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961.
Deferral for low hemoglobin is not associated with increased risk of infection in Danish blood donors 下载免费PDF全文
962.
Sushma Dahal Melinda Jenner Linh Dinh Kenji Mizumoto Cecile Viboud Gerardo Chowell 《Annals of epidemiology》2018,28(5):273-280
Purpose
Our understanding of the temporal dynamics and age-specific mortality patterns of the 1918–1921 influenza pandemic remains scarce due to lack of detailed respiratory mortality datasets in the United States and abroad.Methods
We manually retrieved individual death records from Arizona during 1915–1921 and applied time series models to estimate the age specific mortality burden of the 1918–1921 influenza pandemic. We estimated influenza-related excess mortality rates and mortality rate ratio increase over baseline based on pneumonia and influenza (P&I), respiratory, tuberculosis and all-cause death categories.Results
Based on our analysis of 35,151 individual mortality records from Arizona, we identified three successive pandemic waves in spring 1918, fall 1918–winter 1919 and winter 1920. The pandemic associated excess mortality rates per 10,000 population in Arizona was estimated at 83 for P&I, 86 for respiratory causes, 84 for all-causes and 9 for tuberculosis. Age-specific P&I and tuberculosis excess death rates were highest among 25- to 44-year-olds and individuals ≥65 years, respectively. The 25- to 44-year-olds and 5- to 14-year-olds had highest P&I and tuberculosis mortality impact respectively when considering the ratio over background mortality.Conclusions
The 1918–1921 influenza pandemic killed an estimated 0.8% of the Arizona population in three closely spaced consecutive waves. The mortality impact of the fall 1918 wave in Arizona lies in the upper range of previous estimates reported for other US settings and Europe, with a telltale age distribution of deaths concentrated among young adults. We identified a significant rise in tuberculosis-related mortality during the pandemic, lending support to the hypothesis that tuberculosis was a risk factor for severe pandemic infection. Our findings add to our current understanding of the mortality impact of this pandemic in the US and globally. 相似文献963.
964.
目的:观察从脐血中提取的树突状细胞负载热休克蛋白70-肿瘤抗原肽复合物的细胞表面表型特点及其所激活的细胞毒T淋巴细胞的杀伤活性。方法:实验于2003-10/2005-12在解放军军事医学院兽医研究所完成。①脐血来源于长春市妇产医院足月顺产的非高危妊娠产妇,要求无急慢性感染及血液系统疾病,产妇及其家属均签署知情同意书。热休克蛋白70由本室制备纯化。人骨肉瘤细胞Saos-2(北京肿瘤研究所,批号222RXB013538)。②封闭式采集脐带血,体外分离脐血单个核细胞,调整浓度为1×109L-1,接种于24孔细胞培养板,每孔均加入100μg/L人重组粒-巨噬细胞集落刺激因子、50μg/L白细胞介素4、10μg/L肿瘤坏死因子α。培养14d后,鉴定细胞表面CD1a、HLA-DR的百分率。③用含胎牛血清的IMDM培养Saos-2骨肉瘤细胞至对数生长期,胰酶消化后调整细胞数为5×107L-1。集传20代生长的Saos-2,冻融2次,低渗震荡,离心,上清用盐酸调pH至7.0,过滤后即为肿瘤抗原肽,与热休克蛋白70体外结合。④另取脐血40mL,分离T淋巴细胞,诱导分化至第4天,加入热休克蛋白70-肿瘤抗原肽100μL,促使T淋巴细胞活化为细胞毒T淋巴细胞。⑤效应细胞(细胞毒T淋巴细胞)与靶细胞(Saos-2)按效靶比50∶1,25∶1,12.5∶1,6.25∶1,3.125∶1梯度,四甲基偶氮唑盐法检测细胞毒T淋巴细胞杀伤活性。结果:①细胞形态学观察:细胞因子诱导后第3天,镜下脐血细胞呈均匀散布的细胞聚体,胞体拉长;第7天可见不明显突起;第14天出现具有典型树枝状突起的树突状细胞。②细胞因子诱导后脐血单核细胞表面表型鉴定结果:经细胞因子诱导后,脐血单核细胞CD1a与HLA-DR表达率均较诱导前明显升高[0,(18.43±3.26)%;(4.03±1.66)%,(59.69±8.47)%;P均<0.01]。③细胞毒T淋巴细胞杀伤活性检测结果:培养72h后,细胞毒T淋巴细胞与靶细胞Saos-2效靶比为50∶1时可杀伤决大部分肿瘤细胞,杀伤率为(97.50±11.24)%,效靶比从50∶1至3.125∶1可使靶细胞Saos-2生长呈梯度受到不同程度的抑制。单纯的树突状细胞及未经激活的T淋巴细胞对Saos-2细胞仅有微弱的生长抑制作用。结论:脐血来源的树突状细胞经过热休克蛋白70-肿瘤抗原肽复合物负载致敏后,激活的细胞毒T淋巴细胞对人骨肉瘤细胞Saos-2具有极强的杀伤能力。 相似文献
965.
