医院业务收入变化因素分析

目的研究影响业务收入变化因素,有的放矢抓管理。方法运用因素分析方法综合指数分析某医院2008年和2009年业务收入变动方向和影响程度。结果医院业务收入的增长主要是和该医院采取一系列管理措施增加门诊和住院工作量有关。其次,与该院规范管理,开展增收节支,加强科室成本核算有关。再次,与国家新农合惠民政策有关。结论医院管理科学、医疗水平和服务质量提高、业务收入规范,医院发展呈健康平稳态势。     

华支睾吸虫LAP2基因的生物信息学分析及克隆表达、组织定位

目的利用生物信息学方法分析华支睾吸虫LAP2全长基因的结构和功能,并将该基因克隆至原核表达载体进行表达、纯化,为进一步研究LAP2功能奠定基础。方法利用生物信息学相关软件,分析华支睾吸虫LAP2基因及其蛋白的结构、生物学和免疫学功能特征。针对LAP2的EST序列的编码区设计引物,从华支睾吸虫囊蚴cDNA质粒中扩增目的基因,克隆到原核表达质粒pET-28a(+)中,经PCR、双酶切及DNA测序鉴定的阳性克隆诱导目的蛋白表达、亲和层析纯化、免疫印迹鉴定及组化定位。结果华支睾吸虫LAP2基因全长为1761bp,其编码序列长度为1662bp,编码553个氨基酸,理论分子量是59696.5Da,与人的该基因氨基酸序列相似性为26.7%,一致性仅为15.4%。该基因在大肠杆菌中可被高效表达,纯化的重组蛋白能被感染华支睾吸虫的大鼠血清识别,免疫组化结果表明该重组蛋白定位于华支睾吸虫成虫的肠支及表膜。结论华支睾吸虫LAP2在大肠杆菌中呈高效的可溶性表达,具有良好的抗原活性,可能为华支睾吸虫成虫分泌排泄抗原的组份之一。     

腹腔镜下广泛子宫切除加盆腔淋巴结清扫术与开腹手术的比较

目的比较广泛子宫切除加盆腔淋巴结清除术经腹腔镜与开腹施术两种方式的,临床疗效。方法回顾性分析2009年2月至2010年2月在我院行腹腔镜下广泛子宫切除加盆腔淋巴结清除术的20例子宫颈癌患者（腹腔镜组）的临床资料,同时随机抽取同期行同类开腹手术25例患者（开腹组）作为对照。结果腹腔镜组的手术时间为（279±84）min,明显长于开腹组的（212±65）min;术中出血量（456±218）ml、输血量（42±19）ml、术后体温恢复正常时间（5．2±1．3）d、术后排气时间（35-4-16）h、住院时间（8±20）d均明显少于开腹组的（629±314）ml、（148±35）ml、（6．9±2．3）d、（64±28）h、（14±5）d;切除盆腔淋巴结的数目为（20±4）枚,与开腹组的（18±5）枚相比差异无统计学意义（P〉0．05）,两组间术后盆腔引流液量、拔除导尿管时间、住院费用比较差异均无统计学意义（P〉0．05）。结论腹腔镜下子宫根治术加盆腔淋巴结清除术可达到同类开腹手术的彻底性,并具有创伤小、恢复快等优点。     

妊高征1号治疗妊娠期高血压疾病疗效观察

目的探讨以杜仲颗粒为主的中药加减的妊高征1号治疗妊娠期高血压疾病的临床治疗效果。方法将62例妊娠期高血压疾病患者随机分为两组,妊高征1号组（A组）32例,常规治疗组（B组）30例,观察保守治疗后两组尿蛋白含量、血清中尿酸含量、保守治疗时间及新生儿结局等情况。结果①A组从尿蛋白（一）发展到尿蛋白（＋＋＋）平均需要（14．3±3．5）d,而B组需要（6．5±1．8）d。终止妊娠时A组尿蛋白以轻中度为主,孕周已达到（35．6±3．4）周,继续妊娠会增加孕妇肾脏功能损害;B组以重度为主,孕周为（33．7±2．8）周,二者比较差异有统计学意义（P〈0．05）;②A组保守治疗的时间平均为（26±4）d,B组保守治疗平均时间（14±3）d,二者比较差异有统计学意义（P〈0．05）;③A组与B组相比,新生儿的存活率增加。结论妊高征1号能延缓妊娠期高血压疾病患者尿蛋白加重的病程,减轻肾脏功能损害,延长孕周,提高新生儿的存活率。     

帕金森病人危重疾病性多发性神经病1例临床分析

目的分析1例帕金森病人发生危重疾病性多发性神经病的过程、临床特点及早期诊断方法。方法对1例帕金森病危重疾病性多发神经病进行临床资料分析及相关文献回顾。结果该病人败血症过程不典型、发展快,早期以内环境紊乱为表现,很快引起呼吸肌无力,需用呼吸机辅助呼吸,但肢体活动尚好。在有效抗生素应用、内环境紊乱纠正后,仍然难以撒离呼吸机,行肌酶检查和脑脊液检查正常,肌电图发现四肢感觉与运动神经传导速度下降及波幅降低,提示危重疾病性多发神经病可能。结论帕金森病人发生败血症后,出现脱机困难和肢体无力时,应重视神经系统检查,及时观察病情变化和完善肌电图检查,考虑危重疾病性多发性神经病可能。避免危险因素,预防脓毒血症的发生可能是预防本病发生的有效措施。     

