2种钼簇化合物对酪氨酸酶的抑制作用及对凡纳滨对虾的保鲜效果研究

通过合成2种高核钼簇（NH4）12[Mo36O108（NO）4（H2O）16].33H2O(Mo36)和[Mo36O112（OH2）16（H2bipy）4].28H2O (Mo36-bipy),其对酪氨酸二酚酶活性的抑制作用机理以及对凡纳滨对虾的防黑变保鲜效果进行研究。结果表明Mo36和Mo36-bipy对酪氨酸二酚酶IC50值分别为0.0358 mmol/L和0.0601 mmol/L,Mo36对酪氨酸酶的抑制作用为可逆竞争性抑制,Mo36-bipy对酪氨酸酶的抑制作用为可逆混合性抑制,且Mo36对酪氨酸酶活性的抑制作用效果优于Mo36-bipy。将凡纳滨对虾在4℃环境下贮藏10 d,通过对感官评分、颜色、pH值、TVB-N和菌落总数等指标检测,发现高核钼簇对样品具有一定保鲜效果。其均能适当提升感官分值、L*值,降低pH值与菌落总数。本研究结果为开发一种新型的抗虾体黑变的保鲜剂提供实验基础,并对多金属氧酸盐的应用研究拓展新的研究领域。国家自然科学基金项目(21871110

公司践行社会主义荣辱观与公司的社会责任初探

公司社会责任作为公司道德责任和法律责任的连接点,是道德义务和法律义务的统一体。强化公司社会责任与践行社会主义荣辱观是内在的统一,是我国公司制度改革和发展的方向。公司践行社会主义荣辱观是企业道德建设的需要和构建和谐社会的需要。公司践行社会主义荣辱观,需要正确认识公司的目的与公司社会责任的关系,全面构建公司社会责任法律体系,完善公司治理结构,加强董事会的道德建设

论基本公共服务均等化的宪法价值

基本公共服务均等化要求政府必须为社会公众提供基本的、与经济社会发展水平相适应的、体现公平公正原则的大致均等的公共物品或公共服务,即在基本的公共服务领域政府应尽可能地满足人们的基本物质需要,使人们在分享公共服务中有同样的权利。基本公共服务均等化的宪法基础是人权保障和法治原则,其宪法价值在于,它是尊重和保障人权的重大举措,是促进中央与地方关系法治化的有效路径,是建设社会主义法治国家的必然要求

如何增强我国金融体系的稳定性探讨

金融稳定关乎整个经济的健康发展,银行稳定是我国金融稳定的核心。作为我国金融主体的银行背负着不良资产的历史包袱,面临着银行业逐渐全面开放的日益增大的竞争压力,而且还缺乏有效的稳定机制。近年来人们一直在讨论的存款保险制度的确越来越迫切需要建立,但是,本文认为存款保险制度必须与银行体系市场化改革、金融风险预警系统、金融机构市场退出的法律制度相结合,在一国的内部共同构成一个金融机构特别是银行的风险监督、市场退出和危机处理机制

Rigging and Fabricating Creative Characters

创造力支持的造型技术常用于辅助普通用户的开放式造型过程.针对现有的大多数创造力支持的造型技术针对静止物体造型而设计,无法造型动态模型的问题,提出; 一种造型动态模型的技术,其造型结果是已蒙皮并可直接三维打印的模型.该技术分为模型进化与应用2个阶段.在模型进化阶段,用户从数据库内选择一组绑定的; 模型,迭代地产生一代代新模型,作为建议提示给用户,以激发灵感;在应用阶段,用户选择感兴趣的模型用于动画编辑与三维打印.实验结果表明,文中技术将造; 型、动画编辑与面向三维打印的模型分析集成至统一的框架,极大地帮助了用户的创意建模过程.Creative modeling techniques are commonly used to assist novice users in; open-ended 3D content creation. Most existing creative modeling methods; are mainly designed to model static objects only, not appropriate to; model dynamic models. We present a method for modeling dynamic creative; models which are rigged and fabricatable. There are two stages: models; evolution and application. During the models evolution stage, the users; select a small set of skinned watertight objects, our technique; iteratively synthesizes new creative characters for users to explore.; During the application stage, the users can choose those of interest for; animation or fabrication directly. Experiments demonstrate that the; proposed technique unifies modeling, animation and fabrication together,; facilitating the creative design process.国家自然科学基金; 国家科技支撑计划课

