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1. Choudhary SK, Archin NM, Margolis DM: Hexamethylbisacetamide and disruption of human immunodeficiency virus type 1 latency in CD4(+) T cells. J Infect Dis; 2008 Apr 15;197(8):1162-70
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  • [Title] Hexamethylbisacetamide and disruption of human immunodeficiency virus type 1 latency in CD4(+) T cells.
  • BACKGROUND: Novel therapeutic approaches are needed to attack persistent proviral human immunodeficiency type 1 (HIV-1) infection.
  • RESULTS: HMBA induced outgrowth of HIV-1 from resting CD4(+) T cells recovered from aviremic patients treated with antiretroviral therapy (ART).
  • HMBA signaling via both protein kinase C mu and phosphatidylinositol 3-kinase appeared to contribute to LTR induction.
  • [MeSH-major] Acetamides / pharmacology. CD4-Positive T-Lymphocytes / virology. HIV Infections / virology. HIV-1 / physiology. Virus Latency / drug effects
  • [MeSH-minor] Cyclin-Dependent Kinase 9 / antagonists & inhibitors. Cyclin-Dependent Kinase 9 / metabolism. Gene Expression Regulation, Viral. HIV Long Terminal Repeat. HeLa Cells. Humans. Jurkat Cells. Phosphatidylinositol 3-Kinases / metabolism. Phosphorylation / drug effects. Polymerase Chain Reaction. Promoter Regions, Genetic. Protein Kinase C / metabolism. Protein Kinase Inhibitors / pharmacology. RNA Polymerase II / metabolism. RNA, Small Interfering / genetics. RNA, Viral / chemistry. RNA, Viral / genetics. Sp1 Transcription Factor / metabolism

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  • (PMID = 18419522.001).
  • [ISSN] 0022-1899
  • [Journal-full-title] The Journal of infectious diseases
  • [ISO-abbreviation] J. Infect. Dis.
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / AI045297; United States / NIAID NIH HHS / AI / AI064074; United States / NIAID NIH HHS / AI / P30 AI50410
  • [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 / Acetamides; 0 / Protein Kinase Inhibitors; 0 / RNA, Small Interfering; 0 / RNA, Viral; 0 / Sp1 Transcription Factor; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.- / protein kinase D; EC 2.7.11.13 / Protein Kinase C; EC 2.7.11.22 / CDK9 protein, human; EC 2.7.11.22 / Cyclin-Dependent Kinase 9; EC 2.7.7.- / RNA Polymerase II; LA133J59VU / hexamethylene bisacetamide
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2. Crespo M, Sauleda S, Esteban JI, Juarez A, Ribera E, Andreu AL, Falco V, Quer J, Ocaña I, Ruiz I, Buti M, Pahissa A, Esteban R, Guardia J: Peginterferon alpha-2b plus ribavirin vs interferon alpha-2b plus ribavirin for chronic hepatitis C in HIV-coinfected patients. J Viral Hepat; 2007 Apr;14(4):228-38
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  • Treatment of chronic hepatitis C in human immunodeficiency virus (HIV)-infected patients is associated with low response rates and high incidence of side effects.
  • One hundred twenty-one hepatitis C virus (HCV)-HIV-coinfected patients were randomized to receive interferon alpha-2b (3 MU thrice weekly; n = 61) or peginterferon alpha-2b (1.5 microg/kg/week; n = 60), plus ribavirin (800 mg daily), for 24 (genotype 2 or 3) or 48 weeks (genotype 1 or 4).
  • The difference for HCV genotypes 1 and 4 was 45%vs 14% (P = 0.009) and 50%vs 27% (P = 0.387), respectively, and for genotype 2 or 3, 71%vs 43% (P = 0.12) Viral response at 4, 8 and 12 weeks of treatment was highly predictive of SVR.
  • Among genotype 3 patients, 17 of 20 (85%) whose HCV RNA was already undetectable at 4 weeks had an SVR after 24 weeks of treatment.
  • Hyperlactataemia occurred in 22 patients and was clinically significant in six, two of whom died. mtDNA decreased significantly 4-12 weeks after the start of treatment in patients developing clinically significant hyperlactataemia.
  • Frequent monitoring of virological response may be very helpful to optimize treatment compliance, to tailor treatment duration and to minimize side effects.
