重楼活性单体pp-10通过抑制PI3K/Akt通路诱导人胃癌细胞BGC-823凋亡和自噬

目的:探讨重楼/七叶一枝花(Paris polyphylla)的醇提物单体pp-10诱导人胃癌BGC-823细胞凋亡和自噬及其分子机制。方法:采用MTT法和克隆形成抑制实验观察不同浓度的重楼单体pp-10对人胃癌BGC-823细胞的增殖抑制作用;Hoechst33342染色法检测pp-10作用于人胃癌BGC-823细胞后细胞核形态的改变;Annexin V-FITC/PI双染法检测细胞凋亡;Western blotting检测重楼单体pp-10对细胞凋亡和自噬相关蛋白Caspase-3、Caspase-9、(ADP-核糖)聚合酶(PARP)、Bax、Bcl-2、LC3、P62以及PI3K/Akt信号通路相关蛋白(Akt、p-Akt、m TOR、p-m TOR、P70s6k、p-P70s6k)表达的影响。结果:重楼单体pp-10能显著抑制BGC-823细胞的生长,作用呈时间-效应关系及剂量-效应关系;克隆形成抑制实验表明随着pp-10浓度的增加,细胞克隆形成逐渐减少,与对照组相比有显著差异;在荧光显微镜下观察可见其细胞核固缩、边聚、裂解等细胞凋亡形态学变化;流式细胞术检测显示,随着作用药物浓度的增高,其凋亡率逐渐升高;Western blotting结果表明,随着药物浓度的增加,线粒体相关凋亡信号通路蛋白Caspase9、Caspase3及PARP均出现酶切活化条带,细胞促凋亡蛋白Bax的表达水平增加,抗凋亡蛋白Bcl-2减少,自噬相关蛋白Ⅱ型LC3增加,P62蛋白减少,p-Akt蛋白的表达水平下降,Akt下游蛋白p-m Tor、p-p70S6K表达减少。结论:重楼单体pp-10通过抑制BGC-823细胞增殖,诱导细胞凋亡和自噬,与下调P13K/Akt信号通路有关。     

普洱茶中功能性微生物的筛选及其对普洱茶感官品质的影响

普洱茶的渥堆发酵过程是以晒青毛茶的内含成分为基础,在微生物分泌的胞外酶及湿热作用下,发生一系列化学变化,最终形成普洱茶独特的风味。采用稀释涂布法,根据产酶微生物的特性,经过固体平板初筛和液体茶汤培养基复筛,从普洱茶中分离得到若干株产酶菌株,并从中挑选优良菌株接种普洱茶固体发酵,考察其对普洱茶感官品质的影响。经分子生物学鉴定,D13-16为米曲霉(Aspergillus oryzae),相似度为98.62%;GJ-02为米根霉(Rhizopus cryzae),相似度为98.57%;XW-10和DF-03均为黑曲霉(Aspergillus niger),相似度分别为99.10%和99.92%。结果表明:普洱茶香气的形成主要与蛋白酶产生菌有关,DB-16发酵后香气评分达到31分(对照28,总分40);汤色主要受多酚氧化酶产生菌的影响,DF-03发酵后汤色评分达到19分(对照12,总分20);而这四种功能性微生物均在不同程度上促进了普洱茶滋味的形成。     

CCR9和CCL25蛋白在上皮性卵巢癌中表达及临床意义

目的:探讨CCR9和CCL25蛋白在不同卵巢组织中的表达及其与上皮性卵巢癌患者临床病理因素之间的关系。方法:通过组织芯片结合免疫组织化学法检测78例上皮性卵巢癌组织和30例正常卵巢组织中CCR9和CCL25表达水平,结合上皮性卵巢癌病人的临床病理资料,进行统计分析。结果:CCR9和CCL25在上皮性卵巢癌中高表达,在正常卵巢组织中低表达,二者的表达与上皮性卵巢癌的组织类型、患者年龄无显著相关(P0.05),而与淋巴结转移、组织学分级和临床分期有显著相关(P0.05);上皮性卵巢癌组织中CCR9与CCL25表达相关(P0.05)。结论:CCR9和CCL25在上皮性卵巢癌的发生发展中可能起重要作用,二者可能是上皮性卵巢癌治疗的一个潜在的分子靶点。     

血栓通配合康复训练对缺血性脑卒中恢复期患者肢体康复的疗效

目的:探究血栓通配合康复训练对缺血性脑卒中(cerebral arterial thrombosis,CAT)恢复期患者肢体康复的疗效情况。方法:选取2011年3月-2013年3月我院收治的84例CAT患者按数字表法随机分为观察组和对照组,各42例。对照组单纯采用康复训练治疗,观察组在对照组康复训练的基础上服用血栓通配合治疗,分别观察治疗前、治疗后1个月、3个月、6个月的各项基本指标并对比研究。结果:两组患者治疗前和治疗1月后Barthel评分无明显差异(P0.05);观察组治疗后3、6个月Barthel评分显著高于对照组,差异有统计学意义(P0.05),两组患者治疗前和治疗1月后肢体Fugl-Meyer评分无明显差异(P0.05);观察组治疗后3、6个月肢体Fugl-Meyer评分显著高于对照组,差异有统计学意义(P0.05),且对照组出院时上肢依然未完全恢复。通过对对照组和观察组患者的生活质量评分比较,观察组生活质量的各项评分均明显高于对照组,两组比较差异有统计学意义(P0.05)。结论:对缺血性脑卒中恢复期患者采用血栓通药物配合适当的康复训练疗效较好,术后肢体恢复理想,值得作为治疗CAT的首选方法在临床上推广应用。     

