 was found in the H. pylori-positive relatives of GC patients, which suggest that this genetic polymorphism could play some role in the H. pylori-induced gastroduodenal diseases in Korea.
  • [MeSH-major] Gastrointestinal Diseases / genetics. Helicobacter Infections / complications. Interleukin-1 / genetics. Polymorphism, Genetic. Tumor Necrosis Factor-alpha / genetics
  • [MeSH-minor] Adult. Aged. Duodenal Ulcer / genetics. Duodenal Ulcer / microbiology. Female. Gene Frequency. Genetic Predisposition to Disease. Genotype. Humans. Korea. Male. Middle Aged. Polymerase Chain Reaction. Polymorphism, Restriction Fragment Length. Stomach Neoplasms / genetics. Stomach Neoplasms / microbiology. Stomach Ulcer / genetics. Stomach Ulcer / microbiology

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  • [ErratumIn] Helicobacter. 2006 Jun;11(3):215
  • (PMID = 16579840.001).
  • [ISSN] 1083-4389
  • [Journal-full-title] Helicobacter
  • [ISO-abbreviation] Helicobacter
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interleukin-1; 0 / Tumor Necrosis Factor-alpha
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73. Zhao YP, Wang H, Fang M, Ji Q, Yang ZX, Gao CF: Study of the association between polymorphisms of the COL1A1 gene and HBV-related liver cirrhosis in Chinese patients. Dig Dis Sci; 2009 Feb;54(2):369-76
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  • Polymorphisms -1997T>G, -1663 ins/del T and -1363C>G of the COL1A1 gene were detected by direct sequencing.
  • No polymorphism at -1663 ins/del T was observed in any subject.
  • [MeSH-major] Collagen Type I / genetics. Hepatitis B, Chronic / complications. Liver Cirrhosis / genetics

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  • (PMID = 18536987.001).
  • [ISSN] 1573-2568
  • [Journal-full-title] Digestive diseases and sciences
  • [ISO-abbreviation] Dig. Dis. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Collagen Type I; 0 / collagen type I, alpha 1 chain; 82115-62-6 / Interferon-gamma
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74. Wex T, Kuester D, Vieth M, Treiber G, Krieg A, Roessner A, Malfertheiner P: Helicobacter pylori infection and short-term intake of low-dose aspirin have different effects on alpha-1 antitrypsin/alpha-1 peptidase inhibitor (alpha1-PI) levels in antral mucosa and peripheral blood. Scand J Gastroenterol; 2008;43(10):1194-201
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  • [Title] Helicobacter pylori infection and short-term intake of low-dose aspirin have different effects on alpha-1 antitrypsin/alpha-1 peptidase inhibitor (alpha1-PI) levels in antral mucosa and peripheral blood.
  • OBJECTIVE: Alpha-1 protease inhibitor (alpha1-PI) is the major circulating serine protease inhibitor.
  • The purpose of the study was to investigate alpha1-PI expression in gastroduodenal mucosa and blood with respect to two major etiological risk factors for gastroduodenal diseases, Helicobacter pylori infection and intake of low-dose aspirin.
  • Blood and tissue samples were obtained on days 0, 1, 3 and 7; alpha1-PI levels were determined by enzyme-linked immunosorbent assay (ELISA) and quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) and analyzed for histopathological findings.
  • Alpha-1-PI transcript levels were similarly induced in H. pylori-infected subjects (0.13+/-0.15 versus 0.027+/-0.043 a.u. (arbitrary units), p=0.018).
  • [MeSH-major] Anti-Inflammatory Agents, Non-Steroidal / administration & dosage. Aspirin / administration & dosage. Gene Expression Regulation, Enzymologic / drug effects. Helicobacter Infections / metabolism. alpha 1-Antitrypsin / metabolism
  • [MeSH-minor] Adult. Enzyme-Linked Immunosorbent Assay. Female. Gastric Mucosa / chemistry. Gastric Mucosa / metabolism. Gastric Mucosa / microbiology. Gene Expression / drug effects. Helicobacter pylori. Humans. Male. Pyloric Antrum / chemistry. Reverse Transcriptase Polymerase Chain Reaction. Time Factors


