就诊官兵H7N9禽流感预防知识知晓率调查

<正>人感染H7N9禽流感是由H7N9禽流感病毒引起的急性呼吸道传染病。全军H7N9禽流感防控会议报告指出,截止2014-02-18,共报告H7N9禽流感347例,确诊203例,超过2013年疫情高发水平。早发现、早报告、早诊断、早治疗是有效防控H7N9禽流感的关键。为维护部队战斗力,有效防控军队人员感染H7N9禽流感,强化H7N9禽流感相关知识的宣传力度,自2013年3月—2013年12月,笔者所在医     

人感染H7N9禽流感诊疗方案人感染H7N9禽流感诊疗方案（2014年版）

人感染H7N9禽流感是由H7N9禽流感病毒引起的急性呼吸道传染病,其中重症肺炎病例常可合并急性呼吸窘迫综合征、感染性休克,甚至多器官功能衰竭。早发现、早报告、早诊断、早治疗,加强重症病例救治,注意中西医并重,是有效防控、提高治愈率、降低病死率的关键。     

卫计委印发《医院人感染H7N9禽流感病毒核酸检测标准操作程序》等技术规范

根据人感染H7N9禽流感疫情联防联控工作机制会议议定事项及《关于医院开展人感染H7N9禽流感病毒核酸检测有关工作的通知》(卫办医政函〔2013〕383号,以下简称《通知》)精神,为指导医院做好人感染H7N9禽流感病毒核酸检测工作,国家卫生和计划生育委员会组织制定了《医院人感染H7N9禽流感病毒核酸检测标准     

人感染H7N9禽流感的治疗与用药

目的探讨人感染H7N9禽流感的治疗与用药。方法采用文献检索和网络查询方法,收集H7N9禽流感最新研究动态,发病初期及轻重症患者的治疗与用药原则,重症患者的治疗措施与用药。结果 H7N9禽流感发病初期和轻症患者及早发现和治疗,重症患者采用＂四抗二平衡＂方法和人工肝技术清除体内堆积的炎症因子,合理使用神经氨酸酶抑制剂等,临床治疗效果显著。结论新型重组人感染H7N9禽流感及早发现和正确治疗,正确使用神经氨酸酶抑制剂和对症联用中药治疗效果良好。     

12例人感染H7N9禽流感重症患者的护理

目的:总结12例确诊人感染H7N9禽流感重症患者救治的护理过程。方法:2013年8月-2014年12月救治12例人感染H7N9禽流感患者,予以消毒隔离、呼吸系统、循环系统、消化系统和心理护理等方面的护理措施。结果:经过系统的治疗及精心的护理后,成功抢救人感染H7N9禽流感重症患者,提高危重患者生命率的关键结论:10例患者康复出院,2例患者死亡。     

药界

H7N9禽流感病毒检测试剂盒获批 上海之江生物科技股份有限公司申报的“人感染H7N9禽流感病毒RNA检测试剂盒（荧光PCR法）”和中山大学达安基因股份有限公司申报的“人感染H7N9禽流感病毒RNA检测试剂盒（荧光PCR法）”近日获得国家食品药品监督管理总局批准，     

防范H7N9:不懈怠,不恐慌

禽流感又来了。这次是H7N9。连日来,上海、浙江、江苏、安徽等省市相继确诊多例H7N9禽流感患者,死亡人数不断增加。此次H7N9禽流感病毒在人类身上发现并致人死亡,系全球首次。H7N9新型病毒的突然来袭,不禁让人想起10年前的非典(SARS),不少人也担忧H7N9禽流感会成为"SARS重演"。现在,从中央有关部门到出现疫情的各地,已经进入"备战"状态。国家卫生和计生委要求,确诊人感染H7N9禽流感病例的省份启动疫情信息     

综合医院人感染H7N9禽流感防控述要

根据国家卫计委关于印发《人感染mN9禽流感医院感染预防与控制技术指南（2013年版）》、《人感染H7N9禽流感诊疗方案（2013年第2版）》的通知要求,北京市海淀区羊坊店医院积极行动,及时、有效地采取防控措施,管理体会如下。1医院领导重视。职能部门分工负责主管院长组织召开H7N9禽流感防控工作专题会,传达上级部门防控工作精神和文件内容,布置本院H7N9禽流感防控工作。成立防控工作领导小组与防控工作办公室。职能科室分工明确,医务科负责制定本院《人感染H7N9禽流感防控工作应急预案应急预案》。院感科制定《人感染mN9禽流感隔离、消毒和个人防护应急工作方案》。     