Toxicity Study of VOSO_4 Using NMR-based Metabonomics

通讯作者：陈忠 E-mail: [email protected][中文文摘]采用基于核磁共振(NMR)的代谢组学方法,结合生化指标分析及组织病理学检测,研究了具有类胰岛素活性的硫酸氧钒(VOSO4)对Wistar大鼠的毒性作用.通过不同剂量的VOSO4对Wistar大鼠连续灌胃给药16d,收集大鼠的血清和尿液,并采集样品的1H NMR谱进行多变量数据统计分析来辨识其特征代谢物,然后采用TICL(a web Tool for automatic Interpretation of Compound List)方法建立特征代谢物的代谢网络模型,分析受影响的主要代谢途径及其相互关系.研究结果表明:高剂量组(45mg/kg)和低剂量组(15mg/kg)的特征代谢物含量与对照组存在明显的差异;与对照组相比,高剂量和低剂量组血清中乳酸、肌氨酸酐以及牛磺酸等代谢物的含量增加,尿液中氧化三甲胺(TMAO)、肌酐、牛磺酸和甘氨酸等代谢物的含量增加,并呈现显著的剂量依赖关系;给药组中乙酸和琥珀酸的含量都降低.这些结果说明VOSO4可能影响大鼠体内的糖代谢、脂类代谢及肠道菌群代谢等多个代谢系统,高剂量的VOSO4会导致肝脏毒性和肾脏损伤.[英文文摘]NMR-Based metabonomics combined with clinical biochemical analysis and histopathological examination was applied to investigate the toxicity effects of vanadyl sulfate with insulin-like activity in male Wistar rats. Male Wistar rats were administrated with VOSO4 at doses of 15 and 45 mg/kg body weight by intragastric administration for 16 d. Urine and serum samples were collected and analyzed by 1H NMR experiment. Multivariate analyses were employed to identify the characteristic metabolites for the toxicity effects of vanadyl sulfate.Then the metabolic networks of these characteristic metabolites were built up using TICL (a web Tool for automatic Interpretation of Compound List). The relationship between the characteristic metabolites and the main matebolic pathways perturbed were analyzed and discussed. The differences of metabolic profiles were examined among high-dose (45 mg/kg), low-dose (15 mg/kg) of VOSO4 and control groups. Compared to the control group, increased levels of lactate, creatinine and taurine in serum and increased excretion of trymethylamine-N2-oxide, creatinine, taurine and glycine in urine were found in both high- and low-dose groups which showed an obvious dose-dependent relationship. On the other hand, the concentration of acetate and succinate were decreased in both serum and urine samples of dosed groups. These results indicate that VOSO4 have disturbed the carbohydrate metabolism, lipid metabolism and gut microflora and the high-dosage of VOSO4 may cause liver and kidney injury.卫生部科学研究基金-福建省卫生教育联合攻关计划(No.WKJ2008-2-36);福建省自然科学基金(No.2009J01299)资助项

