首次自杀未遂者和重复自杀未遂者的对照研究

目的探讨首次自杀未遂者和重复自杀未遂者的区别.方法检查126名因自杀未遂而入院的患者,分为首次自杀未遂组和重复自杀未遂组,获得有关的临床资料并进行自杀意图及自杀企图冲动性和致死性的测定,将有关项目作对比分析.结果有51(40.5%)名重复自杀未遂者,与首次自杀未遂者比较,重复自杀未遂者已婚居多、文化程度较低、缺乏固定的经济收入、有较多的既往精神科治疗史、常饮酒、企图自杀前与他人交流少,自杀意图较低,冲动性较高(P均＜0.05).结论对伴有某些危险因素的自杀未遂者应积极进行医学干预,以期减少自杀行为的再次发生.     

硬膜外阻滞下胆系手术胆心反射预防的临床观察

硬膜外阻滞下胆系手术胆心反射预防的临床观察金贵元，奉菊梅硬膜外阻滞麻醉下胆系手术对循环功能影响较大。本文就硬膜外阻滞麻醉下胆系手术胆心反射几种预防措施的临床观察分析如下。资料和方法８１例成年急性（或慢性）胆囊炎、胆石症病人，均在连续硬膜外阻滞下行胆囊...     

企业集团财务管理模式及其选择

企业集团财务管理必须以市场为导向，以资本为纽带，以现代企业制度为保证，合理配置企业集团资产，发挥集团优势，提高资本的运营效率。企业集团公司对集团内成员单位的财务管理模式可分为“集权式”、“分权式”和“集团总部指导下的分散管理”三种。     

局部亚低温治疗急性脑出血的临床研究

目的观察冰帽加双侧颈动脉区冰敷治疗急性脑出血的临床疗效和探讨最佳治疗时机。方法 174例急性脑出血患者随机分为治疗组和对照组 ,每组 87例。对照组给予常规治疗 ,治疗组在常规治疗的基础上同时给予亚低温治疗 ;治疗组中 46例在发病 3小时内治疗 ,41例在发病 3小时后治疗。观察治疗组与对照组以及治疗组中发病 3小时内与发病 3小时后两组的临床疗效和预后情况。结果亚低温治疗组与对照组比较 ,神经功能改善 (P <0 0 5 ) ,生存率及恢复良好率提高 (P <0 0 5 )。发病 3小时内开始治疗者优于 3小时后开始者 (P <0 0 5 )。结论亚低温治疗能有效减轻急性脑出血后的神经功能缺损 ,降低病死率和致残率 ;最佳治疗时机在发病 3小时以内。     

枕下减压扩大硬膜腔修补治疗小脑扁桃体下疝25例临床分析

目的　探讨枕下减压硬膜开放与扩大硬膜腔修补 ,治疗小脑扁桃体下疝的临床意义。方法　传统枕下减压后 ,用人工硬膜行扩大硬膜腔修补后观察愈后及各种并发症的发生情况。结果　硬膜修补组术后恢复明显较快 ,并发症较少 ,住院天数明显缩短。结论　扩大硬膜腔修补治疗小脑扁桃体下疝 ,取得较好的临床效果 ,有非常实用的临床价值     

文拉法辛缓释剂治疗抑郁症的开放性研究

目的观察文拉法辛缓释剂治疗抑郁症的疗效和不良反应。方法采用开放多中心研究方法,收集符合国际疾病诊断分类第十版(ICD-10)抑郁障碍诊断标准的住院或门诊患者,接受可变剂量文拉法辛缓释剂治疗8周。在治疗前和治疗后第2、4、8周末分别进行汉密顿抑郁量表(HAMD)、汉密顿焦虑量表(HAMA)和临床总体印象量表(CGI)检查,评定药物疗效,描述性记录治疗中出现的任何不良反应。结果435例参加研究,406例完成8周试验。从治疗第2周末开始,HAMD总分和各因子分显著下降,并且此后继续下降。治疗8周末,63.3%患者达到临床治愈标准(HAMD17总分≤7分)。HAMD17总分减分率达74.5%。总有效(临床治愈加有效)率为89.6%。反复发作者药物剂量明显高于单次发作者,病程短于1年的患者疗效优于病程超过1年以上的患者。常见的不良反应为中枢神经系统和消化系统反应,如头晕,多汗和恶心等。治疗前后患者的血压无明显改变。结论文拉法辛缓释剂是一种安全有效的抗抑郁药物。     