临床用人感染H7N9禽流感病毒检测试剂盒获批

2013年5月21日,上海之江生物科技股份有限公司申报的“人感染H7N9禽流感病毒RNA检测试剂盒（荧光PCR法）”和中山大学达安基因股份有限公司申报的“人感染HTN9禽流感病毒RNA检测试剂盒（荧光PCR法）”获得国家食品药品监督管理总局批准,标志着我国临床用人感染H7N9禽流感病毒诊断试剂率先批准上市。该诊断试剂均基于荧光PCR方法,可对具有流感样症状的患者或者相关密切接触者的鼻咽拭子、口咽拭子、痰液等呼吸道分泌物样本中的H7N9禽流感病毒RNA进行体外定性检测,检测结果可用于临床辅助诊断患者是否感染H7N9禽流感病毒。     

人感染H7N9禽流感人源化中和抗体论证会在京召开

<正>为做好应对人感染H7N9禽流感疫情的科技支撑工作,"重大新药创制"科技重大专项于2013年4月组织神州细胞工程有限公司等单位实施了人感染H7N9禽流感应急抗体制备和研发项目。目前,该项目进展顺利,已完成人感染H7N9禽流感人源化中和抗体的临床前研究并申报临床试验。为加快推进该项目实施进程,2014年2月12日,新药专项行政责任人、国家卫生和计划生育委员会副主任刘谦同志主持召开"人感染H7N9禽流感人源化中和抗体论证会"。会议听取了项目研发进展情况汇报并进行了充分讨论。与会专家     

Characteristics of human infection with avian influenza viruses and development of new antiviral agents

Since 1997, several epizootic avian influenza viruses (AIVs) have been transmitted to humans, causing diseases and even deaths. The recent emergence of severe human infections with AIV (H7N9) in China has raised concerns about efficient interpersonal viral transmission, polygenic traits in viral pathogenicity and the management of newly emerging strains. The symptoms associated with viral infection are different in various AI strains: H5N1 and newly emerged H7N9 induce severe pneumonia and related complications in patients, while some H7 and H9 subtypes cause only conjunctivitis or mild respiratory symptoms. The virulence and tissue tropism of viruses as well as the host responses contribute to the pathogenesis of human AIV infection. Several preventive and therapeutic approaches have been proposed to combat AIV infection, including antiviral drugs such as M2 inhibitors, neuraminidase inhibitors, RNA polymerase inhibitors, attachment inhibitors and signal-transduction inhibitors etc. In this article, we summarize the recent progress in researches on the epidemiology, clinical features, pathogenicity determinants, and available or potential antivirals of AIV.     

人感染甲型H7N9禽流感病毒致病性研究进展

人感染甲型H7N9禽流感病毒（human-infecting H7N9 avian influenza A virus，hH7N9 AIAV）已跨越禽类与人类之间的宿主屏障而感染人类。2013年至今，hH7N9 AIAV已在中国引起5次大的流行。虽然到目前为止仅存在有限的hH7N9 AIAV感染人际传播病例，但hH7N9 AIAV的高突变率特征似存在引发大流行的可能。此文就hH7N9 AIAV的来源、致病性和抗原分子基础，以及人感染H7N9禽流感的临床特征进行综述，以为hH7N9 AIAV防控提供参考。     

高致病性H7N9禽流感病毒研究进展

摘要：H7N9禽流感病毒在中国出现以来共造成5次流行。在第5次流行中出现了高致病性H7N9变异株,该病 毒株的HA链接肽位置发生了基因插入性突变,导致该病毒对家禽毒力的增强。同时在人感染H7N9禽流感病例中 也相继分离到了该病毒。因此,对高致病性H7N9禽流感病毒病原学及流行病学研究对于该疾病的预防和控制具有 重要意义。本文从高致病性H7N9禽流感病毒的变异来源、流行病学特征及防治措施等方面进行综述,为高致病性 H7N9禽流感的有效防治提供科学策略。     

Therapeutic targeting of adenosine receptors in inflammatory diseases

A novel H7N9 avian influenza A virus (IAV) emerged in China in early 2013 causing > 450 cases of respiratory illness and 175 deaths within a 20-month period. Though avian viruses infect humans infrequently, the lack of human immunity to these viruses raises the possibility of a pandemic if they were to acquire the ability to transmit efficiently. Despite the fact that IAV pathogenicity results from the cytopathic effects and tissue damage caused by both viral replication and an overly robust immune response, current IAV therapeutics only target the viral proteins. This has led to the emergence of drug resistance due to the high mutation rates of viruses. The growing obsolescence of our current influenza therapeutics underscores the need for alternative treatment strategies. One promising area of research is the use of drugs that target the host response to IAV infection. This article describes how gene expression profiling can be used to predict drugs that reverse the destructive effects of the host response to H7N9 and other pathogenic influenza viruses.     

