Gut hormones and the regulation of energy homeostasis

Food intake, energy expenditure and body adiposity are homeostatically regulated. Central and peripheral signals communicate information about the current state of energy balance to key brain regions, including the hypothalamus and brainstem. Hunger and satiety represent coordinated responses to these signals, which include neural and hormonal messages from the gut. In recent years our understanding of how neural and hormonal brain-gut signalling regulates energy homeostasis has advanced considerably. Gut hormones have various physiological functions that include specifically targeting the brain to regulate appetite. New research suggests that gut hormones can be used to specifically regulate energy homeostasis in humans, and offer a target for anti-obesity drugs.     

In situ structure of the complete Treponema primitia flagellar motor

The bacterial flagellar motor is an amazing nanomachine: built from approximately 25 different proteins, it uses an electrochemical ion gradient to drive rotation at speeds of up to 300 Hz (refs 1, 2). The flagellar motor consists of a fixed, membrane-embedded, torque-generating stator and a typically bidirectional, spinning rotor that changes direction in response to chemotactic signals. Most structural analyses so far have targeted the purified rotor, and hence little is known about the stator and its interactions. Here we show, using electron cryotomography of whole cells, the in situ structure of the complete flagellar motor from the spirochaete Treponema primitia at 7 nm resolution. Twenty individual motor particles were computationally extracted from the reconstructions, aligned and then averaged. The stator assembly, revealed for the first time, possessed 16-fold symmetry and was connected directly to the rotor, C ring and a novel P-ring-like structure. The unusually large size of the motor suggested mechanisms for increasing torque and supported models wherein critical interactions occur atop the C ring, where our data suggest that both the carboxy-terminal and middle domains of FliG are found.     

一个基于Swarm的人工生态系统模型

利用Swarm平台，采用自下而上的建模思想，建立了一个人工生态系统，并对局部生态环境下虫害的演化行为以及天敌的抑制作用进行了模拟。针对不同环境条件设定相应的仿真参数，可以得到恰当的害虫种群演化结果，有助于生态管理的科学决策。所建立的人工生态系统模型为局部生态研究提供了一种崭新的实验手段。     

武术运动员血型及指纹的分析

对四川省一级以上的３９ 名武术运动员血型和指纹进行了调查分析,结果表明武术运动员多数血型和指纹指标与一般人比较没有明显差异,故用这两项指标作为选材的依据还有待进一步探讨     

基于声学参量阵理论的超声波防录音屏蔽研究与实现

随着智能设备的快速发展,利用一些录音设备诸如智能手机、录音笔等窃取信息的手段显得更为方便和隐蔽,这对于个人、企业和政府都存在着不小的隐患.传统的对抗方式有背景噪声屏蔽和电磁波屏蔽,但都有其局限性.前者通过播放大音量噪声覆盖对话声音,但这会影响对话的正常进行;后者发射大功率电磁波屏蔽录音设备,但其屏蔽距离与效果都十分有限.针对上述问题,本文提出一种基于声学参量阵理论的超声波防录音屏的方案,可以对录音窃听进行有效屏蔽,同时不妨碍正常对话.根据声学参量阵理论,多个高频的超声波经过非线性系统,会因为非线性作用产生低频声音信号.根据这一原理,首先生成低频宽带噪声信号,然后进行BASK调制将其调制到高频载波上,进行功率放大后由换能器发射向目标录音设备.实验测试结果表明对iPhone6S、华为P10、P20、荣耀9等智能手机的录音功能都可以实现有效屏蔽,最大屏蔽距离1~3 m不等.由于屏蔽原理的普适性,本文的方案可以屏蔽目前大多数型号的智能手机、录音笔等带录音功能的终端.      

水溶液中Co-Sb薄膜的电化学沉积

采用电化学循环伏安法分析了柠檬酸水溶液中Co2+、SbO+的沉积电位,利用恒电位沉积的方法,在不锈钢基片上,从柠檬酸水溶液中沉积出Co-Sb薄膜.运用X射线衍射和扫描电子显微镜对薄膜的结构、组成以及形貌进行了分析.结果表明,在柠檬酸水溶液中,Co2+和SbO+可同时沉积到不锈钢基片上,形成Co-Sb薄膜,在不同的沉积电位下,薄膜形成不同的物相.薄膜的形貌呈现颗粒状,分布比较均匀.薄膜在充满Ar的管式炉中热处理2h,热处理温度为400℃,结果发现薄膜物相组成发生了很大变化,转变为主要由晶体CoSb3组成,还有少量的CoSb形成.     

