甲型H1N1流感的预防

<正>甲型H1N1流感(猪流感)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,墨西哥和美国等国家先后发生人感染新型猪流感病毒疫情。甲型H1N1流感可以人传染人,其传染途径与季     

甲型H1N1流感56例临床分析

甲型H1N1流感为一种新型呼吸道传染病,其病原为新型甲型H1N1流感病毒,病毒基因中包含猪流感、禽流感和人流感3种流感病毒的基因片段,临床表现通常为流感样症状,可发生病毒性肺炎等并发症。本研究收集了我院收治的56例甲型H1N1流感确诊病例,现分析总结如下。     

甲型H1N1流感确诊和疑似病例194例临床诊断分析

甲型H1N1流感是甲型流感的一个亚型，曾在人类历史上造成大规模流行和病人的死亡，2009年春季源于墨西哥的甲型H1N1流感在中国及世界范围内流行，此次流行引起中国10万人以上的感染，近千人死亡，探讨甲型H1N1流感的诊断规律，流行的特点很有意义。     

甲型H1N1流感诊疗方案（2009年第三版）

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,WHO宣布将甲型H1Nl流感大流行警告级别提升为6级,全球进入流感大流行阶段。此次流感为一种新型呼吸道传染病,其病原为新甲型H1N1流感病毒株,病毒基因中包含有猪流感、禽流感和人流感三种流感病毒的基因片段。     

178例甲型H1N1流感临床分析

2009年3月,墨西哥暴发“人感染猪流感”（后更名为甲型H1N1流感）疫情,并迅速在全球范围内蔓延。6月11日,WHO宣布全球进入甲型H1N1流感大流行阶段,截至10月底我国内地31个省市自治区累计报告甲型H1N1流感确诊病例44981例,已治愈33184例。重症病例累计82例,已治愈29例,死亡6例。目前甲型H1N1流感的全部临床表现尚不明确。现将我院收治的甲型H1N1流感确诊患者178例分析如下。     

甲型H1N1流感流行对输血行业的影响

2009年4月暴发的甲型H1N1流感(简称甲型流感)在人和人之间的快速传播,引发了全球公共卫生的高度关注.2009年6月11日,世界卫生组织(WHO)将疫情升至Ⅵ级警告级别,标志着全球"流感大流行的到来".甲型流感流行,对采供血机构及医疗机构各自从事的工作造成不可避免的冲击,为此,了解甲型流感的诊断与治疗的研究动态,将对疾病流行期间开展的采供血与临床输血工作有很好的指导意义.     

1例重症甲型H1N1流感患者的护理体会

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".2009年6月11日,WHO宣布将甲型H1N1流感大流行警告级别提升为6级,全球进入流感大流行阶段.卫生部通报,2010年1月11日~17日,境内31个省份报告甲型H1N1流感确诊病例1 556例,住院治疗348例,死亡27例.2009年12月4日,我院收治1例甲型H1N1流感(危重症)合并重症肺炎、皮下气肿患者,经机械通气、补液抗炎支持治疗,逐步好转,现将护理体会报道如下.     

甲型H1N1流感危重症2例临床分析

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,WHO宣布将甲型H1N1流感大流行警告级别提升为6级,全球进入流感大流行阶段.此次流感为一种新型呼吸道传染病,其病原为新甲型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.我国大部分省份自2009年5月起新型甲型H1N1流行性感冒暴发流行,疫情迅速蔓延.我国卫生部通报指出:截至2009年12月31日,全国31个省份累计报告甲流确诊病例12万余例,治愈11万例,死亡648例.2009年11月20日至12月15北京市京煤集团总医院收治甲型H1N1流感危重症2例,现将临床特点及治疗体会结合文献复习报道如下,以期为今后的甲型H1N1流感危重症救治工作积累经验.     

216例轻症甲型H1N1流感病例分析

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。此次流感为一种新型呼吸道传染病,其病原为新甲型H1N1流感病毒,病毒基因中包含有猪流感、禽流感和人流感三种流感病毒的基因片段。世界卫生组织（WHO）初始将此型流感称为“人感染猪流感”,后将其重新命名为“甲型H1N1流感”。本院2009年7月31日至2009年10月21日共收治北京市朝阳区确诊的216例轻症甲型H1N1流感患者。现将患者资料分析如下。     

