Inflammatory Bowel disease

Natural product-based therapy for Inflammatory bowel disease: Methyl Jasmonate (MeJA), isolated from Jasmine, decreases the expression of oncostatin M, attenuates activation of oncostatin M- oncostatin M receptor pathway in inflamed colon tissues, inhibits inflammatory gene expression, attenuates colonic pathogenesis, and inhibits the progression of inflammatory bowel disease and colitis via down regulation of its target gene, 27/June/2017, 12.23 am
Natural product-based therapy for Inflammatory bowel disease: Methyl Jasmonate (MeJA), isolated from Jasmine, decreases the expression of oncostatin M, attenuates activation of oncostatin M- oncostatin M receptor pathway in inflamed colon tissues, inhibits inflammatory gene expression, attenuates colonic pathogenesis, and inhibits the progression of inflammatory bowel disease and colitis via down regulation of its target gene, 27/June/2017, 12.23 am 960 720 Dr Boomi's Genom-2-Discovery Center

Introduction: What they say: A study from the Kennedy Institute of Rheumatology, University of Oxford, Oxford, UK Translational Gastroenterology Unit, Nuffield Department of Medicine, University of Oxford, Oxford, UK shows…

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Natural product-derived therapy for Inflammatory bowel disease: Salvianolic acid A, isolated from Salvia miltiorrhiza Bunge, decreases the expression of oncostatin M, attenuates activation of oncostatin M- oncostatin M receptor pathway in inflamed colon tissues, inhibits inflammatory gene expression, attenuates colonic pathogenesis, and inhibits the progression of inflammatory bowel disease and colitis via down regulation of its target gene, 20/June/2017, 11.51 pm
Natural product-derived therapy for Inflammatory bowel disease: Salvianolic acid A, isolated from Salvia miltiorrhiza Bunge, decreases the expression of oncostatin M, attenuates activation of oncostatin M- oncostatin M receptor pathway in inflamed colon tissues, inhibits inflammatory gene expression, attenuates colonic pathogenesis, and inhibits the progression of inflammatory bowel disease and colitis via down regulation of its target gene, 20/June/2017, 11.51 pm 960 720 Dr Boomi's Genom-2-Discovery Center

Introduction: What they say: A study from the Kennedy Institute of Rheumatology, University of Oxford, Oxford, UK Translational Gastroenterology Unit, Nuffield Department of Medicine, University of Oxford, Oxford, UK shows…

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Molecular therapy for Inflammatory bowel disease: Zic2 (Zic Family Member 2) promotes NFKB-p50/p65 dimer formation, induces inflammatory gene expression downstream of RelA/p65, inhibits colonic pathogenesis, and stalls the progression of inflammatory bowel disease and colitis via down regulation of its target gene, 16/June/2017, 12.04 am
Molecular therapy for Inflammatory bowel disease: Zic2 (Zic Family Member 2) promotes NFKB-p50/p65 dimer formation, induces inflammatory gene expression downstream of RelA/p65, inhibits colonic pathogenesis, and stalls the progression of inflammatory bowel disease and colitis via down regulation of its target gene, 16/June/2017, 12.04 am 960 720 Dr Boomi's Genom-2-Discovery Center

Introduction: What they say: A study from the Institute for Molecular Medicine, University Medical Center of the Johannes Gutenberg, University of Mainz, Obere Zahlbarer Str, Mainz, Germany shows that increased…

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Vitamin-based therapy for Inflammatory bowel disease: Ascorbate decreases the expression of oncostatin M, attenuates activation of oncostatin M- oncostatin M receptor pathway in inflamed colon tissues, inhibits inflammatory gene expression, attenuates colonic pathogenesis, and inhibits the progression of inflammatory bowel disease and colitis via down regulation of its target gene, 22/June/2017, 11.41 pm
Vitamin-based therapy for Inflammatory bowel disease: Ascorbate decreases the expression of oncostatin M, attenuates activation of oncostatin M- oncostatin M receptor pathway in inflamed colon tissues, inhibits inflammatory gene expression, attenuates colonic pathogenesis, and inhibits the progression of inflammatory bowel disease and colitis via down regulation of its target gene, 22/June/2017, 11.41 pm 960 720 Dr Boomi's Genom-2-Discovery Center

Introduction: What they say: A study from the Kennedy Institute of Rheumatology, University of Oxford, Oxford, UK Translational Gastroenterology Unit, Nuffield Department of Medicine, University of Oxford, Oxford, UK shows…

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Molecular therapy for Inflammatory bowel disease: TCTP (Translationally-controlled tumor protein) promotes NFKB-p50/p65 dimer formation, induces inflammatory gene expression downstream of RelA/p65, inhibits colonic pathogenesis, and stalls the progression of inflammatory bowel disease and colitis via down regulation of its target gene, 12/June/2017, 12.11 am
Molecular therapy for Inflammatory bowel disease: TCTP (Translationally-controlled tumor protein) promotes NFKB-p50/p65 dimer formation, induces inflammatory gene expression downstream of RelA/p65, inhibits colonic pathogenesis, and stalls the progression of inflammatory bowel disease and colitis via down regulation of its target gene, 12/June/2017, 12.11 am 960 720 Dr Boomi's Genom-2-Discovery Center

Introduction: What they say: A study from the Institute for Molecular Medicine, University Medical Center of the Johannes Gutenberg, University of Mainz, Obere Zahlbarer Str, Mainz, Germany shows that increased…

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