胰腺分裂症的内镜诊治方法及临床价值

目的探讨胰腺分裂症(PD)内镜诊治的常规及补救方法、临床疗效和安全性。方法回顾性分析该院2014年1月-2016年12月经内镜下逆行胰胆管造影(ERCP)诊治的17例PD患者的临床病历资料,并电话回访患者症状改善及术后恢复情况。结果 17例PD患者,仅1例进行了再次内镜下治疗,共进行内镜下治疗18例次。内镜下治疗常规策略包括:副乳头括约肌切开术(MiES)、副胰管支架置入术(EDSi)及副乳头括约肌扩张术(MiED)。术中16例次手术过程顺利,2例次经过困难,但最终采用补救方法联合超声内镜(EUS)对接技术使手术成功。术后并发出血1例次,并发支架相关性胰腺炎2例次,无穿孔和发热等其他并发症发生。17例患者无1例失访,随访时间(16.3±9.4)个月,所有患者术后腹痛视觉模拟评分(VAS)较术前明显改善[(2.0±1.2)vs(7.0±1.8)分],差异有统计学意义(P 0.05)。结论内镜诊治PD具有安全、有效、创伤及并发症少等特点,可明显改善患者临床症状,值得临床推广。根据临床情况可选择常规方法诊治,对于插管困难患者,可联合EUS通过对接技术进行补救诊治。     

A sieving method for collecting the metacercariae of trematode parasites from freshwater fish

This study describes a sieving method for the collection of metacercariae from frozen (-20 degrees C) freshwater fish. Digested fish tissue is filtered through a series of sieves; the crude filtrate is then centrifuged. Centrifugation produces a sediment from which metacercariae can be removed. Half of the metracercariae that were obtained from the fish meat that had been frozen for 10 days (-20 degrees C) were dead; the other half were alive and some larvae were moving slowly.     

Tissue Kallikrein Prevents Restenosis After Stenting of Severe Atherosclerotic Stenosis of the Middle Cerebral Artery: A Randomized Controlled Trial

In-stent restenosis (ISR) following intracranial artery stenting affects long-term clinical outcome. This randomized controlled trial sought to identify the long-term efficacy of exogenous tissue kallikrein (TK) for preventing ISR after intracranial stenting of symptomatic middle cerebral artery (MCA) atherosclerotic stenosis.Sixty-one patients successfully treated with intracranial stenting for symptomatic MCA M1 segment stenosis (>70%) were enrolled and randomized into 2 groups: control group and TK group. Patients in the TK group received human urinary kallidinogenase for 7 days, followed by maintenance therapy of pancreatic kallikrein for 6 months. The primary end point was angiographically verified ISR at 6 months, and secondary end points included vascular events and death within 12 months. Endogenous TK plasma concentrations of patients were measured before stenting and at the 6-month follow-up time-point.Patients in the TK group had lower occurrence rates of ISR and vascular events than patients in the control group. There was no difference in endogenous TK levels in plasma at 6 months postoperatively between the TK and control groups. Further subgroup analysis revealed that patients without ISR had higher endogenous TK levels at baseline and lower concentrations at 6 months postoperatively compared with patients who underwent ISR.Exogenous TK is effective for the prevention of ISR after intracranial stenting.     

Initial evidence of endothelial cell apoptosis as a mechanism of systemic capillary leak syndrome

BACKGROUND: Systemic capillary leak syndrome (SCLS) is a rare disorder of unknown etiology that is characterized by acute recurrent attacks of hypovolemic shock commonly following an inflammatory stimulus such as a viral illness. Prophylactic therapy is generally ineffective, and the outcome is frequently fatal. METHODS: In order to investigate the cellular mechanisms leading to SCLS, we examined the effects of sera from two patients with active SCLS on microvascular endothelial cell apoptosis in vitro. Apoptosis was determined by morphologic criteria, DNA fragmentation, annexin V stain, and by a quantitative photometric assay. The apoptotic pathway was investigated by Western blot of endothelial cells lysate after exposure to SCLS sera. RESULTS: The sera from patients with active SCLS mediated profound apoptosis of microvascular endothelial cells shortly after exposure. The exposed microvascular endothelial cells underwent immediate apoptosis as evidenced by morphologic changes, plasma membrane phosphatidylserine exposure, and by DNA fragmentation. Increased Bax/Bcl-2 ratio in endothelial cells exposed to SCLS sera was observed and suggested an oxidation injury as the possible mechanism for endothelial apoptosis. This potential mechanism was further explored by measuring intracellular reactive oxygen species (ROS) following SCLS serum exposure. Sera from both patients caused marked increases in ROS, initially detectable at 1 h and persisted for at least 12 h, with control serum from healthy subjects showing no effect on basal endothelial cell ROS concentrations. CONCLUSION: Components from the sera of patients with active systemic capillary leak syndrome in contrast to healthy subject sera mediate early and extensive endothelial apoptosis in vitro that is associated with oxidation injury. These data represent compelling initial evidence for oxidation-induced apoptosis as a likely mechanism for endothelial injury leading to SCLS.