AFP火箭电泳放射试管测量法

AFP是肝细胞癌的重要标志物之一,快速定量检测具有重要意义。我们在实践中摸索出一种新的快速定量测定AFP的方法——火箭电泳放射试管测量法。该法具有流程短、结果便于计算、操作较简便等优点,灵敏度与火箭电泳放射自显影法相当。现将有关方法和结果报告如下。     

B超诊断肺不张64例报告

分析６４例肺不张及胸腔积液（血）的Ｂ超图象特点．结果皆与Ｘ线诊断相符，但分辨率优于Ｘ线检查．     

急肝效灵口服液对小鼠实验性肝损伤的保护作用

急肝效灵是由丹参、赤芍、泽兰叶、茵陈、柴胡、大黄等十二味中药精制而成的复方制剂，我们用实验性肝损伤模型，通过酶学指标探讨了急肝效灵对肝损伤的有益作用。结果表明急肝效灵不同剂量组均有降低肝损伤后ＳＧＰＴ升高的作用，而以２０ｇ／ｋｇ组效果最为明显，能显著降低硫代乙酰胺及ＣＣｌ４所致ＳＧＰＴ的升高并有减轻病理改变的作用。急肝效灵１０ｇ／ｋｇ，２０ｇ／ｋｇ组还能显著降低扑热息痛所致肝湿重的增高，有缓解炎性损伤的作用。以上结果表明急肝效灵对实验性肝损伤具有保护作用，可能是药物多成分多环节综合作用的结果。     

化瘀生脉方对血管吻合术后内皮细胞愈合影响的实验研究

为研究化瘀生脉方对小血管吻合术后内皮细胞愈合机制的影响。采用SD大鼠尾动脉切断后作端端吻合的模型。按用药不同随机分成化瘀生脉组和空白对照组,每组16只。每组再按血管吻合术后22、4、48小时和7天切取标本时间的不同随机分为4组。样本用扫描电镜观察吻合口处内皮细胞的修复过程。结果显示术后2、24、48小时和7天,化瘀生脉组缝线表面完全覆盖率均高于空白对照组,经成组设计两样本比较的秩和检验,统计学上有显著性差异。术后2、24、48小时,化瘀生脉组在针孔及缝线表面的覆盖成分以纤维素、内皮细胞为主,构成比不同于空白对照组,经χ2检验,其差异有非常显著性意义(P<0.01)。表明化瘀生脉方具有抑制血小板在针孔处聚集的作用,能够促进纤维素对针孔及缝线表面的覆盖,能够促进内皮细胞的生长,从而可以防治术后血栓形成。     

卡托普利改善血管结构与降压效果的关系

为研究血管紧张素转换酶抑制剂对血管与血压作用之间的关系，选用２组自发性高血压大鼠，从胚胎期每天分别给予卡托普利２０ｍｇ／ｋｇ，至１６周龄停药。测定左心室重量／体重比，肠系膜动脉Ⅲ级血管与肾动脉的血管壁／管腔比，并同时观察后肢阻力血管灌注模型对苯肾上腺素的灌注压反应曲线。     

切开复位内固定治疗锁骨骨折

锁骨骨折在临床极为多见，约占全身骨折的５．９８％，通常多采用横“８”字绷带保守治疗，随着人们对生活质量要求的提高，手术适应症较前放宽。我院１９９７年１２月～２００１年１２月共收治１４６例患者，对其中８２例有明显移位的锁骨骨折采用切开复位加克氏针及钢丝内固定术，疗效满意。１临床资料本组８２例，男６４例，女１８例；年龄１８岁～６４岁。锁骨外１／３骨折９例，中１／３骨折３２例，中外１／３骨折３８例，内１／３骨折３例。所有骨折均因车祸或跌伤所致。其中横形骨折１７例，斜形骨折３４例，粉碎性骨折３１例。开放…     

面部炎性皮损与蠕形螨和细菌感染的关系

目的探索颜面部炎性皮损与蠕形螨和细菌感染的关系,寻找防治颜面部炎性皮损有效的药物和方法。方法在邵阳医专检验系281个学生中进行炎性皮损的调查,检查面部蠕形螨及细菌培养并做药物敏感试验。结果共查出面部有炎性皮损者83人,统计显示有面部炎性皮损者蠕形螨感染率为89.17%(74/83),明显高于无面部炎性皮损的蠕形螨感染率15.96%(31/198)(χ2=134.99,P<0.01)。有面部炎性皮损的细菌感染率占93.98%(78/83),明显高于无面部炎性皮损的细菌感染率6.56%(13/198)(χ2=204.07,P<0.01)。共分离出91株细菌,主要为血浆凝固酶阴性葡萄球菌,占分离菌总数的90.01%(82/91),药敏结果提示,最敏感的抗生素是氨基糖苷类的丁胺卡那。结论面部炎性皮损与蠕形螨和细菌感染存在因果关系。     

浅谈导致医疗纠纷增加的原因及对策

医患关系紧张、医疗纠纷增加,是当前医疗服务中一个十分突出的问题。医患之间缺乏信任和理解,医患关系紧张的现状不容乐观。其产生的原因应该是多方面的:医疗资源配置的不合理和国家及社会医疗投入比重降低、医疗机构自身的原因、患者的因素等。解决这些矛盾应该重视调整医疗资源的合理性配置,更多的体现医疗服务的公平性及可及性,加强对医疗机构的监控力度,提高医务人员的自身素质,普及医疗知识的宣传教育,加强医患双方的沟通和理解,建立医患互信的良好关系,完善现有的法律法规,通过人性化、制度化的有效措施缓解医患关系的紧张,减少医疗纠纷的发生,构建和谐医患关系。     

Effects of Serum Containing Xinlikang (心力康) on Angiotensin Ⅱ Induced Hypertrophy in Cultured Neonatal Rat Cardiomyocytes

Objective: To evaluate the effects of Xinlikang (心力康,XLK) on angiotensinⅡ(AngⅡ) induced hypertrophic cultured neonatal rat's cardiomyocyte (CMC). Methods: Primary cultured neonatal rat's CMCs with the purity certified by immunohistochemical technique, were divided into three groups. Rats in the normal control group were untreated; those in the model group were established into hypertrophic models but underwent no treatment; and those in the XLK group were established to hypertrophic models and treated with XLK containing serum obtained from rats with aorta coarctation after 8 days of feeding with XLK. MTT and phase-contrast microscope were used to evaluate the effect of XLK on cell activity, pulsating rhythm and surface area; Atrial natriuretic peptide (ANP) expression was determined by radioimmunoassay; Protein content was determined by Bradford method; and DNA synthesis was detected by flow cytometric assay. Results: Immunohistochemistry results showed that more than 90% of the cells wereα-sarcometin actin stained positive cells. No significant effect of XLK on normal CMC was found. AngⅡcould significantly induce hypertrophy in CMCs, and XLK could significantly decrease the increased surface area and the accelerated pulsating rate in them. ANP expression was 780±38 Mg/L in the model group, and 430±23μg/L in the control group, and the elevated expression of ANP in model rats was significantly decreased in the XLK group;The DNA content in the G0/G1 and G2/M phases was significantly enhanced and at the same time it was accompanied with increase of total protein content in the model rats after being stimulated by AngⅡfor 24 h, showing that serum-containing XLK could also significantly suppress total protein synthesis (P<0. 05). Conclusion: XLK could improve AngⅡmediated pathological growth of CMCs without influencing the growth of normal CMCs, suggesting that XLK is probably an effective drug for treatment of myocardial hypertrophy and heart failure.