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PulseNet China是我国细菌性传染病分子分型实验室监测网络,是中国疾控系统在病原菌监测领域技术进步和科技创新的平台。本文阐述了PulseNet China网络在传染病暴发的早期预警、溯源、突发公共卫生事件应对中的作用,介绍了PulseNet China 工作进展、发展目标以及2012年重点工作,讨论了PulseNet China现阶段存在的问题及对策。 PulseNet China 是我国细菌性传染病分型监测网络化理念创新,是未来我国实验室病原体监测的发展方向和关键支撑技术。PulseNet China将病原菌分子分型监测形成的技术成果和创新转化为我国传染病预防控制的技术手段,是我国转化预防医学的实践,也是为我国传染病预防控制和食品安全以及为我国民生事业做出相应贡献的专业实践。 相似文献
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目的探讨复方苦参注射液联合常规灌肠治疗溃疡性结肠炎的临床疗效。方法选择2009年1月~2011年2月就诊的轻、中度活动期远段UC患者32例,随机分为治疗组17例,复方苦参注射液20raL加入生理盐水250mL中,静脉滴入,每日一次,联合甲硝唑0.4g+地塞米松lOmg+生理盐水lOOmL混合摇匀,每晚睡前保留灌肠,l0d为一个疗程;对照组15例仅使用常规保留灌肠法。结果治疗组和对照组总有效率分别为88.2%和64.3%,两组有明显差异(P〈0.01)。结论复方苦参注射液联合常规灌肠治疗溃疡性结肠炎疗效确切,建议进一步了解此药的作用机制,做临床长期效果观察。 相似文献
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The reliability and validity of the pain items of the Hong Kong version interRAI community health assessment for community‐dwelling elders in Hong Kong 下载免费PDF全文
Justina YW Liu PhD RN Iris Chi DSW Kin‐Sun Chan PhD Claudia KY Lai PhD RN Angela YM Leung PhD RN 《Journal of clinical nursing》2015,24(15-16):2352-2354
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Clinical activity of ASP8273 in Asian patients with non‐small‐cell lung cancer with EGFR activating and T790M mutations 下载免费PDF全文
Haruyasu Murakami Hiroshi Nokihara Hidetoshi Hayashi Takashi Seto Keunchil Park Koichi Azuma Chun‐Ming Tsai James Chih‐Hsin Yang Makoto Nishio Sang‐We Kim Katsuyuki Kiura Akira Inoue Koji Takeda Jin‐Hyoung Kang Tomoki Nakagawa Kentaro Takeda Rio Akazawa Yuichiro Kaneko Masashi Shimazaki Satoshi Morita Masahiro Fukuoka Kazuhiko Nakagawa 《Cancer science》2018,109(9):2852-2862
Epidermal growth factor receptor (EGFR)‐activating mutations confer sensitivity to tyrosine kinase inhibitor (TKI) treatment for non‐small‐cell lung cancer (NSCLC). ASP8273 is a highly specific, irreversible, once‐daily, oral, EGFR TKI that inhibits both activating and resistance mutations. This ASP8273 dose‐escalation/dose‐expansion study (NCT02192697) was undertaken in two phases. In phase I, Japanese patients (aged ≥20 years) with NSCLC previously treated with ≥1 EGFR TKI received escalating ASP8273 doses (25‐600 mg) to assess safety/tolerability and to determine the maximum tolerated dose (MTD) and/or the recommended phase II dose (RP2D) by the Bayesian Continual Reassessment Method. In phase II, adult patients with T790M‐positive NSCLC in Japan, Korea, and Taiwan received ASP8273 at RP2D to further assess safety/tolerability and determine antitumor activity, which was evaluated according to Simon's two‐stage design (threshold response = 30%, expected response = 50%, α = 0.05, β = 0.1). Overall, 121 (n = 45 [33W/12M] phase I, n = 76 [48W/28M]) phase 2) patients received ≥1 dose of ASP8273. In phase I, RP2D and MTD were established as 300 and 400 mg, respectively. As 27 of the 63 patients treated with ASP8273 300 mg achieved a clinical response, ASP8273 was determined to have antitumor activity. The overall response rate at week 24 in all patients was 42% (n = 32/76; 95% confidence interval, 30.9‐54.0). Median duration of progression‐free survival was 8.1 months (95% confidence interval, 5.6, upper bound not reached). The most commonly reported treatment‐related adverse event in phase II was diarrhea (57%, n = 43/76). ASP8273 300 mg was generally well tolerated and showed antitumor activity in Asian patients with both EGFR‐activating and T790M mutations. 相似文献
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HLA frequencies in Black Zimbabweans 总被引:1,自引:0,他引:1
One-hundred-and-nineteen normal Black Zimbabweans were typed for HLA antigens. We found a close similarity between the HLA antigen frequencies in Zimbabweans and Black South Africans (Xhosa), another Bantu-speaking group. The only significant differences noted were for HLA-Aw36, -Bw53, -Cw6, -DR4 and -DQw3 (p less than 0.01). The most common HLA haplotypes in significant positive linkage disequilibrium in the two groups were different. The differences that were noted may be due to gene flow from the San to the Black South Africans, since it is thought that the Zimbabweans had little if any contact with the San. 相似文献
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Ha Ryong Kim Kyuhong Lee Chang We Park Jeong Ah Song Da Young Shin Yong Joo Park Kyu Hyuck Chung 《Archives of toxicology》2016,90(3):617-632
Polyhexamethylene guanidine (PHMG) phosphate was used as a disinfectant for the prevention of microorganism growth in humidifiers, without recognizing that a change of exposure route might cause significant health effects. Epidemiological studies reported that the use of humidifier disinfectant containing PHMG-phosphate can provoke pulmonary fibrosis. However, the pulmonary toxicity of PHMG-phosphate aerosol particles is unknown yet. This study aimed to elucidate the toxicological relationship between PHMG-phosphate aerosol particles and pulmonary fibrosis. An in vivo nose-only exposure system and an in vitro air–liquid interface (ALI) co-culture model were applied to confirm whether PHMG-phosphate induces inflammatory and fibrotic responses in the respiratory tract. Seven-week-old male Sprague–Dawley rats were exposed to PHMG-phosphate aerosol particles for 3 weeks and recovered for 3 weeks in a nose-only exposure chamber. In addition, three human lung cells (Calu-3, differentiated THP-1 and HMC-1 cells) were cultured at ALI condition for 12 days and were treated with PHMG-phosphate at set concentrations and times. The reactive oxygen species (ROS) generation, airway barrier injuries and inflammatory and fibrotic responses were evaluated in vivo and in vitro. The rats exposed to PHMG-phosphate aerosol particles in nanometer size showed pulmonary inflammation and fibrosis including inflammatory cytokines and fibronectin mRNA increase, as well as histopathological changes. In addition, PHMG-phosphate triggered the ROS generation, airway barrier injuries and inflammatory responses in a bronchial ALI co-culture model. Those results demonstrated that PHMG-phosphate aerosol particles cause pulmonary inflammatory and fibrotic responses. All features of fibrogenesis by PHMG-phosphate aerosol particles closely resembled the pathology of fibrosis that was reported in epidemiological studies. Finally, we expected that PHMG-phosphate infiltrated into the lungs in the form of aerosol particles would induce an airway barrier injury via ROS, release fibrotic inflammatory cytokines, and trigger a wound-healing response, leading to pulmonary fibrosis. A simultaneous state of tissue destruction and inflammation caused by PHMG-phosphate had whipped up a “perfect storm” in the respiratory tract. 相似文献