腹泻患儿粪便A群轮状病毒抗原检测的结果分析

目的：了解本地区腹泻婴幼儿的A群轮状病毒感染情况及其流行特点。方法：采用胶体金法对我院2009年10月-2010年9月2104例有腹泻和肠炎特征的婴幼儿粪便进行A群轮状病毒抗原检测。结果：在2104例受检者中,A群轮状病毒感染的总阳性率是24．71％,其中男性感染率24．17％,女性为25．40％。不同年龄组间以1—2岁婴幼儿感染率最高,为32．13％,0-1岁为20．72％,2-5岁为12．03％。感染的季节特征是秋末冬初季（10—12月）阳性率最高,为42．82％,春末夏初季（4．6月）最低,为8．81％。结论：由A群轮状病毒感染引发的急性腹泻主要发生在1-2岁的婴幼儿,各个季节均有发生,以秋末冬初季为高发。     

Temporal relationship of autophagy and apoptosis in neurons challenged by low molecular weight β‐amyloid peptide

Alzheimer's disease (AD) is an aging‐related progressive neurodegenerative disorder. Previous studies suggested that various soluble Aβ species are neurotoxic and able to activate apoptosis and autophagy, the type I and type II programmed cell death, respectively. However, the sequential and functional relationships between these two cellular events remain elusive. Here we report that low molecular weight Aβ triggered cleavage of caspase 3 and poly (ADP‐ribose) polymerase to cause neuronal apoptosis in rat cortical neurons. On the other hand, Aβ activated autophagy by inducing autophagic vesicle formation and autophagy related gene 12 (ATG12), and up‐regulated the lysoso‐mal machinery for the degradation of autophagosomes. Moreover, we demonstrated that activation of autophagy by Aβ preceded that of apoptosis, with death associated protein kinase phosphorylation as the potential molecular link. More importantly, under Aβ toxicity, neurons exhibiting high level of autophagosome formation were absent of apoptotic features, and inhibition of autophagy by 3‐methylade‐nine advanced neuronal apoptosis, suggesting that autophagy can protect neurons from Aβ‐induced apoptosis.     

微生态失调与感染

微生态失调与感染的关系极为密切。引起感染的微生物不一定是致病菌或病原体,微生态失调后,正常微生物群易位或易主也可以引起感染。从微生态的视角去审视感染的发生、发展和结局,将会为感染病的防治提供新的思路。     

Development of [Ile40]HTLV‐I protease inhibition assay using novel fluorogenic and chromogenic substrate

HTLV‐I is a debilitating and/or lethal retrovirus that causes HTLV‐I‐associated myelopathy/tropical spastic paraparesis, adult T‐cell leukemia and several inflammatory diseases. HTLV‐I protease is an aspartic retropepsin involved in HTLV‐I replication and its inhibition could treatHTLV‐I infection. A recombinant L40I mutant HTLV‐I protease was designed and obtained from Escherichia coli, self‐processingand purification by ion‐exchange chromatography. The protease was refolded by a one‐step dialysis and recovered activity. The cleavage efficiency of the [Ile⁴⁰]HTLV‐I protease was at least 300 times higher for a fluorescent substratethan that of our previously reported recombinant His‐tagged non‐mutated HTLV‐I protease. In addition, we designed and synthesized a substrate containing a highly fluorescent Mca moiety in the fragment before the scissile bond, and a chromogenic p‐nitrophenylalanine moiety after the scissile bond that greatly amplified spectrometry detection and improved the HTLV‐I protease inhibition potency assay. The HTLV‐I protease inhibition assay with the [Ile⁴⁰]HTLV‐I protease and fluorogenic substrate requires distinctively less protease, substrate, inhibitor and assay time than our previous methods. This means our new assay is more cost‐effective and more time‐efficient while being reproducible and less labor‐intensive. Copyright © 2011 European Peptide Society and John Wiley & Sons, Ltd.     

游离植皮联合负压封闭引流治疗骨科创面的临床研究

目的:观察游离植皮联合负压封闭引流(vacuumsealingdrainage,后文简称VSD)对骨科创面的疗效,并与植皮后传统加压包扎相比较,为临床实践提供更好的治疗方法。方法:对广州中医药大学第一附属医院创伤骨科2008年3月至2010年2月收治的65例感染创面病例采取手术清创后予VSD引流,合理应用抗生素,创面感染得到控制后,创面干净,肉芽生成良好,外露的肌腱、骨膜表面有新鲜的肉芽组织覆盖,达到植皮的要求后,随机分成两组,其中30例(实验组)采用游离植皮联合VSD法闭合创面,35例(对照组)采用游离植皮加压包扎植皮区,对两组术后的平均换药次数、创面平均愈合时间、植皮成活率情况、平均住院时间(植皮后)、平均抗生素应用次数(植皮后)进行统计学分析,采用t检验和卡方检验,对此两种方法进行评价。结果:植皮联合VSD组与植皮加压包扎组,在平均换药次数、创面平均愈合时间、植皮成活率、平均住院时间(植皮后)、平均抗生素应用次数(植皮后)的对比,有显著性差异(P<0.05)。结论:创面达到游离植皮条件后,游离植皮联合VSD负压引流可以促使皮片黏附,保持创面洁净,避免皮下渗液积聚,有利于皮片的存活,与植皮加压包扎组相比,减少了平均换药次数,缩短创面平均愈合时间及平均住院时间(植皮后),减少抗生素平均应用次数,提高了植皮成活率,说明游离植皮联合VSD组优于游离植皮加压包扎组,游离植皮联合VSD法治疗骨科创面有显著疗效。该手术方法操作简单,术后护理方便,是一种较理想的植皮后的固定方法,有利于创面的愈合,值得临床推广应用。     