奥沙利铂与氟尿嘧啶，亚叶酸钙联合治疗晚期大肠癌的临床观察

目的 研究奥沙利铂与氟尿嘧啶，亚叶酸钙联合治疗晚期大肠癌的疗效和毒副反应。方法 采用奥沙利铂130mg/m^2，静滴2小时，第1天；亚叶酸钙200mg／m^2，静滴2小时，第1—5天；氟尿嘧啶300mg/m^2，静滴4小时，第1—5大；28天为1周期。结果 总有效率为32.7％，毒副反应以骨髓抑制，感觉性神经毒性为主，白细胞减少47．26％Ⅲ级和Ⅳ级为9．09％，感觉性神经毒性为73．32％，Ⅲ级和Ⅳ级为5．05％。结论 奥沙利铂与氟尿嘧啶，亚叶酸钙联合应用治疗晚期大肠癌疗效肯定，毒副反应能耐受。     

脂氧素A4对心肌缺血再灌注损伤的保护作用

Objective To investigate the roles of lipoxin A4, an endegenous lipid mediator with wide anti-inflammatory fea- tures, in attenuating myocardial ischemia-reperfusion injury and the possible mechanisms. Methods Thirty male KM mice were divid- ed randomly into three groups, 10 in each: ischemia-reperfusion group (group A), lipoxin A4 (0.1 mg/kg) group (group B) and Zn- PP (Zinc protoporphyrin Ⅸ, 25 mg/kg)phus lipoxin A4 (0.1 mg/kg)group (group C). A ischemia-reperfusion heart model was de- veloped by ligating the lift anterior descending branch of the coronary artery. A dine of 10% dehydrated alcohol in 0.2 ml for group A, a dose of isochoric lipoxin A4 for group B and a dose of isochoric ZnPP + lipoxin A4 for group C was infused into the ascending aorta through a catheter, which was kpassing the right common carotid artery, 30 minutes after reperfusion. The concentration of serum TNF-α, activities of serum crestine kinase(CK) and lactate dehydrogenase (LDH), activities of myeloperoxidase (MPO) and malond- ialdehyde (MDA) and the cell apoptosis rate in the myocardial tissue were measured 5 hours after reperfusion. Pathological features of the inflammatory infiltration in the myocardium were also observated.Results As compared with group A, the inflammatoryry infiltra- tion in the ischemic and necrotic regions tithe myocardium was reduced, with group C in the intermediate range. The serum activities of CK and LDH wine significantly lower in group B and C than that in group A, and the lowest activities were detected in group B. Similar findings were observed for MPO, an indicator for neutrophil infiltration, and MDA, an indictor for cell injury caused by oxy- gen radicals, in the myocardium. The concentration of TNF-α and the rate of cadiocyte apoptosis were decreased significantly in group B(P < 0.01). ZnPP, an inhibitor of heine oxygenase (HO)-1, attenusted the above protective effects of lipoxin A4 significantly (P<0.05). Conclusion Lipoxin A4 has protective effects against myocardial ischemia-reperfusion injury, and HO-1 may have a potential role in the protectve mechanisms of lipoxin A4, probably pertly by means of reducing the production of reactive oxygen spe- cies and TNF-α, decreasing the activation and infiltration of neutrophils, alleviating inflammatory damage and avoiding apoptosis.