微波配合序贯扩肛治疗陈旧性肛裂患者的临床分析

目的:探讨微波配合序贯扩肛治疗陈旧性肛裂的临床疗效。方法:选取陈旧性肛裂患者78例,随机分为对照组和治疗组,每组各39例。对照组患者采用后卫内括约肌部分切断治疗,治疗组患者采用微波配合序贯扩肛治疗。结果:观察组患者术中出血量、切口愈合时间均少于对照组(P<0.05),并发症发生率低于对照组(P<0.05)。结论:采用微波配合序贯扩肛治疗陈旧性肛裂,临床疗效显著。     

Postoperative development of sarcopenia is a strong predictor of a poor prognosis in patients with adenocarcinoma of the esophagogastric junction and upper gastric cancer

Background

There were few studies assessed the postoperative sarcopenia in patients with cancers. The objective of present study was to assess whether postoperative development of sarcopenia could predict a poor prognosis in patients with adenocarcinoma of esophagogastric junction, (AEG) and upper gastric cancer (UGC).

Lysophosphatidylcholine‐induced cytotoxicity and protection by heparin in mouse brain bEND.3 endothelial cells

A pathological feature in atherosclerosis is the dysfunction and death of vascular endothelial cells (EC). Oxidized low‐density lipoprotein (LDL), known to accumulate in the atherosclerotic arterial walls, impairs endothelium‐dependent relaxation and causes EC apoptosis. A major bioactive ingredient of the oxidized LDL is lysophosphatidylcholine (LPC), which at higher concentrations causes apoptosis and necrosis in various EC. There is hitherto no report on LPC‐induced cytotoxicity in brain EC. In this work, we found that LPC caused cytosolic Ca²⁺ overload, mitochondrial membrane potential decrease, p38 activation, caspase 3 activation and eventually apoptotic death in mouse cerebral bEND.3 EC. In contrast to reported reactive oxygen species (ROS) generation by LPC in other EC, LPC did not trigger ROS formation in bEND.3 cells. Pharmacological inhibition of p38 alleviated LPC‐inflicted cell death. We examined whether heparin could be cytoprotective: although it could not suppress LPC‐triggered Ca²⁺ signal, p38 activation and mitochondrial membrane potential drop, it did suppress LPC‐induced caspase 3 activation and alleviate LPC‐inflicted cytotoxicity. Our data suggest LPC apoptotic death mechanisms in bEND.3 might involve mitochondrial membrane potential decrease and p38 activation. Heparin is protective against LPC cytotoxicity and might intervene steps between mitochondrial membrane potential drop/p38 activation and caspase 3 activation.     

生殖专科机构预防新型冠状病毒肺炎感染的措施

新型冠状病毒肺炎(简称新冠肺炎, COVID-19)是近期流行的一种新发传染病,已造成大量人员感染,其中包括医务人员。为预防生殖医学的医院感染,有效降低新冠肺炎在生殖专科机构传播的风险,通过查询相关文献、指南和规范等,并结合生殖医学特点,制定生殖医学有关的临床区、手术室和实验室及相关人员预防新冠肺炎的措施。     

Proliferation of Hepatocytes and Attenuation from Carbon Tetrachloride Hepatotoxicity by Gadolinium Chloride in Rats

Abstract: Intravenous injection of gadolinium chloride (GdCl₃) at a dose of 10 mg/kg caused an increase in proliferating cell nuclear antigen labeling index and the grade of pyronin positivity (RNA level) in rat liver. In CCl₄-exposed rats, pretreatment with GdCl₃ also showed a preventive effect of the liver injury both biochemically and histologically. Moreover, the proliferative action preceded the attenuative effect of the liver injury. Results suggest that GdCl₃ induces hepatocyte proliferation, and this action of GdCl₃ may modify the development of CCl₄-induced liver injury.     

实验性下腔静脉可扩张性内支撑形态学研究

目的 :通过观察实验犬下腔静脉内放置可扩张性内支撑后血管的形态学变化 ,确定支撑的内皮化进程 ,以期为临床减少内支撑阻塞、合理应用抗凝剂提供组织学的依据。　 方法 :在 14只杂种犬下腔静脉内放置金属内支撑 ,于术后 1个月起 ,逐月取下腔静脉作光镜和电镜检查。　 结果 :术后 1个月左右 ,内支撑基本内皮化 ,5个月完成血管的重构。　 结论 :早期抗凝治疗是防止内支撑阻塞的关键 ,首次提出内支撑放置后血管重构的现象     

In Vivo Molecular Imaging Characterizes Pulmonary Gene Expression During Experimental Lung Transplantation

Experimental gene therapy is a promising strategy to prevent ischemia-reperfusion (I/R) injury and allograft rejection after lung transplantation, and methods will eventually be needed to characterize pulmonary transgene expression in vivo in humans. Therefore, we studied positron emission tomography (PET) as a means of performing in vivo molecular imaging in rodent models of lung transplantation. Rats were transfected endotracheally with adenovirus encoding a fusion gene of a mutant Herpes simplex virus-1 thymidine kinase and the green fluorescent protein gene (the former serving as an imaging reporter gene). Twenty-four hours after transfection, lungs were transplanted in groups representing normal transplantation, I/R injury and acute allograft rejection. Imaging was obtained either 24 h after transplantation to study reperfusion injury or 4 days after transplantation to study graft rejection. After imaging, lungs were excised and analyzed for thymidine kinase activity. Imaging detected transgene expression in transplanted lungs even in the presence of acute rejection or I/R injury. The PET imaging signal correlated with in vitro lung tissue assays of thymidine kinase activity (r(2) = 0.534). Thus, noninvasive molecular imaging with PET is a feasible, sensitive and quantitative method for characterizing pulmonary transgene expression in experimental lung transplantation.     

Plasma and tumor gastrin in patients with primary hyperparathyroidism

It is well known that primary hyperparathyroidism is often associated with peptic ulcer. The purpose of this study is to confirm the relationship between the gastrin-levels before and after parathyroidectomy in fourteen patients with primary hyperparathyroidism, and to determine the localization of gastrin in the surgically resected parathyroid tumor. The results obtained were as follows: 1) Three patients had peptic ulcer (gastric ulcer and duodenal ulcer), the incidence being 21%. 2) The basal serum gastrin levels were 123.0% +/- 68.1 pg/ml before operation and decreased to 90.2 +/- 44.5 pg/ml after operation. In the 3 patients with slightly elevated gastrin levels, the mean level before operation was 209.1 +/- 61.2 pg/ml. The gastrin level decreased to 116.4 +/- 62.0 pg/ml after operation. 3) Gastrin immunoreactivity was detected in 10 out of 14 tumors and its localization was at the periphery of tumor cells. From these results, we conclude that extragastric gastrin secretion from parathyroid tumors may be one of the cause of peptic ulcer in patients with primary hyperparathyroidism.