曲美他嗪对儿童病毒性心肌炎患者血清IL-18和TNF—α的影响

目的探讨曲美他嗪对儿童病毒性心肌炎患者血清IL—18和TNF-α的影响。方法102例儿童病毒性心肌炎患者随机分为对照组44例、治疗组58例;两组病例确诊后均使用黄芪注射液及给予改良极化液静脉注射,每日1次,2周为1个疗程。同时给予口服辅酶Q10、维生素C等药物,持续治疗3个月。治疗组在上述治疗基础上给予曲美他嗪20mg,口服,3次／d,连续3个月。有频发期前收缩的患者,均酌情加用抗心律失常药物。治疗前后测定患者血清IL-18和TNF-α的浓度。结果治疗组可明显降低患者的血清IL-18和TNF-Q的浓度,与对照组比较有明显差异（P〈0．05）。结论曲美他嗪可能通过改善细胞因子IL-18和TNF—α而有助于病情缓解。     

细胞荷载溶瘤病毒

溶瘤病毒是一类仅在肿瘤细胞内特异增殖的新型病毒载体,具有高度的肿瘤靶向性和良好的转染率.局部注射溶瘤病毒治疗体表肿瘤已获得显著疗效,但全身应用后机体的免疫防御机制明显限制了溶瘤病毒的治疗效果.细胞荷载溶瘤病毒可能是克服这一瓶颈的有效策略,为治疗肿瘤提供了新的平台.     

感染人类呼吸道的病毒及其分类新进展

近年来,随着SAPS、禽流感等重大呼吸道传染病的出现,人们对呼吸道病毒感染给予了高度重视,促进了呼吸道病毒学的发展.这主要表现在三个方面,一是对相关病毒如SARS冠状病毒和高致病性禽流感病毒的致病性、基因与抗原变异、疫苗制备等取得了进展;二是发现了一些新的呼吸道病毒如冠状病毒HCoV-NL63和HCoV-HKU1、博卡病毒;三是一些被认为与呼吸道感染关系不大的"老病毒"如某些疱疹类病毒和细小病毒,现在经常出现在呼吸道感染者的样本中.鉴于目前呼吸道病毒的范围比以前有明显扩大,此文就能够感染人类呼吸道的病毒及其分类作一综述.     

Community Study Using a Polymerase Chain Reaction Panel to Determine the Prevalence of Common Respiratory Viruses in Asthmatic and Nonasthmatic Children

We developed a sensitive polymerase chain reaction (PCR) panel, suitable for the detection of seven common respiratory viruses, to study the prevalence of viruses in nasal swabs obtained from clinically stable asthmatic children (n = 21), non-physician diagnosed asthmatic children with exercise-induced bronchoconstriction (EIB) (n = 16), and nonasthmatic, non-EIB controls (n = 33). The PCR panel detected viruses in 43/70 (61.4%) specimens but there were no significant differences in prevalence of these viruses between the three groups of children. These results indicate that clinically stable asthmatic and nonasthmatic children frequently harbor viruses in the upper respiratory tract.     

丙型肝炎病毒ns5b基因的克隆、表达及鉴定

目的：构建HCV ns5b基因的重组原核表达质粒，并获得NS5B蛋白的高效表达，为制备抗NS5B抗体及以其为靶位的抗HCV感染研究创造条件。方法：利用PCR技术扩增HCV ns5b基因，Xho I和Kpn I双酶切后连接到经同样酶切的原核表达载体pRSETA上，转化大肠杆菌JM109菌株，获得阳性重组质粒pRSETA-ns5b，阳性质粒转化BL21(DE3)，IPTG诱导表达，表达产物经SDS-PAGE和Western Blot电泳进行鉴定，并以薄层扫描分析对其定量。结果：成功构建了HCV NS5B蛋白表达载体pRSETA-ns5b，经诱导明显表达出6His-NS5B融合蛋白，表达产物主要以包涵体形式存在，表达量占菌体蛋白25％，Western—Blot结果显示表达蛋白保持活性。结论：HCV NS5B蛋白在体外得到了有效表达。     

