IIEF-5与NEVA检测在阴茎勃起功能障碍诊断中的意义

目的探讨应用国际勃起功能评分5(IIEF-5)问卷表结合夜间阴茎勃起测定系统(NEVA)筛选勃起功能障碍(ED)的可行性及意义。方法148例门诊ED病人,应用IIEF-5问卷表评分,再通过NEVA测定仪监测夜间阴茎勃起情况,次日数据输入主机回放并分析。结果93例为心理性ED;在19~69岁的5个年龄组中,重度ED的比例由11.8%到55.0%,NEVA中度异常者IIEF积分(12.98±2.58)分,NEVA重度异常者IIEF积分(7.32±1.04)分。结论NEVA能有效地鉴别心理性与器质性ED,IIEF-5评分值与NEVA检测阴茎勃起时血容量变化值有相关性。IIEF-5与NEVA检测结合,能提高诊断和评估ED的可靠性。     

Monosodium iodoacetate induces apoptosis via the mitochondrial pathway involving ROS production and caspase activation in rat chondrocytes in vitro

Monosodium iodoacetate (MIA) is an inhibitor of glyceraldehyde‐3‐phosphate dehydrogenase activity, and causes dose‐dependent cartilage degradation resembling the pathological changes of human osteoarthritis (OA). In this study, we assessed the apoptosis induced by MIA and clarified the underlying mechanisms using the primary rat chondrocytes. The apoptosis of primary rat chondrocytes was analyzed by flow cytometry. The levels of mitochondrial membrane potential (ΔΨm) were evaluated using fluorescence spectrophotometer. The production of reactive oxygen species (ROS) was determined by fluorescence spectrophotometer. Apoptosis‐related protein cytochrome c and procaspase‐3 expressions were examined by Western blotting. We found that MIA treatment induces apoptosis in chondrocytes, as confirmed by increases in the percent of apoptotic cells, up‐regulation of cytochrome c and caspase‐3 protein levels. Treatment with MIA increases ROS production and decreases the levels of ΔΨm. The antioxidant, N‐acetylcysteine (NAC), significantly prevented the production of ROS, the reduction of ΔΨm, the release of cytochrome c and the activation of caspase‐3. Further, NAC completely protected the cells from MIA‐induced apoptosis. Together these observations suggest that the mechanisms of MIA‐induced apoptosis are primarily via ROS production and mitochondria‐mediated caspase‐3 activation in primary rat chondrocytes. © 2012 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 31: 364–369, 2013     

丙泊酚对大鼠海马脑片CA1区长时程增强的影响

目的观察不同浓度丙泊酚对离体大鼠海马脑片CA1区长时程增强(LTP)的影响。方法30张海马脑片分为五组,Ⅰ、Ⅱ和Ⅲ组分别应用浓度为30、10和3μmolo/L的丙泊酚,Ⅳ组用脂肪乳,Ⅴ组不用药物作为对照。利用细胞外记录方式,以海马脑片CA1区群峰电位(PS)为观察指标,首先观察丙泊酚对CA1区基础传递的影响,待基线稳定后,记录高频刺激(HFS)后海马脑片CA1区PS的变化情况。结果Ⅰ、Ⅱ、Ⅲ组应用丙泊酚后PS降低,在持续给药后30min恢复至基线。实施HFS后,Ⅲ、Ⅳ和Ⅴ组的PS较HFS前显著升高(P<0.05,P<0.01);而Ⅰ、Ⅱ组PS与HFS前相比差异无显著意义(P>0.05)。HFS后,Ⅰ组PS显著低于Ⅱ、Ⅲ、Ⅳ和Ⅴ组(P<0.01),Ⅱ组PS也低于Ⅲ、Ⅳ和Ⅴ组(P<0.05)。结论丙泊酚可以抑制大鼠离体海马脑片CA1区LTP的形成。     

不同麻醉方法对乳腺癌患者血液流变学的影响

目的比较两种麻醉方法对乳腺癌患者血液流变学的影响。方法32例ASAⅠ~Ⅱ级行择期乳腺癌根治术患者随机分为两组:Ⅰ组为全麻组;Ⅱ组为硬膜外加全麻组,诱导前硬膜外给2%利多卡因5 ml,继之行全麻诱导。全麻用药两组相同,Ⅱ组术中每50分钟硬膜外给2%利多卡因6~8 ml。术后24 h内用0.5%布比卡因镇痛,Ⅰ组术后肌注哌替啶镇痛。分别于麻醉前、麻醉后30、90 min各取桡动脉血10 ml,测血液流变学指标。结果两组麻醉后309、0 min全血高切及低切粘度、红细胞压积及红细胞聚集指数下降(P<0.05),但Ⅱ组这几项指标下降明显且持续时间长,且有血浆粘度及纤维蛋白原浓度的下降(P<0.05)。结论全麻加用硬膜外阻滞对血液流变学的影响更有利于预防术后上肢静脉血栓的形成。     