75. Ramasawmy R, Fae KC, Cunha-Neto E, Müller NG, Cavalcanti VL, Ferreira RC, Drigo SA, Ianni B, Mady C, Goldberg AC, Kalil J: Polymorphisms in the gene for lymphotoxin-alpha predispose to chronic Chagas cardiomyopathy. J Infect Dis; 2007 Dec 15;196(12):1836-43
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  • [Title] Polymorphisms in the gene for lymphotoxin-alpha predispose to chronic Chagas cardiomyopathy.
  • BACKGROUND: Chagas disease, caused by Trypanosoma cruzi infection, displays clinical heterogeneity and may be attributable to differential genetic susceptibility.
  • Chronic Chagas cardiomyopathy (CCC) develops only in a subset of T. cruzi-infected individuals and may lead to heart failure that has a worse clinical course and that leads to reduced life expectancy, compared with heart failure of other etiologies.
  • Clinical, genetic, and epidemiological studies have linked lymphotoxin-alpha (LTA), a proinflammatory cytokine, to coronary artery disease and myocardial infarction.
  • METHODS: We used polymerase chain reaction to genotype the LTA +80A-->C and LTA +252A-->G variants in 169 patients with CCC and in 76 T. cruzi-infected asymptomatic (ASY) patients.
  • Furthermore, homozygosity for the LTA +80A allele correlated with the lowest levels of plasmatic tumor-necrosis factor-alpha.
  • CONCLUSIONS: Our results suggest that the study of genetic variations in patients with Chagas disease may help in the identification of individuals at increased risk of progressing to CCC and, by providing early treatment, reduce the morbidity and mortality associated with this disease.
  • [MeSH-major] Chagas Cardiomyopathy / genetics. Lymphotoxin-alpha / genetics. Trypanosoma cruzi / growth & development
  • [MeSH-minor] Animals. Female. Gene Frequency / genetics. Genetic Predisposition to Disease. Genotype. Haplotypes / genetics. Humans. Male. Middle Aged. Polymorphism, Genetic. Tumor Necrosis Factor-alpha / blood. Tumor Necrosis Factor-alpha / immunology

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  • (PMID = 18190265.001).
  • [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 / Lymphotoxin-alpha; 0 / Tumor Necrosis Factor-alpha
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76. Ota T, Taketani S, Iwai S, Miyagawa S, Furuta M, Hara M, Uchimura E, Okita Y, Sawa Y: Novel method of decellularization of porcine valves using polyethylene glycol and gamma irradiation. Ann Thorac Surg; 2007 Apr;83(4):1501-7
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  • BACKGROUND: Recent tissue-engineered valves are in need of a breakthrough to overcome several limitations against clinical applications.
  • These were evaluated by histologic, biochemical (DNA, solubilized protein and collagen content), mechanical (strength test, transmission electron microscopy) and immunologic (porcine endogenous retrovirus and the alpha-1.3 galactosyl epitope) analyses.
  • The DNA sequence of a porcine endogenous retrovirus and the alpha-1.3 galactosyl epitope were eliminated after the decellularizing process.
  • [MeSH-major] Bioprosthesis. Gamma Rays. Heart Valve Diseases / surgery. Heart Valve Prosthesis Implantation / methods. Polyethylene Glycols / pharmacology. Tissue Engineering / methods
  • [MeSH-minor] Animals. Aortic Valve / cytology. Aortic Valve / radiation effects. Cell Movement / drug effects. Disease Models, Animal. Dogs. Microscopy, Electron, Transmission. Polymerase Chain Reaction. Prosthesis Design. Rats. Sensitivity and Specificity. Swine

