猪细小病毒VP2与大肠杆菌不耐热肠毒素B亚单位在干酪乳杆菌表面共表达

将分别编码猪细小病毒(PPV)主要免疫保护性抗原VP2蛋白与大肠杆菌不耐热肠毒素B亚单位(LTB)基因插入乳酸杆菌细胞表面表达载体pPG中, 成功构建了重组表达载体pPG-VP2-LTB, 将其电转化干酪乳杆菌Lactobacillus casei 393, 获得了表达猪细小病毒VP2-LTB融合蛋白的重组乳酸菌表达系统, 经2%乳糖诱导, SDS-PAGE和Western-blot检测表明, 有大小约78 kD的蛋白得到了表达, 具有与天然病毒蛋白一样的抗原特异性, 全细胞ELISA结果表明, LTB同     

非模式植物蛋白质组学研究进展

蛋白质组学研究是对基因组学研究的重要补充,它是在蛋白质水平定量、动态、整体性研究生物体。该文简要介绍了蛋白质组学的含义,蛋白质组学及植物蛋白质组学产生的科学背景,蛋白质组学的研究内容。概述了非模式植物蛋白质组学的研究进展,主要包括非模式植物个体及群体蛋白质组学,组织和器官蛋白质组学,亚细胞蛋白质组学,响应环境变化的蛋白质组学以及非模式植物生物环境因子的蛋白质组学的研究情况,同时对植物蛋白质组学的发展前景进行了展望。     

The Microtubule-associated Protein EB1 Links AIM2 Inflammasomes with Autophagy-dependent Secretion

Inflammasomes are multi-protein complexes that regulate chronic inflammation-associated diseases by inducing interleukin-1 β (IL-1β) secretion. Numerous components involved in inflammasome activation have been identified, but the mechanisms of inflammasome-mediated IL-1β secretion have not yet been fully explored. Here, we demonstrate that end-binding protein 1 (EB1), which is required for activation of AIM2 inflammasome complex, links the AIM2 inflammasome to autophagy-dependent secretion. Imaging studies revealed that AIM2 inflammasomes colocalize with microtubule organizing centers and autophagosomes. Biochemical analyses showed that poly(dA-dT)-activated AIM2 inflammasomes induce autophagy and IL-1β secretion in an LC3-dependent fashion. Furthermore, depletion of EB1 decreases autophagic shedding and intracellular trafficking. Finally, we found that the 5′-AMP activated protein kinase may regulate this EB1-mediated autophagy-based inflammasome-induced secretion of IL-1β. These findings reveal a novel EB1-mediated pathway for the secretion of IL-1β.     

The association between three AXIN2 variants and cancer risk

Plenty of epidemiological studies have assessed the effects of AXIN2 polymorphisms on the risk of developing cancer, but the available results were somewhat inconclusive. Odds ratios (ORs) with 95% confidence intervals (CIs) were utilized to investigate the relationship between three AXIN2 variants (rs2240308 C/T, rs1133683 C/T, and rs4791171 A/G) and overall cancer susceptibility. In silico tools were undertaken to investigate the correlation of AXIN2 expression with cancer risk and survival time. Furthermore, we explored the serum expression of AXIN2 by enzyme-linked immunosorbent assay. A total of 4167 cancer patients and 3515 control subjects were evaluated. The overall results demonstrated that there was no major association of these polymorphisms on cancer risk. However, stratified analysis by cancer type showed evidence that rs2240308 C/T polymorphism had a lower risk in lung cancer (OR, 0.76; 95% CI, 0.63-0.92; P_{heterogeneity} = 0.865) and prostate cancer (OR, 0.54; 95% CI, 0.35-0.84; P_{heterogeneity} = 0.088) by heterozygote comparison. Similar results were indicated in Asian descendants and population-based studies. In silico analysis showed evidence that AXIN2 expressions in lung cancer and prostate cancer were lower than that in normal counterpart. High expression of AXIN2 may have longer overall survival time than low expression group for lung cancer participants. In addition, individuals who were CC/TC carriers had a higher serum expression level than TT carriers. In conclusion, this pooled analysis suggested that AXIN2 rs2240308 C/T variant may decrease both lung and prostate cancer susceptibility, particularly in Asian descendants and population-based studies. Future large scale and well-designed research are required to validate these effects in more detail.     

