CO作用后大鼠肺血管细胞增殖和凋亡状况的研究

目的：通过研究CO和低氧作用后大鼠肺血管细胞增殖和凋亡状况，探讨低氧肺动脉高压的发病机制及防治措施。方法：应用免疫组织化学，原位末端标记及Western杂交等方法检测常压低氧大鼠肺血管壁细胞增殖，凋亡及c-myc基因的表达状况。结果：正常组，低氧和锡原卟啉组，低浓度CO和血晶素组大鼠肺动脉均存在增殖和凋亡的阳性细胞，两类细胞在肺内呈不均匀散在分布，低氧和锡原卟啉组大鼠肺血管增殖细胞数显著升高而凋亡细胞数显著减少，细胞增殖凋亡比值分别为对照组的5倍或4倍，而低浓度CO和血晶素组肺血管增殖细胞和凋亡细胞系数均显著增加，细胞增殖凋亡比值均为1．2，c-myc在低氧和锡原卟啉组大鼠肺内表达显著增加，在低浓度CO和血晶素组大鼠肺内表达减少。结论：增殖和凋亡现象共存在于正常和处理大鼠的肺血管细胞中，也许c-myc等基因的异常表达导致了细胞增殖和凋亡的失衡，进而调节了慢性低氧肺血管结构的改建。     

先天性心脏病患儿术后多脏器功能障碍的预后分析

目的 探讨小儿先天性心脏病(先心病)术后多脏器功能障碍(MODS)预后情况及其影响因素,为对此类患儿进行针对性护理提供依据.方法 收集先心病术后并发MODS 77例患儿的临床资料.结果 11例放弃治疗出院,66例中44例救治存活,22例死亡.出现时间最早、累及最多的脏器为心脏;病死率最高的为累及中枢神经系统的患儿(57.69%),其次是累及血液系统的患儿(55.56%);患儿的病死率与累及脏器的数量呈显著正相关(P＜0.01).死亡患儿手术体外循环时间和主动脉阻断时间显著长于存活患儿(均P＜0.05),术中意外及术后心肺复苏发生率显著高于存活患儿(均P＜0.05).结论 先心病术后患儿应加强心功能监护,特别是体外循环时间＞120 min,主动脉阻断时间＞60 min及术中发生过意外情况、术后采取过心肺复苏术的患儿;尽早采取有利措施避免其他脏器功能受损是提高患儿存活率的关键.     

慢性低O2高CO2时NO-sGC-cGMP细胞信号转导通路变化及与肺动脉高压的关系

目的 :探讨慢性低O2 高CO2 性肺动脉高压发生与发展中NO sGC cGMP细胞信号转导通路的变化和作用。方法 :雄性Sprague Dawley大鼠随机分为对照组与低O2 高CO2 肺动脉高压 1w、2w及 4w组。用比色法测定血浆NO含量 ,酶动力学法测定肺组织sGC活性 ,12 5 I 放射免疫法检测肺组织cGMP含量。结果 :低O2 高CO2 1w、2w、4w组mPAP较对照组均明显升高 (P均 <0 .0 1)。而血浆NO含量、肺组织sGC活性和肺组织cGMP含量均显著降低 (分别P <0 .0 5,P <0 .0 1或P <0 .0 0 1)。mPAP与血浆NO含量 (r =-0 .80 7,P <0 .0 1)、与肺组织sGC活性 (r=-0 .754,P <0 .0 1)、与肺组织cGMP含量 (r=-0 .62 1,P <0 .0 1)之间均存在显著负相关。结论 :低O2 高CO2 引起的NO sGC cGMP转导通路的遏制性变化导致肺动脉舒张性降低是形成肺动脉高压的重要机制     

嘌呤霉素肾病大鼠肾小球中nephrin、Podocin和α-actinin与蛋白尿的关系

目的动态观察肾小球足细胞及裂孔隔膜分子nephrin,podocin和α-actinin在嘌呤霉素(puromycinaminonucleoside,PAN)大鼠肾病模型肾组织中表达的时相变化,探讨这些分子间及这些分子与蛋白尿发生的关系。方法用间接免疫荧光染色及实时定量PCR方法,检测PAN注射后12h、1d、36h、2d、5d、10d、15d及20d大鼠肾小球中nephrin,podocin和α-actinin分子分布和表达。结果(1)PAN注射后1d、2d及5d时,尿蛋白量无明显改变;10d时尿蛋白量明显增加(P=0.02);20d时恢复至对照组水平。(2)对照组大鼠肾小球中nephrin和podocin沿肾小球毛细血管袢呈连续线状分布,α-actinin沿肾小球毛细血管袢呈点线状分布。PAN注射1d后,nephrin和podocin的分布即发生改变,表现为断续、非线性分布。nephrin和podocin的分布改变随着尿蛋白的增多而加重,尿蛋白恢复时也逐渐恢复。20d时,α-actinin沿肾小球毛细血管袢呈连续线性分布。(3)免疫荧光定量分析结果表明,在PAN注射后36h(P=0.04)、2d(P=0.03)及5d(P=0.04)时,肾小球中podocin的免疫荧光染色强度明显下降,于第10d降至最低(P=0.006);自15d时逐渐恢复(P=0.007),20d后podocin的免疫荧光强度恢复至对照组水平。nephrin的免疫荧光染色强度在PAN注射第5天后出现下降(P=0.002),持续下降至第10天(P=     