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  • [CommentIn] Ann Thorac Surg. 2008 Jun;85(6):2163; author reply 2163-4 [18498860.001]
  • (PMID = 17383366.001).
  • [ISSN] 1552-6259
  • [Journal-full-title] The Annals of thoracic surgery
  • [ISO-abbreviation] Ann. Thorac. Surg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 30IQX730WE / Polyethylene Glycols
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77. Boyer JF, Balard P, Authier H, Faucon B, Bernad J, Mazières B, Davignon JL, Cantagrel A, Pipy B, Constantin A: Tumor necrosis factor alpha and adalimumab differentially regulate CD36 expression in human monocytes. Arthritis Res Ther; 2007;9(2):R22
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  • [Title] Tumor necrosis factor alpha and adalimumab differentially regulate CD36 expression in human monocytes.
  • In chronic inflammatory diseases, such as rheumatoid arthritis, inflammation acts as an independent cardiovascular risk factor and the use of anti-inflammatory drugs, such as anti-tumor necrosis factor alpha (anti-TNFalpha), may decrease this risk.
  • Further studies are needed to investigate the clinical implications of these results in accelerated atherosclerosis observed in rheumatoid arthritis.
  • [MeSH-major] Anti-Inflammatory Agents / pharmacology. Antibodies, Monoclonal / pharmacology. Antigens, CD36 / drug effects. Monocytes / drug effects. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Adalimumab. Antibodies, Monoclonal, Humanized. Arthritis, Rheumatoid / complications. Arthritis, Rheumatoid / metabolism. Arthritis, Rheumatoid / physiopathology. Atherosclerosis / etiology. Atherosclerosis / metabolism. Atherosclerosis / physiopathology. Cells, Cultured. Electrophoretic Mobility Shift Assay. Flow Cytometry. Gene Expression / drug effects. Humans. Immunoglobulin Fab Fragments / pharmacology. PPAR gamma / metabolism. RNA, Messenger / drug effects. Reactive Oxygen Species / analysis. Reactive Oxygen Species / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 17335569.001).
  • [ISSN] 1478-6362
  • [Journal-full-title] Arthritis research & therapy
  • [ISO-abbreviation] Arthritis Res. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens, CD36; 0 / Immunoglobulin Fab Fragments; 0 / PPAR gamma; 0 / RNA, Messenger; 0 / Reactive Oxygen Species; 0 / Tumor Necrosis Factor-alpha; FYS6T7F842 / Adalimumab
  • [Other-IDs] NLM/ PMC1906797
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78. Arrigo AP, Simon S, Gibert B, Kretz-Remy C, Nivon M, Czekalla A, Guillet D, Moulin M, Diaz-Latoud C, Vicart P: Hsp27 (HspB1) and alphaB-crystallin (HspB5) as therapeutic targets. FEBS Lett; 2007 Jul 31;581(19):3665-74
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  • This review summarizes the current knowledge about Hsp27 and alphaB-crystallin and the implications, either positive or deleterious, of these proteins in pathologies such as neurodegenerative diseases, myopathies, asthma, cataracts and cancers.
  • [MeSH-major] Heat-Shock Proteins / metabolism. Inflammation / drug therapy. Molecular Chaperones / metabolism. Neoplasm Proteins / metabolism. Neoplasms / drug therapy. alpha-Crystallin B Chain / metabolism

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  • (PMID = 17467701.001).
  • [ISSN] 0014-5793
  • [Journal-full-title] FEBS letters
  • [ISO-abbreviation] FEBS Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / CRYAB protein, human; 0 / HSP27 Heat-Shock Proteins; 0 / HSPB1 protein, human; 0 / Heat-Shock Proteins; 0 / Molecular Chaperones; 0 / Neoplasm Proteins; 0 / alpha-Crystallin B Chain
  • [Number-of-references] 104
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79. Chen A, Liao WP, Lu Q, Wong WS, Wong PT: Upregulation of dihydropyrimidinase-related protein 2, spectrin alpha II chain, heat shock cognate protein 70 pseudogene 1 and tropomodulin 2 after focal cerebral ischemia in rats--a proteomics approach. Neurochem Int; 2007 Jun;50(7-8):1078-86
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  • [Title] Upregulation of dihydropyrimidinase-related protein 2, spectrin alpha II chain, heat shock cognate protein 70 pseudogene 1 and tropomodulin 2 after focal cerebral ischemia in rats--a proteomics approach.
  • In recent years, there are an increasing number of proteomics studies that investigated the alterations in the protein expression relevant to human diseases but none for stroke.
  • Two spots were identified as spectrin alpha II chain (rat fragment, also known as alpha-fodrin or non-erythroid alpha chain, SPNA-2); and one spot each for heat shock cognate protein 70 pseudogene 1 (HSC70-ps1, also known as heat shock protein 8 pseudogene 1), and tropomodulin 2 (Tmod2).
  • [MeSH-minor] Animals. Disease Models, Animal. Gene Expression Regulation, Enzymologic. Male. Pseudogenes. Rats. Rats, Wistar. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 17196711.001).
  • [ISSN] 0197-0186
  • [Journal-full-title] Neurochemistry international
  • [ISO-abbreviation] Neurochem. Int.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / HSP70 Heat-Shock Proteins; 0 / Intercellular Signaling Peptides and Proteins; 0 / Nerve Tissue Proteins; 0 / collapsin response mediator protein-2; 12634-43-4 / Spectrin
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80. Stamatiou R, Paraskeva E, Boukas K, Gourgoulianis KI, Molyvdas PA, Hatziefthimiou AA: Azithromycin has an antiproliferative and autophagic effect on airway smooth muscle cells. Eur Respir J; 2009 Sep;34(3):721-30
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  • Azithromycin is used in long-term, low-dose treatment of airway diseases where airway wall remodelling is present.
  • Since it improves total score symptom and respiratory function of such patients, we hypothesise that azithromycin's additional clinical benefits are due to an inhibition of airway smooth muscle cell (SMC) proliferation.
  • Induction of autophagy was studied by indirect immmunofluorescence and/or Western blotting with antibodies against human smooth muscle alpha-actin, beclin 1, light chain 3 and caspase 3.

