浅谈皮肤科来华留学研究生培养的心得体会及建议

来华留学生培养是中国高等教育的重要组成部分,是提高中国高等教育的国际知名度、中国大学国际化程度的环节之一.皮肤科留学研究生的培养在来华留学生中有一定的需求,但大多数以东南亚来源国和非洲国家为主,其文化背景、医学基础知识差异大,很多不懂中文,缺乏统一的英文或英汉皮肤性病学教材等,这些都给带教老师带来了较大的挑战.该文分享...     

甘草泻心汤对贝赫切特病患者疗效及血清细胞因子水平的影响

目的：观察甘草泻心汤对贝赫切特病（BD）患者的疗效及血清细胞因子水平的影响。方法：将52例BD患者分为治疗组（甘草泻心汤加强的松治疗）与对照组（强的松治疗）,疗程8周,观察疗效及BD患者治疗前、治疗后细胞因子白细胞介素-6（IL-6）、白细胞介素-10（IL-10）、肿瘤坏死因子-α（TNF-α）及干扰素-γ（IFN-γ）水平的变化：并设30例健康体检者为健康组？结果：治疗组}临床痊愈20例（76．92％）,有效5例,无效1例,总有效率96．15％;对照组临床痊愈1l例（42．31％）,有效9例,无效6例,总有效率76．92％。2组临床痊愈率及总有效率比较,差异均有显著性意义（P〈0．05）。BD患者治疗前血清IL-6、IL-10、TNF-α、IFN-γ水平高于健康组（P〈0．05）,治疗组治疗后血清IL-6、IL-10、TNF-α较治疗前降低（P〈0．05）,治疗组治疗后血清IFN-γ水平较健康组增高（P〈0．05）。52例BD患者,共有3例发生不良反应,不良反应均较轻微,主包括食欲减退、腹胀、轻度血压增高、轻度浮肿等,对症处理或停药1周后可恢复正常。本次研究中未有病例退出实验.结论：甘草泻心汤能改善BD患者的临床症状,可影响BD患者体内细胞因子IL-6、IL-10、TNF-α、IFN-γ的水平,提高糖皮质激素疗效、     

品管圈活动在降低血液透析过程中低血压发生率的探讨研究

目的研究品管圈(quality control circle,QCC)活动在降低血液透析过程中低血压发生率的应用价值。方法选取在本院实施血液透析患者60例,将其随机分为研究组与对照组,每组患者30例。将常规血液透析护理应用于对照组患者中,研究组患者则开展QCC活动,比较组间患者在透析过程中低血压发生率。结果研究组低血压发生率为3.3%,对照组为23.3%,研究组结果显著低于对照组,差异存在统计学意义(P<0.05)。结论QCC活动的开展能有效降低血液透析患者血透过程中低血压的发生率,进而提升患者生存质量,提高患者满意度,具有一定临床应用价值。     

老年系统性红斑狼疮住院患者111例主诉分析

系统性红斑狼疮(SLE)是一种侵犯多系统、多器官的自身免疫性疾病,其发病在不同年龄、性别、种族和地区存在明显差异〔1,2〕,好发于育龄女性,占病人的90%～95%,但也见于儿童和老人〔3〕。其临床表现、病程及预后变化多样,以周期性静止     

学科交叉融合培养模式对八年制医学生科研能力的影响分析

自2004年首批临床医学八年制专业获批以来,各大高校八年制科研培养模式仍处于摸索阶段。学科交叉融合和多学科协同是提升科研创新能力、培养拔尖人才的重要方式。本研究选取华中科技大学同济医学院附属协和医院2011级、2012级已发表学术论文的八年制学生为研究对象,分为实验组和对照组,其中实验组学生为学科交叉融合模式培养,对照组则为传统的专科导师制模式培养。分别比较了两组学生以第一作者发表学术论文的篇数和总影响因子。结果表明,学科交叉融合培养模式有助于提高八年制医学生的科研能力,对培养拔尖创新医学人才有重要意义。     

系统性红斑狼疮的精神障碍

神经系统受累是系统性红斑狼疮患者残疾、死亡的重要原因之一,临床表现为一系列高度异质性的神经精神症状.其中精神症状主要包括精神病、急性意识错乱状态、情绪障碍、认知功能障碍和焦虑症.然而,当前仍缺乏相关的诊断标准和治疗准则,导致对精神狼疮患者的诊断不足和治疗不当.因此,本文围绕精神狼疮展开综述,促进患者及临床医生对其的认识...     

规范抗乙肝病毒治疗与肝癌术后肿瘤复发的关系

目的 通过肝癌多学科协作（multi-disciplinary team,MDT）诊治模式下实施规范抗乙肝病毒方案在肝癌病人中的应用,探讨抗乙肝治疗与肝癌术后生存率及肿瘤复发的关系。方法 回顾性分析2015年1月至2017年12月经我院肝癌MDT讨论后实施规范抗乙肝治疗病人（治疗组,36例）和未进行规范抗乙肝治疗病人（对照组,34例）的临床资料,比较两组病人肝癌术后肿瘤复发情况及1、3、5年内生存率。结果两组病人一般情况、实验室指标、肿瘤大小及术前HBV-DNA差异无统计学意义（P> 0.05）,手术后为期5年的随访中治疗组病人1、3、5年肿瘤复发率分别为8.3%、33.3%、41.6%;对照组1、3、5年肿瘤复发率分别为11.7%、41.1%、64.7%,差异均具有统计学意义（P <0.05）。治疗组病人1、3、5年生存率分别为91.6%、66.7%、58.3%;对照组1、3、5年生存率分别为88.2%、58.8%、29.5%,差异均具有统计学意义（P <0.05）。结论 HBV相关性肝癌病人在经过肝癌MDT制定方案,术前和术后实施规范抗乙肝病毒治疗,可有效降低肝癌...     