心肌挫伤诊断指标的实验研究

目的：探讨心肌挫伤的病理生理学改变,提出早期的诊断指标并评价相关指标的真实性及诊断价值。方法：选用新西兰大白兔36只,采用撞击法制备心前区闭合性损伤模型。测定伤前及伤后1、6、12、24、48 h的心电图、超声心动图、漂浮导管、肌钙蛋白Ⅰ、CK-MB改变,依据病理结果,将创伤动物分为心肌挫伤组和非心肌挫伤组,比较上述诊断指标最早出现阳性结果的时间及其真实性和诊断价值。结果：心肌挫伤后1 h心电图出现ST-T改变等非特异性改变且阳性结果动物数量最多,灵敏度为58.8%,特异度为75%,阴性预测值为56.2%。伤后1 h超声心动图提示EF下降、室壁异常运动、肺动脉估测压差升高等,伤后6 h阳性结果动物数量最多,灵敏度为93.3%,特异度为78.6%,阴性预测值为91.7%。漂浮导管检测提示,伤后1 h中心静脉压及肺动脉压明显升高且阳性结果动物数量最多,灵敏度为100%,特异度为83.3%,阴性预测值为100%。伤后6 h肌钙蛋白Ⅰ明显升高且阳性结果动物数量最多,灵敏度为94.1%,特异度为100%,阴性预测值为92.3%。伤后6 h CK-MB明显升高,12 h血清CK-MB阳性结果动物数量最多,灵敏度为88.2%,特异度为66.7%,阴性预测值为80%。结论：漂浮导管、超声心动图、心电图均能较早检测出心肌挫伤,而肌钙蛋白Ⅰ和CK-MB则稍晚。漂浮导管检测心肌挫伤的真实性和诊断价值最好,其次为肌钙蛋白Ⅰ和超声心动图对肺动脉估测压差的检测,CK-MB和心电图真实性和诊断价值较差。     

S-52, a novel nootropic compound, protects against β-amyloid induced neuronal injury by attenuating mitochondrial dysfunction

Accumulating evidence suggests that β‐amyloid (Aβ)‐induced oxidative DNA damage and mitochondrial dysfunction may initiate and contribute to the progression of Alzheimer's disease (AD). This study evaluated the neuroprotective effects of S‐52, a novel nootropic compound, on Aβ‐induced mitochondrial failure. In an established paradigm of moderate cellular injury induced by Aβ, S‐52 was observed to attenuate the toxicity of Aβ to energy metabolism, mitochondrial membrane structure, and key enzymes in the electron transport chain and tricarboxylic acid cycle. In addition, S‐52 also effectively inhibited reactive oxygen species accumulation dose dependently not only in Aβ‐harmed cells but also in unharmed, normal cells. The role of S‐52 as a scavenger of free radicals is involved in the antioxidative effect of this compound. The beneficial effects on mitochondria and oxidative stress extend the neuroprotective effects of S‐52. The present study provides crucial information for better understanding the beneficial profiles of this compound and discovering novel potential drug candidates for AD therapy. © 2012 Wiley Periodicals, Inc.     

Huperzine A alleviates synaptic deficits and modulates amyloidogenic and nonamyloidogenic pathways in APPswe/PS1dE9 transgenic mice

Huperzine A (HupA) is a potent acetylcholinesterase inhibitor (AChEI) used in the treatment of Alzheimer's disease (AD). Recently, HupA was shown to be active in modulating the nonamyloidogenic metabolism of β-amyloid precursor protein (APP) in APP-transfected human embryonic kidney cell line (HEK293swe). However, in vivo research concerning the mechanism of HupA in APP transgenic mice has not yet been fully elucidated. The present study indicates that the loss of dendritic spine density and synaptotagmin levels in the brain of APPswe/presenilin-1 (PS1) transgenic mice was significantly ameliorated by chronic HupA treatment and provides evidence that this neuroprotection was associated with reduced amyloid plaque burden and oligomeric β-amyloid (Aβ) levels in the cortex and hippocampus of APPswe/PS1dE9 transgenic mice. Our findings further demonstrate that the amelioration effect of HupA on Aβ deposits may be mediated, at least in part, by regulation of the compromised expression of a disintegrin and metalloprotease 10 (ADAM10) and excessive membrane trafficking of β-site APP cleavage enzyme 1 (BACE1) in these transgenic mice. In addition, extracellular signal-regulated kinases 1/2 (Erk1/2) phosphorylation may also be partially involved in the effect of HupA on APP processing. In conclusion, our work for the first time demonstrates the neuroprotective effect of HupA on synaptic deficits in APPswe/PS1dE9 transgenic mice and further clarifies the potential pharmacological targets for this protective effect, in which modulation of nonamyloidogenic and amyloidogenic APP processing pathways may be both involved. These findings may provide adequate evidence for the clinical and experimental benefits gained from HupA treatment.