  • [MeSH-major] HIV. HIV Infections / complications. Hepacivirus. Hepatitis C, Chronic / complications. Hepatitis C, Chronic / drug therapy. Interferon-alpha / administration & dosage. Ribavirin / administration & dosage
  • [MeSH-minor] Adolescent. Adult. Antiviral Agents / administration & dosage. Antiviral Agents / adverse effects. Cell Nucleus / genetics. Cell Nucleus / metabolism. DNA / metabolism. DNA, Mitochondrial / blood. DNA, Mitochondrial / metabolism. Drug Therapy, Combination. Female. Humans. Male. Middle Aged. Polyethylene Glycols. Recombinant Proteins. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 17381714.001).
  • [ISSN] 1352-0504
  • [Journal-full-title] Journal of viral hepatitis
  • [ISO-abbreviation] J. Viral Hepat.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antiviral Agents; 0 / DNA, Mitochondrial; 0 / Interferon-alpha; 0 / Recombinant Proteins; 0 / peginterferon alfa-2b; 30IQX730WE / Polyethylene Glycols; 49717AWG6K / Ribavirin; 9007-49-2 / DNA; 99210-65-8 / interferon alfa-2b
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3. Pizzimenti S, Barrera G, Calzavara E, Mirandola L, Toaldo C, Dianzani MU, Comi P, Chiaramonte R: Down-regulation of Notch1 expression is involved in HL-60 cell growth inhibition induced by 4-hydroxynonenal, a product of lipid peroxidation. Med Chem; 2008 Nov;4(6):551-7
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  • As a result, Notch1 signalling inhibition is an attractive goal in leukaemia therapy.
  • 4-Hydroxynonenal (HNE), an aldehyde produced during lipid peroxidation, is involved in several pathological and physiological conditions, including inflammation; atherosclerosis; and neurodegenerative and chronic liver diseases.
  • The expression of Hes1, a Notch1 target gene, was concomitantly down-regulated by HNE treatment, reflecting Notch1 signalling inhibition.
  • Moreover, DAPT treatment reversed the HNE-induced differentiation.
  • [MeSH-major] Aldehydes / pharmacology. Lipid Peroxidation / drug effects. Receptor, Notch1 / genetics. Receptor, Notch1 / physiology
  • [MeSH-minor] Amyloid Precursor Protein Secretases / antagonists & inhibitors. Apoptosis / drug effects. Blotting, Western. Cell Differentiation / drug effects. Cell Proliferation / drug effects. Down-Regulation. Enzyme Inhibitors / pharmacology. Gene Expression. Glyceraldehyde-3-Phosphate Dehydrogenases / metabolism. HL-60 Cells. Humans. RNA / biosynthesis. RNA / isolation & purification. Reverse Transcriptase Polymerase Chain Reaction. Triglycerides / pharmacology. gamma-Aminobutyric Acid / analogs & derivatives. gamma-Aminobutyric Acid / pharmacology

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  • (PMID = 18991739.001).
  • [ISSN] 1573-4064
  • [Journal-full-title] Medicinal chemistry (Shāriqah (United Arab Emirates))
  • [ISO-abbreviation] Med Chem
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Aldehydes; 0 / Enzyme Inhibitors; 0 / NOTCH1 protein, human; 0 / Receptor, Notch1; 0 / Triglycerides; 29343-52-0 / 4-hydroxy-2-nonenal; 56-12-2 / gamma-Aminobutyric Acid; 63231-63-0 / RNA; 93349-26-9 / 1,2-dilinolenoyl-3-(4-aminobutyryl)propane-1,2,3-triol; EC 1.2.1.- / Glyceraldehyde-3-Phosphate Dehydrogenases; EC 3.4.- / Amyloid Precursor Protein Secretases
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4. De Rycke L, Kruithof E, Van Damme N, Hoffman IE, Van den Bossche N, Van den Bosch F, Veys EM, De Keyser F: Antinuclear antibodies following infliximab treatment in patients with rheumatoid arthritis or spondylarthropathy. Arthritis Rheum; 2003 Apr;48(4):1015-23
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  • [Title] Antinuclear antibodies following infliximab treatment in patients with rheumatoid arthritis or spondylarthropathy.
