二尖瓣瓣膜成形术治疗非风湿性二尖瓣关闭不全的临床效果

目的 探讨二尖瓣瓣膜成形术(MVP)治疗非风湿性二尖瓣关闭不全的临床效果.方法 选择2006年1月至2013年11月内蒙古医科大学附属医院非风湿性二尖瓣关闭不全患者43例,病因包括先天性瓣叶脱垂、缺血性改变、退行性改变、感染性病变.手术方式为单纯瓣叶部分切除、单纯腱索短缩或转移、瓣膜裂修补、瓣叶部分切除+双孔成形、腱索短缩或转移+瓣膜裂修补、术中均放置二尖瓣成形环,同期冠状动脉旁路移植术,术中采用注水试验和食管内超声评价成形效果.结果 术前超声心动图示二尖瓣均为中大量关闭不全,术中食管内超声发现中量关闭不全2例,改行二尖瓣置换术.43例患者中术后在院死亡1例.出院后随访1 ～83个月,平均(43±17)个月,无再次手术者,无死亡者,超声心动图示40例二尖瓣瓣膜成形术患者中无或少量二尖瓣关闭不全27例,少量到中量关闭不全13例.结论 应用二尖瓣瓣膜成形术治疗非风湿性二尖瓣关闭不全是可行的,可以取得良好的效果.     

食管射频消融术后发热的影响因素分析

目的　探讨食管内镜下射频消融术（radiofrequency ablation,RFA）后患者发热的独立危险因素。方法　2016年1月—2021年4月,因早期食管癌就诊于长海医院消化内科,且病变范围超过食管3/4环周的51例病例纳入病例对照研究。患者均行RFA治疗,按术后是否发热分成发热组（n=15）和未发热组（n=36）,主要收集患者一般情况、消化道肿瘤家族史、病变长度、病变范围、消融能量和消融次数用于单因素分析,其中P<0.1的变量再进一步纳入多因素Logistic回归分析探究RFA术后发热的独立危险因素。结果　单因素分析发现,病变长度（t=-3.89,P<0.001）、病变范围（χ2=11.52,P=0.001）和消融能量（P=0.001）在2组间差异有统计学意义。Pearson相关性显示,病变长度与病变环周长度存在明显正相关（r=0.71,P<0.001）,而病变范围由病变环周长度决定,因此最终将病变长度和消融能量这两个变量纳入Logistic回归方程。Logistic回归分析结果显示,食管病变长度每增加1 cm,患者发生RFA术后发热的风险是前者的1.21倍（95%CI：1.01～1.43,P=0.037）;术中使用12 J消融能量者,发生RFA术后发热的风险是使用10 J消融能量者的0.43倍（95%CI：0.22～0.85,P=0.015）。结论　病变长度和消融能量是导致食管RFA术后发热的独立危险因素。长节段早期食管癌者更易发生RFA术后发热,术中使用低消融能量者更易发生RFA术后发热。     

内镜黏膜下剥离术切除胃内异位胰腺伴导管内乳头状黏液性肿瘤1例

异位胰腺伴导管内乳头状黏液性肿瘤形成是一种罕见的疾病,国内鲜见报道,主要位于胃、肝内胆管和小肠。本文报道1例病例,病变位于胃壁,术前超声内镜显示病变位于黏膜下层,内部回声局部呈中高回声,可见囊腔样无回声区,经内镜黏膜下剥离术完整切除,术后病理为异位胰腺伴导管内乳头状黏液性肿瘤（胃型）。     

城市固体废物产生量与经济增长脱钩关系的实证研究——以北京市为例

采用脱钩理论的3种评价方法 (脱钩指数法、IPAT模型法以及弹性分析法)对北京市城市固体废物产生量与经济增长之间的状态进行对比分析,发现:3种评价方法的原理不同,但评价结果基本一致,但Tapio(2005)提出的弹性分析法模型在指标细分上存在问题;北京市1979—2011年城市固体废物产生量总体实现相对脱钩,但通过分析个别年份状态数据发现要真正实现城市固体废物的减量化需要管理制度的改进,以及市民环保素质的提升。     

淮安市清河区公厕空间布局探讨

运用人群密度分析法和人口分布分析法,对淮安市清河区公共厕所的布局、质量、数量进行分析,并提出了公厕布局方案。     

The common characteristics and mutual effects of heart failure and atrial fibrillation: initiation,progression, and outcome of the two aging-related heart diseases

Heart Failure Reviews - Atrial fibrillation (AF) and heart failure (HF) are common chronic diseases noted in humans. AF and HF share several risk factors, such as age, hypertension, obesity,...     

