体操运动员技术风格个性化形成的主要影响因素

根据运动员的成才特点，阐述了科学选材、运动训练及教练员执教能力对形成运动员技术风格个性化过程中所起的作用。     

钢-混凝土连续组合梁桥的理论分析和试验研究

根据完全剪力连接的连续组合梁桥的构造特点及各部分受力机理,做出合理假设,提出分层平面框架计算模型该计算模型用于沈阳市东西快速干道工程某段连续组合梁桥,计算值与静载试验实测值非常接近,证明了本计算模型用于钢-混凝土连续组合梁桥正确实用的.     

图书馆培训实用手册

在今天这样一个信息爆炸的时代，每天都有成千上万水平参差不齐的新的网页诞生。用户或读者面对这些铺天盖地的资源不知所惜，无从下手。如何通过电子媒介来管理这些信息成为一个十分重要的问题。图书馆员就是要成为这些信息的把关者和提供者，图书馆员应当学会利用网络引导用户快捷方便地获得所需资料，为用户提供高质量的服务。图书馆员工的素质对于图书馆的发展就显得尤为重要了。随之而来的必要和迫切的问题就是如何建立并长期维护一个行之有效的图书馆员工培训系统。     

对河南农村劳动力向小城镇转移趋势的调查研究

“人口城镇化”是社会发展的必然趋势。本文从河南沁阳等九个“小城镇”的实际调查材料出发,较详细地讨论了农村劳动力向小城镇转移的流量,形成、就业层次和社会影响,说明中国的“人口城镇化”方向关键在于积极发展小城镇。     

构建和谐社会的重要任务:和谐社区建设

社区是进行一定的社会活动、具有互动关系和共同文化维系力的人类群体及其活动区域,大力发展社区建设是社会发展进步的客观要求,也是构建和谐社会的重要保证.要在充分认识和谐社区建设的重要性基础上,按照胡锦涛同志"6·25讲话"精神开拓和激发建设和谐社区的新途径和新活力,为和谐社会建设做出应有的贡献.     

How do Shp2 mutations that oppositely influence its biochemical activity result in syndromes with overlapping symptoms?

Activating and inactivating mutations of SHP-2 are responsible, respectively, for the Noonan (NS) and the LEOPARD (LS) syndromes. Clinically, these developmental disorders overlap greatly, resulting in the apparent paradox of similar diseases caused by mutations that oppositely influence SHP-2 phosphatase activity. While the mechanisms remain unclear, recent functional analysis of SHP-2, along with the identification of other genes involved in NS and in other related syndromes (neurofibromatosis-1, Costello and cardio-facio-cutaneous syndromes), strongly suggest that Ras/MAPK represents the major signaling pathway deregulated by SHP-2 mutants. We discuss the idea that, with the exception of LS mutations that have been shown to exert a dominant negative effect, all disease-causing mutations involved in Ras/MAPK-mediated signaling, including SHP-2, might lead to enhanced MAPK activation. This suggests that a narrow range of MAPK signaling is required for appropriate development. We also discuss the possibility that LS mutations may not simply exhibit dominant negative activity. Received 30 November 2006; received after revision 8 February 2007; accepted 13 March 2007     

Targeted inhibition of Livin resensitizes renal cancer cells towards apoptosis

Cancer cells are typically characterized by apoptosis deficiency. In order to investigate a possible role for the anti-apoptotic livin gene in renal cell cancer (RCC), we analyzed its expression in tumor tissue samples and in RCC-derived cell lines. In addition, we studied the contribution of livin to the apoptotic resistance of RCC cells by RNA interference (RNAi). Livin gene expression was detected in a significant portion of RCC tumor tissue specimens (13/14, 92.9%) and tumor-derived cell lines (12/15, 80.0%). Moreover, targeted inhibition of livin by RNAi markedly sensitized RCC cells towards proapoptotic stimuli, such as UV irradiation or the chemotherapeutic drugs etoposide, 5-fluorouracil, and vinblastine. These effects were specific for livin expressing tumor cells. We conclude that livin can contribute significantly to the apoptosis resistance of RCC cells. Targeted inhibition of livin could represent a novel therapeutic strategy to increase the sensitivity of renal cancers towards pro-apoptotic agents. Received 30 November 2006; received after revision 22 February 2007; accepted 20 March 2007     

中部地区教育投资效应实证分析

利用面板数据模型着重分析中部地区之间教育投资效应差异及其原因.得出结论:由于对教育的投资力度不同,导致了中部地区发展的不平衡.     

Mutations in LMF1 cause combined lipase deficiency and severe hypertriglyceridemia

Hypertriglyceridemia is a hallmark of many disorders, including metabolic syndrome, diabetes, atherosclerosis and obesity. A well-known cause is the deficiency of lipoprotein lipase (LPL), a key enzyme in plasma triglyceride hydrolysis. Mice carrying the combined lipase deficiency (cld) mutation show severe hypertriglyceridemia owing to a decrease in the activity of LPL and a related enzyme, hepatic lipase (HL), caused by impaired maturation of nascent LPL and hepatic lipase polypeptides in the endoplasmic reticulum (ER). Here we identify the gene containing the cld mutation as Tmem112 and rename it Lmf1 (Lipase maturation factor 1). Lmf1 encodes a transmembrane protein with an evolutionarily conserved domain of unknown function that localizes to the ER. A human subject homozygous for a deleterious mutation in LMF1 also shows combined lipase deficiency with concomitant hypertriglyceridemia and associated disorders. Thus, through its profound effect on lipase activity, LMF1 emerges as an important candidate gene in hypertriglyceridemia.