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。     

92例重型肝炎并发自发性细菌性腹膜炎的诊断与治疗

目的探讨重型肝炎并发自发性细菌性腹膜炎(SBP)的诊断和抗生素使用。方法回顾性分析2002年7月~2005年6月间收治的92例并发SBP的重型肝炎患者的临床资料。结果92例患者中,发热72例(78.26%),腹胀85例(92.39%),腹痛38例(41.30%),反跳痛35例(38.04%),83例(90.21%)外周血中性粒细胞(PMN)分类≥0.75,40例(45.98%)腹水PMN计数≥250个/mm3,79例(90.80%)腹水PMN比值≥0.50,11例(12.00%)腹水细菌培养阳性,共分离出细菌17株,G-杆菌占52.9%(9/17),其对头孢曲松、头孢哌酮、头孢他啶、左旋氧氟沙星及泰能敏感,对丁胺卡那、氧哌嗪青霉素敏感性较低。临床治疗显示,联合使用头孢他啶和甲硝唑效果较好,并较少出现继发真菌感染。结论重型肝炎并发SBP患者的临床表现不典型,腹水培养阳性率低,外周血和腹水PMN比值是诊断SBP比较可靠的参数。治疗SBP,可首选二联使用头孢他啶与甲硝唑,疗程约10~14日。     

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.     

CD14+单核细胞人类白细胞抗原DR表达率与脓毒症关系的研究

目的了解烧伤延迟复苏时CDl4^＋单核细胞人类白细胞抗原DR（HLA—DR）表达率的变化，分析其与脓毒症的关系。方法选择烧伤面积大于30％TBSA的25例烧伤延迟复苏患者，于伤后1、3、7、14、28d取外周血，其中7例患者住院期间并发脓毒症，于脓毒症发生后连续2d亦取其外周血。另取20例健康体检者外周血作为对照。流式细胞仪检测CD14^＋单核细胞HLA．DR表达率，酶联免疫吸附测定法检测血浆中肿瘤坏死因子α（TNF—α）、白细胞介素10（IL-10）的浓度。结果非脓毒症患者伤后1、3、7、14、28dCD14^＋单核细胞HLA—DR表达率分别为（15±6）％、（74±5）％、（264±17）％、（284-16）％、（474-16）％，明显低于健康体检者[（924±10）％，P〈0．01]；脓毒症患者发生脓毒症后1、2d，该指标亦明显低于健康体检者及非脓毒症患者伤后1、7、14、28d（P〈0．01）。脓毒症患者TNF—d检出率及TNF—α、IL-10浓度，均高于非脓毒症患者和健康体检者（P〈0．05或P〈0．01）。伤后1、7、28d，外周血CD14^＋单核细胞HLA—DR表达率与IL—10浓度呈显著负相关（r分别为-0．9963、-0．7459、-0．8474，P〈0．01）。结论烧伤延迟复苏患者免疫功能低下，促炎性介质释放量增加，并发脓毒症时则更为严重。外周血CD14^＋单核细胞HLA—DR表达率可作为动态检测患者免疫功能状态的有效指标。     

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。     

沐舒坦治疗重型颅脑损伤后肺部感染的临床分析

目的:探讨沐舒坦对重型颅脑损伤后肺部感染的治疗作用.方法:选择GCS3～8分重型颅脑损伤后肺部感染的患者90例,随机选45例(实验组)加用沐舒坦治疗,另45例(对照组)未予沐舒坦治疗。所有患者其他治疗措施均基本相同。结果:实验组有42例感染控制,感染控制时间平均(7.8±2.6)d:对照组有35例感染控制,感染控制时间平均(14.1±3.2)d。实验组肺部感染控制率显著高于对照组(P<0.05),而控制感染平均时间显著短于对照组(P<0.05)。结论:沐舒坦治疗重型颅脑损伤后肺部感染有较好的临床疗效,值得临床推广应用。     

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。