YR-黏和染色体模型初探(上)

30nm螺线管是如何形成300nm染色线的?高度重复序列占人类第22号染色体DNA量的41.9％［1］,它们的功能是什么?全身着丝粒或弥散型着丝粒染色体是怎样形成的? 姐妹染色体由前期到中期为什么不分开?同源染色体联会是怎样形成的?联会复合体的中央区是什么?为什么通过花粉管会导入外源遗传物质?高等生命是怎样从原始生命进化而来的?在此,我们给出一个新的五级染色体模型：YR－黏和染色体模型。它不仅能解释以上问题,同时能解释多线染色体、灯刷染色体 以及一些经典遗传现象。 Abstract:How is the 300nm(nanometer)chromonema compacted with 30nm solenoid?What are the functions of repeat family sequence?How does the holocentromere or polycentromere chromosome form?What is the reason that non?separation of sister chromatid occur from prophase to metaphase?How do the synaptonemal complex(SC)occur?What are the compositions in the central region of SC?How to explain the transmission of heterologous?DNA by pollen tube pathway?How did the higher organism evolve from primitive forms?Hereon we provide a new five degree chromosome model-YR-cohesion chromosome model which will give a better answer to the questions above,as well as polytene chromosome,puff,and lampbrush chromosome and many other genetic phenomena.     

Snapshot of HIV pathogenesis in China

Several reviews have focused on the nature of HIV infection and its spread in various geographical regions of China. In contrast, this review provides a comprehensive update on the prevalence of multiple HIV- 1 subtypes, consequent emergence of recombinant and novel forms of HIV- 1 in China, and the implications this may have on HIV diversity and the development of effective vaccines. In addition it also examines the dissemination of primary drug resistance in therapy naive patients, as well as co-infections with two other important viruses-hepatitis B and C. The main purpose of this review is to provide a current snapshot of HIV-1 pathogenesis in China and possibly shed some light on the future of HIV evolution, and potential challenges for future vaccine and anti-retroviral therapeutics against HIV strains in this area.     

大熊猫NADH-辅酶Q氧化还原酶铁硫蛋白亚基6基因（NDUFS6）的序列分析

NADH-Q还原酶是线粒体内膜上氧化呼吸链的复合体Ⅰ.在哺乳动物中,它结构十分复杂,由不少于45个亚基组成,分为以黄素单核苷酸为辅基的黄素蛋白和以铁硫族(Fe-S)为辅基的铁硫蛋白.     

Identification of neurons responsible for feeding behavior in the Drosophila brain

Drosophila melanogaster feeds mainly on rotten fruits,which contain many kinds of sugar.Thus,the sense of sweet taste has evolved to serve as a dominant regulator and driver of feeding behavior.Although several sugar receptors have been described,it remains poorly understood how the sensory input is transformed into an appetitive behavior.Here,we used a neural silencing approach to screen brain circuits,and identified neurons labeled by three Gal4 lines that modulate Drosophila feeding behavior.These three Gal4 lines labeled neurons mainly in the suboesophageal ganglia(SOG),which is considered to be the fly’s primary taste center.When we blocked the activity of these neurons,flies decreased their sugar consumption significantly.In contrast,activation of these neurons resulted in enhanced feeding behavior and increased food consumption not only towards sugar,but to an array of food sources.Moreover,upon neuronal activation,the flies demonstrated feeding behavior even in the absence of food,which suggests that neuronal activation can replace food as a stimulus for feeding behavior.These findings indicate that these Gal4-labeled neurons,which function downstream of sensory neurons and regulate feeding behavior towards different food sources is necessary in Drosophila feeding control.