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2018~2020年深圳市龙岗区流行性腮腺炎流行病学特征分析
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作者 谢远声 陈立平 《中国实用医药》 2023年第21期167-169,共3页
目的分析2018~2020年深圳市龙岗区流行性腮腺炎流行病学特征。方法以抽样方式选取2018年1月~2020年12月深圳市龙岗区462例流行性腮腺炎患者的临床资料,分析不同性别及年龄患者的发病情况,不同季节患者的发病情况,不同教育程度患者的发... 目的分析2018~2020年深圳市龙岗区流行性腮腺炎流行病学特征。方法以抽样方式选取2018年1月~2020年12月深圳市龙岗区462例流行性腮腺炎患者的临床资料,分析不同性别及年龄患者的发病情况,不同季节患者的发病情况,不同教育程度患者的发病情况。结果2018~2020年深圳市龙岗区1~3岁、4~9岁、10~20岁、21~75岁男性的流行性腮腺炎发病率分别为7.3%、38.5%、49.2%、5.0%,女性分别为4.5%、37.0%、47.0%、11.5%。1~3岁、4~9岁、10~20岁男性的流行性腮腺炎发病率高于女性,21~75岁男性的流行性腮腺炎发病率低于女性。2018~2020年深圳市龙岗区4~6月流行性腮腺炎的发病率高于1~3月、7~9月、10~12月。2018、2019、2020年深圳市龙岗区的流行性腮腺炎发病率分别为33.3%、34.6%、32.0%,差异不大。2018~2020年深圳市龙岗区小学、初中、高中教育程度流行性腮腺炎发病率分别为23.8%、40.0%、21.6%,高于文盲、大专及以上教育程度的5.6%、8.9%。结论2018~2020年深圳市龙岗区流行性腮腺炎中男性患者数量明显更高,4~6月属于高发期,小学、初中、高中教育程度患者数量更高,均属于其流行病学特征,进而为深圳市龙岗区流行性腮腺炎疾病的治疗提供重要的参考依据。 展开更多
关键词 2018~2020年 深圳市龙岗区 流行性腮腺炎 流行病学特征 学生类型 流行性季节
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中西医结合防治病毒性疾病的优势 被引量:4
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作者 纪鹏程 李爽 +1 位作者 谢院生 陈香美 《中国中西医结合杂志》 CAS CSCD 北大核心 2022年第2期232-235,共4页
很多病毒性疾病传染性强、预后差、危害大。中医药在乙型脑炎、流行性出血热、甲型病毒性肝炎、SARS、H1N1流感、新冠肺炎等病毒性疾病的防治中发挥了重要作用,在改善症状、缩短病程、延缓疾病进展、提高临床治愈率、降低病死率等方面,... 很多病毒性疾病传染性强、预后差、危害大。中医药在乙型脑炎、流行性出血热、甲型病毒性肝炎、SARS、H1N1流感、新冠肺炎等病毒性疾病的防治中发挥了重要作用,在改善症状、缩短病程、延缓疾病进展、提高临床治愈率、降低病死率等方面,优于单纯西医治疗。本文总结分析中医药防治病毒性疾病的作用,为临床提供参考。 展开更多
关键词 中医药 中西医结合 病毒性疾病
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Role of microRNA-181a in the apoptosis of tubular epithelial cell induced by cisplatin 被引量:10
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作者 Zhu Han-yu Liu Mo-yan +4 位作者 Hong Quan Zhang Dong Geng Wen-jia xie yuan-sheng Chen Xiang-mei 《Chinese Medical Journal》 SCIE CAS CSCD 2012年第3期523-526,共4页
Background Cisplatin (DDP) is one of most effective and most commonly used therapeutic agent in treating tumors,it can accumulate in the kidney and lead to acute renal failure.MicroRNA-181a can induce cell apoptosis... Background Cisplatin (DDP) is one of most effective and most commonly used therapeutic agent in treating tumors,it can accumulate in the kidney and lead to acute renal failure.MicroRNA-181a can induce cell apoptosis by suppressing the expression of Bcl-2 family.In the present study,we investigated the role of microRNA-181a in the apoptosis of tubular epithelial cell induced by DDP.Methods HK-2 cells were cultured,transfected with microRNA-181a inhibitor for 48 hours,and stimulated with 50 μmol/L cisplatin for 24 hours.MicroRNA-181a expression was analyzed by real time PCR,and cell apoptosis was detected by flow cytometry.Moreover,Bcl-2 and Bcl-2-associated X protein (Bax) expression were measured by Western blotting.Results MicroRNA-181a expression significantly down-regulated in cells transfected with microRNA-181a inhibitor,compared with that in untransfectd cells (21.19±2.01 vs.38.87±1.97,P 〈0.05).Cell apoptosis induced by DDP significantly decreased in cells transfected with MicroRNA-181a inhibitor.Compared with DDP treated cells alone,Bcl-2 expression strikingly was up-regulated and Bax expression was down-regulated in cells transfected with microRNA-181a inhibitor.Conclusion One pathway of DDP induces apoptosis of tubular epithelial cell by suppressing Bcl-2 expression is achieved by regulating the target gene of MicroRNA-181a. 展开更多
关键词 MicroRNA-181a CISPLATIN tubular epithelial cell APOPTOSIS
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Tissue inhibitor of metalloproteinase-1 counteracts glucolipotoxicity in the pancreatic β-cell line INS-1 被引量:2
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作者 JIANG Hong-wei ZHU Han-yu +5 位作者 WANG Jian-zhong FU Bo LU Yang HONG Quan xie yuan-sheng CHEN Xiang-mei 《Chinese Medical Journal》 SCIE CAS CSCD 2011年第2期258-261,共4页
Background Glucolipotoxicity might play an important role in the β cell decompensation stage during the development of obesity-associated type 2 diabetes.Tissue inhibitor of metalloproteinase-1 (TIMP-1) inhibits ma... Background Glucolipotoxicity might play an important role in the β cell decompensation stage during the development of obesity-associated type 2 diabetes.Tissue inhibitor of metalloproteinase-1 (TIMP-1) inhibits matrix metalloproteinase (MMP) activity and regulates proliferation and apoptosis of a variety of cell types,including pancreatic β-cells.In the present study,we investigated whether TIMP-1 counteracts glucolipotoxicity in the pancreatic β-cell line INS-1.Methods INS-1 cells were incubated in normal or high glucose,with or without palmitate (0.4 mmol/L),in the presence of TIMP-1 or MMP inhibitor GM60001.In some experiments,cells were pretreated with phosphatidylinositol-3 (Pl-3) kinase inhibitor,LY294002 or wortmannin.The amount of dead INS-1 cells was determined by HO342 and propidium iodide staining.Akt phosphorylation was evaluated by Western blotting analysis to investigate a possible mechanism of TIMP-1's action.Results TIMP-1 protected INS-1 cells from glucolipotoxicity independent of MMP inhibition.TIMP-1 stimulated Akt phosphorylation.Inhibition of the PI-3 kinase pathway abolished the survival effect of TIMP-1.Conclusion TIMP-1 may counteract glucolipotoxicity induced β-cell death via a PI-3 kinase pathway. 展开更多
关键词 GLUCOLIPOTOXICITY tissue inhibitor of metalloproteinase-1 pancreatic β-cell line INS-1
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