大流行流感与甲型H1N1流感

目的对大流行流感和甲型H1N1进行综述。方法参考国内外近期的有关文献和WHO的相关报道,介绍了流感病毒的基本知识、大流行流感的定义和发展,以及甲型H1N1流感的特点和流行现状等。结果与结论大流行流感具有传播性强、危害大等特点,2009年的甲型H1N1流感为21世纪的第1次大流感,应加以重视。     

海南州首例甲型H1N1流感病例的发现与处置

<正>2009年3月在墨西哥等国家发生的甲型H1N1流感疫情蔓延迅速,已成为全球高度关注的重大公共卫生事件。6月11日世界卫生组织将这次流感流行的警告级别提高到6级[1],2009年5月10日,四川省报告1例甲型H1N1流感疑似病例,被国家确诊为中国内地首例甲型H1N1流感病例[2],2009年9月5日青海省首次确诊为甲型H1N1流感病例[3],2009年9月24日,海南州首次确诊为甲型H1N1流感病例。     

郑州市2009-2010年甲型H1N1流感流行特征分析

目的掌握郑州市2009-2010年甲型H1N1流感流行特点,为控制疫情暴发采取相应措施提供依据。方法收集和分析郑州市2009-2010年报告的全部甲型H1N1流感病例资料。结果两年内全市共报告甲型H1N1流感病例1400例,重症病例168例,死亡14例,发病初期是以境外输入为主,后来在学校内出现聚集性病例,而后从学生向其他人群扩散。重症和死亡病例中,孕妇和患基础性疾病者所占比例较高。结论结合不同阶段的疫情特点采取有针对性的防控措施,起到了较好的控制效果。     

甲型H1N1流感门诊筛查流程实施体会

自2009年4月以来,墨西哥、美国等国家相继发生甲型H1N1流感疫情,4月27日世界卫生组织宣布,此次爆发的甲型H1N1流感可能成为40年来首个世界范围内流感大流行。我国已将甲型H1N1流感纳入《中华人民共和国传染病防治法》规定的乙类传染病,并采取甲类传染病的预防、控制措施,同时将甲型H1N1流感纳入《中华人民共和国国境卫生检疫法》规定的检疫传染病管理。2009年4月30日,按国家卫生部的通知,在佳木斯大学领导的重视和督导下,我院立即建立了发热门诊,开展发热病人的筛查工作。     

贵阳市2009年甲型H1N1流感疫情分析

甲型H1N1流感是一种新型呼吸道传染病,2009年4月首先在墨西哥、美国等地开始流行,随后在全世界迅速传播。我国在5月11日诊断首例输入性甲型H1N1流感病例,疫情在全国快速蔓延。贵阳市9月出现本土病例之后,疫情蔓延。本文对贵阳市2009年甲型H1N1流感疫情进行分析,现将结果报告如下。     

清新县甲型H1N1流感流行因素分析

[目的]通过系统监测调查,及时掌握我县甲型H1N1流感的疫情动态和流行规律,分析其流行因素,为我县完善甲型H1N1流感的防控工作提供科学依据.[方法]在清新县中部、南部、北部地区选择6个镇作为监测点,抽取普通人群静脉血,用酶联免疫试验检测甲型H1N1 IgG抗体进行血清学调查,同时以面对面问卷方式进行流行病学调查.[结果]共调查1325人,甲型H1N1流感抗体阳性190人,阳性率为14.34％;我县甲型H1N1流感病毒感染以轻症患者和隐性感染者为主;生活聚集性人群甲型H1N1IgG抗体高于非聚集人群(P＜0.05),甲型H1N1流感疫苗接种率为2.49％,免疫效果为57.58％;感冒患者就诊率为70.66％;甲型H1N1确诊0例.[结论]疫苗接种率及免疫效果、医疗诊断的准确率、生活聚集人群的易感性、以轻症感染和隐性感染为主的感染状况是影响我县甲型H1N1流感流行的主要因素,应加强人群甲型H1N1流感疫苗的接种,加强对临床医生甲型H1N1流感知识的培训,幼托机构、学校等聚集性场所仍然是我县甲型H1N1流感防控的重点场所.     

某市甲型H1N1流感后流行期防控策略研讨

目的分析汕头市甲型H1N1流感疫情特征,预测流行趋势,研讨防控对策。方法运用描述性流行病学方法,对汕头市2009年至2010年甲型H1N1流感疫情特征进行统计分析,总结不同流行阶段的防控措施,提出后流行期防控策略。结果 2009至2010年汕头市共确诊甲型H1N1流感病例240例,疫情按时间分布可分为输入散发期、社区扩散期、社区流行期、快速下降期和后流行期五个阶段。病例分布在除南澳县之外的6个区县,报告病例集中在主城区。人群分布以6～20岁年龄组(76.25%)和学生(83.02%)为主,男女性别比为1.55∶1。暴发疫情3起,1起发生在中学,2起发生在小学。死亡病例3例,其中1例为幼童,1例伴有基础性疾病。结论根据甲型H1N1流感疫情不同阶段的流行特点,采取不同防控策略,有效控制了甲型H1N1流感疫情传播,汕头市已经进入后流感流行阶段。未来应密切关注甲型H1N1流感抗原基因的重组与变异情况,建立健全各类中小学校和幼托机构的甲型H1N1流感预警机制,提高对低高龄或有基础性疾病人群的甲型H1N1流感疫苗接种率,加强医疗机构救治能力,减少危重病例病死率。     