Liquid chromatography-electrospray ionization tandem mass spectrometry analysis of 7-ethylguanine in human liver DNA

Considerable evidence in the literature demonstrates the exposure of humans to an unknown ethylating agent. Previous studies have demonstrated the presence of 7-ethyl-Gua and 3-ethyl-Ade in urine, 7-ethyl-dGuo and O4-ethyl-dThd in human lung, and ethylvaline in hemoglobin. Some studies also report higher levels of ethyl adducts in smokers than in nonsmokers, and there is convincing evidence for an uncharacterized ethylating agent in cigarette smoke. To further investigate this question, we have developed a liquid chromatography-electrospray ionization tandem mass spectrometry-selected reaction monitoring method for analysis of 7-ethyl-Gua in human liver DNA. To our knowledge, there are no previous reports of MS analyses of 7-ethyl-Gua in human tissues. [15N 5]7-Ethyl-Gua was synthesized and used as the internal standard. Human liver DNA was heated to release 7-ethyl-Gua. After partial purification by solid-phase extraction, analysis was carried out using the transition m/z 180 [M+H]+-->m/z 152 [Gua+H]+ for 7-ethyl-Gua and m/z 185-->m/z 157 for the internal standard. The method was accurate and precise. The detection limit was approximately 8-9 fmol/micromol Gua, starting with 1-2 mg of DNA. Clear coeluting peaks for 7-ethyl-Gua and the internal standard were observed in the human liver DNA samples. Twenty-six human liver DNA samples (0.77+/-0.40 mg) were analyzed, and 25 were positive for 7-ethyl-Gua. The mean level of 7-ethyl-Gua was 42.2+/-43.0 fmol/micromol Gua (8.4+/-8.6 adducts per 10(9) nucleotides). These results demonstrate that 7-ethyl-Gua is a common DNA adduct in human liver with likely endogenous sources that require further investigation.     

Rapid analysis of proteomic biomarkers expressed in human endometrial stromal cells during decidualization

Decidualization of human endometrial stromal (ES) cells plays a critical role in successful uterine implantation. Therefore, monitoring of the behavior of human ES cells may provide the clue for early detection of a uterine abnormality such as sterility and abortion. Monitoring of decidualization in vitro cell culture system fundamentally depends on expression of the definite biomarkers. In this study, we tried to uncover novel marker proteins of 8-bromo-cyclic adenosine monophosphate (8-Br-cAMP)-induced decidualization in human ES cells using the surface enhanced laser desorption/ionization time-of-flight mass spectrometry (SELDI-TOF-MS). Samples were divided into three groups; control human ES cells (n=7), ES cells treated with 8-Br-cAMP (n=7 per each treatment, treated for 3, 6, 9, or 12 days), and cells from which 8-Br-cAMP was withdrawn for 3 days (n=7) or 6 days (n=7) after 8-Br-cAMP treatment for 6 days. Differential expressions between non-decidual control cells and 8-Br-cAMPinduced decidual cells were observed in the peaks of 9787.058 Da, 10115.45 Da, and 24031.25 Da, detected by H4 ProteinChip, and in the peaks of 10833.08 Da, 22440.88 Da, and 32777.38 Da, detected by CM10 ProteinChip. The expression patterns of these decidual markers are expected to provide invaluable information in monitoring cellular development, and further identification of these proteins may hopefully offer precious means for clinical research and therapeutic purposes.     

静脉用人免疫球蛋白在重症甲型流感患儿治疗的临床观察

目的 观察静脉用人免疫球蛋白治疗重症甲型流感患儿的临床疗效.方法 回顾性总结本院2009年8月至2012年12月确诊的24例重症甲型流感患儿病例,随机分为治疗组（12例）和对照组（12例）,对照组予抗感染、抗病毒、雾化吸入等常规治疗,治疗组加于静脉用人免疫球蛋白治疗,对两组患儿疗效进行对照分析.结果 治疗组经治疗后,疗效明显优于对照组,两者比较,差异有统计学意义（P＜0.05）.结论 静脉用人免疫球蛋白治疗儿童甲型流感患儿有显著疗效,值得临床应用推广.     