甲基化CpG结合域蛋白1在胰腺癌组织中的表达和意义

目的：检测甲基化CpG结合域蛋白I（MBD1）蛋白在胰腺癌组织中的表达，并探讨其临床意义。方法：应用S-P免疫组织化学法检测38例胰腺癌、17例胰腺癌旁组织、8例胰腺良性肿瘤、3例慢性胰腺炎和6例正常胰腺组织中MBD1蛋白的表达。结果：MBD1在胰腺癌组织、正常胰腺组织、胰腺良性肿瘤、胰腺癌旁组织中的表达阳性率分别是76．32％（29/38）、16．67％（1／6）、25．0％（2／8）、29．41％（5／17），3例慢性胰腺炎标本中未见表达；胰腺癌阳性表达率明显高于正常胰腺、慢性炎症、良性肿瘤和癌旁对照组织（P〈0．05）。MBD1表达水平的高低与病人的性别、年龄、肿瘤部位、肿瘤大小、分化程度和TNM分期无显著性差异（P〉0．05）；而与淋巴结转移密切相关，有淋巴结转移者胰腺癌组织MBD1的表达阳性率为92．31％（24／26），高于无淋巴结转移者的41．67％（5／12）（P〈0．01）。结论：胰腺癌中MBD1呈高水平表达，并与胰腺癌的高转移侵袭活性有关，其机制可能与MBD1介导抑制多个甲基化相关抑癌基因的表达有关。MBD1的转录调控机制有待进一步研究。     

多层螺旋CT泌尿系成像在上尿路梗阻诊断中的应用

目的 探讨多层螺旋CT泌尿系成像（MSCTU）在上尿路梗阻性疾病中的诊断价值。方法 对17例经B超或IVU检查显示上尿路梗阻患者行螺旋CT扫描，并行3D重建，将诊断结果与手术结果进行对照。结果 MSCTU诊断输尿管结核4例，肾盂输尿管连接部狭窄6例。输尿管末端狭窄2例，输尿管阴性结石3例。输尿管肿瘤1例，腔静脉后输尿管1例，均显示出梗阻部位及尿路扩张的形态。手术结果与MSCTU诊断相符。结论 SCTU是一种安全有效的非侵袭性的影像学检查方法，特别对患肾功能严重受损的上尿路梗阻性疾病患者具有特殊诊断价值。     

年龄与成年人肾细胞癌临床分期的相关性分析

目的 探讨年龄与成年人肾细胞癌（renalcell carcinoma，RCC）临床分期的相关性。方法 回顾性分析310例病理确诊的成年RCC患者的临床资料，按年龄大小分为10岁以下组（≤40岁）、40-60岁组、60岁以上组（≥60岁），对三组患者的症状表现、病理学特点、淋巴结转移进行比较，以此了解年龄与成年人RCC临床分期的相关性。结果 40岁以下组偶发癌所占的比例明显低于10-60岁组（X^2=3．294，P=0．070），60岁以上组则显著低于40-60岁组（X^2=3．950，P=0．047）；分化不良RCC的发生率随年龄增长逐渐降低（11．6％vs．5．2％vs．2．7％），且40岁以下组与60岁以上组相比较差异有显著性意义（P=0．038）；淋巴结转移的发生率同样随年龄的增长而降低，且40岁以下组与其他两组相比较差异均有显著性意义（P〈0．05）；三组临床分期的构成比差异有显著性意义（P〈0．01）．Ⅰ期所占的比例随年龄增长逐渐降低，Ⅱ期在10岁以下组中所占的比例明显低于其他两组．而Ⅰ期＋Ⅱ期在40-60岁组中的比例则明显高于其他两组。结论 偶发癌在各年龄组的不同比例值是导致不同年龄组患者临床分期出现差异的主要因素；淋巴结转移及分化不良RCC是导致这种差异的次要因素。     

RIPK3‐Mediated Necroptosis Promotes Donor Kidney Inflammatory Injury and Reduces Allograft Survival

Kidney transplant injury occurs with ischemia and alloimmunity. Members of the receptor interacting protein kinase family (RIPK1,3) are key regulators of “necroptosis,” a newly recognized, regulated form of necrosis. Necroptosis and apoptosis death appear to be counterbalanced as caspase‐8 inhibition can divert death from apoptosis to necrosis. Inhibition of necroptosis in donor organs to limit injury has not been studied in transplant models. In this study, necroptosis was triggered in caspase inhibited tubular epithelial cells (TEC) exposed to tumor necrosis factor alpha in vitro, while RIPK1 inhibition with necrostatin‐1 or use of RIPK3^?/? TEC, prevented necroptosis. In vivo, short hairpin RNA silencing of caspase‐8 in donor B6 mouse kidneys increased necroptosis, enhanced high‐mobility group box 1 release, reduced renal function and accelerated rejection when transplanted into BALB/c recipients. Using ethidium homodimer perfusion to assess necrosis in vivo, necrosis was abrogated in RIPK3^?/? kidneys postischemia. Following transplantation, recipients receiving RIPK3^?/? kidneys had longer survival (p = 0.002) and improved renal function (p = 0.03) when compared to controls. In summary, we show for the first time that RIPK3‐mediated necroptosis in donor kidneys can promote inflammatory injury, and has a major impact on renal ischemia–reperfusion injury and transplant survival. We suggest inhibition of necroptosis in donor organs may similarly provide a major clinical benefit.

     

“黑皮”，绝对劣品后遗症

为了变美而使用化妆品，不曾想却伤害了自己的肌肤。本刊记者提醒爱美女孩应引以为戒！[编者按]