关于HCMV 潜伏感染与激活感染研究的新进展

人巨细胞病毒(HCMV)是疱疹病毒科中最大的病毒,结构复杂,其感染在人群中非常普遍,近年来免疫妥协(immunocompromised)群体尤其是移植群体中的HCMV潜伏感染和激活感染越来越受到临床重视。本文就HCMV的感染与免疫、HCMV的致病机制、宿主的抗感染与免疫、HCMV的免疫逃逸、HCMV的潜伏与激活及HCMV相关研究的困境与展望近年来此方面研究新进展作一简要综述。     

High‐fat diet‐induced dysbiosis mediates MCP‐1/CCR2 axis‐dependent M2 macrophage polarization and promotes intestinal adenoma‐adenocarcinoma sequence

High‐fat diet (HFD) is a well‐known risk factor for gut microbiota dysbiosis and colorectal cancer (CRC). However, evidence relating HFD, gut microbiota and carcinogenesis is limited. Our study aimed to demonstrate that HFD‐induced gut dysbiosis promoted intestinal adenoma‐adenocarcinoma sequence. In clinical study, we found that HFD increased the incidence of advanced colorectal neoplasia (AN). The expression of monocyte chemoattractant protein 1 (MCP‐1), CC chemokine receptor 2 (CCR2) and CD163 in CRC patients with HFD was significantly higher than that in CRC patients with normal diet. When it comes to the Apc^min/+ mice, HFD consumption could induce gut dysbiosis and promote intestinal carcinogenesis, accompanying with activation of MCP‐1/CCR2 axis that recruited and polarized M2 tumour‐associated macrophages. Interestingly, transfer of faecal microbiota from HFD‐fed mice to another batch of Apc^min/+ mice in the absence of HFD could also enhance carcinogenesis without significant body weight gain and induced MCP‐1/CCR2 axis activation. HFD‐induced dysbiosis could also be transmitted. Meanwhile, antibiotics cocktail treatment was sufficient to inhibit HFD‐induced carcinogenesis, indicating the vital role of dysbiosis in cancer development. Conclusively, these data indicated that HFD‐induced dysbiosis accelerated intestinal adenoma‐adenocarcinoma sequence through activation of MCP‐1/CCR2 axis, which would provide new insight into better understanding of the mechanisms and prevention for HFD‐related CRC.     

外泌体在病毒感染诊断和治疗中的作用研究 *

外泌体是多泡体与细胞质膜融合后释放的细胞外囊泡.它们携带有源自分泌细胞的功能性蛋白质,脂质和核酸,能够介导细胞间通信,并在生物体的致病过程中发挥重要作用.当前,对外泌体在病毒感染中的作用机制研究,以及外泌体作为病毒感染诊断和治疗的潜在标志物研究仍处于初级阶段.首先阐述了外泌体的组成和生物学发生机制;然后重点阐述了外泌体在病毒感染中的作用机制,尤其是其在免疫调节中的作用;最后探讨了外泌体作为病毒感染诊断和治疗的潜在标志物的可能性及其应用前景.     

Macroautophagy is repressed during mitosis – seeing is believing

ABSTRACT

For the last two decades there has been wide ranging debate about the status of macroautophagy during mitosis. Because metazoan cells undergo an “open” mitosis in which the nuclear envelope breaks down, it has been proposed that macroautophagy must be inhibited to maintain genome integrity. While many studies have agreed that the number of autophagosomes is greatly reduced in cells undergoing mitosis, there has been no consensus on whether this reflects decreased autophagosome synthesis or increased autophagosome degradation. Reviewing the literature we were concerned that many studies relied too heavily on autophagy assays that were simply not appropriate for a relatively brief event such as mitosis. Using highly dynamic omegasome markers we have recently shown unequivocally that autophagosome synthesis is repressed at the onset of mitosis and is restored once cell division is complete. This is accomplished by CDK1, the master regulator of mitosis, taking over the function of MTORC1, to ensure autophagy is repressed during mitosis.