术前同步放化疗在Ⅱ B期宫颈癌患者中的临床研究

目的 探讨Ⅱ B期宫颈癌患者术前同步放化疗的可行性及疗效.方法 回顾性分析56例ⅡB期宫颈癌患者的治疗过程.按照治疗方式的不同分为2组,术前同步放化疗组(26例)和单纯放疗组(30例),比较2组患者不良反应及远期疗效.结果 与单纯放疗组比较,同步放化疗组骨髓抑制发生率、恶心及呕吐发生率高于单纯放疗组(P＜0.05),但经过对症处理,不影响治疗进程.与单纯放疗组比较,术前同步放化疗组3年的局部复发率明显降低,3年生存率提高(P＜0.05),而1年的局部复发率、1年生存率两组无明显差异.结论 Ⅱ B期宫颈癌患者术前行同步放化疗可降低肿瘤复发率,提高3年生存率.     

基于深度学习的睑板腺腺体分割方法研究

目的:探讨应用深度学习技术解决睑板腺腺体自动分割问题的效果与价值。方法:采集并筛选出193幅红外睑板腺图像构建图像数据库,由3名临床医师对图像进行人工标记;引入UNet++网络与自动数据增广策略构建睑板腺腺体自动分割模型,采用精确率、敏感性、特异性、准确率和交并比分析该模型的可行性与有效性。结果:以人工标注结果为金标准,基于UNet++的睑板腺腺体自动分割模型取得94.31%的准确率,敏感性、特异性分别为82.15%和96.13%,腺体分割表现具有较好的稳定性,模型处理单张图像的平均用时仅为0.11s。结论:引入深度学习技术实现睑板腺腺体的自动分割,具有良好的准确性、稳定性和高效性,可服务于睑板腺功能障碍患者腺体形态参数的计算,辅助相关疾病的临床诊断和筛查,提高诊断效率。     

基于视网膜神经血管单元损伤及其耦联失衡防治糖尿病视网膜病变的研究进展

糖尿病视网膜病变(DR)作为常见的糖尿病并发症之一,是导致失明的主要原因。传统上,DR主要被认为是一种微血管疾病,随着研究的进展,目前认为神经-胶质-血管单元(NVU)破坏及其耦联机制(coupling)失衡在DR发病的早期起到了关键作用。了解NVU的细胞和分子基础,以及糖尿病如何改变正常的细胞通讯和破坏细胞环境,对DR的早期防治具有重要的意义。本文总结视网膜NVU及其参与DR发病分子机制,基于视网膜NVU修复的DR治疗,并对DR未来发展前景及问题进行探讨。     

Prolonged exposure to resistin inhibits glucose uptake in rat skeletal muscles

AIM: To assess the effects and mechanisms of the action of resistin on basal and insulin-stimulated glucose uptake in rat skeletal muscle cells. METHODS: Rat myoblasts (L6) were cultured and differentiated into myotubes followed by stimulation with single commercial resistin (130 ng/mL, 0-24 h) or cultured supernatant from 293-T cells transfected with resistin-expressing vectors (130 ng/mL, 0-24 h). Liquid scintillation counting was used to quantitate [3H] 2-deoxyglucose uptake. The translocation of insulin-sensitive glucose transporters GLUT4 and GLUT1, synaptosomal-associated protein 23 (SNAP23) and GLUT protein content, as well as the tyrosine phosphorylation status and protein content of insulin receptor substrate (IRS)-1, were assessed by Western blotting. RESULTS: Treatment of L6 myotubes with single resistin or cultured supernatant containing recombinant resistin reduced basal and insulin-stimulated 2-deoxyglucose uptake and impaired insulin-stimulated GLUT4 translocation. While SNAP23 protein content was decreased, no effects were noted in GLUT4 or GLUT1 protein content. Resistin also diminished insulin-stimulated IRS-1 tyrosine phosphorylation levels without affecting its protein content. The effects of recombinant resistin from 293-T cells transfected with resistin-expressing vectors were greater than that of single resistin treatment. CONCLUSION: Resistin regulated IRS-1 function and decreased GLUT4 translocation and glucose uptake in response to insulin. The downregulated expression of SNAP23 may have been partly attributed to the decrease of glucose uptake by resistin treatment. These observations highlight the potential role of resistin in the pathophysiology of type 2 diabetes related to obesity.     

Synthesis and anti-diabetic activity of （RS）-2-ethoxy-3-{4-[2-（4-trifluoro-methanesulfonyloxy-phenyl）-ethoxy]-phenyl}-propionic acid

AIM: To synthesize and study the anti-diabetic activity of (RS)-2-ethoxy-3-{4-[2-(4-trifluoromethanesulfonyloxy-phenyl)-ethoxy]-phenyl}-propionic acid (compound I). METHODS: Compound I was prepared in 6 steps, using 4-(2-hydroxy-ethyl)-phenol as the starting material. The in vitro selectivity and potency of target compound I, rosiglitazone and WY-14643 on human PPARalpha and PPARgamma were determined in reporter gene assays. In vivo, rosiglitazone and compound I were administered orally to KK(Ay) mice for 14 d. Insulin tolerance tests and oral glucose tolerance tests were performed on the 10th and 14th day of treatment, respectively. At the end of the treatment, sera were collected for biochemical analysis. RESULTS: In vitro, compound I significantly activated both PPARalpha and PPARgamma. In vivo, compound I corrected the impaired insulin and glucose tolerance of KK(Ay) mice, and produced a significant reduction in plasma triglyceride levels after 14 d of treatment. The effect produced was significant compared with the control group. CONCLUSION: Both in vitro and in vivo anti-diabetic activity studies for compound I were conducted and the data suggest that this compound is a potentially effective anti-diabetic agent.     

