重症H1N1流感的护理问题及相关支持

2009年3月,墨西哥暴发＂人感染猪流感＂疫情,并迅速在全球范围内蔓延。世界卫生组织（WHO）初始将此型流感称为＂人感染猪流感＂,后将其更名为＂甲型H1N1流感＂。我国从2009年9月“甲流”呈明显上升趋势,河南省平顶山市也不例外,我科为我市定点收治“甲流”单位,从2009年9月开始收治发热待查患者,从2009年10月成立“甲流”病区,收治确诊甲型H1N1流感患者。     

甲型H1N1流感危重症患者的护理体会

2009年，随着甲型H1N1流感（以下简称“甲流”）疫情在我国各地陆续发生，我区也于9月出现了“甲流”疫情。与许多内地城市情况不同，     

西藏首例甲型H1N1流感死因浅析及启示

2009年3月以来,全球许多国家出现甲型H1N1流感暴发流行,包括我国在内也相继出现暴发流行,甚至引起人类死亡。2009年10月4日,西藏墨竹工卡县发生首例甲型H1N1流感（以下简称“甲流”）死亡病例,这也是我国报告的首例死于“甲流”的病例。为总结经验,及时发现“甲流”重症和危重症病例,减少病死率,现将死亡病例的死亡经过报告如下,并对死因作初步分析。     

甲型H1N1流感的抗病毒治疗

2009年4月初,甲型H1N1流感开始在墨西哥和美国出现,2009年6月11日WHO将甲型H1N1流感大流行警告级别提升至6级,表明此次流感疫情已经进入大流行阶段,目前,甲型H1N1流感正在令球流行.     

有效应对甲型H1N1流感的一些启示

自2009年3月以来，一种新型呼吸道传染病在墨西哥暴发，随即在世界范围内传播，使众多民众受到感染甚至危及了生命。经研究确定，引发本次疫情的病原为新型甲型流感病毒，世界卫生组织将其命名为“甲型H1N1流感”（以下简称“甲流”）。     

重症甲型H1N1流感32例临床分析

<正>2009年3月,墨西哥、美国爆发甲型H1N1流感,之后疫情迅速蔓延。截至2009年12月27日,共有超过208个国家和地区向世界卫生组织(WHO)报告了经实验室确诊的甲型H1N1流感病例,超过12220人死亡。作为嘉兴市定点医院,我院自2009年11月17日至2010年1月10日收治了32例甲型H1N1流感重症及危重症病例,在第一时间给予规范     

H1N1与肥胖

随着甲型H1N1流感在全球的肆虐,各国防控“甲流的”措施空前严密,各类高危人群纷纷被纳入重点保护对象。在卫生部公布的《甲型H1N1流感诊疗方案（2009年第三版）》中,首次将肥胖者列为甲流重症高危人群。     

儿童甲型H1N1流感重症病例早期诊断及救治策略

自2009年3月墨西哥暴发“人感染猪流感”疫情以来，迅速在全球蔓延，世界卫生组织（WHO）后将其更名为“甲型H1N1流感”，并于6月11日宣布将警戒级别提升为6级，预示全球进入流感大流行阶段。我国卫生部高度重视甲型H1N1流感在国内的有效防控，但至9月入秋后国内疫情发生重大变化，     

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。     

新型H1N1流感实验室检测方法

2009年3月,墨西哥暴发“人感染猪流感”疫情,并迅速在全球范围内蔓延。世界卫生组织（WHO）初始将此型流感称为“人感染猪流感”,后将其更名为“甲型H1N1流感”。6月11日,     

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。