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  • (PMID = 19386688.001).
  • [ISSN] 1399-3003
  • [Journal-full-title] The European respiratory journal
  • [ISO-abbreviation] Eur. Respir. J.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 83905-01-5 / Azithromycin
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81. Amaral AU, Leipnitz G, Fernandes CG, Seminotti B, Schuck PF, Wajner M: Alpha-ketoisocaproic acid and leucine provoke mitochondrial bioenergetic dysfunction in rat brain. Brain Res; 2010 Apr 9;1324:75-84
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  • [Title] Alpha-ketoisocaproic acid and leucine provoke mitochondrial bioenergetic dysfunction in rat brain.
  • Patients affected by maple syrup urine disease (MSUD) present severe neurological symptoms and brain abnormalities, whose pathophysiology is poorly known.
  • In the present study we investigated the in vitro effects of leucine (Leu), alpha-ketoisocaproic acid (KIC) and alpha-hydroxyisovaleric acid (HIV), respectively, the branched-chain amino, keto and hydroxy acids that most accumulate in MSUD, on brain bioenergetic homeostasis, evaluating respiratory parameters obtained by oxygen consumption, membrane potential (Psim), NAD(P)H content, swelling and citric acid cycle enzyme activities in mitochondrial preparations from rat forebrain using glutamate plus malate, succinate or alpha-ketoglutarate as respiratory substrates.
  • Furthermore, KIC and Leu, but not HIV, decreased state 3 using alpha-ketoglutarate.
  • A KIC-induced selective inhibition of alpha-ketoglutarate dehydrogenase activity was also verified, with no alteration of the other citric acid cycle activities.
  • The ADP/O ratio and the mitochondrial NAD(P)H levels were also reduced by KIC using glutamate/malate and alpha-ketoglutarate.
  • In addition, KIC caused a reduction in the Psim when alpha-ketoglutarate was the substrate.
  • The present data indicate that KIC acts as an uncoupler of oxidative phosphorylation and as a metabolic inhibitor possibly through its inhibitory effect on alpha-ketoglutarate dehydrogenase activity, while Leu acts as a metabolic inhibitor.
  • It is suggested that impairment of mitochondrial homeostasis caused by the major metabolites accumulating in MSUD may be involved in the neuropathology of this disease.
  • [MeSH-major] Brain / drug effects. Central Nervous System Agents / toxicity. Keto Acids / toxicity. Leucine / toxicity. Mitochondrial Diseases / chemically induced
  • [MeSH-minor] Animals. Electron Transport / drug effects. Homeostasis / drug effects. Ketoglutarate Dehydrogenase Complex / metabolism. Maple Syrup Urine Disease. Membrane Potential, Mitochondrial / drug effects. Mitochondrial Swelling / drug effects. NADP / metabolism. Oxygen Consumption / drug effects. Prosencephalon / drug effects. Prosencephalon / physiopathology. Rats. Rats, Wistar. Valerates / toxicity

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  • [Copyright] Copyright (c) 2010 Elsevier B.V. All rights reserved.
  • (PMID = 20153737.001).
  • [ISSN] 1872-6240
  • [Journal-full-title] Brain research
  • [ISO-abbreviation] Brain Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Central Nervous System Agents; 0 / Keto Acids; 0 / Valerates; 4026-18-0 / 2-hydroxyisovaleric acid; 53-59-8 / NADP; 816-66-0 / alpha-ketoisocaproic acid; EC 1.2.4.2 / Ketoglutarate Dehydrogenase Complex; GMW67QNF9C / Leucine
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82. Sardinha LR, Mosca T, Elias RM, do Nascimento RS, Gonçalves LA, Bucci DZ, Marinho CR, Penha-Gonçalves C, Lima MR, Alvarez JM: The liver plays a major role in clearance and destruction of blood trypomastigotes in Trypanosoma cruzi chronically infected mice. PLoS Negl Trop Dis; 2010;4(1):e578
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  • Intravenous challenge with Trypanosoma cruzi can be used to investigate the process and consequences of blood parasite clearance in experimental Chagas disease.
  • Following clearance, the number of infiltrating cells in the hepatic tissue notably increased: initially (at 24 h) as diffuse infiltrates affecting the whole parenchyma, and at 48 h, in the form of large focal infiltrates in both the parenchyma and perivascular spaces.
  • [MeSH-major] Chagas Disease / immunology. Chagas Disease / parasitology. Liver / immunology. Liver / parasitology. Trypanosoma cruzi / immunology
  • [MeSH-minor] Animals. CD4-Positive T-Lymphocytes / immunology. CD8-Positive T-Lymphocytes / immunology. Female. Immunohistochemistry. Interferon-gamma / metabolism. Interleukin-2 Receptor alpha Subunit / metabolism. Interleukin-2 Receptor beta Subunit / metabolism. Killer Cells, Natural / immunology. Mice. Mice, Inbred C57BL. Polymerase Chain Reaction