内生真菌SEF15927对截短侧耳素的微生物羟化研究

目的 研究植物内生真菌SEF15927对截短侧耳素的转化作用.方法 利用液体培养生长细胞对截短侧耳素进行生物转化.发酵液经乙酸乙酯萃取和硅胶柱层析分离获得一个羟化产物.运用质谱和核磁共振光谱鉴定结构.结果 转化产物为2-羟基截短侧耳素.结论 植物内生真菌SEF15927为一具有高转化率的截短侧耳素羟化菌株,     

桑叶提取物降血脂作用的动物试验研究

目的了解桑叶提取物降血脂效果。方法以100、200、400mg／kg．bw剂量的桑叶提取物连续给大鼠灌胃30d，次日采血测定TC、TG及HDL—C的含量。结果受试样品组大鼠血清的TC、TG含量低于模型对照组。而其HDL—C含量高于模型对照组。结论桑叶提取物具有降低血脂的作用。     

C型钠尿肽抑制大鼠胃窦环行肌自发性收缩活动

目的：研究钠尿肽对胃动力的作用及其可能的机制．方法：用四道记录仪记录胃窦环行肌条的自发性收缩活动;利用放射免疫技术测定cGMP的产生量;利用放射自显影技术分析钠尿肽受体在胃内的分布情况．结果：钠尿肽受体在大鼠胃的不同部位均有分布,但在胃窦部最多。ANP、BNP和CNP均能抑制胃窦环行肌条的自发性收缩,其中,CNP的作用尤为明显并呈剂量依赖关系．CNP的这种抑制性作用被鸟苷酸环化酶抑制剂LY83583所削弱,而用cGMF敏感的磷酸酯酶抑制剂zaparinist预处理时CNP的抑制作用明显增加．CNP明显提高胃窦环行肌cGMP的浓度．用非选择性钾通道阻断剂TEA预处理后发现CNP对胃窦环行肌自发性收缩活动的抑制作用明显减弱．结论：钠尿肽受体在大鼠的胃窦分布最多．CNP明显抑制大鼠胃窦环行肌的自发性收缩活动．CNP对大鼠胃窦环行肌自发性收缩活动的抑制效应是通过cGMP途径实现的．钾通道也参与CNP对大鼠胃窦平滑肌的舒张过程。     

评价抗快速室性心律失常药物的心电生理-电药理学方法

用冠状动脉Harris二期结扎并部分再灌注及吻合支缝扎法造成犬急性心肌梗塞，5－8天后，辅以心脏程控制激技术（PES）进行心电生理检查及复制快速室性心律失常，研制成犬在体心脏心电生理－电药理学实验模型，并观察了普鲁卡因胺（PA）对该实验模型的电生理影响。结果表明。PA能显著延长QTc间期，RERP，NERP及IERP，缩小IDR和VDR，抑制心室PES诱发的室速和室颤，并能有效地预防犬心肌梗塞后再次急性缺血所导致的自发性室颤，表明PA有抗缺血性快速室性心律失常的心电生理－电药理作用。结果同时表明，该心电生理－电药理学实验的犬模型具有很高的可靠性，重复性及临床相关性，是一种有价值的评价抗快速室性心律失常药物的心电生理一电药理学方法。     

二烯丙基二硫对人胃癌MGC803细胞G_2/M期的阻滞作用

目的　探讨二烯丙基二硫 (DADS)对人胃癌MGC80 3细胞G2 /M期的阻滞作用及分子机制。方法　体外培养MGC80 3细胞 ,采用MTT比色实验、细胞计数法 ,流式细胞光度术和Westernblot分析DADS对MGC80 3细胞的抑制增殖作用 ,细胞周期分布的影响及细胞周期相关蛋白的表达。结果　MTT法显示 ,2 0mg·L-1DADS、30mg·L-1DADS作用MGC80 3细胞 72h后 ,生长抑制率分别达2 5 7%、5 8 6 %。细胞计数法表明常规培养MGC80 3细胞群体倍增时间为 2 9 92h ,30mg·L-1DADS作用MGC80 3细胞后 ,其细胞群体倍增时间延长到 5 5 5 8h。流式细胞仪分析结果显示DADS呈浓度依赖性将MGC80 3细胞阻滞在G2 /M期。 30mg·L-1DADS作用MGC80 3细胞 36h ,与对照组相比 ,可使G2 /M期细胞增加到 4倍多。Westernblot分析表明在G2 /M期阻滞同时有Cdc2 5C蛋白表达下降 ,但CDK1蛋白表达不受DADS作用的影响。结论　DADS对MGC80 3细胞的抑制增殖作用与G2 /M期阻滞有关 ,DADS对MGC80 3细胞G2 /M期阻滞的分子机制可能与降低Cdc2 5C蛋白水平有关