VIRUSES, NEURODEVELOPMENTAL DISORDER AND CHILDHOOD PSYCHOSIS

Four cases are described of prepubertal boys in whom the convergence of neurodevelopmental disorder, viral infection and psychosis seemed more than coincidental. Review of the literature highlights the possibility that viral infection of the central nervous system may play a contributory role in childhood psychosis. Whilst it is essential to avoid a reductionist stance when investigating these difficult conditions, the emergence of potent anti-viral treatments and sophisticated methods of identifying the presence of viral infection should encourage us to consider more carefully the relevance of viruses in childhood psychosis.     

The multitude and diversity of environmental carcinogens

We have recently proposed that lifestyle-related factors, screening and aging cannot fully account for the present overall growing incidence of cancer. In order to propose the concept that in addition to lifestyle related factors, exogenous environmental factors may play a more important role in carcinogenesis than it is expected, and may therefore account for the growing incidence of cancer, we overview herein environmental factors, rated as certainly or potentially carcinogenic by the International Agency for Research on Cancer (IARC). We thus analyze the carcinogenic effect of microorganisms (including viruses), radiations (including radioactivity, UV and pulsed electromagnetic fields) and xenochemicals. Chemicals related to environmental pollution appear to be of critical importance, since they can induce occupational cancers as well as other cancers. Of major concerns are: outdoor air pollution by carbon particles associated with polycyclic aromatic hydrocarbons; indoor air pollution by environmental tobacco smoke, formaldehyde and volatile organic compounds such as benzene and 1,3 butadiene, which may particularly affect children, and food pollution by food additives and by carcinogenic contaminants such as nitrates, pesticides, dioxins and other organochlorines. In addition, carcinogenic metals and metalloids, pharmaceutical medicines and cosmetics may be involved. Although the risk fraction attributable to environmental factors is still unknown, this long list of carcinogenic and especially mutagenic factors supports our working hypothesis according to which numerous cancers may in fact be caused by the recent modification of our environment.     

Using a magnetic field to redirect an oncolytic adenovirus complexed with iron oxide augments gene therapy efficacy

Adenovirus (Ad) is a widely used vector for cancer gene therapy but its therapeutic efficacy is limited by low coxsackievirus and adenovirus receptor (CAR) expression in tumors and non-specifically targeted infection. Ad infectivity and specificity can be markedly improved by creating Ad-magnetic nanoparticles cluster complexes and directing their migration with an external magnetic field (MGF). We electrostatically complexed GFP-expressing, replication-incompetent Ad (dAd) with PEGylated and cross-linked iron oxide nanoparticles (PCION), generating dAd-PCION complexes. The dAd-PCION showed increased transduction efficiency, independent of CAR expression, in the absence or presence of an MGF. Cancer cell killing and intracellular oncolytic Ad (HmT)-PCION replication significantly increased with MGF exposure. Site-directed, magnetically-targeted delivery of the HmT-PCION elicited significantly greater therapeutic efficacy versus treatment with naked HmT or HmT-PCION without MGF in CAR-negative MCF7 tumors. Immunohistochemical tumor analysis showed increased oncolytic Ad replication in tumors following infection by HmT-PCION using an MGF. Whole-body bioluminescence imaging of tumor-bearing mice showed a 450-fold increased tumor-to-liver ratio for HmT-PCION with, versus without, MGF. These results demonstrate the feasibility and potential of external MGF-responsive PCION-coated oncolytic Ads as smart hybrid vectors for cancer gene therapy.     

A systematic review of viral exposures as a risk for rheumatoid arthritis

Objective

Different viral exposures have been implicated in the etiology of rheumatoid arthritis (RA). Evidence relating to the association between putative viral exposures and the development of RA was reviewed.