拟南芥bHLH家族转录因子DYT1在花药发育过程中调控胼胝质降解(英文)

胼胝质的合成和降解是雄配子体减数分裂过程中的一个重要特征,对后期花粉成熟有重要作用.在此研究中,分离到了一个雄性不育突变体msl57,该突变体的绒毡层分化及胼胝质降解过程出现异常,导致花粉败育.图位克隆和遗传分析表明:MSl57基因与bHLI-I家族转录因子DYTI(At4g21330)是同一基因.因此,将ms157突变体改名为dyt1-2.反式激活作用实验揭示了DYTI的激活功能域位于基因的250 ～504bp之间.通过酵母双杂交实验发现DYT1蛋白在体内可以形成同源二聚体来执行其功能.RT-PCR及定量PCR分析表明胼胝质酶相关基因A6的表达在突变体背景下严重下调.因此,DVF1通过调控胼胝质的降解来影响花药发育过程.     

浑善达克沙漠化防治重点生态系统功能区防风固沙功能动态特征分析

浑善达克沙漠化防治重点生态系统功能区是位于内蒙古地区维护国家北方生态安全屏障的重要区域.本文基于气象、遥感数据,运用RWEQ(Revised Wind Erosion Equation)模型,定量分析了1990—2015年浑善达克防风固沙功能区生态系统结构与防风固沙功能的时空变化特征,揭示了生态系统结构变化对防风固沙服务功能的影响.结果表明:26年间各生态系统间转换强烈,以草地生态系统转出为主,2005年之前主要向农田生态系统和荒漠生态系统转变,2005年以后得益于生态建设工程的实施和禁牧封育等措施,主要向草地、森林生态系统转变.研究区以微度和轻度土壤侵蚀为主,风蚀情况整体好转.农田生态退耕、荒漠化程度减轻、草地质量提高等生态系统转换有益于提升防风固沙功能.同时,也揭示了该功能区内生态退耕对防风固沙服务功能的影响,两者呈显著负相关.     

Platelet-derived growth factor stimulates synthesis of PtdIns(3,4,5)P3 by activating a PtdIns(4,5)P2 3-OH kinase.

Although the hormone-stimulated synthesis of 3-phosphorylated inositol lipids is known to form an intracellular signalling system, there is no consensus on the crucial receptor-regulated event in this pathway and it is still not clear which of the intermediates represent potential output signals. We show here that the key step in the synthesis of 3-phosphorylated inositol lipids in 3T3 cells stimulated by platelet-derived growth factor is the activation of a phosphatidylinositol(4,5)-bisphosphate (3)-hydroxy (PtdIns(4,5)P2 3-OH) kinase. A similar conclusion has been applied to explain the actions of formyl-Met-Leu-Phe on neutrophils, and it may be that receptors that couple through intrinsic tyrosine kinases or through G proteins stimulate the same step in 3-phosphorylated inositol lipid metabolism. The close parallel between these two mechanisms for the activation of PtdIns(4,5)P2 3-OH kinase and those described for the activation of another key signalling enzyme, phospholipase C (ref. 7), focuses attention on the product of the PtdIns(4,5)P2 3-OH kinase, PtdIns(3,4,5)P3, as a possible new second messenger.     

语言自主性学习理论评述

人本主义心理学认为学习者具有发展潜能的能力和动力，研究者应促进其个性发展和潜能发挥；社会认知学派通过所构建的研究框架确定学习自主性程度，采用五个维度描述自主学习状态，认为自主学习能力习得是将外部学习技能内化为个人能力的过程；信息加工理论指出完整意义上的自主学习过程经历四个阶段，还构建了自主学习内在机制；元认知理论认为循序渐进的发展过程直接影响自主性学习能力的发展。对各理论学派教育哲学理念进行全面梳理，利于研究者借鉴其成果，从而提出本土化之理论。     

Targeting C-reactive protein for the treatment of cardiovascular disease

Complement-mediated inflammation exacerbates the tissue injury of ischaemic necrosis in heart attacks and strokes, the most common causes of death in developed countries. Large infarct size increases immediate morbidity and mortality and, in survivors of the acute event, larger non-functional scars adversely affect long-term prognosis. There is thus an important unmet medical need for new cardioprotective and neuroprotective treatments. We have previously shown that human C-reactive protein (CRP), the classical acute-phase protein that binds to ligands exposed in damaged tissue and then activates complement, increases myocardial and cerebral infarct size in rats subjected to coronary or cerebral artery ligation, respectively. Rat CRP does not activate rat complement, whereas human CRP activates both rat and human complement. Administration of human CRP to rats is thus an excellent model for the actions of endogenous human CRP. Here we report the design, synthesis and efficacy of 1,6-bis(phosphocholine)-hexane as a specific small-molecule inhibitor of CRP. Five molecules of this palindromic compound are bound by two pentameric CRP molecules, crosslinking and occluding the ligand-binding B-face of CRP and blocking its functions. Administration of 1,6-bis(phosphocholine)-hexane to rats undergoing acute myocardial infarction abrogated the increase in infarct size and cardiac dysfunction produced by injection of human CRP. Therapeutic inhibition of CRP is thus a promising new approach to cardioprotection in acute myocardial infarction, and may also provide neuroprotection in stroke. Potential wider applications include other inflammatory, infective and tissue-damaging conditions characterized by increased CRP production, in which binding of CRP to exposed ligands in damaged cells may lead to complement-mediated exacerbation of tissue injury.