沙丘稀有种准噶尔无叶豆花部综合特征与传粉适应性

植物花部特征进化与传粉适应性一直是进化生态学领域关注的核心问题之一。以古尔班通古特沙漠自然生长的准噶尔无叶豆为对象,对其花部特征和传粉特性进行了野外观察和室内的分析研究。结果表明:种群花期历时21 d,花序花期历时7-12 d,单花花期一般3 d,若遇阴雨天气,花期可延长1-2 d,整个花期龙骨瓣一直保持闭合状态。单花10枚花药在旗瓣微张时已全部完成散粉。准噶尔无叶豆主要靠分泌花蜜、鲜艳的花色以及旗瓣基部的黄色辐射状纹理结构吸引传粉者。准噶尔无叶豆花期的有效传粉者为4种蜂类昆虫,它们的平均访花频率为(7.75±0.57)次·花^-1·d^-1,访花高峰期表现为三峰型: 13:00-14:00,16:00-17:00和19:00-20:00。准噶尔无叶豆人工套袋实验表明该种为自交亲和型,主动自交少见,生殖成功依赖传粉者。胚珠成功受精至果实完全成熟阶段存在自交衰退,柱头角质层结构和花粉刷结构是准噶尔无叶豆在进化过程中形成的减少自交,倾向异交的机制。     

眼镜蛇毒对大鼠脊髓乙酰胆碱酯酶表达的影响

目的 探讨眼镜蛇毒对大鼠腰髓乙酰胆碱酯酶（AchE）表达的影响。方法 将蛇毒注射到大鼠左小腿下部,采用亚铁氰化铜法示AchE,观察大鼠腰髓前角AchE阳性神经元在眼镜蛇毒中毒组、生理盐水组、正常对照组的变化。结果 蛇毒组大鼠AchE阳性神经元比对照组表达增强。结论 眼镜蛇毒对腰髓的AchE阳性神经元表达有上调作用。     

南方红豆杉响应不同传粉式样的结实表现

采用开花前雌株短枝套袋隔离传粉、花期人工授粉、风媒传粉 对照 及其传粉障碍等几种传粉式样 ,比较不同传粉 授粉 方式对南方红豆杉 Taxus chinensis var.mairei 结实的影响 ;在风媒传粉条件下 ,研究了南方红豆杉不同种植行向、树冠不同方位、上下内外不同层面的结实表现 .结果表明 :南方红豆杉存在孤雌生殖现象 ,平均单枝结实率为 2 8.7% ,与风媒传粉相比较 ,存在极显著差异 P<0 .0 1 ;人工授粉能显著提高结实率 P<0 .0 5 2 0 .7% ;2～ 3月份开花期 ,江汉平原盛行东北风 ,在风媒传粉条件下 ,东西向种植的南方红豆杉有更多的授粉机会 ,其结实情况极显著优于南北向种植的 P<0 .0 1 ;东西向种植的南方红豆杉树冠果实的空间分布 ,受传粉条件包括风向、冠层方位及距传粉源的距离、冠层内外上下层次等因素的影响 ,方位间的结实量按东南西北方位依次为 :2 30 .375粒、185 .6 2 5粒、12 8.813粒、10 5 .4 38粒 ,呈递减趋势 ,冠外层结实量普通高于冠内层 ,树冠东向下外层结实量最高 4 16 .75粒 ,北向下内层最低 2 2 .0 0粒 .     

A simian replication-defective adenoviral recombinant vaccine to HIV-1 gag

In animal models, E1-deleted human adenoviral recombinants of the serotype 5 (AdHu5) have shown high efficacy as vaccine carriers for different Ags including those of HIV-1. Humans are infected by common serotypes of human adenovirus such as AdHu5 early in life and a significant percentage has high levels of neutralizing Abs to these serotypes, which will very likely impair the efficacy of recombinant vaccines based on the homologous virus. To circumvent this problem, a novel replication-defective adenoviral vaccine carrier based on an E1-deleted recombinant of the chimpanzee adenovirus 68 (AdC68) was developed. An AdC68 construct expressing a codon-optimized, truncated form of gag of HIV-1 induces CD8(+) T cells to gag in mice which at the height of the immune response encompass nearly 20% of the entire splenic CD8(+) T cell population. The vaccine-induced immune response provides protection to challenge with a vaccinia gag recombinant virus. Induction of transgene-specific CD8(+) T cells and protection against viral challenge elicited by the AdC68 vaccines is not strongly inhibited in animals preimmune to AdHu5 virus. However, the response elicited by the AdHu5 vaccine is greatly attenuated in AdHu5 preimmune animals.     

Genetic metabolic polymorphisms and the risk of cancer: a review of the literature

The purpose of this paper is to systematically analyse the design and results of epidemiological studies on the association between various types of cancer (lung, bladder, breast, colon, stomach) and four genetically-based metabolic polymorphisms, involved in the metabolism of several carcinogens (glutathione-S-transferase M1, debrisoquine hydroxylase, N acetyltransferase, aryl hydrocarbon hydroxylase). These inherited polymorphisms usually cause modifications in the quality or quantity of the relevant enzymes. Such enzymes are involved in the activation/inactivation of known carcinogens and seem to modify the extent to which carcinogens interact with DNA in target tissues. Two enzymes, debrisoquine hydroxylase and aryl hydrocarbon hydroxylase, activate procarcinogens to carcinogens (phase I enzymes). The other two, glutathione-S-transferase M1 and N-acetyltransferase, mainly detoxity carcinogenic substances (phase II enzymes). Because of their role as host factors (modulating the action of carcinogens), it has been hypothesized that subjects presenting a specific phenotype for such polymorphisms could be at a greater risk of developing various types of cancer. A number of epidemiological studies have investigated such associations, often with discordant results. We examine and discuss the design of the studies, and present a meta-analysis of the available data.     

