小儿毒蛇咬伤49例

目的总结小儿毒蛇咬伤的综合防治措施。方法对1997年1月-2006年12月收治49例毒蛇咬伤患儿，记录性别、年龄、居住地、受伤及就诊时间、受伤部位、受伤后的局部症状及全身情况、治疗过程及预后，并进行综合分析。结果小儿蛇咬伤病例集中于夏秋湿热季节，乡村小儿发生率多见（占81．6％），从发生至来院时间平均38．4h，93．9％未看见毒蛇或不能描述毒蛇的特征。按照Downey系统分类，3、4级重型伤员所占比重较大（占59．2％）。蛇咬伤局部可出现肿胀、疼痛、瘀斑、伤口感染、局部坏死伴组织缺失、骨筋膜室综合征等表现，亦可导致器官功能损害等并发症；均行针对性的综合治疗，无死亡病例。结论加强预防知识教育、早期诊断和综合对症处理可有效降低小儿蛇伤后病死率和病残率。     

苯酮尿症的分子研究及其基因型-表型相关性的研究进展

苯酮尿症(phenlketonuria,PKU)主要是由于编码苯丙氨酸羟化酶(PAH)的基因突变,导致肝脏PAH活性降低或缺乏所致。各国应用分子生物学等技术对PAH基因突变进行了广泛研究,到目前为止,有498突变基因被确定,其中致病性的突变有460余种;研究者们应用体外表达预测酶活性和测定体内苯丙氨酸氧化率等方法研究基因型-表型的相关性,希望通过基因型来预测未知的表型,以便指导PKU的分类和治疗。该文综述了PAH基因突变在不同地区、人种和民族的特点,同时对基因型-生化代谢表型以及基因型-智能表型的相关关系的研究进行综合分析。     

Hepatitis D: advances and challenges

Hepatitis D virus (HDV) infection causes the most severe form of viral hepatitis with rapid progression to cirrhosis, hepatic decompensation, and hepatocellular carcinoma. Although discovered > 40 years ago, little attention has been paid to this pathogen from both scientific and public communities. However, effectively combating hepatitis D requires advanced scientific knowledge and joint efforts from multi-stakeholders. In this review, we emphasized the recent advances in HDV virology, epid...     

基于发布/订阅系统的安全管理平台设计

本文就如何建立高效液相色谱法测定含量的色谱条件与溶液浓度进行了论述，系统地阐述了确定的理由，并列举了质量标准制订和实际测定中存在的一些问题。     

多西他赛联合卡培他滨方案在新辅助化疗三阴乳腺癌与非三阴乳腺癌中的近期疗效观察

目的探讨三阴乳腺癌(triple-negative breast cancer,TNBC)与非三阴乳腺癌患者应用多西他赛联合卡培他滨(DX)方案行新辅助化疗的临床疗效及不良反应。方法选择2008年7月—2013年8月收治的102例乳腺癌患者,其中TNBC 27例,非TNBC75例,均应用DX方案新辅助化疗。观察临床疗效和毒副反应发生情况。结果TNBC患者总有效率与非TNBC患者比较差异无统计学意义(P>0.05)。TNBC患者病理完全缓解率、临床完全缓解率高于非TNBC患者(P<0.01,P<0.05)。毒副反应主要表现为胃肠道反应、骨髓抑制及手足综合征等,TNBC与非TNBC患者毒副反应发生率比较差异无统计学意义(P>0.05)。结论 TNBC患者较非TNBC患者对DX方案新辅助化疗更敏感,且未增加毒副反应发生率。     

左旋千金藤立定对溴隐亭诱导的哺乳期大鼠促乳素水平低下的拮抗作用

目的:研究左旋千金藤立定(SPD)对溴隐亭(Bro)诱导的促乳素(PRL)水平低下的对抗作用。方法:哺乳期母鼠sc Bro 0.5mg·kg~(-1)·d~(-1),PRL显著降低,乳腺组织发育不良,而且仔鼠体重增长缓慢。用放免法测定母鼠PRL,检查乳腺发育状况,评价SPD的对抗作用。结果:SPD30及100mg·kg~(-1)·d~(-1)ip,能够显著对抗Bro诱导的母鼠PRL降低,分娩后d15PRL为11±4及23±6μg·L~(-1)(生理盐水为7±2),而且乳腺组织发育正常,仔鼠在出生后d11—15内迅速生长发育。结论:SPD能阻断大鼠脑垂体前叶的D_2受体,是一个D_2受体的拮抗剂。     