Calpain is a mediator of preservation-reperfusion injury in rat liver transplantation

Proteases as well as alterations in intracellular calcium have important roles in hepatic preservation-reperfusion injury, and increased calpain activity recently has been demonstrated in liver allografts. Experiments were designed to evaluate (i) hepatic cytosolic calpain activity during different periods of cold ischemia (CI), rewarming, or reperfusion, and (ii) effects of inhibition of calpain on liver graft function using the isolated perfused rat liver and arterialized orthotopic liver transplantation models. Calpain activity was assayed using the fluorogenic substrate Suc-Leu-Leu-Val-Tyr-7-amino-4-methyl coumarin (AMC) and expressed as mean ± SD pmol AMC released/min per mg of cytosolic protein. Calpain activity rose significantly after 24 hr of CI in University of Wisconsin solution and further increased with longer preservation. Activity also increased within 30 min of rewarming, peaking at 120 min. Increased durations of CI preceding rewarming resulted in significantly higher activity (P < 0.01). Calpain activity increased rapidly upon reperfusion and was significantly enhanced by previous CI (P < 0.01). Calpain inhibition with Cbz-Val-Phe methyl ester significantly decreased aspartate aminotransferase released in the isolated perfused rat liver perfusate (P < 0.05). Duration of survival after orthotopic liver transplantation using livers cold-preserved for 40 hr was also significantly increased (P < 0.05) with calpain inhibitor. In conclusion, calpain proteases are activated during each phase of transplantation and are likely to play an important role in the mechanisms of preservation-reperfusion injury.     

Glucocorticoid induces apoptosis in rat leydig cells.

The aim of the present study was to investigate whether glucocorticoid induces apoptosis in rat Leydig cells. To determine whether there are developmental differences in glucocorticoid sensitivity, Leydig cells were isolated at distinct stages of their differentiation [mesenchymal-like progenitors (PLC), immature Leydig cells (ILC), and adult Leydig cells (ALC)] from 21-, 35-, and 90-d-old Sprague Dawley rats, respectively. Glucocorticoid induction of apoptosis was evaluated after both in vitro and in vivo exposures. In the first set of experiments, PLC, ILC, and ALC were treated with 100 nM corticosterone (CORT) for either 4 or 24 h in vitro and then assessed for labeling with the apoptotic marker annexin V. PLC exposed to CORT had levels of annexin V-fluorescein isothiocyanate labeling that were unchanged relative to control values at both time points (P > 0.05). In contrast, CORT-treated ILC and ALC had increased frequencies of apoptosis: in ALC, a 22.1 +/- 1.7% incidence after 4 h and 30.5 +/- 2.3% after 24 h compared with 7.4 +/- 0.8% in untreated controls (P < 0.05). Similar trends were observed for ILC. Ultrastructural analysis confirmed that the increase in annexin V labeling was associated with characteristic signs of apoptosis, including nuclear fragmentation and formation of apoptotic bodies. A second line of experiments examined whether apoptosis was evident in purified Leydig cells after administration of CORT in vivo. Male rats were subjected to bilateral adrenalectomy and were treated with CORT by ip injection twice daily at doses ranging from 2.5-7.5 mg/100 g BW starting 3 d after surgery. The frequency of Leydig cell apoptosis was measured at 12, 24, 48, and 72 h after the first injection. Administration of the 2.5-mg dose raised circulating CORT 5-10 times above normal basal concentrations, and LH levels sampled at these times were not altered in the treated animals. Increased Leydig cell apoptosis was measurable after 24 h of treatment, with an incidence of 21.1 +/- 1.8% in ALC compared with 5.7 +/- 0.8% in untreated controls (P < 0.05). Sharp reductions in immunocytochemical staining intensity were observed in the treated animals for a Leydig cell marker, 11beta-hydroxysteroid dehydrogenase, which occurred concurrently with decreased serum T levels. This was consistent with the hypothesis that CORT-mediated induction of apoptosis leads to declines in Leydig cell numbers, thereby affecting T production. These results suggest that excessive exposure to CORT initiates apoptosis in rat Leydig cells, potentially contributing to suppression of circulating T levels during stress and other conditions in which glucocorticoid concentrations are elevated.