  • OBJECTIVE: To investigate the effect of infliximab treatment on antinuclear antibodies (ANAs), anti-double-stranded DNA (anti-dsDNA), antinucleosome, antihistone, and anti-extractable nuclear antigen (anti-ENA) antibodies in rheumatoid arthritis (RA) and spondylarthropathy (SpA) patients.
  • Anti-dsDNA antibodies were detected by IIF on Crithidia luciliae and by enzyme-linked immunosorbent assay (ELISA) and were further isotyped with gamma, mu, and alpha chain-specific conjugates at various time points.
  • After infliximab treatment, these numbers shifted to 51 of 62 (P < 0.001) and 31 of 35 (P < 0.001), respectively.
  • After infliximab treatment, 7 RA patients (P = 0.016) and 6 SpA patients (P = 0.031) became positive for anti-dsDNA antibodies.
  • All 7 anti-dsDNA-positive RA patients had IgM and IgA anti-dsDNA antibodies.
  • Three of the 6 anti-dsDNA-positive SpA patients had IgM and IgA anti-dsDNA antibodies, and 2 had IgM anti-dsDNA antibodies alone.
  • In both diseases, the IgM anti-dsDNA antibodies appeared before the IgA anti-dsDNA antibodies.
  • The development of antinucleosome, antihistone, or anti-ENA antibodies following infliximab treatment was observed in some patients, but the numbers were not statistically significant.
  • CONCLUSION: Infliximab treatment may induce ANAs, and especially IgM and IgA anti-dsDNA antibodies, in RA and SpA patients.
  • [MeSH-major] Antibodies, Antinuclear / immunology. Antibodies, Monoclonal / therapeutic use. Antirheumatic Agents / therapeutic use. Arthritis, Rheumatoid / drug therapy. Arthritis, Rheumatoid / immunology. Spondylitis, Ankylosing / drug therapy. Spondylitis, Ankylosing / immunology
  • [MeSH-minor] Adult. Aged. DNA / immunology. Drug Therapy, Combination. Female. Fluorescent Antibody Technique, Indirect. Humans. Infliximab. Infusions, Intravenous. Male. Methotrexate / therapeutic use. Middle Aged


5. Egli RJ, Di Criscio A, Hempfing A, Schoeniger R, Ganz R, Hofstetter W, Leunig M: In vitro resistance of articular chondrocytes to 5-Aminolevulinic acid based photodynamic therapy. Lasers Surg Med; 2008 Apr;40(4):282-90
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  • [Title] In vitro resistance of articular chondrocytes to 5-Aminolevulinic acid based photodynamic therapy.
  • OBJECTIVE: 5-Aminolevulinic acid based photodynamic therapy (5-ALA-PDT) has revealed promising results in the treatment of inflammatory joint diseases due to the sensitivity of inflamed synovial tissue.
  • As no data yet exist, the aim of the present study was to assess in vitro the response of the chondrocytes to 5-ALA-PDT and to compare with osteoblasts and synovial tissue derived cells.
  • After incubation with 0.5 mM 5-ALA and application of light at a dose of 20 J/cm2, chondrocytes were functionally not affected (collagen type II and aggrecan mRNA, glycosaminoglycan synthesis) whereas a decrease in the proportion of viable cells was observed in osteoblasts and synovial cells (2+/-2% and 14+/-8%, respectively; chondrocytes 91+/-13%).
  • Chondrocytes showed a 58% reduction of 5-ALA uptake using [3H]5-ALA as compared to osteoblasts and a lower mitochondrial content as assessed by the activity of the mitochondrial marker enzyme citrate synthase (9.2+/- 3.6 mU/mg protein) than osteoblasts (32.6+/-10.5 mU/mg) and synovial cells (60.0+/-10.8 mU/mg).
  • CONCLUSION: 5-ALA-PDT might represent a treatment strategy in inflammatory joint diseases without endangering the cartilage function.
  • [MeSH-major] Aminolevulinic Acid / pharmacology. Chondrocytes / drug effects. Photochemotherapy / methods. Photosensitizing Agents / pharmacology
  • [MeSH-minor] Animals. Cattle. Cell Survival. Cells, Cultured. Drug Resistance. In Vitro Techniques. Osteoblasts / drug effects. Reverse Transcriptase Polymerase Chain Reaction. Synovial Membrane / cytology. Synovial Membrane / drug effects

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  • (PMID = 18412230.001).