基于"欧盟草药专论"解析中药欧盟注册关键问题

欧盟2004/24/EC法令针对传统草药药品实行简化注册程序,很大程度降低了草药药品上市门槛,但法令为其额外设定的注册条件,如草药在欧盟至少药用15年历史要求、适应症限制、给药途径限制等,对非欧洲本土来源的中药产品而言仍面临诸多挑战.鉴于"欧盟草药专论"的评价与草药药品简化注册中安全性和有效性的审评标准基本一致,首次从欧盟草药专论的角度,跟踪欧盟草药专论最新评价进展,对影响欧盟草药专论建立的关键因素以及中药产品简化注册过程中的关键问题进行深入分析,并提出建议与对策,以期为中药产品欧盟注册提供一定指导和参考.     

Silencing of Nesprin‐2 inhibits the differentiation of myofibroblasts from fibroblasts induced by mechanical stretch

Mechanical force plays a pivotal role in the pathogenesis of hypertrophic scar (HTS). Dermal fibroblasts and myofibroblasts are the key cells involved in HTS. Myofibroblasts in HTS possess different biochemical and biophysical characteristics by which myofibroblasts are often distinguished from fibroblasts. The role of mechanotransducers outside the nucleus in the pathogenesis of HTS has been reported in many studies. However, the role of Nesprin‐2 in HTS is not clear. Hence, we aim to construct a cell model of HTS and explore the role of Nesprin‐2 in this process. Myofibroblasts and fibroblasts were isolated from HTS and healthy skin tissues of the same patient. Fibroblasts were exposed to cyclic stretch with 10% magnitude and a frequency of 0.1 Hz for 3 days, 5 days, and 7 days, respectively. After the cell model was confirmed, fibroblasts transfected with siRNA targeting human Nesprin‐2 were exposed to cyclic stretch. The mechanical behaviour and biochemical reaction of the dermal fibroblasts were analysed. The stretched fibroblasts at day 5 showed the same mechanotransductive and biochemical features as unstretched myofibroblasts. Mechanical strain could induce the myofibroblasts differentiation and a cell model of HTS was established successfully at day 5. The expressions of lamin A/C, alpha‐smooth muscle actin, transforming growth factor beta 1, and collagen type I in fibroblasts were reduced by the silencing of Nesprin‐2. Mechanical strain could induce the myofibroblasts differentiation and silencing of Nesprin‐2 could block the mechanical stimulation of terminal myofibroblasts differentiation. Nesprin‐2 might be a potential target to treat the HTS.     

IL‐27 improves adoptive CD8+ T cells’ antitumor activity via enhancing cell survival and memory T cell differentiation

IL‐27 is an anti‐inflammatory cytokine that triggers enhanced antitumor immunity, particularly cytotoxic T lymphocyte responses. In the present study, we sought to develop IL‐27 into a therapeutic adjutant for adoptive T cell therapy using our well‐established models. We have found that IL‐27 directly improved the survival status and cytotoxicity of adoptive OT‐1 CD8⁺ T cells in vitro and in vivo. Meanwhile, IL‐27 treatment programs memory T cell differentiation in CD8⁺ T cells, characterized by upregulation of genes associated with T cell memory differentiation (T‐bet, Eomes, Blimp1, and Ly6C). Additionally, we engineered the adoptive OT‐1 CD8⁺ T cells to deliver IL‐27. In mice, the established tumors treated with OT‐1 CD8⁺ T‐IL‐27 were completely rejected, which demonstrated that IL‐27 delivered via tumor antigen–specific T cells enhances adoptive T cells’ cancer immunity. To our knowledge, this is the first application of CD8⁺ T cells as a vehicle to deliver IL‐27 to treat tumors. Thus, this study demonstrates IL‐27 is a feasible approach for enhancing CD8⁺ T cells’ antitumor immunity and can be used as a therapeutic adjutant for T cell adoptive transfer to treat cancer.