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Hantaan virus was discovered in Korea during the 1970s while other similar viruses were later reported in Asia and Europe. There was no information about hantavirus human infection in the Americas until 1993 when an outbreak was described in the United States. This event promoted new studies to find hantaviruses in the Americas. At first, many studies were conducted in Brazil, Argentina, Chile, Uruguay and Paraguay, while other Latin American countries began to report the presence of these agents towards the end of the 20th century. More than 30 hantaviruses have been reported in the Western Hemisphere with more frequent cases registered in the southern cone (Argentina, Chile, Uruguay, Paraguay, Bolivia and Brazil). However there was an important outbreak in 2000 in Panama and some rare events have been described in Peru, Venezuela and French Guiana. Since hantaviruses have only recently emerged as a potential threat in the tropical zones of the Americas, this review compiles recent hantavirus reports in Central America, the Caribbean islands and the northern region of South America. These studies have generated the discovery of new hantaviruses and could help to anticipate the presentation of possible future outbreaks in the region.  相似文献   
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目的 探讨丹参多酚酸(Salvianolate Acid,SAL)和三七总皂苷(Panax Notoginseng Saponins,PNS)合用保护氧糖剥夺/复氧复糖(Oxygen-Glucose Deprivation/Reoxygenation,OGD/R)损伤后星形胶质细胞线粒体、促进神经营养因子表达的作用及机制。方法 大鼠星形胶质细胞原代培养,建立OGD/R损伤模型。Cell counting kit-8(CCK-8)法检测星形胶质细胞活力,流式细胞仪检测活性氧(reactive oxygen species,ROS)释放量、胞内Ca2+ 浓度、线粒体膜电位(mitochondrial membrane potential,MMP)变化,实时定量PCR(real time polymerase chain reaction,RT-PCR)和蛋白质免疫印迹(western blot,WB)法检测HIF-1α、PI3K/Akt/mTOR信号通路蛋白及脑源性神经营养因子(brain-derived neurotrophic factor,BDNF)、神经生长因子(nerve growth factor,NGF)、胰岛素样生长因子(insulin-like growth factors,IGF-1α)的表达情况。结果 胶质细胞OGD/R条件确定为OGD4h/R24h,给药浓度确定为SAL 25 μg·mL-1、PNS 6.25 μg·mL-1。与OGD/R组相比,SAL 25 μg·mL-1、PNS 6.25 μg·mL-1、SAL 25 μg·mL-1与PNS 6.25 μg·mL-1合用均能增强损伤后星形胶质细胞活力(P<0.05),升高MMP,降低ROS释放量(P<0.05),降低损伤后星形胶质细胞HIF-1α蛋白和mRNA的表达,升高磷脂酰肌醇激酶(PI3K)磷酸化水平(P<0.05);SAL还可升高mTOR蛋白磷酸化水平(P<0.05),PNS可提高Akt磷酸化水平(P<0.05),增加损伤星形胶质细胞BDNF mRNA 表达(P<0.05);SAL、SAL与PNS合用能增加损伤后星形胶质细胞 BDNF、NGF、IGF-1α mRNA 表达(P<0.05)。结论 丹参多酚酸和三七总皂苷组分合用可保护OGD/R损伤后星形胶质细胞线粒体、促进胶质细胞表达神经营养因子BDNF、NGF、IGF-1α。  相似文献   
998.
This study tested a recently proposed “Basal Cell Shrinkage” hypothesis of pemphigus acantholysis through a quantitative analysis of individual and cooperative effects of pemphigus vulgaris (PV) IgG, Fas-ligand (Fas-L) and tumor necrosis factor-α (TNFα) on keratinocyte (KC) volume (i.e. cell size) and adhesive properties. Exposure of KC monolayers and MatTek EpiDermFT? tissues cultures to the physiologic concentrations of Fas-L, TNFα or IgGs from two PV patients resulted in various degrees of reversible changes, which were not observed in control cultures either exposed to normal IgG or left intact. Within 12–24 h of exposure, basal cells in experimental cultures lost their ability to form stress fibers, retracted cytoplasmic aprons and formed keratin aggregates, indicating that their cytoskeleton collapsed. The cell volume decreased significantly (p < 0.05) as the polygonal cell shape changed to a round one. The shrunk cells detached from their neighbors and the substrate, resulting in a reciprocal increase of both the areas of acantholysis and the number of detached KCs, respectively. Since in the skin of PV patients, KCs are targeted by autoantibodies concomitantly with being exposed to autocrine and paracrine pro-apoptotic and pro-inflammatory cytokines, we combined PV IgG with Fas-L and/or TNFα in the cell culture experiments. This amplified several fold an ability of PV IgG to cause basal cell shrinkage and detachment. The obtained results demonstrated for the first time that PV IgG works together with Fas-L and TNFα to induce acantholysis via basal cell shrinkage, which provides a novel mechanism explaining successful treatment of PV patients with TNFα inhibitors.  相似文献   
999.
After the 2011 declaration of rinderpest disease eradication, we surveyed 150 countries about rinderpest virus stocks. Forty-four laboratories in 35 countries held laboratory-attenuated strains, field strains, or diagnostic samples. Vaccine and reagent production and laboratory experiments continued. Rigorous standards are necessary to ensure that stocks are kept under safe conditions.  相似文献   
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BackgroundIndividuals with cystic fibrosis (CF) have difficulty maintaining optimal vitamin D status due to pancreatic insufficiency-induced malabsorption, inadequate sunlight exposure, and poor intake of vitamin D containing foods. Vitamin D deficiency may increase the risk of pulmonary exacerbations of CF. The objective of this study was to assess factors impacting vitamin D status in patients with CF recently hospitalized for a pulmonary exacerbation of CF.MethodsThis was a pre-planned analysis of vitamin D intake in patients enrolled in a multi-center, double-blind, randomized controlled study examining vitamin D therapy for pulmonary exacerbation of CF. Demographic information, responses from a habitual sun exposure questionnaire and food frequency questionnaire, and vitamin D supplement usage were queried and compared to serum 25-hydroxyvitamin D (25(OH)D) concentrations.ResultsA total of 48 subjects were included in this analysis. Subjects were taking approximately 1,200 IU of vitamin D daily. Reported vitamin D intake, age, race, employment, and education were not significantly associated with vitamin D status in this population. However, smoking status, sunlight exposure in the last 3 years, and skin type (in the bivariate model) were all significantly associated with vitamin D status (all p<0.05).ConclusionsSunlight exposure was the most predictive determinant of vitamin D status in patients with CF prior to pulmonary exacerbation. Subjects reported vitamin D intake below the recommended amounts. The role and mode of optimizing vitamin D status prior to a pulmonary exacerbation needs further investigation.  相似文献   
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