高原地区重症和危重症甲型H1N1流感患者心理护理体会

甲型H1N1流感是由甲型H1N1流感病毒引起的一种新型急性呼吸道传染病,病毒基因中包含有猪流感、禽流感和人流感3种流感病毒的基因片段。人群普遍易感,甲型H1N1流感患者为主要传染源。该病主要通过飞沫经呼吸道传播,通常表现为流感样症状,体征主要包括咽部充血和扁桃体肿大,     

大学校园内甲型H1N1流感的护理及预防

甲型H1N1流感是一种由新的甲型H1N1流感病毒引起的急性呼吸道传染病,其病原体是一种新型的甲型H1N1流感病毒,在人群中传播。与以往或目前的季节性流感病毒不同,该病毒毒株包含有猪流感、禽流感和人流感3种流感病毒的基因片段。人群对甲型H1N1流感病毒普遍易感,并可以人传染人,人感染甲型H1N1流感后的早期症状与普通流感相似,包括发热、咳嗽、喉痛、身体疼痛、头痛、发冷和疲劳等,有些还会出现腹泻或呕吐、肌肉痛或疲倦、眼睛发红等^[1]。     

重症甲型H1N1流感1例临床分析

甲型H1N1流感为一种新型呼吸道传染病,其病原菌为新甲型H1N1流感病毒株,病毒基因中包含有猪流感、禽流感和人流感3种流感病毒的基因片段。2009年12月我院收治了重症甲型H1N1流感患儿1例,现将该病的救治与药学监护报道如下。     

甲型H1N1流感116例治疗及临床护理体会

甲型H1N1流感是由新型甲型H1N1流感病毒引起的一种新型呼吸道传染病。2009年10～12月我院传染病区收治甲型H1N1流感116例,现将治疗及护理体会报道如下。     

甲型H1N1流感疑似病例的治疗与护理

甲型H1N1流感为急性呼吸道传染病,其病原体是一种新型的甲型H1N1流感病毒。在人群中传播,普遍易感,并且可以人传染人。人感染甲型H1N1后的早期症状与普通流感相似,包括发热、咳嗽、喉痛、身体疼痛、发热和疲劳等。有些人还会出现腹泻或呕吐,肌肉痛或疲倦眼睛发红等。     

甲型H1N1流感中医药预防方案(2009版)

甲型H1N1流感是甲型(A型)流感病毒引起的猪或人的一种急性、人畜共患呼吸道传染性疾病。2009年3月墨西哥和美国等先后发生人感染甲型H1N1流感病毒,人感染甲型H1N1流感后的临床早期症状与流感类似,有发烧、咳嗽、疲劳、食欲不振等,还可以出现腹泻和呕吐等症状。病情可迅速进展,突然高热、肺炎,重者可以出现呼吸衰竭、多器官损伤,导致死亡。     

甲型H1N1流感疫苗预防接种的护理

甲型H1N1流感为急性呼吸道传染病,与以往或目前的季节性流感病毒不同,该病毒毒株包含有猪流感、禽流感和人流感三种流感病毒的基因片段.人群对甲型H1N1流感病毒普遍易感,人感染甲流后的早期症状与普通流感相似,包括发热、咳嗽、喉痛、身体疼痛、头痛和疲劳等,有些还会出现腹泻或呕吐、肌肉痛或眼睛发红等.其发病突然、蔓延迅速,常引起地方性甚至全球性大流行.     

甲型H1N1流感简介

甲型H1N1流感是一种新型流感病毒,且能够传染人,通过呼吸道传播,临床主要表现为流感样症状,多数患者症状比较轻。病毒对奥司他韦和扎那米韦敏感,早发现、早诊断是防控与治疗的关键。     

预防流感，远离病毒侵扰

甲型H1N1流感为急-陛呼吸道传染病，其病原体是一种新型的甲型H1N1流感病毒，早期被称为猪流感。与以往或目前的季节性流感病毒不同。该病毒毒株包含有猪流感、禽流感和人流感三种流感病毒的基因片段。人群对甲型H1N1流感病毒普遍易感，并可以人传染人，人感染甲流后的早期症状与普通流感相似，包括发热、咳嗽、咽痛、身体疼痛、头痛、发冷和疲劳等。有些还会出现腹泻或呕吐、肌肉痛或疲倦、眼睛发红等。     

县级医院甲型H1N1流感预防控制管理体会

甲型H1N1流感是一种新型甲型H1N1流感病毒引起的急性呼吸道传染病,可通过近距离飞沫和接触传播。临床早期症状与流感类似,重者可以出现呼吸衰竭、多器官损伤,导致死亡。我院是一所综合性医院,是我县唯一收治甲型H1N1流感病人的定点医院。为有效应对甲型H1N1流感疫情,全力做好甲型H1N1流感患者的医疗救治和防止医院感染,我院认真落实国家有关甲型H1N1流感防治工作的精神,扎实做好各项防范应对措施,成功救治一名甲型H1N1流感确诊病例,无二代病例的发生。     

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。