Genetic Polymorphism of Angiotensin II Type 1 Receptors and Their Effect on the Clinical Outcome of Captopril Treatment in Arab Iraqi Patients with Acute Coronary Syndrome (Mid Euphrates)

Genetic variation in the angiotensin II type 1 receptor (AT1R) has an important effect on the outcome of acute coronary syndrome (ACS) initiated treatment with captopril. This study aims to investigate the impact of genetic polymorphism of AT1R (rs5186 and rs275651) on the ACS outcome in Iraqi patients treated with captopril. A total of 250 Iraqi individuals with ACS were included in this case—control study and they were divided into two study groups; Study group 1 included 125 participants who were prescribed captopril, 25 mg twice daily and study group 2 included 125 participants who received no captopril as part of their ACS treatment (control study). The AT1R gene (rs5186) CC genotype was found to be associated with ST-elevation myocardial infarction (STEMI) (Odd’s ratio (O.R) = 1.2, P = 0.7), while AC was associated with Non-ST-elevation myocardial infarction (NSTEMI) and unstable angina (UA) (O.R = 1.2, P = 0.8). AC genotype is more prone to have Percutaneous coronary intervention (PCI) after ACS attack (O.R = 1.2, P = 0.6). CC genotype had a risk to get less improvement (O.R = 1.6, P = 0.5), so might require higher doses of captopril during acute coronary insult. The AT1R gene (rs275651) AA genotype was associated with UA (O.R = 1.3, P = 0.9). AA and AT genotypes were more prone to have PCI after ACS attack (O.R = 3.9 P = 0.2, O.R = 3.5, P = 0.3 respectively) and thus requiring higher doses of captopril. We conclude that the AT1R rs5186, rs275651 genetic polymorphisms might partially affect the clinical outcome of ACS patients treated with captopril and might have captopril resistance which requires higher doses.     

中国北方汉族青年ACE 基因I/ D多态性频率分布特征

通过分析与探讨汉族普通人群ACE基因I／D多态频率分布特征，试图为中国优秀耐力运动员的基因选材研究提供中国人相关人群ACE基因I／D多态频率分布的基础数据。选择18-22岁汉族学生216名作为研究对象，观察其ACE基因I／D多态频率分布。结果显示：北方汉族青年的ACE基因I／D多态频率分布，与国内相关研究结果一致，与欧美人群有非常显著差异。研究认为：从种族单一性、样本数量和年龄段的选择等因素考虑．研究结果不仅可以作为北方汉族青年ACE基因I／D多态频率分布的代表，而且对于杰出耐力的多态性标记研究来讲是理想的对照群体。     

长期运动训练对运动性低血色素大鼠组织转铁蛋白及转铁蛋白受体基因表达的影响

了解发生运动性低血色素时转铁蛋白及转铁蛋白受体基因表达的变化对深入研究运动性贫血的发生机制具有重要的意义.实验结果表明:长期运动训练导致运动性低血色素大鼠肌肉组织中转铁蛋白和转铁蛋白受体基因表达均显著增加,表明运动训练造成的运动性低血色素大鼠肌肉中铁代谢紊乱,肌肉应激性使转铁蛋白以及转铁蛋白受体表达增加,以促进肌肉对铁的吸收;运动性低血色素大鼠肝脏组织中转铁蛋白基因表达均显著下降,这可能是由于肝脏铁储量增加而导致的转铁蛋白基因表达的适应性的降低有关;运动训练导致运动性低血色素大鼠转铁蛋白和转铁蛋白受体表达具有组织特异性,转铁蛋白受体基因表达与组织铁代谢关系密切.     

探寻与运动能力有关的基因研究进展

对目前运动能力基因定位研究进展进行了综述.结果发现,与有氧能力有关的基因主要包括ACE、CKMM、ADRA2A及mtDNA的D-loop和MTND5,此外,家系研究提示1p、2p、4q、6p、8q、11p、14q染色体区域可能有与运动能力有关的基因;与肌肉力量有关的基因主要涉及GDF8、 CNTF.但这些基因的作用机制尚不清楚.同时,就今后研究趋势作了展望.     

Advances in the phylogenesis of Agaricales and its higher ranks and strategies for establishing phylogenetic hypotheses

We present an overview of previous research results on the molecular phylogenetic analyses in Agaricales and its higher ranks (Agaricomycetes/Agaricomycotina/Basidiomycota) along with the most recent treatments of taxonomic systems in these taxa. Establishing phylogenetic hypotheses using DNA sequences, from which an understanding of the natural evolutionary relationships amongst clades may be derived, requires a robust dataset. It has been recognized that single-gene phylogenies may not truly represent organismal phylogenies, but the concordant phylogenetic genealogies from multiple-gene datasets can resolve this problem. The genes commonly used in mushroom phylogenetic research are summarized.     