季节性流感疫苗接种对大流行流感的影响研究

加拿大研究发现,季节性流感疫苗接种增加2009年大流行甲型流感(H1N1)感染的危险性,而澳大利亚研究未能证实这个发现.雪貂实验结果表明,以前的季节性流感感染能防御大流行甲型流感(H1N1),但以前的季节性流感疫苗接种则不能.模型研究显示,流感感染可导致对不同亚型的暂时性免疫.这些观察可以解释加拿大和澳大利亚的不一致发...     

西藏拉萨140例甲型H1N1流感病例的病原学与流行病学分析

目的了解2009年西藏拉萨140例甲型H1N1流感住院病例的病原学特点及流行病学分析,为早期诊断、防控甲型H1N1流感提供依据。方法回顾分析西藏拉萨2009年9月至10月甲型H1N1流感患者的相关信息。结果 140例甲型流感病例全部治愈出院、治愈率达100%。结论在甲型H1N1流感流行时期,如能做到消灭控制传染源、切断传播途径、保护易感者。早期发现、早期隔离、早期治疗,本病病程有自限性,未发生合并症者预后良好.     

甲型H1N1流感暴发流行915例发热病历分析

目的：掌握甲型H1N1流感暴发流行情况,采取有效措施,控制甲型H1N1流感在学校内传播及蔓延。方法：对本校2009年9～12月门诊记录的体温37.5℃以上、以呼吸道症状为主的发热大学生的所有资料进行回顾性调查分析。结果：4个月内本校大学生流感样发热915例,发病率为7.08%;11月为发热高峰期;男生发热人数多与女生,差异有统计学意义;体温多为38.1～39.0℃。结论：要控制甲型H1N1流感在学校流行,必须及时采取隔离传染源、切断传播途径、保护易感人群各项有效可行措施。     

Vascular sphingosine-1-phosphate S1P1 and S1P3 receptors

The sphingolipid sphingosine-1-phosphate (S1P) acts on five subtypes of G-protein- coupled receptors, termed S1P(1) (formerly endothelial differentiation gene-1 [Edg-1]), S1P(2) (Edg-5), S1P(3) (Edg-3), S1P(4) (Edg-6) and S1P(5) (Edg-8), and possibly several other "orphan" receptors, such as GPR3, GPR6 and GPR12. These receptors are coupled to different intracellular second messenger systems, including adenylate cyclase, phospholipase C, phosphatidylinositol 3-kinase/protein kinase Akt, mitogen-activated protein kinases, as well as Rho- and Ras-dependent pathways. Consistently with this receptor multiplicity and pleiotropic signaling mechanisms, S1P influences numerous cell functions. S1P(1)1, S1P(2) and S1P(3) receptors are the major S1P receptor subtypes in the cardiovascular system, where they mediate the effects of S1P released from platelets, and possibly other tissues (such as brain). Thus S1P(1) and S1P(3) receptors enhance endothelial and vascular smooth muscle cell proliferation and migration, playing a key role in developmental and pathological angiogenesis. In contrast, S1P(2) receptors inhibit migration of these cell types, probably because of their unique stimulatory effect on a GTPase-activating protein inhibiting the activity of Rac. S1P receptors can also cause relaxation and constriction of blood vessels. The former effect is mediated by pertussis toxin-sensitive receptors (possibly S1P(1)) located on the endothelium and stimulating phosphatidylinositol 3-kinase/Akt/endothelial nitric oxide synthase (eNOS). The vasoconstricting effect of S1P is likely to be mediated by S1P(2) and/or S1P(3) receptors, via Rho-Rho-kinase, and is more potent in coronary and cerebral blood vessels. Finally, S1P also protects endothelial cells from apoptosis through activation of phosphatidylinositol 3-kinase/Akt/eNOS via S1P(1) and S1P(3) receptors. The variety of these effects, taken together with the existence of multiple receptor subtypes, provides an abundance of therapeutic targets that currently still await the development of selective agents.     

Antimykobakterielle 1-Phenyl-1-alkylaminoalkane

Antimycobacterial 1-Phenyl-1-alkylaminoalkanes Synthesis and testing for antimycobacterial properties (M. tuberculosis H 37 Ra, Middlebrook-7H9-broth) of 1-phenyl-1-alkylaminoalkanes, which differ from antimycobacterial N-alkylbenzylamines by an additional alkyl chain in α-position, is described. By variation of both alkyl chains and introduction of one or two Cl-substituents in the aromatic ring the activity increases up to an optimum within the homologous series. Overstepping optimal lipophilicity or ramification of the alkyl chains decrease activity. Compounds 19, 20, 33-35, 51-53, 61-63, 65-67, 70-73, 96 and 102 - 104 inhibit the growth of M. tuberculosis in concentrations of 2 to 4 μg/ml.     