新疆棉田土壤固氮菌遗传多样性分析

利用ERIC-PCR和16SrDNA全序列测定方法,研究了新疆棉田土壤中分离获得的58株固氮菌的遗传多样性及系统发育。采用平均连锁法(UPGMA)分析ERIC-PCR的聚类结果表明在Watson距离为0.65左右时可以将供试菌株分为9个大群。选取ERIC-PCR各群中代表菌株进行16SrRNA全序列测定分析,结果表明这些菌株分别属于Enterobacter、Bacillus、Acinetobacter、Pseudomonas、Serratia和Yersinia6个属。     

陆地棉新型核雄性不育系21A的初步研究

利用辐射诱变和回交育种成功培育出21A雄性不育系,经遗传分析和等位性测验发现,该不育性受1对隐性基因控制,它与国内发现的msc1、msc2、msc3、msc74个陆地棉隐性不育基因彼此是非等位基因;采用NCⅡ遗传交配设计,用21A不育系作母本,5个常规棉品种作父本,配制杂交组合,对10个组合的F1产量和品质性状的竞争优势和配合力进行分析,结果表明,该不育系杂种优势明显,一般配合力高,易于筛选优良的杂交组合,在生产优质杂交种方面具有很大的利用价值。     

线粒体CytC的释放机制及其在细胞凋亡中的作用

描述了细胞色素C(CytC)从线粒体释放的机制及其在细胞凋亡中的作用,主要阐述了细胞凋亡信号转导途径中的线粒体-CytC途径及AIF途径;CytC在细胞凋亡中的作用及介导细胞凋亡的方式。探讨了线粒体CytC的泄漏机制,对非特异性释放模式(MPTP假说和线粒体膨胀假说)、特异性释放模式(专一性通道假说)进行了阐述,最后分析了研究CytC与细胞凋亡分子机制的意义并提出细胞凋亡分子机制中一些未完全研究清楚的问题。     

单核细胞趋化蛋白-1与2型糖尿病大血管病变

单核细胞趋化蛋白-1(monocyte chemoattractant protein-1;MCP-1)属于炎症趋化因子CC亚族成员,它能趋化T淋巴细胞、单核细胞,诱导内皮细胞、单核细胞释放黏附因子,使单核/巨噬细胞向病变处聚集。这些免疫及炎症过程有可能导致2型糖尿病大血管病变的发生、发展。本文就单核细胞趋化蛋白-1促使动脉粥样硬化的机制、及其干预治疗,单核细胞趋化蛋白-1表达上调的影响因素,深入了解单核细胞趋化蛋白-1与2型糖尿病大血管病变的关系。     

Elevated CO2 changes the interactions between nematode and tomato genotypes differing in the JA pathway

Interactions between the root‐knot nematode Meloidogyne incognita and three isogenic tomato (Lycopersicon esculentum) genotypes were examined when plants were grown under ambient (370 ppm) and elevated (750 ppm) CO₂. We tested the hypothesis that, defence‐recessive genotypes tend to allocate ‘extra’ carbon (relative to nitrogen) to growth under elevated CO₂, whereas defence‐dominated genotypes allocate extra carbon to defence, and thereby increases the defence against nematodes. For all three genotypes, elevated CO₂ increased height, biomass, and root and leaf total non‐structural carbohydrates (TNC):N ratio, and decreased amino acids and proteins in leaves. The activity of anti‐oxidant enzymes (superoxide dismutase and catalase) was enhanced by nematode infection in defence‐recessive genotypes. Furthermore, elevated CO₂ and nematode infection did not qualitatively change the volatile organic compounds (VOC) emitted from plants. Elevated CO₂ increased the VOC emission rate only for defence‐dominated genotypes that were not infected with nematodes. Elevated CO₂ increased the number of nematode‐induced galls on defence‐dominated genotypes but not on wild‐types or defence‐recessive genotypes roots. Our results suggest that CO₂ enrichment may not only increase plant C : N ratio but can disrupt the allocation of plant resources between growth and defence in some genetically modified plants and thereby reduce their resistance to nematodes.     

CpG island hypermethylation of multiple tumor suppressor genes associated with loss of their protein expression during rat lung carcinogenesis induced by 3-methylcholanthrene and diethylnitrosamine

The epigenetic mechanisms underlying the tumorigenesis caused by polycyclic aromatic hydrocarbons and nitrosamine compounds such as 3-methylcholanthrene (MCA) and diethylnitrosamine (DEN) are currently unknown. We reported previously that dynamic changes in DNA methylation occurred during MCA/DEN-induced rat lung carcinogenesis. Here, we used the same animal model to further study the evolution of methylation alterations in tumor suppressor genes (TSGs) DAPK1, FHIT, RASSF1A, and SOCS-3. We found that none of these genes were methylated in either normal or hyperplasia tissue. However, as the severity of the cancer progressed through squamous metaplasia and dysplasia to carcinoma in situ (CIS) and infiltrating carcinoma, so methylation became more prevalent. Particularly dramatic increases in the level of methylation, the average number of methylated genes, and the incidence of concurrent methylation in three genes were observed in CIS and infiltrating carcinoma. Similar but less profound changes were seen in squamous metaplasia and dysplasia. Furthermore, methylation status was closely correlated to loss of protein expression for these genes, with protein levels markedly declining along the continuum of carcinogenesis. These results suggest that progressive CpG island hypermethylation leading to inactivation of TSGs might be a vital molecular mechanism in the pathogenesis of MCA/DEN-induced multistep rat lung carcinogenesis.