ACE基因多态性与有氧耐力运动关系研究

目前普遍认为ACE(血管紧张素转换酶)的水平和心血管的形态、功能密切相关。ACE基因的多态性是人耐力素质优劣的决定性因素之一。为了解运动员血管紧张素转换酶(ACE)基因插入或缺失(I/D）多态性情况，探讨ACE基因多态性与有氧耐力可能的关系，用聚合酶链反应(PCR)技术检测20例运动员和20例健康对照者的ACE基因多态性。结果位于ACE基因16内含子的L／D多态性经PCR扩增后呈三种基因型：纯合子插入型(II）、纯合子缺失型(DD)和杂合子插入或缺失型(ID)。耐力运动员组Ⅱ基因型和Ⅰ等位基因频率显著高于健康对照组。结果表明ACE基因可能在运动员的有氧耐力中起重要作用。     

1016名学生PTC尝味能力基因频率的调查

目的:了解味盲基因频率和基因型频率在不同群体中的分布,从而为人种学及人类群体遗传学提供基本数据,并用于研究某些疾病。方法:本文是运用阈值法研究满、汉、回三民族人的尝味能力,并计算了味盲者和尝味者的基因频率。结果:三民族味盲基因频率分别为:满族:0.4588.汉族:0.2845 回族:0.4431。结论:满、汉、回三民族人对PTC尝味能力在统计学上存在显著差异,不同的民族有不同的基因库。     

L-ficolin突变体原核表达载体的构建及表达产物的鉴定

目的构建L-ficolin突变体的原核表达载体，为研究L-ficolin的糖结合位点奠定基础。方法设计L-ficolin突变体基因上、下游引物，分别引入EcoRⅠ和XhoⅠ酶切位点。以插入L—ficolin M2（Val144Phe）和M6（Glu 307Asp）点突变的完整编码区基因的质粒pCDNA3-L-ficolin为模板，通过PCR扩增获得突变体的基因片段，将其克隆入原核表达载体pGEX—KG．然后通过酶切和序列测定对其进行鉴定；将此表达载体转化入表达菌BL21（DE3）pLvSs诱导表达。并采用SDS—PAGE对表达产物进行鉴定。结果经酶切及序列分析表明．成功地构建了重组原核表达载体pGEX-KG—L—ficolin—M2、pGEX-KG-L-ficolin—M6，SDS—PAGE显示目的蛋白大量表达。结论L—ficolin突变体融合蛋白可以在大肠杆菌中大量表达。为研究L-ficolin的糖结合位点打下基础。     

Study of Resistin gene expression in peripheral blood mononuclear cell and its gene polymorphism in a small range population

INTRODUCTION Recently discovered as an endocrine organ, adi-pose tissue can secrete many cytokines such as Re-sistin, adiponectin and free fatty acids, and receives much attention in the study of insulin resistance and type 2 diabetes mellitus (T2DM). As a peptide hor-mone secreted by adipocyte, Resistin is considered to be the linkage between obesity and insulin resistance (Steppan et al., 2001). Most studies on Resistin in-vestigate adipose tissue. In this experiment we de-tected t…     

Ultrabithorax is a key regulator for the dimorphism of wings,a main cause for the outbreak of planthoppers in rice

Rice planthoppers, the most devastating rice pests, occur in two wing forms: the short-wing form for rapid population growth and long-wing form for long-distance migration, which together create the mechanism for outbreak. Here we show that Ultrabithorax (Ubx) is a key regulator for switching between the long- and short-wing forms of rice planthoppers. Ubx is expressed in both forewing and hindwing pads, which is different from the canonical model of Ubx expression. In brown planthoppers, expression of Ubx (NlUbx) is regulated by nutritional status of the rice host. High-quality young plants induce NlUbx expression leading to the short-wing form; low-quality ripe plants reduce NlUbx expression resulting in long-wing form. We also showed that NlUbx is regulated by the insulin receptors NlInR1 and NlInR2. The default expression of NlInR1 inhibits NlUbx resulting in long-wings, while high-quality hosts induce NlInR2 expression, which represses NlInR1 thus promoting NlUbx expression to produce short-wings.