  • [ISSN] 0196-8092
  • [Journal-full-title] Lasers in surgery and medicine
  • [ISO-abbreviation] Lasers Surg Med
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Photosensitizing Agents; 88755TAZ87 / Aminolevulinic Acid
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6. Krogh-Madsen M, Arendrup MC, Heslet L, Knudsen JD: Amphotericin B and caspofungin resistance in Candida glabrata isolates recovered from a critically ill patient. Clin Infect Dis; 2006 Apr 1;42(7):938-44
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  • BACKGROUND: Consecutive Candida glabrata isolates recovered from a patient in an intensive care unit were resistant to amphotericin B (minimum inhibitory concentration, up to 32 mu g/mL; determined by Etest [AB Biodisk]).
  • METHODS: Different broth microdilution tests, Etests, and time-kill studies for antifungals were performed in different media.
  • For the clonality studies, arbitrarily primed polymerase chain reaction (PCR) was performed with the 4 isolates, 8 isolates obtained from nonrelated patients, and a reference strain.
  • CONCLUSIONS: We have documented the emergence of amphotericin B-resistant and caspofungin-resistant C. glabrata isolates during treatment of a critically ill liver transplant recipient.
  • We recommend that important fungal strains recovered from patients who are receiving antifungal therapy should be tested for susceptibility to the antifungal drug used, because resistance can be present initially or may occur during treatment.
  • [MeSH-major] Amphotericin B / pharmacology. Antifungal Agents / pharmacology. Candida glabrata / drug effects. Peptides, Cyclic / pharmacology
  • [MeSH-minor] Aged. Animals. Candidiasis / drug therapy. Critical Illness. Echinocandins. Female. Humans. Mice. Microbial Sensitivity Tests. Polymerase Chain Reaction


7. Ludwiczek S, Theurl I, Muckenthaler MU, Jakab M, Mair SM, Theurl M, Kiss J, Paulmichl M, Hentze MW, Ritter M, Weiss G: Ca2+ channel blockers reverse iron overload by a new mechanism via divalent metal transporter-1. Nat Med; 2007 Apr;13(4):448-54
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  • Hereditary hemochromatosis and transfusional iron overload are frequent clinical conditions associated with progressive iron accumulation in parenchymal tissues, leading to eventual organ failure.
  • We have discovered a new mechanism to reverse iron overload-pharmacological modulation of the divalent metal transporter-1 (DMT-1).
  • We show that the L-type calcium channel blocker nifedipine increases DMT-1-mediated cellular iron transport 10- to 100-fold at concentrations between 1 and 100 microM.
  • Modulation of DMT-1 function by L-type calcium channel blockers emerges as a new pharmacological therapy for the treatment of iron overload disorders.
  • [MeSH-major] Calcium Channel Blockers / pharmacology. Cation Transport Proteins / metabolism. Hemochromatosis / prevention & control. Iron Overload / drug therapy. Nifedipine / pharmacology
  • [MeSH-minor] Animals. Biological Transport, Active / drug effects. COS Cells. Cercopithecus aethiops. Electrophysiology. Humans. Immunoblotting. Iron / metabolism. Iron / urine. Liver / metabolism. Mice. Mice, Knockout. Microarray Analysis. Reverse Transcriptase Polymerase Chain Reaction


8. Mozer-Lisewska I, Słuzewski W, Ali Youseif K, Figlerowicz M, Kowala-Piaskowska A: Virus genotype 1b and long-term response to interferon alpha monotherapy in children with chronic hepatitis C. Eur J Pediatr; 2003 Nov;162(11):755-9
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  • Interferon alpha (IFN-alpha) remains the basic modality in the treatment of chronic hepatitis C in children, but the effects of therapy are still unsatisfactory.
  • The IFN-treated group received a dosage 3 MU of IFN-alpha three times a week for 24 weeks.
  • In the IFN-treated group ALT normalisation was observed by the end of treatment in 9/20 patients, but after 6 months 10 patients (50%) had sustained ALT normalisation and in 4 of them the virus was eliminated.
  • CONCLUSION: The negative predictive effect of HCV genotype 1b in the course of IFN-alpha treatment may be not valid in children and other features have to be taken into account in the assessment of the efficacy of therapy.