正清风痛宁配合西药治疗类风湿关节炎30例

笔者于2001年3月至2007年5月,采用正清风痛宁与甲氨蝶呤治疗类风湿关节炎30例,并与单纯用西药治疗30例进行对照观察,收到满意效果,现将结果报道如下。     

内皮素对黑素瘤A375细胞转化生长因子-β1及磷酸化Smad 3蛋白表达的调节

Objective To investigate the effects ofendothelin-1 (ET-1) and endothelin-3 (ET-3) on the expression of transformation growth factor-beta 1 (TGF-β1) and phosphorylation of Smad 3 in malignant melanoma cell line, A375. Methods Cultured A375 cells were classified into 5 groups, i.e. control group (no stimulation), ET-1 group (stimulated with ET-1), ET-1+BQ123 group (treated with ET-1 and BQ123),ET-1 + BQ788 group (treated with ET-1 and BQ788), ET-3 group (stimulated with ET-3), to receive different stimulation. The working concentrations were 0, 0.1, 1, 10, 100 nmol/L for ET-1 and ET-3, 10 μmol/L for BQ123 and BQ788. After another 12- and 24-hour culture, ELISA, RT-PCR and Western blot were used to detect the expression of TGF-β1 protein and mRNA as well as phosphorylated Smad 3 (P-Smad 3). Results The expression of TGF-β1 in A375 cells was up-regulated by ET-1, but down-regulated by ET-3, and both of the effects were in a concentration-dependent manner. Under the stimulation with ET-1 and ET-3 of 100 nmol/L, the level of TGF-β1 reached 1289.38 ± 89.42 ng/L per 105 cells and 85.09 ± 9.37 ng/L per 105 cells, respectively, significantly different from that in unstimulated cells (both P < 0.05). BQ123 signifi-cantly blocked the up-regnlatory effect of ET-1 on the expression TGF-β1 protein(P < 0.05), but BQ788 had no significant influence on the effect, so was the case with TGF-β1 mRNA. Western blot revealed that ET-1significantly elevated the expression of P-Smad 3 in A375 cells (P <0.05), and the elevation was significantly inhibited by BQ123, but not by BQ788. The expression of P-Smad 3 was statistically decreased by ET-3 in A375 cells (P <0.05). Conclusions The expression of TGF-β1 could be enhanced by ET-1, but suppressed by ET-3. It is likely that endothelin receptor A mediates the phosphorylation of Smad 3 induced by ET-1.     

内皮素对黑素瘤A375细胞转化生长因子-β1及磷酸化Smad 3蛋白表达的调节

Objective To investigate the effects ofendothelin-1 (ET-1) and endothelin-3 (ET-3) on the expression of transformation growth factor-beta 1 (TGF-β1) and phosphorylation of Smad 3 in malignant melanoma cell line, A375. Methods Cultured A375 cells were classified into 5 groups, i.e. control group (no stimulation), ET-1 group (stimulated with ET-1), ET-1+BQ123 group (treated with ET-1 and BQ123),ET-1 + BQ788 group (treated with ET-1 and BQ788), ET-3 group (stimulated with ET-3), to receive different stimulation. The working concentrations were 0, 0.1, 1, 10, 100 nmol/L for ET-1 and ET-3, 10 μmol/L for BQ123 and BQ788. After another 12- and 24-hour culture, ELISA, RT-PCR and Western blot were used to detect the expression of TGF-β1 protein and mRNA as well as phosphorylated Smad 3 (P-Smad 3). Results The expression of TGF-β1 in A375 cells was up-regulated by ET-1, but down-regulated by ET-3, and both of the effects were in a concentration-dependent manner. Under the stimulation with ET-1 and ET-3 of 100 nmol/L, the level of TGF-β1 reached 1289.38 ± 89.42 ng/L per 105 cells and 85.09 ± 9.37 ng/L per 105 cells, respectively, significantly different from that in unstimulated cells (both P < 0.05). BQ123 signifi-cantly blocked the up-regnlatory effect of ET-1 on the expression TGF-β1 protein(P < 0.05), but BQ788 had no significant influence on the effect, so was the case with TGF-β1 mRNA. Western blot revealed that ET-1significantly elevated the expression of P-Smad 3 in A375 cells (P <0.05), and the elevation was significantly inhibited by BQ123, but not by BQ788. The expression of P-Smad 3 was statistically decreased by ET-3 in A375 cells (P <0.05). Conclusions The expression of TGF-β1 could be enhanced by ET-1, but suppressed by ET-3. It is likely that endothelin receptor A mediates the phosphorylation of Smad 3 induced by ET-1.