Author
Michael Karin
Other affiliations: Sanford-Burnham Institute for Medical Research, University of California, Los Angeles, University of California, Berkeley ...read more
Bio: Michael Karin is an academic researcher from University of California, San Diego. The author has contributed to research in topics: IκB kinase & Signal transduction. The author has an hindex of 236, co-authored 704 publications receiving 226485 citations. Previous affiliations of Michael Karin include Sanford-Burnham Institute for Medical Research & University of California, Los Angeles.
Papers published on a yearly basis
Papers
More filters
Patent•
10 Jun 2016TL;DR: In this article, a non-human animal model for non-alcoholic steatohepatitis (NASH)-induced heptocellular carcinoma, methods of screening for agents for treating heptocyte carcinoma and compositions for treating the same were provided.
Abstract: The invention provides a non-human animal model for non-alcoholic steatohepatitis (NASH)-induced heptocellular carcinoma, methods of screening for agents for treating heptocellular carcinoma, methods of screening for targets useful in suppressing NASH progression to heptocellular carcinoma, methods of treating heptocellular carcinoma, and compositions for treating the same.
1 citations
TL;DR: In this article , the authors compared the frequency of esophageal function abnormalities between patients with LSBE and those with SSBE and determined their clinical predictors, such as hypercontractile disorders or hypocontractile disorders.
Abstract: Background/Aims Presently, there is paucity of information about clinical predictors, especially esophageal motor abnormalities, for long segment Barrett’s esophagus (LSBE) as compared with short segment Barrett’s esophagus (SSBE). The aims of this study are to compare the frequency of esophageal function abnormalities between patients with LSBE and those with SSBE and to determine their clinical predictors. Methods This was a multicenter cohort study that included all patients with a diagnosis of BE who underwent high-resolution esophageal manometry. Motility disorders were categorized as hypercontractile disorders or hypocontractile disorders and their frequency was compared between patients with LSBE and those with SSBE. Multivariable logistic regression modeling was used to calculate the odds of being diagnosed with LSBE relative to SSBE for demographics, comorbidities, medication use, endoscopic findings, and the type of motility disorders. Results A total of 148 patients with BE were identified, of which 89 (60.1%) had SSBE and 59 (39.9%) LSBE. Patients with LSBE had a significantly larger hiatal hernia and higher likelihood of erosive esophagitis than patients with SSBE (P = 0.002). Patients with LSBE had a significantly lower mean LES resting pressure, distal contractile integral, distal latency, and significantly higher failed swallows and hypocontractile motility disorders than those with SSBE (P < 0.05). Hiatal hernia and hypocontractile motility disorder increased the odds of LSBE by 38.0% and 242.0%, as opposed to SSBE. Conclusions The presence of a hypocontractile motility disorder increased the risk for LSBE. Furthermore, the risk for LSBE was directly associated with the length of the hiatal hernia.
1 citations
1 citations
1 citations
TL;DR: In this article, the authors summarized recent studies on fructose biology and pathology and discussed new opportunities for prevention and treatment of diseases associated with high-fructose consumption, including obesity and type 2 diabetes mellitus.
1 citations
Cited by
More filters
TL;DR: Recognition of the widespread applicability of these concepts will increasingly affect the development of new means to treat human cancer.
51,099 citations
28 Jul 2005
TL;DR: PfPMP1）与感染红细胞、树突状组胞以及胎盘的单个或多个受体作用，在黏附及免疫逃避中起关键的作�ly.
Abstract: 抗原变异可使得多种致病微生物易于逃避宿主免疫应答。表达在感染红细胞表面的恶性疟原虫红细胞表面蛋白1（PfPMP1）与感染红细胞、内皮细胞、树突状细胞以及胎盘的单个或多个受体作用，在黏附及免疫逃避中起关键的作用。每个单倍体基因组var基因家族编码约60种成员，通过启动转录不同的var基因变异体为抗原变异提供了分子基础。
18,940 citations
TL;DR: Attention is focussed on the ROS/RNS-linked pathogenesis of cancer, cardiovascular disease, atherosclerosis, hypertension, ischemia/reperfusion injury, diabetes mellitus, neurodegenerative diseases, rheumatoid arthritis, and ageing.
12,240 citations
TL;DR: New insights into innate immunity are changing the way the way the authors think about pathogenesis and the treatment of infectious diseases, allergy, and autoimmunity.
10,685 citations
TL;DR: The mechanisms of ROS generation and removal in plants during development and under biotic and abiotic stress conditions are described and the possible functions and mechanisms for ROS sensing and signaling in plants are compared with those in animals and yeast.
Abstract: Several reactive oxygen species (ROS) are continuously produced in plants as byproducts of aerobic metabolism. Depending on the nature of the ROS species, some are highly toxic and rapidly detoxified by various cellular enzymatic and nonenzymatic mechanisms. Whereas plants are surfeited with mechanisms to combat increased ROS levels during abiotic stress conditions, in other circumstances plants appear to purposefully generate ROS as signaling molecules to control various processes including pathogen defense, programmed cell death, and stomatal behavior. This review describes the mechanisms of ROS generation and removal in plants during development and under biotic and abiotic stress conditions. New insights into the complexity and roles that ROS play in plants have come from genetic analyses of ROS detoxifying and signaling mutants. Considering recent ROS-induced genome-wide expression analyses, the possible functions and mechanisms for ROS sensing and signaling in plants are compared with those in animals and yeast.
9,908 citations