  • [MeSH-major] Hepacivirus / genetics. Hepatitis C, Chronic / diagnosis. Hepatitis C, Chronic / drug therapy. Interferon-alpha / administration & dosage
  • [MeSH-minor] Case-Control Studies. Child. Child, Preschool. Dose-Response Relationship, Drug. Drug Administration Schedule. Female. Follow-Up Studies. Humans. Liver Function Tests. Long-Term Care. Male. Probability. Prospective Studies. RNA, Viral / analysis. Reference Values. Reverse Transcriptase Polymerase Chain Reaction. Risk Assessment. Severity of Illness Index. Treatment Outcome. Viral Load

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  • (PMID = 12937972.001).
  • [ISSN] 0340-6199
  • [Journal-full-title] European journal of pediatrics
  • [ISO-abbreviation] Eur. J. Pediatr.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Germany
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9. Audard V, Georges B, Vanhille P, Toly C, Deroure B, Fakhouri F, Cuvelier R, Belenfant X, Surin B, Aucouturier P, Mougenot B, Ronco P: Renal lesions associated with IgM-secreting monoclonal proliferations: revisiting the disease spectrum. Clin J Am Soc Nephrol; 2008 Sep;3(5):1339-49
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  • [Title] Renal lesions associated with IgM-secreting monoclonal proliferations: revisiting the disease spectrum.
  • BACKGROUND AND OBJECTIVES: Since the first description of pathology of the kidney in Waldenström disease in 1970, there have been few reports on kidney complications of IgM-secreting monoclonal proliferations.
  • Here, we aimed to revisit the spectrum of renal lesions occurring in patients with a serum monoclonal IgM.
  • DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: Fourteen patients with a circulating monoclonal IgM and a kidney disease related to B cell proliferation were identified retrospectively.
  • Demographic, clinical, and laboratory data were assessed for each patient at the time of kidney biopsy.
  • For five patients, the diagnosis of monoclonal IgM preceded the kidney disease by 28.8 mo (range 12 to 60).
  • Seven patients had Waldenström disease, two had a small B cell non-Hodgkin lymphoma, one had an IgM-excreting multiple myeloma, one had a marginal zone B cell lymphoma, and three had an IgM-related disorder.
  • Renal lesions included (1) intracapillary monoclonal deposits disease with granular, electron-dense IgM thrombi occluding capillary lumens (5);.
  • (3) lambda light chain amyloidosis (2) associated with mu deposits in one patient;.
  • Remission of the nephrotic syndrome was attained in three of seven patients, and renal function improved after chemotherapy.
  • CONCLUSIONS: Although renal complications of IgM proliferations are rare, a wide spectrum of kidney lesions is observed, without correlation with the type of hematologic disorder.
  • [MeSH-major] Antibodies, Monoclonal / analysis. B-Lymphocytes / immunology. Cell Proliferation. Immunoglobulin M / analysis. Kidney Diseases / immunology. Lymphoproliferative Disorders / immunology
  • [MeSH-minor] Aged. Amyloidosis / immunology. Female. Glomerulonephritis, Membranoproliferative / immunology. Humans. Lymphoma, B-Cell / immunology. Lymphoma, B-Cell, Marginal Zone / immunology. Male. Middle Aged. Multiple Myeloma / immunology. Nephrotic Syndrome / immunology. Retrospective Studies. Treatment Outcome. Waldenstrom Macroglobulinemia / immunology

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  • (PMID = 18632851.001).
  • [ISSN] 1555-905X
  • [Journal-full-title] Clinical journal of the American Society of Nephrology : CJASN
  • [ISO-abbreviation] Clin J Am Soc Nephrol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Immunoglobulin M
  • [Other-IDs] NLM/ PMC2518806
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10. Mu H, Ohashi R, Yan S, Chai H, Yang H, Lin P, Yao Q, Chen C: Adipokine resistin promotes in vitro angiogenesis of human endothelial cells. Cardiovasc Res; 2006 Apr 1;70(1):146-57
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVE: Resistin may be associated with obesity and cardiovascular diseases.
  • Capillary-like tube formation was studied with a Matrigel model.
  • Several gene expression levels were determined by real-time PCR.
  • RESULTS: Resistin induced both endothelial proliferation and migration in a dose- and time-dependent manner with the maximal effect at 40 ng/ml.