Formin mDia1 contributes to migration and epithelial-mesenchymal transition of tubular epithelial cells exposed to TGF-β1

Renal tubular epithelial cells may undergo epithelial-mesenchymal transition (EMT) in response to stimuli, such as transforming growth factor (TGF)-β1, leading to myofibroblast activation and renal fibrosis. The formin mDia1 is required for nucleation and polymerization of actin and the microtubule cytoskeleton. The present study sought to explore the role of mDia1 in EMT of tubular epithelial cells. A rat model of unilateral ureteral obstruction (UUO) was established. The expression of TGF-β1, collagen I, collagen III, and mDia1 in the kidneys was examined at day 7 after surgery. The effect of mDia1 on EMT was explored in NRK-52E cells by exposing them to TGF-β1. Increased expression of TGF-β1, collagen I, collagen III, and mDia1 was found in obstructive kidneys of UUO model rats. Exposing rat tubular epithelial cells to TGF-β1 promoted collagen I and collagen III expression but had no effect on mDia1 expression. Silencing mDia1 expression impeded epithelial cell migration as well as reduced TGF-β1, collagen, and Profilin1 expression, whereas mDia1 overexpression exerted an opposite effect. Furthermore, mDia1 regulated the expression of vimentin, α-smooth muscle actin, and E-cadherin and focal adhesion-kinase (FAK)/Src activation through Profilin1. Inhibition of the mDia1 activator RhoA by fasudil reversed EMT, and FAK/Src activation induced by mDia1. In conclusion, mDia1 regulated tubular epithelial cell migration, collagen expression, and EMT in NRK-52E cells exposed to TGF-β1. Thus, suppression of mDia1 activation might be a strategy to counteract renal fibrosis.     

新疆贫困地区维吾尔族农民肥胖与血脂异常相关性研究

肥胖及血脂异常研究很少涉及低收入地区。本研究分析了新疆低收入地区维吾尔族农民体质指数(BMI)、超重及肥胖与多种血脂分子异常的关系,探讨贫困地区筛查高危人群的适宜策略。在新疆喀什农村对3 286名年龄≥18岁个体(男1 585人,女1 701人) 进行问卷检查、体格检查及多项血脂分子的检测。数据采用Pearson相关性、ROC、Logistic回归等统计学分析。结果显示,在男女性中,随着BMI的增加,甘油三酯(TG)、总胆固醇(TC)、低密度脂蛋白胆固醇(LDLC)的血浓度呈现递增趋势（P<0.01）;男/女性TG、LDLC、TC血浓度均与BMI有显著相关性(P<0.01)。单项或多项血脂异常率均随BMI增加而上升;同一个体2个血脂指标同时异常的高危组合分别是TG+HDLC(高密度脂蛋白胆固醇)和TC+TG。Logistic联合多变量ROC曲线分析表明, 单项指标HDLC(AUC=089)在血脂异常诊断中的权重最高;而组合指标TG+HDLC(AUC=095)的权重高于其它任何组合。单因素Logistic回归分析发现,超重和肥胖是代谢综合征相关血脂指标TG、TC和HDLC异常的危险因素(P<0.05)。上述结果表明,在南疆农村贫困维吾尔族人群中,男女性超重与肥胖者均与血脂指标异常升高相关;HDLC、TG和 TC 任意两个指标同时异常,为血脂异常的高危状态。肥胖伴有“TG+HDLC”异常升高可能是血脂异常相关疾病的“集合危险因素”,在贫困地区具有临床筛查参考价值。     

