Single-step transvenous extraction of a passive fixation lead with delayed perforation of the right ventricle

Delayed pacemaker lead perforation is a very rare complicationand most of the published reports involve active fixation leads.The authors report an uneventful transvenous extraction of apassive fixation lead, which had a delayed perforation of theright ventricle, disclosed two months after pacemaker implantation.     

Delayed esophageal perforation after laparoscopic fundoplication in a patient with diabetes mellitus: a case report

A 55-year-old man on hemodialysis for diabetic nephropathy suffered from vomiting and hematoemesis. He was diagnosed to have reflux esophagitis with Los Angeles classification grade D, which was accompanied by a shortened esophagus and stricture. His reflux esophagitis was proton pump inhibitor resistant. Therefore, we performed laparoscopic Toupet fundoplication. Delayed esophageal perforation occurred on the ninth day postoperatively, for which he had to be reoperated. To our knowledge, there is no previous report of delayed esophageal perforation after laparoscopic fundoplication. Esophageal perforation might have been caused by denudation or attenuation of the abdominal esophagus.     

甲状旁腺腺瘤9例临床特点及延误诊断分析

目的 探讨甲状旁腺腺瘤患者的临床特点和延误诊断的原因。方法 回顾性分析2000年1月至2005年6月华中科技大学同济医学院协和医院收治的经手术确诊的9例甲状旁腺腺瘤患者的资料。结果 9例中男性4例，女性5例。误诊时间8个月至11年。9例患者均有骨骼系统临床表现，同时兼有泌尿系统、消化系统表现者各有7例和6例。所有患者均有低血磷和血碱性磷酸酶升高，8例有高血钙和高尿钙。7例患者血清甲状旁腺素（PTH）明显升高。^99m锝-甲氧基异丁基异腈（^99mTc-MIBI）甲状旁腺显像是最佳定位检查。结论 完整的病史，细致的体检和实验室检查对于甲状旁腺腺瘤的诊断十分重要。     

结核性肛周脓肿延误诊断临床分析(附5例报告)

2015年12月至2017年12月,航空总医院普外科收治的320例肛周脓肿患者中5例患者术后30d内切口未愈合,最终诊断为结核性肛周脓肿;其中3例并发肺结核,给予2R-H-E-Z/4R-H-E抗结核药物化疗方案治疗后,切口均愈合,平均愈合时间(25.5±3.6)d,无复发。分析延误诊断原因主要为:结核性肛周脓肿临床较少见,临床表现缺乏特异性,医务人员对此病的认识不足,未对患者病史进行详细分析,未进行脓液抗酸杆菌检查及肛周病变组织病理学检查。对于肛周脓肿的患者,应仔细询问患者病史,常规进行脓液分泌物抗酸杆菌检查、组织病理学检查。确诊为结核性肛周脓肿后应给予规范抗结核药物化疗方案治疗6个月至1年。     

水通道蛋白4对一氧化碳中毒后迟发性脑病大鼠神经损伤的影响

目的 探讨水通道蛋白4(Aquaporin 4,AQP4)对一氧化碳(Carbon monoxide,CO)中毒后迟发性脑病(Delayed encephalopathy,DEACMP)大鼠神经损伤的影响。方法 将210只雄性SD大鼠随机分为空白对照(Blank control,BC)组、CO中毒(CO)组、钠-钾-氯共转运体(Na⁺-K⁺-Cl^- cotransporter,NKCC)抑制剂处理(布美他尼)组、p38-丝裂原活化蛋白激酶(Mitogen activated protein kinase,MAPK)抑制剂处理(MAPK)组和AQP4特异性抑制剂处理(AQP4抑制剂)组,每组各42只; 根据造模后不同时间点将每组大鼠进一步分为染毒3、6、12、24、48、72 h和7 d后共7个亚组,每亚组各6只; 取大鼠脑前额叶皮质组织,计算脑皮质含水量,采用HE法观察脑皮质形态; 采用免疫组化链霉菌抗生物素蛋白-过氧化物酶(Streptavidin-perosidase,SP)染色法测定大鼠脑皮质AQP4,p38 MAPK,NKCC1、胶质纤维酸性蛋白(Glial fibrillary acidic protein,GFAP)和S100钙结合蛋白B(S100 calcium binding protein B,S100B)蛋白表达水平。结果 与BC组比较,CO组大鼠在染毒3、6、12、24、48、72 h后尾静脉COHB水平和脑皮质含水量显著升高,脑皮质AQP4,p38 MAPK,NKCC1,GFAP和S100B蛋白表达水平显著升高,染毒7 d后恢复正常(P<0.05); 与CO组比较,布美他尼组、MAPK组和AQP4抑制剂组大鼠脑皮质含水量显著降低,脑皮质AQP4,p38 MAPK,NKCC1,GFAP和S100B蛋白表达水平显著降低,且AQP4抑制剂组变化更明显(P<0.05)。结论 p38-MAPK/NKCC信号通路可能参与调控CO中毒DEACMP大鼠脑皮质AQP4表达,抑制AQP4表达可有效减轻大鼠脑水肿并改善预后,有望成为预防和治疗DEACMP的新靶点。     

