ABSTRACT
The cultivation of research ability can promote eight-year medical students to explore the uncharted academic fields and solve complex clinical problems. One of the firts pilot universities to provide eight-year programs, Xiangya Medical College of Central South University builds on its profound experience in medical education, and establishes a curriculum structure aiming at improving the students' research ability. In the general education stage, cross-disciplinary courses are set up. In the core medical education stage, basic medical innovation experiment extracurricular research courses are set up, and a two-year overseas exchange program is set up in the postgraduate training stage. Different evaluation methods are also designed to meet the specific needs in each stage. This program has achieved preliminary effects.
ABSTRACT
High mobility group box-1 (HMGB1) is an evolutionarily conserved protein,which widely exists in mammals.HMGB 1 contains the nucleus localization sequences.Intracellular and extracellular HMGB1 shows different biological functions.Extracellular HMGB1 is closely related to sepsis,cancer,rheumatoid immune,atherosclerosis,ischemia-reperfusion injury and so on.The mobilization of HMGB 1 from the nucleus to the cytoplasm and subsequent release involves the processes of post-translation modification,active secretion and nuclear localization.
ABSTRACT
High mobility group box 1 (HMGB1) is an evolutionarily conserved non-histone chromatin-binding protein. During infection or injury, activated immune cells and damaged cells release HMGB1 into the extracellular space, where HMGB1 functions as a proinflammatory mediator and contributes importantly to the pathogenesis of inflammatory diseases. Recent studies reveal that inflammasomes, intracellular protein complexes, critically regulate HMGB1 release from activated immune cells in response to a variety of exogenous and endogenous danger signals. Double stranded RNA dependent kinase (PKR), an intracellular danger-sensing molecule, physically interacts with inflammasome components and is important for inflammasome activation and HMGB1 release. Together, these studies not only unravel novel mechanisms of HMGB1 release during inflammation, but also provide potential therapeutic targets to treat HMGB1-related inflammatory diseases.
Subject(s)
Humans , HMGB1 Protein , Chemistry , Metabolism , Inflammasomes , Metabolism , Macrophages , Allergy and Immunology , Metabolism , eIF-2 Kinase , MetabolismABSTRACT
<p><b>OBJECTIVE</b>To observe the expression of extracellular matrix metalloproteinase inducer (EMMPRIN) in the unstable plaque of patients with acute coronary syndrome (ACS), and the impact of leukotriene B4 (LTB4) on the EMMPRIN expression in macrophages.</p><p><b>METHODS</b>The EMMPRIN expression was detected by immunohistochemistry in 11 unstable plaques from patients with ACS. Protein expression of EMMPRIN was evaluated by Western blot on macrophages differentiated from THP-1 which were stimulated with LTB4 in the absence or presence of LTB4 antagonist U75302. There are 8 study groups: 1-THP-1, 2-8-the macrophages derived from THP-1, 2-6-macrophages were stimulated by LTB4 (0, 10(-10), 10(-9), 10(-8) and 10(-7) mol/L) for 24 h, 7-8-the macrophages were pretreated by 10(-6) mol/L or 10(-7) mol/L U75302 2 h before the LTB4 (10(-7) mol/L) stimulation.</p><p><b>RESULTS</b>Abundant EMMPRIN expression was detected in macrophages and smooth muscle cells of unstable plaques from ACS patients. As to the THP-1 derived macrophages, EMMPRIN expression was significantly upregulated in a concentration-dependent manner in LTB4 stimulated groups, which was significantly higher in group 3-6 than in the THP-1 group (group 1) and macrophages group (group 2) (all P < 0.05) and pretreatment with U75302 significantly reduced the LTB4 induced upregulation of EMMPRIN in a dose-dependent manner (P < 0.05).</p><p><b>CONCLUSION</b>EMMPRIN expression is enhanced in macrophages and smooth muscle cells on unstable coronary artery plaques from ACS patients. LTB4 could stimulate EMMPRIN expression on THP-1 derived macrophages suggesting that LTB4 and EMMPRIN might be both involved in the formation and progression of unstable plaques, future studies are warranted to explore if LTB4 and EMMPRIN antagonists are effective or not for treating patients with ACS.</p>
Subject(s)
Humans , Acute Coronary Syndrome , Metabolism , Pathology , Basigin , Metabolism , Cell Line , Leukotriene B4 , Metabolism , Pharmacology , Macrophages , Metabolism , Myocytes, Smooth Muscle , Metabolism , Plaque, Atherosclerotic , MetabolismABSTRACT
The status of marine bioresources and the marine eco-environment issues were summarized and discussed, and the strategies for the development of Chinese marine bioresources in the future were proposed. The degradation of marine eco-environment and unreasonable exploitation of the resources resulted in acute decline of Chinese marine bioresources. The feasible stratagies for the sustainable use of marine bioresources should be to intensify the basic research on marine bioresources science, to strengthen the protection of the marine environment and conservation of marine living resources, and to exploit and utilize marine bioresources scientifically and reasonably by using high-technology including marine biotechnology.