重型颅脑损伤的手术治疗

目的探讨重型颅脑损伤梯度减压的手术方法对预防术中脑膨出、降低死亡率及致残率的效果。方法对100例重型颅脑损伤患者采用分次减压手术方式及去骨瓣后，硬膜与颞肌筋膜瓣减张缝闭硬膜切口方法。结果40例脑肿胀患者术中脑嘭出6例占15．0％，死亡19例占47．5％；60例脑内血肿病人未发生脑膨出，死亡12例占20％。结论脑外伤后脑血管调节麻痹及血肿压迫继发脑水肿易造成脑膨出.术中分次减压降低了骨窗部位脑组织的顺应性，从而降低了局部的压力梯度，避免脑血管急性扩张，能有效防止脑膨出，降低死亡率及致残率。     

The vagal nerve as a link between the nervous and immune system in the instance of polymicrobial sepsis

Background The role of the vagal nerve in the autonomic nervous system is widely well known. Recently, an additional function was revealed serving as a connector between the nervous and immune system. This connection is called the “cholinergic inflammatory pathway.” Through stimulation of the acetylcholine receptors located upon the macrophages, the “unspecific” immune system can be directly influenced. Methods The vagal nerve was completely transected directly posterior to its passage through the diaphragm. The effect of complete vagotomy was analyzed using a murine model of polymicrobial peritonitis (colon ascendens stent peritonitis, CASP). Survival and clinical course of vagotomized or sham-operated mice were analyzed in the CASP model. Results After CASP surgery, vagotomy led to a significantly increased mortality (64.7%) in comparison to sham-vagotomized animals (34%). No difference in the bacterial load of various tissues (lung, liver, spleen, blood, lavage fluid, and kidney) from septic animals with or without vagotomy was observed. Vagotomized animals reveal elevated serum cytokine levels (TNF, IL-6, IL-10, and MCP-1) 20 h after the induction of polymicrobial peritonitis. Conclusion The vagal nerve is therefore an important modulator of the immune system. W. Kessler and T. Traeger contributed equally to this work Best of Forum Papers presented at the Annual Meeting of the German Society of Surgery, 2–5 May 2006, Berlin, Germany     

44例老年重症哮喘的院前急救体会

目的探讨老年重症哮喘急性发作的院前急救措施。方法在常规平喘治疗基础上,治疗组用甲基泼尼松龙80mg加入5%葡萄糖溶液(0.9%氯化钠溶液)40ml中静脉注射,对照组用地塞米松10mg加入5%葡萄糖溶液(0.9%氯化钠溶液)20ml中静脉注射,观察治疗前、后两组患者临床疗效评分变化。结果治疗组比对照组起效快,疗效好,两组疗效间差异有显著性意义(P<0.01)。结论甲基泼尼松龙是老年重症哮喘院前急救的首选方法,尽早使用,有利于提高抢救成功率。     

Molecular basis of severe myoclonic epilepsy in infancy

Severe myoclonic epilepsy (SMEI) or Dravet syndrome is caused by mutations of the SCN1A gene that encodes voltage-gated sodium channel alpha-1 subunit. Recently, we generated and characterized a knock-in (KI) mice with an SCN1A nonsense mutation that appeared in three independent SMEI patients. The SCN1A-KI mice well reproduced the SMEI disease phenotypes. Both homozygous and heterozygous knock-in mice developed epileptic seizures within the first postnatal month. In heterozygous knock-in mice, trains of evoked action potentials in inhibitory neurons exhibited pronounced spike amplitude decrement late in the burst but not in pyramidal neurons. We further showed that in wild-type mice the Nav1.1 protein is expressed dominantly in axons and moderately in somata of parbalbumin (PV) – positive inhibitory interneurons. Our immunohistochemical observations of the Nav1.1 are clearly distinct to the previous studies, and our findings has corrected the view of the Nav1.1 protein distribution. The data indicate that Nav1.1 plays critical roles in the spike output from PV interneurons and further, that the specifically altered function of these inhibitory circuits may contribute to epileptic seizures in the mice. These information should contribute to the understanding of molecular pathomechanism of SMEI and to develop its effective therapies.     