Toxicity Study of VOSO4 Using NMR-based Metabonomics

NMR-Based metabonomics combined with clinical biochemical analysis and histopathological examination was applied to investigate the toxicity effects of vanadyl sulfate with insulin-like activity in male Wistar rats. Male Wistar rats were administrated with VOSO4 at doses of 15 and 45 mg/kg body weight by intragastric administration for 16 d. Urine and serum samples were collected and analyzed by H-1 NMR experiment. Multivariate analyses were employed to identify the characteristic metabolites for the toxicity effects of vanadyl sulfate. Then the metabolic networks of these characteristic metabolites were built up using TICL (a web Tool for automatic Interpretation of Compound List). The relationship between the characteristic metabolites and the main matebolic pathways perturbed were analyzed and discussed. The differences of metabolic profiles were examined among high-dose (45 mg/kg), low-dose (15 mg/kg) of VOSO4 and control groups. Compared to the control group, increased levels of lactate, creatinine and taurine in serum and increased excretion of trymethylamine-N-2-oxide, creatinine, taurine and glycine in urine were found in both high- and low-dose groups which showed an obvious dose-dependent relationship. On the other hand, the concentration of acetate and succinate were decreased in both serum and urine samples of dosed groups. These results indicate that VOSO4 have disturbed the carbohydrate metabolism, lipid metabolism and gut microflora and the high-dosage of VOSO4 may cause liver and kidney injury

Trisomy 21-induced Dysregulation of Microglial Homeostasis in Alzheimer’s Brains is Mediated by USP25

阿尔茨海默病（Alzheimer’s disease, AD）是一种最为常见的与记忆、认知能力退化相关的渐进性神经退行性疾病。唐氏综合征（Down’s syndrome, DS）是早发型阿尔茨海默病的一个重要风险因素，作为最常见的智力障碍遗传疾病，厦门大学医学院神经科学研究所王鑫教授团队揭示了治疗阿尔茨海默病和唐氏综合征新的治疗靶点，并且在小鼠模型上利用USP25小分子抑制剂成功地改善了阿尔茨海默病小鼠的认知功能，缓解了神经退行性病变的病理进程。该研究工作由王鑫教授指导完成，厦门大学医学院助理教授郑秋阳和博士生李桂林完成主要实验工作，王世华、朱琳、高月、邓青芳、张洪峰、张丽珊、吴美玲、狄安洁参与了部分研究工作。厦门大学医学院许华曦、赵颖俊和孙灏教授在研究过程中给予大力帮助和支持，清华大学董晨教授提供了Usp25基因敲除小鼠，厦门大学附属妇女儿童医院周裕林教授和郑良楷博士帮助收集了脑组织样品。Down syndrome (DS), caused by trisomy of chromosome 21, is the most significant risk factor for early-onset Alzheimer’s disease (AD); however, underlying mechanisms linking DS and AD remain unclear. Here, we show that triplication of homologous chromosome 21 genes aggravates neuroinflammation in combined murine DS-AD models. Overexpression of USP25, a deubiquitinating enzyme encoded by chromosome 21, results in microglial activation and induces synaptic and cognitive deficits, whereas genetic ablation of Usp25 reduces neuroinflammation and rescues synaptic and cognitive function in 5×FAD mice. Mechanistically, USP25 deficiency attenuates microglia-mediated proinflammatory cytokine overproduction and synapse elimination. Inhibition of USP25 reestablishes homeostatic microglial signatures and restores synaptic and cognitive function in 5×FAD mice. In summary, we demonstrate an unprecedented role for trisomy 21 and pathogenic effects associated with microgliosis as a result of the increased USP25 dosage, implicating USP25 as a therapeutic target for neuroinflammation in DS and AD.This work was supported by the National Natural Science Foundation of China (31871077, 81822014, and 81571176 to X.W.; 81701130 to Q.Z.), the National Key R&D Program of China (2016YFC1305900 to X.W.), the Natural Science Foundation of Fujian Province of China (2017J06021 to X.W.), the Fundamental Research Funds for the Chinese Central Universities (20720150061 to X.W.), and the BrightFocus Foundation (A2018214F to Yingjun Zhao). 该研究工作得到国家重点研发计划项目、国家自然科学基金、福建省自然科学基金、厦门大学校长基金的资助和支持