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  • [Cites] Infect Immun. 2004 Apr;72(4):2350-7 [15039360.001]
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  • (PMID = 20052269.001).
  • [ISSN] 1935-2735
  • [Journal-full-title] PLoS neglected tropical diseases
  • [ISO-abbreviation] PLoS Negl Trop Dis
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interleukin-2 Receptor alpha Subunit; 0 / Interleukin-2 Receptor beta Subunit; 82115-62-6 / Interferon-gamma
  • [Other-IDs] NLM/ PMC2793026
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83. Villaverde J, Maqueda C, Undabeytia T, Morillo E: Effect of various cyclodextrins on photodegradation of a hydrophobic herbicide in aqueous suspensions of different soil colloidal components. Chemosphere; 2007 Sep;69(4):575-84
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  • The irradiation of NFL aqueous solutions in the presence of CDs showed that the higher the formation constant of NFL-CD complexes (Kc) and their solubility, the higher their photocatalytic effects, following the CDs in the order: RAMEB>HPBCD>beta-CD>alpha-CD>gamma-CD.

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  • (PMID = 17462707.001).
  • [ISSN] 0045-6535
  • [Journal-full-title] Chemosphere
  • [ISO-abbreviation] Chemosphere
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Colloids; 0 / Cyclodextrins; 0 / Environmental Pollutants; 0 / Herbicides; 0 / Pyridazines; 0 / Soil; 0 / Solutions; KES1HB07E4 / norflurazone
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84. Herndler-Brandstetter D, Veel E, Laschober GT, Pfister G, Brunner S, Walcher S, Parson W, Lepperdinger G, Grubeck-Loebenstein B: Non-regulatory CD8+CD45RO+CD25+ T-lymphocytes may compensate for the loss of antigen-inexperienced CD8+CD45RA+ T-cells in old age. Biol Chem; 2008 May;389(5):561-8
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  • The age-related decline in immune system functions is responsible for the increased prevalence of infectious diseases and the low efficacy of vaccination in elderly individuals.
  • [MeSH-major] Aged / physiology. Aging / immunology. Antigens, CD45 / immunology. CD8-Positive T-Lymphocytes / immunology. Interleukin-2 Receptor alpha Subunit / immunology
  • [MeSH-minor] Adult. Cell Differentiation / immunology. Cell Separation. Cells, Cultured. DNA, Complementary / biosynthesis. DNA, Complementary / genetics. Flow Cytometry. Gene Expression Regulation / immunology. Gene Expression Regulation / physiology. Genes, T-Cell Receptor / immunology. Humans. In Situ Hybridization. Phenotype. Reverse Transcriptase Polymerase Chain Reaction. Stimulation, Chemical. Telomere / ultrastructure

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  • (PMID = 18953723.001).
  • [ISSN] 1431-6730
  • [Journal-full-title] Biological chemistry
  • [ISO-abbreviation] Biol. Chem.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / DNA, Complementary; 0 / Interleukin-2 Receptor alpha Subunit; EC 3.1.3.48 / Antigens, CD45
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85. Watanabe N: [Tumor necrosis factor alpha (TNFalpha)]. Nihon Rinsho; 2005 Aug;63 Suppl 8:83-5
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  • [Title] [Tumor necrosis factor alpha (TNFalpha)].
  • [MeSH-major] Tumor Necrosis Factor-alpha / analysis
  • [MeSH-minor] Animals. Biomarkers / blood. Enzyme-Linked Immunosorbent Assay. Humans. Inflammation / diagnosis. Inflammation / etiology. Parasitic Diseases / diagnosis. Polymerase Chain Reaction / methods. Shock, Septic / diagnosis