性别差异对脓毒症大鼠肝脏Toll样受体4和髓样分化蛋白-2基因表达的影响

目的探讨性别差异对脓毒症大鼠肝脏组织Toll样受体4(TLR4)和髓样分化蛋白- 2(MD-2)基因表达的影响。方法以脂多糖(LPS)按5 mg/kg体重由大鼠腹腔注射制作脓毒症动物模型,注射后2 h留取肝脏组织检测TLR4、MD-2和肿瘤坏死因子-α(TNF-α)基因表达,同时测定各组大鼠血浆中丙氨酸氨基转移酶(ALT)及雌二醇含量。结果正常雌雄性大鼠肝脏组织均可表达少量TLR4、MD-2、TNF-α基因,其中雌性组分别为0．175±0．034、0．211±0．044、0．201±0．068; 雄性组分别为0．205±0．061、0．243±0．049、0．243±0．063,两组数据差异无统计学意义(P> 0．05),但LPS刺激后雌性大鼠肝脏组织上述指标分别为0．615±0．089、0．708±0．181、0．730± 0．118,血浆中ALT含量为(81．07±10．72)U／L;雄性组分别为0．723±0．091、1．123±0．272、 0．881±0．156,ALT含量为(106．39±14．21)U／L,雌性组各项指标均明显低于雄性大鼠(P< 0．05)。相关分析表明雌性及雄性脓毒症大鼠肝脏组织TLR4及TNF-α基因表达与相应性别大鼠血浆中雌二醇含量呈显著负相关(P<0．05)。结论 LPS刺激后大鼠肝脏组织TLR4、MD-2及 TNF-α基因表达存在性别差异,内源性雌激素的作用可能导致雌性脓毒症大鼠肝脏组织损伤较雄性轻。     

重症肺炎患者中性粒细胞胞吐作用的改变

目的　研究重症肺炎患者中性粒细胞的功能改变。方法　采用免疫化学法测定 32例重症肺炎患者中性粒细胞胞吐作用和氧化酶反应的变化 ,并与健康对照组比较。结果　重症肺炎患者血液中性粒细胞的基础和PMA刺激的胞吐作用均明显下降 (P <0 .0 1) ;重症肺炎患者的基础和PMA刺激的反应性氧属 (ROS)产生明显增加 ;重症肺炎患者肺部中性粒细胞释放乳铁蛋白、髓过氧化物酶 (MPO)和ROS增加 ,PMA刺激后相似 ;肺炎的严重性与血液中性粒细胞释放乳铁蛋白呈负相关。结论　重症肺炎患者中性粒细胞胞吐作用明显受损 ,与预后相关。     

重型颅脑损伤后凝血功能变化的研究

目的研究重型颅脑损伤后凝血功能的变化及临床意义。方法对本院2005年3月至2006年2月收治的26例重型单纯性颅脑损伤患者（GCS≤8分）进行前瞻性研究，监测其入院当时、入院第2天、第3天及第7天的部分凝血活酶时间（APTT），凝血酶原时间（PT），纤维蛋白原（FIB）及凝血时间（TT）的变化。并检测14例单纯头部外伤患者在入院时的APTT、PT、FIB和TT值。结果APTT在入院3天明显升高。1周后仍未达到正常（P〈0．05）；PT在入院当天即升高（P〈0．05），1周左右逐步恢复正常；FIB在入院当天即升高，第3天下降（P〈0．05），1周左右逐步恢复正常。有3例按照DIC诊断标准诊断为DIC，结果在观察期间均死亡。结论重型颅脑损伤后可发生凝血功能异常，且外凝性凝血途径的启动早于内源性凝血途径。伤后早期即可发生高凝状态，至第3天左右向低凝状态转变，1周左右恢复正常。     

综合医院医务人员感染SARS情况对比分析

目的：分析在防治SARS工作初期、后期医务人员感染SARS的差异和采取的对策，为减少综合医院内医务人员SARS的感染提供参考。方甚：对本院自2003年3月24日至6月2日SARS诊断治疗任务中发生的医务人员的感染原因和采取的对策进行回顾性分析。结果：防治SARS工作初期，急诊科交叉感染和在SARS隔离病房等与SARS患者密切接触的工作岗位，共有17名医务人员感染，及时隔离治疗，均已痊愈，未造成医护人员的进一步交叉感染：经加强防护培训，改善工作条件，在防治SARS工作后期，仅发生2名护工感染，亦已痊愈，派出非典医疗队实现零感染。结论：综合医院内医务人员感染SARS的问题严峻，加强医院内的全员防护培训，按岗分区管理，改善医务人员的工作条件和病人的隔离观察环境，做好监督检查，积极应对，可以减少医务人员的SARS感染。     

Splanchnic metabolism associated with liver metastasis

Metastatic liver disease can modify the metabolic response to critical illness. Systemic lactic acidosis may arise from an increased production due to inadequate peripheral tissue oxygen transport, altered metabolic function such as depressed pyruvate oxidation or insufficient hepatic clearing capacity due to tumor replacement of functional liver mass. Hepatic venous catheterization in a patient with extensive metastatic melanoma to the liver and adult respiratory distress syndrome indicated a marked disparity between whole body and liver oxygenation which may arise due to a markedly stepped up splanchnic oxygen utilization unmatched by a proportionate rise in regional oxygen delivery. Since some neoplasms may exhibit increased metabolic activity, it is suspected that these metastatic lesions may have contributed to the observed regional hypermetabolism thereby worsening hepatic hypoxia and exacerbating lactic acidosis. This case also illustrates the difficulties in interpreting global indicators of metabolic function and oxygenation in critically ill patients.