Single Immunization of Newborn Mice with Heterologous Type-II Collagen Induces Arthritic Disease

Collagen-induced arthritis (CIA) is a widely accepted model of autoimmune disease with significant similarities to rheumatoid arthritis in humans. CIA is provoked in susceptible strains upon immunization of adult mice with native type-II collagen in complete Freund's adjuvant (CFA). Neonatal exposure to antigen is supposed to result in T cell clone deletion and induction of tolerance. Here we report that the neonatal injection of bovine type-II collagen (bCII) to ICR (CD-2) mice triggers the development of autoimmune chronic joint inflammation. Compared with standard CIA significant joint swelling was not observed and anti-collagen antibodies were not detected if the second challenge with the antigen was not supplied. Histopathologic examination of the joints showed cell infiltration, synovial hyperplasia and at the later period bone destruction. Mice immunized as neonates expressed Ag-specific proliferative response and delayed type hypersensitivity (DTH) reaction to bCII.     

The effect of acute and repeated ischemic preconditioning on recovery following exercise-induced muscle damage

ObjectivesThe aim of this investigation was to determine if acute or repeated applications of ischemic preconditioning (IPC) could enhance the recovery process, following exercise induced muscle damage (EIMD).DesignRandomized control trial.MethodsTwenty-three healthy males were familiarised with the muscle damaging protocol (five sets of 20 drop jumps from a 0.6 m box) and randomly allocated to one of three groups: SHAM (3 × 5 min at 20 mmHg), Acute IPC (3 × 5 min at 220 mmHg) and Repeated IPC (3 days x 3 × 5 min at 220 mmHg). The indices of muscle damage measured included creatine kinase concentration ([CK]), thigh swelling, delayed onset muscle soreness, counter movement jumps (CMJ) and maximal voluntary isometric contraction (MVIC).ResultsBoth acute and repeated IPC improved recovery in MVIC versus SHAM. Repeated IPC led to a faster MVIC recovery at 48 h (101.5%) relative to acute IPC (92.6%) and SHAM (84.4%) (P < 0.05). Less swelling was found for both acute and repeated IPC vs. SHAM (P < 0.05) but no group effects were found for CMJ, soreness or [CK] responses (P > 0.05).ConclusionTaken together, repeated IPC can enhance recovery time of MVIC more than an acute application, and both reduce swelling following EIMD, relative to a SHAM condition.     

Evolution of the stroke paradigm: A review of delayed recanalization

While the time window for reperfusion after ischemic stroke continues to increase, many patients are not candidates for reperfusion under current guidelines that allow for reperfusion within 24 h after last known well time; however, many case studies report favorable outcomes beyond 24 h after symptom onset for both spontaneous and medically induced recanalization. Furthermore, modern imaging allows for identification of penumbra at extended time points, and reperfusion risk factors and complications are becoming better understood. Taken together, continued urgency exists to better understand the pathophysiologic mechanisms and ideal setting of delayed recanalization beyond 24 h after onset of ischemia.