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  • (PMID = 16149458.001).
  • [ISSN] 0047-1852
  • [Journal-full-title] Nihon rinsho. Japanese journal of clinical medicine
  • [ISO-abbreviation] Nippon Rinsho
  • [Language] jpn
  • [Publication-type] Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Tumor Necrosis Factor-alpha
  • [Number-of-references] 15
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86. Hao F, Pei XY, Zhang XL, Zhang SB, Lai XH, Wang HH: [Molecular cloning, expression, purification and properties of isocitrate lyase gene from Mycobacterium tuberculosis H37Rv]. Zhonghua Jie He He Hu Xi Za Zhi; 2005 Dec;28(12):845-8
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  • METHODS: The icl gene was amplified by polymerase chain reaction (PCR) from Mycobacterium tuberculosis H(37)Rv strain genomic DNA and cloned into pET28-a(+) vector.
  • The CD spectrum showed that the percentages for alpha- helix, beta- sheet, beta- turn, and random coil were 43.8%, 31.9%, 3.4%, and 20.9%, respectively.

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  • (PMID = 16409788.001).
  • [ISSN] 1001-0939
  • [Journal-full-title] Zhonghua jie he he hu xi za zhi = Zhonghua jiehe he huxi zazhi = Chinese journal of tuberculosis and respiratory diseases
  • [ISO-abbreviation] Zhonghua Jie He He Hu Xi Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Bacterial Proteins; EC 4.1.3.1 / Isocitrate Lyase
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87. Zaima N, Sugawara T, Goto D, Hirata T: Trans geometric isomers of EPA decrease LXRalpha-induced cellular triacylglycerol via suppression of SREBP-1c and PGC-1beta. J Lipid Res; 2006 Dec;47(12):2712-7
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  • Dietary mono- or di-trans fatty acids with chain lengths of 18-22 increase the risk of cardiovascular diseases because they increase LDL cholesterol and decrease HDL cholesterol in the plasma.
  • Dietary PUFAs, especially eicosapentaenoic acid (EPA) in marine oils, improve serum lipid profiles by suppressing liver X receptor alpha (LXRalpha) activity in the liver.

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  • (PMID = 17005995.001).
  • [ISSN] 0022-2275
  • [Journal-full-title] Journal of lipid research
  • [ISO-abbreviation] J. Lipid Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / DNA Primers; 0 / DNA-Binding Proteins; 0 / Orphan Nuclear Receptors; 0 / PPARGC1B protein, human; 0 / RNA, Messenger; 0 / Receptors, Cytoplasmic and Nuclear; 0 / Sterol Regulatory Element Binding Protein 1; 0 / Triglycerides; 0 / liver X receptor; AAN7QOV9EA / Eicosapentaenoic Acid
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88. Kokot A, Sindrilaru A, Schiller M, Sunderkötter C, Kerkhoff C, Eckes B, Scharffetter-Kochanek K, Luger TA, Böhm M: alpha-melanocyte-stimulating hormone suppresses bleomycin-induced collagen synthesis and reduces tissue fibrosis in a mouse model of scleroderma: melanocortin peptides as a novel treatment strategy for scleroderma? Arthritis Rheum; 2009 Feb;60(2):592-603
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  • [Title] alpha-melanocyte-stimulating hormone suppresses bleomycin-induced collagen synthesis and reduces tissue fibrosis in a mouse model of scleroderma: melanocortin peptides as a novel treatment strategy for scleroderma?
  • OBJECTIVE: Recently, we found that human dermal fibroblasts (HDFs) express melanocortin 1 receptors (MC-1R) that bind alpha-melanocyte-stimulating hormone (alpha-MSH).
  • In search of novel therapies for scleroderma (systemic sclerosis [SSc]), we used the bleomycin (BLM) model to investigate the effects of alpha-MSH on collagen synthesis and fibrosis.
  • METHODS: Collagen expression in HDFs was determined by real-time reverse transcription-polymerase chain reaction (RT-PCR) and Western blot analyses.
  • The effect of alpha-MSH in the BLM mouse model of scleroderma was assessed by histologic, immunohistochemical, real-time RT-PCR, and protein analyses.
  • RESULTS: Treatment with alpha-MSH (and related peptides) suppressed BLM-induced expression of type I and type III collagen in HDFs, and this effect was cAMP-dependent.
  • Neither BLM nor alpha-MSH altered Smad signaling, but antioxidants inhibited BLM-induced collagen expression in vitro.
  • In addition, alpha-MSH suppressed BLM-induced oxidative stress and enhanced the expression of superoxide dismutase 2 (SOD2) and heme oxygenase 1 (HO-1).
  • In the BLM mouse model, alpha-MSH reduced skin fibrosis and collagen content and increased tissue levels of SOD2 and HO-1.
  • CONCLUSION: Alpha-melanocyte-stimulating hormone and related peptides that exert their effects via MC-1R may provide a novel antifibrogenic therapeutic tool for the treatment of fibrotic diseases such as scleroderma.
  • [MeSH-major] Collagen / drug effects. Fibrosis / drug therapy. Hormones / pharmacology. Receptors, Melanocortin / drug effects. Scleroderma, Systemic / drug therapy. alpha-MSH / pharmacology
  • [MeSH-minor] Adult. Aged. Animals. Antibiotics, Antineoplastic / toxicity. Antioxidants / pharmacology. Bleomycin / toxicity. Dermis / drug effects. Dermis / metabolism. Dermis / pathology. Disease Models, Animal. Drug Antagonism. Fibroblasts / drug effects. Fibroblasts / metabolism. Gene Expression / drug effects. Heme Oxygenase-1 / genetics. Heme Oxygenase-1 / metabolism. Humans. Infant, Newborn. Male. Mice. Middle Aged. Oxidative Stress / drug effects. Pro-Opiomelanocortin / genetics. Pro-Opiomelanocortin / metabolism. RNA, Messenger / metabolism. Signal Transduction / drug effects. Superoxide Dismutase / genetics. Superoxide Dismutase / metabolism. Young Adult