Stable overexpression of human metallothionein-IIA in a heart-derived cell line confers oxidative protection

Metallothionein (MT) is a metal binding protein and cardioprotective. In order to understand the molecular mechanisms underlying the role of MT in the heart, in the current study we established a stable MT-IIA over-expressing cardiac cell line, and evaluated its anti-oxidative property. Rat heart-derived H9c2 cell line was stably transfected with a vector in which the human MT-IIA gene was placed under the control of the constitutively active β-actin promoter. The transfected cell line (H9c2MT7) exhibited similar growth kinetics and morphology. Western blotting analysis showed that H9c2MT7 had a remarkable increased MT protein level compared with the parent cell line H9c2. Addition of 25 μM ZnSO₄ had an undetectable effect on the induction of endogenous MT, but it likely stabilized the MT protein that is expressed only in H9c2MT7 cells. H9c2MT7 cells showed marked reduction in reactive oxygen species production when exposed to hydrogen peroxide or subjected to hypoxia/reoxygenation challenge evaluated by dihydroethidium staining. In addition, transfection of MT conferred cellular resistance to cadmium toxicity. In summary, we have established a stable human MT-IIA over-expressing cardiac cell line; and this cell line showed a markedly increased oxidative protection and would be useful for dissection of the mechanisms of MT in the cardiac protection.     

人甲型H7N9禽流感全病毒灭活疫苗和裂解疫苗在小鼠中的免疫原性研究

 目的   比较人甲型H7N9禽流感全病毒灭活疫苗和裂解疫苗在小鼠中的免疫原性,为该疫苗的类型选择提供初步依据。 方法   采用相同血凝素含量（5 μg）的H7N9全病毒灭活和裂解疫苗（含或不含氢氧化铝佐剂共4种类型）,分别对BALB/c小鼠进行1针或2针免疫。免疫后,用血凝抑制（hemagglutination inhibition,HI）试验检测血清抗体滴度,比较不同类型疫苗的免疫效果。 结果   小鼠免疫1针全病毒灭活疫苗后,全部血清阳转,HI抗体几何平均滴度（geometric mean titer,GMT）为149;免疫2针后,抗体GMT为243。小鼠免疫1针裂解疫苗后无抗体阳转;免疫2针后全部抗体阳转,GMT为139。两种疫苗添加铝佐剂后,诱导的HI抗体GMT仅略有增加。 结论   H7N9全病毒灭活疫苗在小鼠中的免疫原性较强。在同样类型和剂量的情况下,裂解疫苗需要免疫两次才能达到与全病毒疫苗相同的效果。铝佐剂对免疫原性提升不明显。     

N-Glycosylation during translation is essential for human arylacetamide deacetylase enzyme activity

Human arylacetamide deacetylase (AADAC) can hydrolyze clinical drugs such as flutamide, phenacetin, and rifamycins. AADAC is a glycoprotein, but the role of glycosylation remains unclear. In the present study, we investigated the effect of glycosylation on AADAC enzyme activity. Immunoblot analysis of mutant AADACs that contained an asparagine (N, Asn) to glutamine (Q, Gln) substitution at either residue 78 or 282 (N78Q or N282Q) showed a different migration compared with the wild-type protein. A mutant AADAC that contained N to Q substitutions at both residue 78 and 282 (N78Q/N282Q) showed a similar migration to AADAC in human liver microsomes (HLM) treated with endoglycosidase H (Endo H), which produces deglycosylated proteins. This result indicated that AADAC was glycosylated at both N78 and N282. Mutant types of AADAC with the N282Q and the N78Q/N282Q substitutions showed dramatically lower phenacetin hydrolase activity than did the wild-type protein. The treatment of wild-type AADAC-expressing HuH-7 cells with tunicamycin, which produces unglycosylated protein, decreased AADAC enzyme activity. However, the treatment of the HLM with Endo H caused no decrease of AADAC activity. Thus, the oligosaccharide chain, per se, was not important for AADAC activity in the mature form. The mutant types of AADAC containing the N282Q and the N78Q/N282Q substitutions were not detected by immunoblotting analysis after non-reducing SDS-PAGE, suggesting that the glycosylation of AADAC at N282 was important for proper protein folding. Overall, this study found that the translational, but not post-translational, N-glycosylation of AADAC plays a crucial role in regulating AADAC enzyme activity.