病毒性脑炎患者外周血和脑脊液西尼罗病毒E基因的检测

西尼罗病毒(WNV)是单股正链RNA病毒,属于黄病毒科黄病毒属,其传播媒介和储存宿主是蚊虫[1].人感染WNV会出现感冒样症状,部分患者为脑膜脑炎、坏死性脑干炎等神经系统症状[2,3].本研究对重庆地区不明病因的78例病毒性脑炎(VE)患者血液和脑脊液进行wNV E基因片段检测.     

麻醉诱导期间异丙酚与利多卡因的相互作用

目的探讨麻醉诱导期间不同利多卡因浓度对睫毛反射、意识消失时异丙酚血药浓度和心血管系统的影响。方法选择38例择期手术病人应用微机控制靶控输注利多卡因维持不同目标浓度(Ct)，其后从另一接口输注异丙酚，逐渐增加异丙酚目标浓度直至意识消失。根据利多卡因目标浓度将病人分为5组，分别为A组Oug·ml     

缺血对蛙坐骨神经干传导速度的影响

目的 通过测定传导速度研究缺血对神经干功能的影响，方法 将２０只牛蛙左右后肢分为两组，左后肢为供血组，右后肢为缺血组，对两组坐骨神经干分别每隔５分钟测定一次声望地速度（共１３次，６０分钟）取０，３０，６０分钟三个时相的传导速度进行组内与组间比较，实验组块缺血时间与传导速度进行相关性分析，统计学处理用双侧ｔ检验，相关性分析，结果：（１）对照组内神经传导速度比较显示差异地显著性（Ｐ〉０．０５），实验组     

重庆地区博尔纳病病毒种系发生分析

目的了解重庆地区博尔纳病病毒(Borna disease virus,BDV)基因特征及其种系发生。方法采用荧光定量巢式实时逆转录聚合酶链反应(fluorescence quantitative nested RT-PCR,FQ-nRT-PCR)检测健康牛、山羊、猪各50例以及病毒性脑炎(viral encephalitis,VE)患者20例外周血单核细胞(peripheral blood mononuclear cells,PBMCs)BDV p24片段,检出阳性序列和前期检出的5例重庆地区山羊和神经精神患者阳性BDV p24基因序列,与GenBank中5个国家7个动物种属33例BDV p24基因序列进行比对,分析其核苷酸和氨基酸序列同源性,重建基因系统发生树。结果10例BDV p24核苷酸序列一部分(1例VE患者)形成重庆独立支系,另一部分(7例动物和2例VE患者)汇聚至德国-瑞士-奥地利-日本-重庆混合支系。与BDV标准病毒株Strain V、H1766及He/80比对,9例核苷酸和氨基酸序列同源相似性分别为94%～100%和82%～100%,1例为95%～98%和89%～93%。结论重庆地区动物和人宿...     

聚乙二醇化重组人G-CSF在以CHOP为基础方案的非霍奇金淋巴瘤中的应用

背景与目的：由环磷酰胺、长春新碱、多柔比星和泼尼松组成的CHOP方案是侵袭性非霍奇金淋巴瘤(non-Hodgkin's lymphoma, NHL)的标准化疗方案,其发生粒细胞减少性发热(febrile neutropenia, FN)的风险为10%~20%。近年来聚乙二醇化粒细胞集落刺激因子(pegylated recombinant human granulocyte colony stimulating factor, PEG-rhG-CSF)在临床中逐渐广泛应用。该研究旨在明确PEG-rhG-CSF在接受CHOP方案为基础化疗的非霍奇金淋巴瘤患者中预防性应用的疗效和安全性。方法：该研究回顾性分析了75例患者,其中36例接受了初级预防,39例接受了次级预防,所有患者均完成所有治疗并纳入数据分析。结果：在初级预防组中,52.8%的患者未再发生4度中性粒细胞缺乏或FN,63.9%未导致化疗减量。在次级预防组,61.5%的患者未再发生4度中性粒细胞缺乏或FN,66.7%未导致化疗减量。多因素分析显示,高龄(大于等于65岁)和3/4期是预防后仍然出现严重中性粒细胞缺乏并导致化疗减量的独立高危因素。安全性方面,短暂的腰骶部1~2级疼痛是主要的不良反应。结论：PEG-rhG-CSF的预防性应用不但使用方便,并且显示了良好的预防效果和耐受性,值得临床推荐。     

Response-adapted therapy for limited stage diffuse large B-cell lymphoma based on interim PET-CT: preliminary results of a phase 2 study

Background

Limited stage diffuse large B-cell lymphoma is curable with R-CHOP (rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone or prednisolone) immunochemotherapy. For patients achieving complete response by interim 18F-fluorodeoxyglucose PET-CT, a previous study showed therapy could be safely de-escalated by omitting the subsequent chemotherapy or radiotherapy. We aimed to adapt the therapy on the basis of the response as assessed by the interim PET-CT.

医学网络教学发展探讨

随着网络教学在医学教育实践中的广泛应用，网络教学在推动医学教育改革中发挥着重要作用。文章结合医学网络教学的实践对其特点、现状及发展进行了探讨。     

出院后持续健康教育对精神分裂症患者家属家庭功能及生活质量的影响

目的 探索出院后持续健康教育对改善精神分裂症患者家属的家庭功能及生活质量的影响.方法 采用抛币法将62例患者家属分为观察组和对照组,入院时对两组进行健康教育,出院后对观察组进行为期9月的家庭随访,对照组常规门诊随访.在出院前和出院后9月分别对两组采用家庭功能评定量表、生活质量综合评定问卷进行评定.结果 家庭功能总分与生活质量的各维度分呈显著相关关系(P＜0.05);两组患者家属的家庭功能评分和生活质量综合评分比较,出院前无统计学意义(P＞0.05),出院9月后观察组明显优于对照组(P＜0.05).结论 出院后持续健康教育改善了精神分裂症患者家属的家庭功能,并提高了生活质量.     

Multiple receptor tyrosine kinase activation attenuates therapeutic efficacy of the fibroblast growth factor receptor 2 inhibitor AZD4547 in FGFR2 amplified gastric cancer

Fibroblast growth factor receptor 2 (FGFR2)-targeted therapy has attracted considerable attention as novel anticancer agents in gastric cancer (GC). However, intrinsic or acquired drug resistance has emerged as a major challenge to their clinical use. In this study, we demonstrated that several receptor tyrosine kinase (RTK), including EGFR, HER3 and MET, activations contributed to AZD4547 (a selective FGFR2 inhibitor) hyposensitivity in FGFR2 amplified GC cells. The rescue effect was abrogated by inhibiting these RTKs with their targeted tyrosine kinase inhibitors (TKIs). In addition, synergy in growth inhibition was observed when the GC cells were treated with a combination of AZD4547 and cetuximab (an EGFR monoclonal antibody) both in vitro and in vivo. More importantly, tissue microarray analysis revealed that these resistance-conferring RTKs were highly expressed in FGFR2 positive GC patients. Taken together, these observations demonstrated RTKs including EGFR, HER3 and MET activations as novel mechanisms of hyposensitivity to AZD4547. It will be clinically valuable to investigate the involvement of RTK-mediated signaling in intrinsicor acquired resistance to FGFR2 TKIs in GC. A combination targeted therapeutic strategy may be recommended for treating FGFR2 amplified GC patients with these RTK activations.