  • [MeSH-major] Coronary Vessels. Endothelial Cells / cytology. Neovascularization, Physiologic / drug effects. Resistin / pharmacology
  • [MeSH-minor] Antibodies, Monoclonal / pharmacology. Biomarkers / analysis. Capillaries. Cell Movement / drug effects. Cell Proliferation / drug effects. Cells, Cultured. Collagen. Dose-Response Relationship, Drug. Drug Combinations. Extracellular Signal-Regulated MAP Kinases / metabolism. Humans. Laminin. Lung. Matrix Metalloproteinase 1 / analysis. Matrix Metalloproteinase 1 / genetics. Matrix Metalloproteinase 2 / analysis. Matrix Metalloproteinase 2 / genetics. Proteoglycans. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction. Stimulation, Chemical. Umbilical Veins. Vascular Endothelial Growth Factor Receptor-1 / analysis. Vascular Endothelial Growth Factor Receptor-1 / genetics. Vascular Endothelial Growth Factor Receptor-2 / analysis. Vascular Endothelial Growth Factor Receptor-2 / genetics. p38 Mitogen-Activated Protein Kinases / metabolism

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  • (PMID = 16515776.001).
  • [ISSN] 0008-6363
  • [Journal-full-title] Cardiovascular research
  • [ISO-abbreviation] Cardiovasc. Res.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / K08 HL076345; United States / NIDCR NIH HHS / DE / R01 DE15543; United States / NIBIB NIH HHS / EB / R01 EB-002436; United States / NHLBI NIH HHS / HL / R01 HL065916; United States / NHLBI NIH HHS / HL / R01 HL072716; United States / NHLBI NIH HHS / HL / R01 HL083471; United States / NCCIH NIH HHS / AT / R21 AT003094
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Biomarkers; 0 / Drug Combinations; 0 / Laminin; 0 / Proteoglycans; 0 / RNA, Messenger; 0 / Resistin; 119978-18-6 / matrigel; 9007-34-5 / Collagen; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-1; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; EC 3.4.24.24 / Matrix Metalloproteinase 2; EC 3.4.24.7 / Matrix Metalloproteinase 1
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11. Shiratori Y, Nakata R, Shimizu N, Katada H, Hisamitsu S, Yasuda E, Matsumura M, Narita T, Kawada K, Omata M, IFN-beta Research Group: High viral eradication with a daily 12-week natural interferon-beta treatment regimen in chronic hepatitis C patients with low viral load. IFN-beta Research Group. Dig Dis Sci; 2000 Dec;45(12):2414-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High viral eradication with a daily 12-week natural interferon-beta treatment regimen in chronic hepatitis C patients with low viral load. IFN-beta Research Group.
  • Virological sustained response (SR) is achieved in 31-49% of patients with chronic hepatitis C with combination therapy using interferon (IFN)-alpha and ribavirin for 24-48 weeks.
  • In all, 112 patients were enrolled and received a daily administration of 6 MU of natural IFN-beta intravenously for 12 weeks.
  • Serum HCV-RNA before treatment was assessed by the competitive reverse-transcription polymerase chain reaction assay.
  • Virological SR was obtained in 37% (41/112) of all the patients; 88% of those with a low viral load, and 22% of patients with a high viral load.
  • In patients with HCV subtype 1b, virological SR was obtained in patients with the mutant-type (> or =4 amino acid mutations in the NSSA2209-48) having a low viral load (4/4), but not in those having a high viral load (0/3).
  • The results suggest that a daily intravenous administration of natural IFN-beta for 12 weeks showed high therapeutic efficacy in patients with a low viral load despite the shorter treatment period and that the therapeutic efficacy depends on viral load rather than on the number of NS5A2209-48 amino acid mutations.
  • [MeSH-major] Hepatitis C, Chronic / therapy. Interferon-beta / administration & dosage
  • [MeSH-minor] Adolescent. Adult. Aged. Drug Administration Schedule. Female. Humans. Injections, Intravenous. Male. Middle Aged. RNA, Viral / blood. Treatment Outcome

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  • (PMID = 11258568.001).