Artemisinin autoinduction is caused by involvement of cytochrome P450 2B6 but not 2C9 总被引:10,自引:0,他引:10
Simonsson US Jansson B Hai TN Huong DX Tybring G Ashton M 《Clinical pharmacology and therapeutics》2003,74(1):32-43
AIM: Our goal was to investigate whether artemisinin autoinduction is caused by an increase in cytochrome P450 (CYP) 2B6 or CYP2C9 activities, we evaluated the effects of multiple-dose artemisinin administration on S-mephenytoin N-demethylation in healthy subjects. METHODS: Fourteen subjects, 6 poor metabolizers of CYP2C19 and 8 extensive metabolizers, received a single oral dose of 200 mg racemic mephenytoin (CYP2B6 in vivo marker) before (day -28) and during multiple-dose artemisinin administration (250 mg/d orally for 9 days and 500 mg on the tenth day). A 500-mg single dose of artemisinin was administered on day -28. The CYP2C9 in vivo marker tolbutamide was administered on day -28 and on days 7, 12, and 17 to monitor the minor involvement of CYP2C9 in S-mephenytoin N-demethylation. RESULTS: Artemisinin oral clearance increased 5.3-fold (P <.001) by the tenth day of administration. Its pharmacokinetics was not different in the 2 CYP2C19 phenotypes. The oral clearance of R-mephenytoin increased 1.7-fold (P <.05) in both phenotypes during the period of artemisinin administration. The area under the concentration-time curve ratio of S-nirvanol/S-mephenytoin, an index of CYP2B6 activity, increased 1.9-fold (P <.05) in CYP2C19 poor metabolizers during artemisinin multiple-dose administration, whereas the urinary excretion ratio of hydroxytolbutamide plus carboxytolbutamide/tolbutamide remained constant during the study period. CONCLUSIONS: These results indicate that artemisinin induces the N-demethylation of S-mephenytoin probably by an increased capacity of CYP2B6. The autoinduction phenomenon of artemisinin may, therefore, be attributed, at least in part, to induction of CYP2B6, because this is the isozyme primarily involved in its metabolism. In addition, artemisinin alters the disposition of R-mephenytoin by an unidentified isozyme. 相似文献
966.
967.
968.
Zhanzhan Xu Yu Zhou Yexuan Cao Thi Lan Anh Dinh Jing Wan Min Zhao 《Medical oncology (Northwood, London, England)》2016,33(11):130
Ovarian cancer is the first leading cause of mortality in gynecological malignancies. To identify key genes and microRNAs in ovarian cancer, mRNA microarray dataset GSE36668, GSE18520, GSE14407 and microRNA dataset GSE47841 were downloaded from the Gene Expression Omnibus database. Differentially expressed genes (DEGs) and microRNAs (DEMs) were obtained using GEO2R. Functional and pathway enrichment analysis were performed for DEGs using DAVID database. Protein–protein interaction (PPI) network was established by STRING and visualized by Cytoscape. Following, overall survival (OS) analysis of hub genes was performed by the Kaplan–Meier plotter online tool. Module analysis of the PPI network was performed using MCODE. Moreover, miRecords was applied to predict the targets of the DEMs. A total of 345 DEGs were obtained, which were mainly enriched in the terms related to cell cycle, mitosis, and ovulation cycle process. A PPI network was constructed, consisting of 141 nodes and 296 edges. Sixteen genes had high degrees in the network. High expression of four genes of the 16 genes was associated with worse OS of patients with ovarian cancer, including CCNB1, CENPF, KIF11, and ZWINT. A significant module was detected from the PPI network. The enriched functions and pathways included cell cycle, nuclear division, and oocyte meiosis. Additionally, a total of 36 DEMs were identified. The expression of KIF11 was negatively correlated with that of has-miR-424 and has-miR-381, and it was also the potential target of two microRNAs. In conclusion, these results identified key genes, which could provide potential targets for ovarian cancer diagnosis and treatment. 相似文献
969.
970.
神经科和精神科门诊抑郁障碍患者的临床和就诊特点 总被引:2,自引:0,他引:2
目的:比较综合医院神经科和精神专科医院门诊抑郁障碍患者的临床特点和就诊特点。方法:分别选择首次就诊于世纪坛医院神经科门诊的47例(综合医院组)和北大精神卫生研究所门诊的65例抑郁障碍患者(专科医院组),采用自编调查表和汉密顿抑郁量表(HAMD-17)调查。自编调查表资料包括年龄、性别、婚姻状况、居住地、病程、首发年龄、个性特征、月收入、就医途径(首诊医院)、前3位主诉、对疾病认识、医疗费用(从患者发病开始计起至调查日止,让患者及家属尽量回忆充分)。汉密顿抑郁量表包含17项,采用0~4分的5级评分法:0无,1轻度,2中度,3重度,4很重。结果:112例患者均完成量表测试和调查,全部进入结果分析。①87%的综合医院组的抑郁障碍患者第一主诉为躯体不适;57%专科医院组的抑郁障碍患者第一主诉为情绪低落。②94%的综合医院组患者首诊选择综合医院;42%的专科医院组患者首诊选择综合医院。③综合医院组汉密顿抑郁量表评分低于专科医院组,属于中度抑郁;而专科医院组基本为重度抑郁。综合医院组患者汉密顿抑郁量表总评分及迟滞和认知障碍的因子分显著低于专科医院组患者,差异有显著性意义。④83%的综合医院组患者认为自己所患不是精神疾病;39%的专科患者认为自己所患为精神疾病。⑤两组在年龄、文化程度、婚姻状况、既往史等方面也有显著差异。结论:综合医院抑郁障碍患者较专科医院患者年龄偏大、多伴有躯体疾病,抑郁程度相对较轻,对情绪问题的自知力差。 相似文献