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  • (PMID = 19180474.001).
  • [ISSN] 0004-3591
  • [Journal-full-title] Arthritis and rheumatism
  • [ISO-abbreviation] Arthritis Rheum.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antioxidants; 0 / Hormones; 0 / RNA, Messenger; 0 / Receptors, Melanocortin; 11056-06-7 / Bleomycin; 581-05-5 / alpha-MSH; 66796-54-1 / Pro-Opiomelanocortin; 9007-34-5 / Collagen; EC 1.14.99.3 / Heme Oxygenase-1; EC 1.15.1.1 / Superoxide Dismutase
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89. Díez-Marqués ML, Ruiz-Torres MP, Griera M, López-Ongil S, Saura M, Rodríguez-Puyol D, Rodríguez-Puyol M: Arg-Gly-Asp (RGD)-containing peptides increase soluble guanylate cyclase in contractile cells. Cardiovasc Res; 2006 Feb 1;69(2):359-69
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  • RGDS effects on sGC regulation were due to the specific interaction with alpha(5)beta(1) integrin.
  • Elucidation of this novel mechanism provides a rationale for future pharmacotherapy in certain vascular diseases.
  • [MeSH-minor] Aorta. Cells, Cultured. Enzyme Activation. Gene Expression. Humans. Mesangial Cells. Mitogen-Activated Protein Kinase 8 / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • [CommentIn] Cardiovasc Res. 2006 Feb 1;69(2):302-3 [16412404.001]
  • (PMID = 16360131.001).
  • [ISSN] 0008-6363
  • [Journal-full-title] Cardiovascular research
  • [ISO-abbreviation] Cardiovasc. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Oligopeptides; 99896-85-2 / arginyl-glycyl-aspartic acid; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 8; EC 4.6.1.2 / Guanylate Cyclase
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90. Sun YY, Wang CY, Hsu MF, Juan SH, Chang CY, Chou CM, Yang LY, Hung KS, Xu J, Lee YH, Hsu CY: Glucocorticoid protection of oligodendrocytes against excitotoxin involving hypoxia-inducible factor-1alpha in a cell-type-specific manner. J Neurosci; 2010 Jul 14;30(28):9621-30
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  • [Title] Glucocorticoid protection of oligodendrocytes against excitotoxin involving hypoxia-inducible factor-1alpha in a cell-type-specific manner.
  • Glucocorticoids are commonly used in treating diseases with white matter lesions, including demyelinating diseases and spinal cord injury (SCI).
  • We report here a novel mechanism of methylprednisolone (MP), a synthetic glucocorticoid widely used for treating multiple sclerosis and SCI, in protecting oligodendrocytes (OLGs) against AMPA-induced excitotoxicity, which has been implicated in the white matter injuries and diseases.
  • MP transactivation of Epo expression involves dual transcription factors: glucocorticoid receptor (GR) and hypoxia-inducible factor-1alpha (HIF-1alpha).
  • Coimmunoprecipitation, chromatin immunoprecipitation analysis, yeast two-hybrid analysis, and structure modeling of three-dimensional protein-protein interactions confirm that MP induces interaction between GR DNA binding domain and HIF-1alpha PAS domain, with subsequent recruitment of HIF-1beta to transactivate Epo expression in OLGs.
  • In contrast, MP activates GR but does not induce GR-HIF-1alpha interaction, HIF-1alpha binding to Epo enhancer/promoter, or Epo expression in cultured cortical neurons.
  • The OLG-specific GR-HIF-1alpha transactivation of Epo provides novel insights into the development of more effective therapies for diseases affecting the white matter.
  • [MeSH-major] Cell Death / drug effects. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Methylprednisolone / pharmacology. Oligodendroglia / drug effects. alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid / toxicity
  • [MeSH-minor] Analysis of Variance. Animals. Cells, Cultured. Chromatin Immunoprecipitation. Computer Simulation. Erythropoietin / genetics. Erythropoietin / metabolism. Immunoprecipitation. Rats. Rats, Sprague-Dawley. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 20631191.001).
  • [ISSN] 1529-2401
  • [Journal-full-title] The Journal of neuroscience : the official journal of the Society for Neuroscience
  • [ISO-abbreviation] J. Neurosci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 11096-26-7 / Erythropoietin; 77521-29-0 / alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; X4W7ZR7023 / Methylprednisolone
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91. Qian J, Cuerrier D, Davies PL, Li Z, Powers JC, Campbell RL: Cocrystal structures of primed side-extending alpha-ketoamide inhibitors reveal novel calpain-inhibitor aromatic interactions. J Med Chem; 2008 Sep 11;51(17):5264-70
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  • [Title] Cocrystal structures of primed side-extending alpha-ketoamide inhibitors reveal novel calpain-inhibitor aromatic interactions.
  • When Ca(2+) homeostasis is disrupted, calpain overactivation causes unregulated proteolysis, which can contribute to diseases such as postischemic injury and cataract formation.
  • Here, we present crystal structures of rat calpain 1 protease core (muI-II) bound to two alpha-ketoamide-based calpain inhibitors containing adenyl and piperazyl primed-side extensions.
  • An unexpected aromatic-stacking interaction is observed between the primed-side adenine moiety and the Trp298 side chain.