A role for VEGF as a negative regulator of pericyte function and vessel maturation

Angiogenesis does not only depend on endothelial cell invasion and proliferation: it also requires pericyte coverage of vascular sprouts for vessel stabilization. These processes are coordinated by vascular endothelial growth factor (VEGF) and platelet-derived growth factor (PDGF) through their cognate receptors on endothelial cells and vascular smooth muscle cells (VSMCs), respectively. PDGF induces neovascularization by priming VSMCs/pericytes to release pro-angiogenic mediators. Although VEGF directly stimulates endothelial cell proliferation and migration, its role in pericyte biology is less clear. Here we define a role for VEGF as an inhibitor of neovascularization on the basis of its capacity to disrupt VSMC function. Specifically, under conditions of PDGF-mediated angiogenesis, VEGF ablates pericyte coverage of nascent vascular sprouts, leading to vessel destabilization. At the molecular level, VEGF-mediated activation of VEGF-R2 suppresses PDGF-Rbeta signalling in VSMCs through the assembly of a previously undescribed receptor complex consisting of PDGF-Rbeta and VEGF-R2. Inhibition of VEGF-R2 not only prevents assembly of this receptor complex but also restores angiogenesis in tissues exposed to both VEGF and PDGF. Finally, genetic deletion of tumour cell VEGF disrupts PDGF-Rbeta/VEGF-R2 complex formation and increases tumour vessel maturation. These findings underscore the importance of VSMCs/pericytes in neovascularization and reveal a dichotomous role for VEGF and VEGF-R2 signalling as both a promoter of endothelial cell function and a negative regulator of VSMCs and vessel maturation.     

国内手机图书馆的现状与服务

手机通信的飞速发展,造就了手机图书馆的崛起,也为图书馆的发展开辟了新的服务领域。详细介绍了手机图书馆的发展情况、服务功能以及用户在移动图书馆中享受图书馆的短消息服务、Web手机上网服务等,探讨了3G时代进一步拓展手机图书馆服务功能的对策。     

A new acute transforming feline retrovirus and relationship of its oncogene v-kit with the protein kinase gene family

A new acute transforming feline retrovirus, the Hardy-Zuckerman 4 feline sarcoma virus (HZ4-FeSV), has been isolated from a feline fibrosarcoma. The viral genome of HZ4-FeSV contains a new oncogene designated v-kit, has the structure 5' delta gag-kit-delta pol-delta env 3' and specifies a gag-kit polyprotein of relative molecular mass 80,000. The predicted kit amino-acid sequence displays partial homology with tyrosine-specific protein kinase oncogenes. HZ4-FeSV appears to have been generated by transduction of feline c-kit sequences with feline leukaemia virus.     

c-Myc regulates mammalian body size by controlling cell number but not cell size.

Overexpression of the proto-oncogene c-myc has been implicated in the genesis of diverse human tumours. c-Myc seems to regulate diverse biological processes, but its role in tumorigenesis and normal physiology remains enigmatic. Here we report the generation of an allelic series of mice in which c-myc expression is incrementally reduced to zero. Fibroblasts from these mice show reduced proliferation and after complete loss of c-Myc function they exit the cell cycle. We show that Myc activity is not needed for cellular growth but does determine the percentage of activated T cells that re-enter the cell cycle. In vivo, reduction of c-Myc levels results in reduced body mass owing to multiorgan hypoplasia, in contrast to Drosophila c-myc mutants, which are smaller as a result of hypotrophy. We find that c-myc substitutes for c-myc in fibroblasts, indicating they have similar biological activities. This suggests there may be fundamental differences in the mechanisms by which mammals and insects control body size. We propose that in mammals c-Myc controls the decision to divide or not to divide and thereby functions as a crucial mediator of signals that determine organ and body size.