Sulfation of iodothyronines by human sulfotransferase 1C1 (SULT1C1)*

Sulfation is an important component of human thyroid hormone metabolism. The role of the human sulfotransferase 1C1 (SULT1C1) is not known. Because SULT1C1 is present in the adult thyroid, intra-thyroidal sulfation of thyroid hormones and their metabolites might occur. We tested this hypothesis by determining the ability of recombinant human SULT1C1 to catalyze iodothyronine sulfation. Apparent K(m) values for 3,3',5-triiodothyronine (T(3)), 3, 3'-diiodothyronine (3,3'-T(2)), 3',5',3-triiodothyronine (rT(3)), and 3,3',5,5'-tetraiodothyronine (T(4)) with SULT1C1 were 28.7, 10.3, 10.2, and 59.3 microM, respectively. Thermal stability and responses to inhibitors also were tested with T(3) as the substrate. Enzyme aliquots were measured simultaneously to determine SULT1C1 substrate preferences at optimal iodothyronine concentrations. SULT1C1 activity obtained with T(3) was used as 100%, and the activities with 3,3'-T(2), rT(3), T(4), and 3,5-diiodothyronine (3, 5-T(2)) were 614, 314, 25, and 4%, respectively. We report for the first time the characterization of human SULT1C1 with T(3) and the preferences of the enzyme for various iodothyronines. The presence of SULT1C1 in the adult thyroid gland raises the possibilities that the enzyme can contribute to intraglandular thyroid hormone processing and iodide reutilization.     

Phenotype of the Cyp1a1/1a2/1b1-/- triple-knockout mouse

Crossing the Cyp1a1/1a2(-/-) double-knockout mouse with the Cyp1b1(-/-) single-knockout mouse, we generated the Cyp1a1/1a2/1b1(-/-) triple-knockout mouse. In this triple-knockout mouse, statistically significant phenotypes (with incomplete penetrance) included slower weight gain and greater risk of embryolethality before gestational day 11, hydrocephalus, hermaphroditism, and cystic ovaries. Oral benzo[a]pyrene (BaP) daily for 18 days in the Cyp1a1/1a2(-/-) produced the same degree of marked immunosuppression as seen in the Cyp1a1(-/-) mouse; we believe this reflects the absence of intestinal CYP1A1. Oral BaP-treated Cyp1a1/1a2/1b1(-/-) mice showed the same "rescued" response as that seen in the Cyp1a1/1b1(-/-) mouse; we believe this reflects the absence of CYP1B1 in immune tissues. Urinary metabolite profiles were dramatically different between untreated triple-knockout and wild-type; principal components analysis showed that the shifts in urinary metabolite patterns in oral BaP-treated triple-knockout and wild-type mice were also strikingly different. Liver microarray cDNA differential expression (comparing triple-knockout with wild-type) revealed at least 89 genes up- and 62 genes down-regulated (P-value < or = 0.00086). Gene Ontology "classes of genes" most perturbed in the untreated triple-knockout (compared with wild-type) include lipid, steroid, and cholesterol biosynthesis and metabolism; nucleosome and chromatin assembly; carboxylic and organic acid metabolism; metal-ion binding; and ion homeostasis. In the triple-knockout compared with the wild-type mice, response to zymosan-induced peritonitis was strikingly exaggerated, which may well reflect down-regulation of Socs2 expression. If a single common molecular pathway is responsible for all of these phenotypes, we suggest that functional effects of the loss of all three Cyp1 genes could be explained by perturbations in CYP1-mediated eicosanoid production, catabolism and activities.     

间质作用因子1通过正调控窖蛋白1抑制FBJ-S1-H的迁移性

目的证明间质作用因子(stromal interaction molecule1,Stim1)在FBJ诱导的小鼠骨肉瘤细胞中的抑癌作用。方法在Stim1高表达的FBJ-S1-H细胞采用Stim1以siRNA干扰技术得到Stim1沉默的几株S1-H单克隆细胞株,通过细胞行为学方法和RT-PCR技术对其mRNA进行研究,通过明胶酶谱法对细胞基质金属酶活性进行研究。结果通过细胞行为学方法证明,Stim1的沉默提高了细胞的迁移性,通过对mRNA表达的研究发现,Stim1沉默引起了多种基因表达的变化,其中包括基质金属酶9(matrix mexalloprotelnase 9,MMP-9)的升高,窖蛋白(caveolinl,Cav1),甾醇调控因子Srebf1的降低等,提高单克隆细胞中的Cav1含量可以使细胞迁移性降低。结论实验结果证明在FBJ-S1-H细胞中,Stim1能够抑制细胞的移动性,沉默Stim1的表达能够提高细胞的迁移性。