  • [ISSN] 0163-2116
  • [Journal-full-title] Digestive diseases and sciences
  • [ISO-abbreviation] Dig. Dis. Sci.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Viral; 77238-31-4 / Interferon-beta
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12. Tanabe Y, Sakamoto N, Enomoto N, Kurosaki M, Ueda E, Maekawa S, Yamashiro T, Nakagawa M, Chen CH, Kanazawa N, Kakinuma S, Watanabe M: Synergistic inhibition of intracellular hepatitis C virus replication by combination of ribavirin and interferon- alpha. J Infect Dis; 2004 Apr 1;189(7):1129-39
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  • Treatment of hepatitis C virus (HCV) infection with interferon (IFN)- alpha and ribavirin combination therapy results in superior clinical antiviral responses than does monotherapy with IFN.
  • To explore the virological basis of the effects of combination therapy, we analyzed the effects of IFN- alpha and ribavirin, singly and in combination, on intracellular HCV replication by use of an HCV replicon system.
  • Therapy with ribavirin showed weak suppression of HCV replication at a lower concentration (IC(50), 126 mu mol/L).
  • The nucleotide sequence diversity of the replicon was increased significantly by therapy with ribavirin, suggesting that error-prone HCV replication was induced by the drug.
  • Importantly, use of a clinically achievable concentration of ribavirin (approximately 10 mu mol/L) in combination with IFN showed strong synergistic inhibitory effects on HCV replication.
  • Our results suggest that the direct effects of ribavirin on the genetic stability of the HCV subgenome and its synergistic action combined, with IFN-alpha, may explain the improved clinical responses to combination therapy.
  • [MeSH-major] Antiviral Agents / pharmacology. Hepacivirus / drug effects. Hepatitis C / virology. Interferon-alpha / pharmacology. Ribavirin / pharmacology. Virus Replication / drug effects
  • [MeSH-minor] Amino Acid Sequence. Base Sequence. Blotting, Northern. Cell Line, Tumor. Drug Synergism. Drug Therapy, Combination. Humans. Molecular Sequence Data. Point Mutation. RNA, Viral / chemistry. RNA, Viral / genetics. Recombinant Proteins. Replicon / drug effects. Reverse Transcriptase Polymerase Chain Reaction. Sequence Alignment. Transfection

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  • (PMID = 15031779.001).
  • [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 / Antiviral Agents; 0 / Interferon-alpha; 0 / RNA, Viral; 0 / Recombinant Proteins; 49717AWG6K / Ribavirin; 99210-65-8 / interferon alfa-2b
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13. Witzig TE, Wahner-Roedler DL: Heavy chain disease. Curr Treat Options Oncol; 2002 Jun;3(3):247-54
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  • [Title] Heavy chain disease.
  • The heavy chain diseases (HCDs) are rare B-cell malignancies that are distinguished by the production of a monoclonal immunoglobulin heavy chain (HC) without an associated light chain by the malignant B-cells.
  • There are three types of HCD defined by the class of immunoglobulin (Ig) HC produced: IgA (alpha-HCD), IgG (gamma-HCD), and IgM (mu-HCD).
  • Alpha-HCD is the most common and occurs most commonly as intestinal malabsorption in a young adult from a country bordering the Mediterranean Sea.
  • Treatment consists of antibiotics and improved nutrition and hygiene.
  • If there is no response to antibiotics or if aggressive non-Hodgkin's lymphoma (NHL) is diagnosed, the patient should be treated with chemotherapy.
  • Gamma- and mu-HCD are rare and essentially are found in patients with a B-cell NHL that produces an abnormal Ig heavy chain.
  • These patients occasionally may be diagnosed with a monoclonal gammopathy of undetermined significance (MGUS).
  • Patients with MGUS with NHL should be administered chemotherapy.
  • Screening the serum and urine of patients with lymphoplasmacytoid NHL would likely identify more patients with gamma- or mu-HCD.
  • [MeSH-major] Heavy Chain Disease / therapy
  • [MeSH-minor] Adult. Aged. Gene Rearrangement, B-Lymphocyte, Heavy Chain / genetics. Humans. Immunoglobulin Heavy Chains / genetics. Incidence. Middle Aged. Radiotherapy

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  • (PMID = 12057070.001).
  • [ISSN] 1527-2729
  • [Journal-full-title] Current treatment options in oncology
  • [ISO-abbreviation] Curr Treat Options Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunoglobulin Heavy Chains
  • [Number-of-references] 36
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