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  • (PMID = 18702462.001).
  • [ISSN] 1520-4804
  • [Journal-full-title] Journal of medicinal chemistry
  • [ISO-abbreviation] J. Med. Chem.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / NS053801-02; United States / NINDS NIH HHS / NS / R21 NS053801; United States / NINDS NIH HHS / NS / R21 NS053801-02
  • [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 / Amino Acids, Aromatic; 0 / Carbamates; 0 / Dipeptides; 0 / Glycoproteins; 0 / calpain inhibitors; EC 3.4.22.- / Calpain
  • [Other-IDs] NLM/ NIHMS86262; NLM/ PMC2631982
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92. Bauman DR, Steckelbroeck S, Williams MV, Peehl DM, Penning TM: Identification of the major oxidative 3alpha-hydroxysteroid dehydrogenase in human prostate that converts 5alpha-androstane-3alpha,17beta-diol to 5alpha-dihydrotestosterone: a potential therapeutic target for androgen-dependent disease. Mol Endocrinol; 2006 Feb;20(2):444-58
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  • [Title] Identification of the major oxidative 3alpha-hydroxysteroid dehydrogenase in human prostate that converts 5alpha-androstane-3alpha,17beta-diol to 5alpha-dihydrotestosterone: a potential therapeutic target for androgen-dependent disease.
  • Androgen-dependent prostate diseases initially require 5alpha-dihydrotestosterone (DHT) for growth.
  • Candidate enzymes that posses 3alpha-HSD activity are type 3 3alpha-HSD (AKR1C2), 11-cis retinol dehydrogenase (RODH 5), L-3-hydroxyacyl coenzyme A dehydrogenase , RODH like 3alpha-HSD (RL-HSD), novel type of human microsomal 3alpha-HSD, and retinol dehydrogenase 4 (RODH 4).
  • The data show that the major oxidative 3alpha-HSD in normal human prostate is RL-HSD and may be a new therapeutic target for treating prostate diseases.
  • [MeSH-major] 3-alpha-Hydroxysteroid Dehydrogenase (B-Specific) / metabolism. Androgens / metabolism. Androstane-3,17-diol / metabolism. Dihydrotestosterone / metabolism. Prostate / enzymology. Prostatic Diseases / enzymology