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In order to effectively improve the fine management level of animal experimental operating room and ensure the smooth development of animal experimental research, operating room of Experimental Animal Center of Beijing Friendship Hospital has established a WeChat reservation platform. The operating room implements an appointment system, and pushes the appointment information to the experimental participants through the WeChat platform, so that the appointment information can be publicized in a timely and effective manner. The platform provides a standardized operating room application procedure for experimental participants in relevant departments. Through the analysis of appointment information, platform managers can timely understand and grasp the focus and needs of animal experimental operating room management. This paper analyzed and summarized the running condition of WeChat reservation platform in the past one year, in order to promote the communication and discussion of related problems.

Hospital established a good animal experiment platform and a complete set of animal experiment management systems. In good operation, document management is a key element. This paper aimed to improve the management of animal laboratory documents from the perspective of the laboratory accreditation and testing institution accreditation auditor of the China National Accreditation Service for Conformity Assessment (CNAS), and provides a reference for the improvement of the management level of relevant practitioners.

Activation of TGFB (transforming growth factor β) promotes liver fibrosis by activating hepatic stellate cells (HSCs), but the mechanisms of TGFB activation are not clear. We investigated the role of ECM1 (extracellular matrix protein 1), which interacts with extracellular and structural proteins, in TGFB activation in mouse livers. We performed studies with C57BL/6J mice (controls), ECM1-knockout (ECM1-KO) mice, and mice with hepatocyte-specific knockout of EMC1 (ECM1Δhep). ECM1 or soluble TGFBR2 (TGFB receptor 2) were expressed in livers of mice after injection of an adeno-associated virus vector. Liver fibrosis was induced by carbon tetrachloride (CCl 4) administration. Livers were collected from mice and analyzed by histology, immunohistochemistry, in situ hybridization, and immunofluorescence analyses. Hepatocytes and HSCs were isolated from livers of mice and incubated with ECM1; production of cytokines and activation of reporter genes were quantified. Liver tissues from patients with viral or alcohol-induced hepatitis (with different stages of fibrosis) and individuals with healthy livers were analyzed by immunohistochemistry and in situ hybridization. ECM1-KO mice spontaneously developed liver fibrosis and died by 2 months of age without significant hepatocyte damage or inflammation. In liver tissues of mice, we found that ECM1 stabilized extracellular matrix–deposited TGFB in its inactive form by interacting with αv integrins to prevent activation of HSCs. In liver tissues from patients and in mice with CCl 4 -induced liver fibrosis, we found an inverse correlation between level of ECM1 and severity of fibrosis. CCl 4 -induced liver fibrosis was accelerated in ECM1Δhep mice compared with control mice. Hepatocytes produced the highest levels of ECM1 in livers of mice. Ectopic expression of ECM1 or soluble TGFBR2 in liver prevented fibrogenesis in ECM1-KO mice and prolonged their survival. Ectopic expression of ECM1 in liver also reduced the severity of CCl 4 -induced fibrosis in mice. ECM1, produced by hepatocytes, inhibits activation of TGFB and its activation of HSCs to prevent fibrogenesis in mouse liver. Strategies to increase levels of ECM1 in liver might be developed for treatment of fibrosis. [ABSTRACT FROM AUTHOR]