高浓度氟引起SH-SY5Y神经细胞中α7尼古丁受体水平降低

目的：观察氟中毒对神经细胞中α7尼古丁受体的影响。方法：体外培养SH-SY5Y神经细胞，在培养液中加人不同浓度的氟化物，培养48h后测定细胞MTT水平；用放射配体结合实验测定α7尼古丁受体亚型含量；用Westem Bloting方法测定α7尼古丁受体亚单位蛋白水平。结果：经氟处理的神经细胞中MTT水平降低，α7尼古丁受体最大结合容量降低，α7尼古丁受体亚单位蛋白含量减少。结论：氟中毒可引起SH—SY5Y神经细胞中α7尼古丁受体表达降低。     

掌板关节囊松解术治疗压砸伤术后掌指关节屈曲障碍

Objective To discuss the application of volar plate joint capsule release to treat metacarpophalangeal joint flexion contracture caused by severe crush injury to the palm. Methods From September 2005 to June 2008, 8 cases with post-traumatic metacarpophalangcal joint flexion contracture caused by severe crush injury was treated with volar plate joint capsule release. Postoperatively the patients underwent keritherapy and functional exercise. They were followed up to evaluate recovery of metacarpopha]angeal joint flexion. Results All 8 patients had metacarpophalangeal joint flexion contracture of the middle finger. The joint flexion function was improved remarkably after the surgery. The joint movement limitation decreased to 0° to30°and the functional impairment reduced to 0% to 18%. Conclusion V olar plate joint capsule release is an excenent method to treat metacarpophalangeal joint flexion eontraeture caused by severe palm crush injuiy. It is easy to operate and leads to reliable results.     

第一掌背动脉逆行筋膜皮瓣修复示指软组织缺损

目的 介绍一种新型逆行筋膜皮瓣修复示指皮肤缺损。方法 我院于1997～2003年，采用第一掌背动脉逆行筋膜皮瓣修复示指皮肤缺损9例，该皮瓣以第一掌背动脉在第二掌骨背侧的纵轴为轴线，以筋膜为蒂，蒂部设计在皮瓣的远侧，供血动脉为示指桡侧指动脉。结果 皮瓣全部成活，随访半年以上5例，修复后指腹两点辨别觉为6mm～11mm(平均7．9mm)，外形满意，患均恢复原工作。结论 切取第一掌背动脉逆行岛状筋膜皮瓣修复示指皮肤缺损安全可行，是修复示指皮肤大面积缺损的较理想方法。     

Subcutaneously administered recombinant human β-interferon in the treatment of chronic hepatitis B virus infection

Background: Treatment of chronic replicative hepatitis B virus (HBV) infection is aimed at stopping viral replication and preventing the development of chronic liver disease. β-Interferon treatment has been less well studied than α-interferon. Methods: The efficacy and tolerability of a 6-month course of subcutaneously administered human recombinant β-interferon (rINF-β_ser) was studied and the results of a low-dose regime compared with a high-dose regime. Twenty patients (17 men and three women), aged 24–54 years, with chronic hepatitis B virus infection (all hepatitis B surface antigen-positive with detectable HBV-DNA in their sera for at least 3 months prior to therapy) were randomized into two treatment groups of 10 patients each. The low-dose group received 6×10⁶ U/dose and the high-dose group received 30×10⁶ U/dose, both groups receiving their respective doses three times a week initially for 1 month and continuing for a total of 6 months. Results: The treatment was well tolerated in both groups. None of the patients required dosage reduction or cessation of treatment because of side-effects. HBV-DNA decreased in all patients during treatment, demonstrating the anti-viral efficacy of rINF-β_ser, and was undetectable in 20 and 40% of patients receiving low-dose and high-dose regimes, respectively, at the end of 6 months treatment (P=N.S.). One year after completion of treatment, HBV-DNA was undetectable in 50 and 30% of patients in the low-dose and high-dose groups, respectively (P=N.S.). However, only one patient achieved seroconversion with loss of the hepatitis B surface antigen and appearance of an anti-hepatitis B ‘e’ antigen at the end of 18 months. Conclusion: This study shows that subcutaneously administered rINF-β_ser is well tolerated, but the optimal dose and duration of treatment still needs to be defined by further studies.     

内皮超极化因子的研究进展

内皮超极化因子（EDHF）是由内皮释放的NO和PGI_2以外的另一种舒张因子,它通过使平滑肌细胞膜超极化而舒张血管,是内皮依赖性血管松驰的第3种重要机制。EDHF可能是花生四烯酸的细胞色素P450代谢产物EET-s,乙酰胆碱、缓激肽等激动剂作用于内皮细胞,使细胞内游离钙浓度升高,合成和（或）释放EDHF,作用于平滑肌细胞膜,激活钙依赖性钾通道,使细胞膜超极化,抑制电压依赖性钙通道的开放,引起血管松弛。在大血管中NO-cGMP松弛机制可能占主导地位,并且抑制EDHF生成;而在阻力小血管,EDHF则可能是引起血管松弛的主要因素。     

康复新液联合奥美拉唑对HP阴性胃溃疡的疗效分析

目的分析康复新液联合奥美拉唑治疗幽门螺杆菌(HP)阴性胃溃疡患者的疗效。 方法选取HP阴性胃溃疡患者108例,随机均分为对照组和联合组。对照组接受奥美拉唑针剂治疗,联合组接受康复新液联合奥美拉唑针剂治疗。比较两组临床疗效、血清胃蛋白酶原(PG)、高迁移率族蛋白B1(HMGB1)、细胞炎症因子水平及不良反应发生率。 结果联合组治疗总有效率高于对照组(P＜0.05)。与治疗前比较,两组治疗后PGⅠ、PGⅡ、HMGB1、白细胞介素-6、肿瘤坏死因子-α及C反应蛋白均有降低,且联合组较对照组降低更明显(P＜0.05)。两组患者治疗期间总不良反应发生率比较,差异无统计学意义(P＞0.05)。 结论康复新液联合奥美拉唑针剂可提高HP阴性胃溃疡患者的临床疗效,值得临床应用推广。