孕产期妇女甲型H1N1流感防治进展

与季节性流感和历次流感大流行相似,甲型H1N1流感大流行过程中,孕妇感染甲型H1N1流感的风险增高,孕妇甲型H1N1流感的患病率、病死率增高,易继发严重并发症.因此,基于疗效-风险评估,无接种禁忌证的孕妇,妊娠各期均应接种甲型H1N1流感疫苗.出现流感样症状或与甲型H1N1流感患者密切接触的孕妇,都应接受神经氨酸酶抑制剂(更推荐奥司他韦)治疗或预防,无需等待实验室检查结果证实甲型H1N1流感感染.感染甲型H1N1流感的哺乳产妇,神经氨酸酶抑制剂对接受授乳的婴儿是安全的.甲型H1N1流感流行期间,孕妇应采取非药物预防措施,降低感染甲型H1N1流感的风险.     

Shh、Ptch、Gli1与CyclinB1-CDK1在肝癌发生发展过程中的改变

目的观察大鼠诱发肝癌过程中Shh信号通路相关蛋白及细胞周期蛋白的表达变化,探讨其在肝癌发生发展过程中的作用。方法利用二乙基亚硝胺(DEN)制备诱发性大鼠肝癌模型,通过HE染色观察肝组织的形态学变化,应用免疫组织化学方法检测Shh、Ptch、Gli1、CyclinB1、CDK1蛋白在诱发性肝癌发生过程中的表达变化。结果根据HE染色结果将实验动物分为正常对照组、肝细胞损伤期、肝细胞增生-硬化期和肝细胞癌变期。Shh、Ptch、Gli1蛋白阳性表达细胞主要分布在增生结节、癌结节、小叶间胆管上皮细胞和癌周组织中,其阳性表达率均随肝癌发生发展过程逐渐增高的趋势;CyclinB1和CDK1阳性表达的细胞主要分布于门管区、肝小叶的周边及癌结节内,在肝细胞增生-硬化期和肝细胞癌变期大鼠肝组织中表达均高于正常对照组。结论 Shh信号通路被激活后,可通过影响CyclinB1和CDK1蛋白的表达促进细胞G2/M期转变,完成有丝分裂,导致细胞失控性增殖,促进肝癌的发生发展。     

Anti-Sc1 in pregnancy

Anti-Sc1 was detected in a gravida-2 patient at 12 weeks' gestation. At 29 weeks, the antibody was found to be of the IgG3 subclass with a titer of 16, score 36, by the indirect antiglobulin test, and it produced 7 percent lysis by antibody-dependent cellular cytotoxicity (ADCC) assay, a finding that suggested an unaffected fetus. The titer remained constant throughout the pregnancy, as did the IgG subclass and activity in the ADCC assay. At delivery of the full-term infant, the cord hemoglobin was 13.5 g per dL and the direct antiglobulin test was positive (3+) with anti-IgG. The infant did not require transfusion. A sample taken 9 weeks after delivery showed 44 percent lysis in the ADCC assay. The anti-Sc1 titer was 32, score 65.     