我国肺形侧耳栽培菌株交配型分析

为分析我国栽培肺形侧耳的遗传多样性,对肺形侧耳菌株的交配型进行测定,测试的肺形侧耳菌株包括俗称为秀珍菇和凤尾菇的菌株。结果显示,我国栽培的秀珍菇与凤尾菇菌株间可以发生性亲和,属于同一生物学物种,但它们之间的交配型特异性低,36个菌株中只含4种A交配型和3种B交配型,暗示我国栽培的肺形侧耳种质资源基因匮乏。     

松墨天牛在秦巴林区不同寄主上的危害规律

松墨天牛Monochamus alternatus是次期性蛀干害虫,也是松材线虫病的主要传播媒介,廓清该害虫在秦巴林区不同寄主上的危害程度和发生规律,对于控制松材线虫病的扩散蔓延具有重要意义.本研究对秦巴林区遭受松材线虫病严重危害的3种主要松树(油松Pinus tabuliformis、华山松P.armandii和马尾松P.massoniana)进行了冬季疫木野外解析,并在统计不同胸径、不同高度疫木树干上松墨天牛侵入孔和幼虫数量的基础上,采用聚集度指标分析方法,对该害虫在不同寄主上的危害差异进行了比较研究.结果表明,松墨天牛在3种寄主上的危害程度具有显著差异,以华山松受害最重,其次分别为马尾松和油松;越冬幼虫在油松上主要危害皮下1～2 cm的边材;在华山松和马尾松上危害比较多样,以髓心部位受害最重,其后依次为心材、边材和树皮;在油松和华山松上,松墨天牛主要在树干7m以下部分危害,而在马尾松上主要危害树干7m以上部分,且虫口数量均与寄主胸径呈显著正相关.松墨天牛侵入孔和越冬幼虫在不同寄主树干上均呈聚集性分布.本研究揭示了松墨天牛在秦巴林区3种主要寄主上的危害规律,对于进一步开展大尺度地理范围松墨天牛的寄主选择性及危害规律研究提供了基础信息,也为秦巴林区松墨天牛的有效防治和松材线虫病的蔓延控制提供了新的重要信息.     

Low-dose Cd induces hepatic gene hypermethylation, along with the persistent reduction of cell death and increase of cell proliferation in rats and mice

BACKGROUND: Cadmium (Cd) is classified as a human carcinogen probably associated with epigenetic changes. DNA methylation is one of epigenetic mechanisms by which cells control gene expression. Therefore, the present study genome-widely screened the methylation-altered genes in the liver of rats previously exposed to low-dose Cd. METHODOLOGY PRINCIPAL FINDINGS: Rats were exposed to Cd at 20 nmol/kg every other day for 4 weeks and gene methylation was analyzed at the 48(th) week with methylated DNA immunoprecipitation-CpG island microarray. Among the 1629 altered genes, there were 675 genes whose promoter CpG islands (CGIs) were hypermethylated, 899 genes whose promoter CGIs were hypomethylated, and 55 genes whose promoter CGIs were mixed with hyper- and hypo-methylation. Caspase-8 gene promoter CGIs and TNF gene promoter CGIs were hypermethylated and hypomethylated, respectively, along with a low apoptosis rate in Cd-treated rat livers. To link the aberrant methylation of caspase-8 and TNF genes to the low apoptosis induced by low-dose Cd, mice were given chronic exposure to low-dose Cd with and without methylation inhibitor (5-aza-2'-deoxyctidene, 5-aza). At the 48(th) week after Cd exposure, livers from Cd-treated mice displayed the increased caspase-8 CGI methylation and decreased caspase-8 protein expression, along with significant increases in cell proliferation and overexpression of TGF-β1 and cytokeratin 8/18 (the latter is a new marker of mouse liver preneoplastic lesions), all which were prevented by 5-aza treatment. CONCLUSION/SIGNIFICANCE: These results suggest that Cd-induced global gene hypermethylation, most likely caspase-8 gene promoter hypermethylation that down-regulated its expression, leading to the decreased hepatic apoptosis and increased preneoplastic lesions.