Dysbiosis Signature of Fecal Microbiota in Colorectal Cancer Patients

The human gut microbiota is a complex system that is essential to the health of the host. Increasing evidence suggests that the gut microbiota may play an important role in the pathogenesis of colorectal cancer (CRC). In this study, we used pyrosequencing of the 16S rRNA gene V3 region to characterize the fecal microbiota of 19 patients with CRC and 20 healthy control subjects. The results revealed striking differences in fecal microbial population patterns between these two groups. Partial least-squares discriminant analysis showed that 17 phylotypes closely related to Bacteroides were enriched in the gut microbiota of CRC patients, whereas nine operational taxonomic units, represented by the butyrate-producing genera Faecalibacterium and Roseburia, were significantly less abundant. A positive correlation was observed between the abundance of Bacteroides species and CRC disease status (R?=?0.462, P?=?0.046?<?0.5). In addition, 16 genera were significantly more abundant in CRC samples than in controls, including potentially pathogenic Fusobacterium and Campylobacter species at genus level. The dysbiosis of fecal microbiota, characterized by the enrichment of potential pathogens and the decrease in butyrate-producing members, may therefore represent a specific microbial signature of CRC. A greater understanding of the dynamics of the fecal microbiota may assist in the development of novel fecal microbiome-related diagnostic tools for CRC.     

寄主植物对棉铃虫越冬蛹抗寒能力的影响

通过对滞育蛹过冷却点的测定 ,初步明确寄主对棉铃虫Helicoverpaarmigera的越冬抗寒性有影响 ,幼虫取食棉花时产生的滞育蛹的过冷却点低于取食玉米的滞育蛹的过冷却点 ,即前者的抗寒能力高于后者 ;但用Bt棉喂养后的棉铃虫滞育蛹抗寒能力下降     

酵母多肽对几种细胞DNA合成的影响

<正> 我们用国内的新鲜酵母为材料,从中分离纯化到一种多肽——酵母多肽,其分子量为14kD。在低血清培养体系中能促使人成纤维细胞(HFB)和人脐静脉内皮细胞(HUVEC)的DNA合成。当培养液中酵母多肽的浓度为1μg/mL时能引起最大的刺激作用。但此多肽对胎牛心脏内皮细胞(FBHEC)的DNA合成则无作用。     

Synthesis and Mechanistic Studies of a Novel Homoisoflavanone Inhibitor of Endothelial Cell Growth

Preventing pathological ocular angiogenesis is key to treating retinopathy of prematurity, diabetic retinopathy and age-related macular degeneration. At present there is no small molecule drug on the market to target this process and hence there is a pressing need for developing novel small molecules that can replace or complement the present surgical and biologic therapies for these neovascular eye diseases. Previously, an antiangiogenic homoisoflavanone was isolated from the bulb of a medicinal orchid, Cremastra appendiculata. In this study, we present the synthesis of a novel homoisoflavanone isomer of this compound. Our compound, SH-11052, has antiproliferative activity against human umbilical vein endothelial cells, and also against more ocular disease-relevant human retinal microvascular endothelial cells (HRECs). Tube formation and cell cycle progression of HRECs were inhibited by SH-11052, but the compound did not induce apoptosis at effective concentrations. SH-11052 also decreased TNF-α induced p38 MAPK phosphorylation in these cells. Intriguingly, SH-11052 blocked TNF-α induced IκB-α degradation, and therefore decreased NF-κB nuclear translocation. It decreased the expression of NF-κB target genes and the pro-angiogenic or pro-inflammatory markers VCAM-1, CCL2, IL8, and PTGS2. In addition SH-11052 inhibited VEGF induced activation of Akt but not VEGF receptor autophosphorylation. Based on these results we propose that SH-11052 inhibits inflammation induced angiogenesis by blocking both TNF-α and VEGF mediated pathways, two major pathways involved in pathological angiogenesis. Synthesis of this novel homoisoflavanone opens the door to structure-activity relationship studies of this class of compound and further evaluation of its mechanism and potential to complement existing antiangiogenic drugs.     

Ephrin‐A3 reverse signaling regulates hippocampal neuronal damage and astrocytic glutamate transport after transient global ischemia

Increasing evidence indicates that the Eph receptors and their ephrin ligands are involved in the regulation of interactions between neurons and astrocytes. Moreover, astrocytic ephrin‐A3 reverse signaling mediated by EphA4 receptors is necessary for controlling the abundance of glial glutamate transporters. However, the role of ephrin‐A3 reverse signaling in astrocytic function and neuronal death under ischemic conditions remains unclear. In the present study, we found that the EphA4 receptor and its ephrin‐A3 ligand, which were distributed in neurons and astrocytes, respectively, in the hippocampus showed a coincident up‐regulation of protein expression in the early stage of ischemia. Application of clustered EphA4 decreased the expressions of astrocytic glutamate transporters together with astrocytic glutamate uptake capacity through activating ephrin‐A3 reverse signaling. In consequence, neuronal loss was aggravated in the CA1 region of the hippocampus accompanied by impaired hippocampus‐dependent spatial memory when clustered EphA4 treatment was administered prior to transient global ischemia. These findings indicate that EphA4‐mediated ephrin‐A3 reverse signaling is a crucial mechanism for astrocytes to control glial glutamate transporters and prevent glutamate excitotoxicity under pathological conditions.