A novel role of sphingosine 1-phosphate receptor S1pr1 in mouse thrombopoiesis

Millions of platelets are produced each hour by bone marrow (BM) megakaryocytes (MKs). MKs extend transendothelial proplatelet (PP) extensions into BM sinusoids and shed new platelets into the blood. The mechanisms that control platelet generation remain incompletely understood. Using conditional mutants and intravital multiphoton microscopy, we show here that the lipid mediator sphingosine 1-phosphate (S1P) serves as a critical directional cue guiding the elongation of megakaryocytic PP extensions from the interstitium into BM sinusoids and triggering the subsequent shedding of PPs into the blood. Correspondingly, mice lacking the S1P receptor S1pr1 develop severe thrombocytopenia caused by both formation of aberrant extravascular PPs and defective intravascular PP shedding. In contrast, activation of S1pr1 signaling leads to the prompt release of new platelets into the circulating blood. Collectively, our findings uncover a novel function of the S1P–S1pr1 axis as master regulator of efficient thrombopoiesis and might raise new therapeutic options for patients with thrombocytopenia.Billions of anucleated platelets circulate in mammalian blood to prevent blood loss in case of tissue injury. The lifespan of platelets is short (4–6 d in mice and 5–9 d in humans; Leeksma and Cohen, 1955; Robinson et al., 2000); as a consequence, several million platelets have to be produced every hour to maintain their physiological blood counts and to avoid the risk of bleeding. In mammals, platelets are generated in BM from megakaryocytes (MKs), polyploid, terminally differentiated myeloid cells with a typical morphology and diameters of up to 100 µm.The production of platelets from MKs involves several sequential developmental and maturation steps. MKs develop from hematopoietic stem and progenitor cells, which give rise to an increasingly restricted lineage culminating in the formation of megakaryocytic precursors that generate MKs. During their differentiation and maturation, MKs localize to the perivascular niche, where they interact with sinusoidal BM endothelial cells (Avecilla et al., 2004; Patel et al., 2005a). Once they have settled in the perivascular microenvironment, mature MKs form dynamic transendothelial pseudopods, which extend into the lumen of BM sinusoids. These intravascular pseudopodial extensions, termed proplatelets (PPs), continue to elongate and become tapered into multiple platelet-size beads connected to each other and with their maternal MKs by thin cytoplasmic bridges (Italiano et al., 1999; Patel et al., 2005a). The release of platelets, the final step of platelet formation, then occurs within the blood, where new platelets are shed as fragments from the tips of intravascular PPs (Stenberg and Levin, 1989; Choi et al., 1995; Italiano et al., 1999; Junt et al., 2007).MKs are a rare cell population, constituting <0.01% of all BM cells. This contrasts with the high demand of platelet production, implying that the differentiation of MKs (termed megakaryocytopoiesis) and the subsequent assembly and release of platelets by MKs (termed thrombopoiesis) are highly efficient and tightly controlled processes. Among the factors that modulate megakaryocytopoiesis, thrombopoietin (TPO) is the major regulator of MK expansion from hematopoietic stem and progenitor cells, whereas chemokines, including stromal-derived factor-1 (SDF-1), primarily initiate the relocation of maturing MKs to the perivascular microenvironment (Avecilla et al., 2004). In contrast, the molecular pathways that control the final steps of thrombopoiesis, particularly the guidance signals that direct megakaryocytic pseudopodial extensions into the vascular lumen and trigger the intravascular release of new platelets, are entirely unknown.The bioactive sphingolipid sphingosine 1-phosphate (S1P) and the receptors responsive to this mediator regulate important biological functions of various hematopoietic cell types (Spiegel and Milstien, 2003, 2011; Schwab et al., 2005; Massberg et al., 2007), including cell migration in the BM compartment (Ishii et al., 2009; Allende et al., 2010). Here we report that S1P and the MK S1P receptor S1pr1 receptor are indispensable for normal BM thrombopoiesis. Using mouse mutants and by multiphoton intravital microscopy (MP-IVM), we demonstrate that a transendothelial S1P gradient navigates megakaryocytic PP extensions into the lumen of BM sinusoids. In the blood, PP extensions are exposed to high S1P concentrations, which initiate the subsequent shedding of platelets into the circulation. Both processes involve the S1P receptor S1pr1, triggering activation of the Gi/Rac GTPase signaling. Correspondingly, lack of S1pr1 on MKs, but not of other S1P receptors, results in severe thrombocytopenia. Thus, we have identified the S1P–S1pr1 pathway as a key nodal point integrating guidance cues that navigate directional PP elongation and enabling the final step of thrombopoiesis, the shedding of new platelets into the blood stream.     

STAT1 promotes megakaryopoiesis downstream of GATA-1 in mice

Thrombocytosis is associated with inflammation, and certain inflammatory cytokines, including IFN-gamma, stimulate megakaryocyte and platelet production. However, the roles of IFN-gamma and its downstream effector STAT1 in megakaryocyte development are poorly understood. We previously reported that STAT1 expression was significantly downregulated in Gata1-knockdown murine megakaryocytes, which also have impaired terminal maturation. Here, we show that ectopic expression of STAT1, or its target effector IRF-1, rescued multiple defects in Gata1-deficient megakaryopoiesis in mice, inducing polyploidization and expression of a subset of platelet-expressing genes. Enforced expression of STAT1, IRF-1, or GATA-1 enhanced phosphorylation of STAT1, STAT3, and STAT5 in cultured Gata1-deficient murine megakaryocytes, with concomitant megakaryocyte maturation. In contrast, enhanced thrombopoietin signaling, conferred by enforced expression of constitutively active JAK2 or c-MPL, induced phosphorylation of STAT3 and STAT5, but not STAT1, and failed to rescue megakaryocyte maturation. Finally, megakaryocytes from Stat1(-/-) mice were defective in polyploidization. Together, these findings reveal a unique role for STAT1 in megakaryopoiesis and provide new insights into how GATA-1 regulates this process. Our studies elucidate potential mechanisms by which various inflammatory disorders can cause elevated platelet counts.