Pr-SNTX,a short-chain three-finger toxin from Papuan pigmy mulga snake,is an antagonist of muscle-type nicotinic acetylcholine receptor (α2βδε)

Three-finger toxins (3FTxs) are one of the major components in snake venoms. In this study, we isolated a cDNA encoding a short-chain 3FTx, Pr-SNTX, from Pseudechis rossignolii. The amino acid sequence of Pr-SNTX is nearly identical to that of its ortholog in Pseudechis australis. Pr-SNTX protein inhibited muscle-type (α₂βδε), but not neuronal α7 nicotinic acetylcholine receptor (nAChR) activity.     

Sub-Cellular Distribution of Zinc in Different Vegetative Organs and Their Contribution to Grains Zinc Accumulation in Rice Under Different Nitrogen and Zinc Supply

Journal of Plant Growth Regulation - Zinc is an important micronutrient for the growth and development of human body and plants. Proper use of nitrogen fertilizer and foliar application of Zn have...     

二种稻飞虱对寄主及氮肥、密度适应性的比较研究

本试验采用二因素最优设计,研究了白背飞虱[Sogatellafurcifera（Horvath）]和褐飞虱[Nilaparvatalugens(Stal）]的种群数量同栽插密度及施氮水平的关系,并考察了它们对寄主品种的适应性。结果表明：二种飞虱对寄主品种的适应性除受到品种自身特性的影响外,还随寄主生育状况及管理水平对田间小气候的影响而变化,表现出时间状态的差异;并得出了二种稻飞虱种群数量同施氮水平和栽插密度关系的回归方程。     

激活淋巴细胞cDNA单链库的构建

介绍一种激活淋巴细胞cDNA单链库构建方法,此库具有良好的模板活性. 用PCR法从此库中克隆了多种中国人源性的细胞因子.     

基于增强回归树与区域增温敏感性指数的城市升温效应空间分异

热岛效应已成为城市化进程中备受关注的城市生态环境问题。有关城市热岛效应的研究对区域在地表升温过程中的空间分异关注尚不足。通过设计区域增温敏感性指数,借助增强回归树（boosted regression tree,BRT）机器学习算法,量化城市不同区域在地表升温过程中的敏感性差异。结果表明：（1）上海市各辖区增温敏感性从高至低依次是：黄浦区、杨浦区、虹口区、静安区、普陀区、徐汇区、长宁区、宝山区、闵行区、浦东新区、嘉定区、奉贤区、松江区、青浦区、金山区、崇明区;（2）区域增温敏感性在不同的温度梯度下具有明显差异,在高温梯度下区域间指数值的差异最大;（3）地表覆被的增温敏感性存在明显的区域分异特性;（4）基于BRT的增温敏感性指数具有较好的指示意义和较高的灵敏度。在城市热环境持续恶化背景下,探讨城市异质空间中地表温度变化的敏感性可为城市热环境调控提供科学依据。     

Smc5/6-Mms21 Prevents and Eliminates Inappropriate Recombination Intermediates in Meiosis

Repairing broken chromosomes via joint molecule (JM) intermediates is hazardous and therefore strictly controlled in most organisms. Also in budding yeast meiosis, where production of enough crossovers via JMs is imperative, only a subset of DNA breaks are repaired via JMs, closely regulated by the ZMM pathway. The other breaks are repaired to non-crossovers, avoiding JM formation, through pathways that require the BLM/Sgs1 helicase. “Rogue” JMs that escape the ZMM pathway and BLM/Sgs1 are eliminated before metaphase by resolvases like Mus81-Mms4 to prevent chromosome nondisjunction. Here, we report the requirement of Smc5/6-Mms21 for antagonizing rogue JMs via two mechanisms; destabilizing early intermediates and resolving JMs. Elimination of the Mms21 SUMO E3-ligase domain leads to transient JM accumulation, depending on Mus81-Mms4 for resolution. Absence of Smc6 leads to persistent rogue JMs accumulation, preventing chromatin separation. We propose that the Smc5/6-Mms21 complex antagonizes toxic JMs by coordinating helicases and resolvases at D-Loops and HJs, respectively.     

P16 and P53 Play Distinct Roles in Different Subtypes of Breast Cancer

Breast cancers are heterogeneous and complex diseases, and subtypes of breast cancers may involve unique molecular mechanisms. The p16^INK4a and p53 pathways are two of the major pathways involved in control of the cell cycle. They also play key roles in tumorigenesis. However, whether the roles of these pathways differ in the subtypes of breast cancer is unclear. Therefore, p16 and p53 expression were investigated in different breast cancer subtypes to ascertain their contributions to these cancers. A total of 400 cases of non-invasive ductal carcinoma in situ (DCIS) and invasive ductal carcinoma (IDC), including the major molecular subtypes luminal-A, luminal-B, Her-2, and triple-negative subtypes, and 50 cases of normal controls were compared. Luminal-A cancers expressed the lowest level of p16 among the subtypes in DCIS, and the level of p16 expression was up-regulated in the luminal-A of IDC (P<0.008). Triple-negative breast cancers were characterized by a correlation of p53 overexpression with a high level of p16 expression. Luminal lesion types with high p16 expression in DCIS were found to be more likely to develop into aggressive breast cancers, possibly promoted by p53 dysfunction. Taken together, the present study suggest that p16 expression in luminal-A breast cancers is associated with their progression from DCIS to IDC, and both p53 and p16 expressions are important for the development of triple-negative breast cancers in DCIS and IDC.