椎板后移回植的椎管扩大术治疗椎管狭窄症

作者报告棘突劈开、椎板后移回植的椎管扩大术治疗椎管狭窄症１８２例，使椎管容积扩大３４．８％，横径扩大３．８ｍｍ，矢径扩大６．１ｍｍ。随访２年９个月，优良率８６．６％，椎板愈合率９６．９％。本文探讨少数椎板迟延愈合的原因和预防措施，如斜切椎板、缝合固定和腰背筋膜与棘上韧带悬吊缝合等。术后卧床１０～１２周，用石膏型保护。作者认为本法能有效的预防术后脊柱不稳，顽固性腰痛等并发症。     

甲氟哌酸药代动力学研究

本文报道国产甲氟哌酸片剂的人体药代动力学研究结果。血、尿药物浓度用微生物打孔法测定。健康志愿者口服甲氟哌酸400mg片剂后,体内药物转运过程符合一室开放模型。甲氟哌酸的血药浓度达峰时间、峰浓度为1.27小时和4.76μg/ml。T_(1/2)Ka和T_(1/2)Ke分别为0.22和10.40小时。研究结果表明,甲氟哌酸吸收快,达峰迅速,血清峰浓度有所提高,消除半衰期长,体内分布广泛,值得在临床推广使用。     

十二指肠钩虫不同蚴龄感染小白鼠的实验研究

用蚴龄20d、40d 和60d 的幼虫,分别感染了3～4个月的小白鼠,每鼠经左腹部感染幼虫300条。在感染24h,3组幼虫均移行至肺脏,但在70d 后肺部仍有幼虫;自感染9d 后蚴龄20d 先移行至小肠,于11d 后蚴龄40d 和蚴龄60d 亦达小肠;感染24h 至70d 各部位组织均可检出未发育的Ⅲ期幼虫。     

Potential contribution of nuclear factor-kappaB to cerebral vasospasm after experimental subarachnoid hemorrhage in rabbits.

Nuclear factor-kappaB (NF-kappaB) plays a key role in inflammation, which is involved in the development of cerebral vasospasm after subarachnoid hemorrhage (SAH). In the present study, we assessed the potential role of NF-kappaB in regulation of cerebral vasospasm. Nuclear factor-kappaB DNA-binding activity was measured in cultured vascular smooth muscle cells (VSMCs) treated with hemolysate and pyrrolidine dithiocarbamate (PDTC, 80 micromol/L), an inhibitor of NF-kappaB. Forty-two rabbits were divided into three groups: control, SAH, and PDTC groups (n=14 for each group). The caliber of the basilar artery was evaluated. Nuclear factor-kappaB DNA-binding activity and the gene expression levels of cytokines and adhesion molecules in the basilar artery were measured. Immunohistochemical study was performed to assess the expression and localization of tumor necrosis factor (TNF)-alpha, intercellular adhesion molecule (ICAM)-1, and myeloperoxidase (MPO). It was observed that NF-kappaB DNA-binding activity was significantly increased by treatment with hemolysate in cultured VSCMs, but this increase was suppressed by pretreatment with PDTC. Severe vasospasm was observed in the SAH group, which was attenuated in the PDTC group. Subarachnoid hemorrhage could induce increases of NF-kappaB DNA-binding activity and the gene expression levels of TNF-alpha, interleukin (IL)-1 beta, ICAM-1, and vascular cell adhesion molecule (VCAM)-1, which were reduced in the PDTC group. Immunohistochemical study demonstrated that the expression levels of TNF-alpha, ICAM-1, and MPO were all increased in the SAH group, but these increases were attenuated in the PDTC group. Our results suggest that NF-kappaB is activated in the arterial wall after SAH, which potentially leads to vasospasm development through induction of inflammatory response.     

聚乳酸骨固定材料的研究

用聚乙烯醇(PVA)的二甲基亚砜(DMSO)溶液对水热反应法合成的超细羟基磷灰石(HAP)进行表面改性，用溶液分散复合法分别制备了HAP含量均为0．03g／mE的聚乳酸(PLLA)／HAP和PLIA／HAP-PVA复合物，并经过挤出成型得到φ=5mm的棒材。重点研究了热拉伸取向的拉伸规律及表面改性前后HAP粒子在PLLA基质中的分散情况。结果表明，经PVA改性的HAP粒子在PLLA基质中的分散要明显优于未经改性的HAP粒子。拉伸取向后PLLA／HAP-PVA复合材料的弯曲强度达262MPa。     

结防机构与医疗机构合作提高肺结核患者发现率

目的了解目前医疗机构与结防机构间合作提高肺结核患者发现方法的实施效果及存在问题。方法采用回顾性调查方法,调查各县区结防门诊根据转诊登记资料、追踪登记表和日常对医疗机构的督导记录;搜集综合医疗机构结核患者发现、报告以及转诊情况数据,搜集医疗机构发现患者到结防机构后诊断复核情况。结果①城市和农村地区医疗机构发现肺结核患者的报告和转诊情况有差异,报告情况城市好于农村,转诊情况农村好于城市;②医疗机构发现肺结核患者的查痰率低仅为13.3%;③结防机构对医疗机构发现未到结防机构就诊肺结核患者的追踪率为94.1%,不同追踪方式追踪到位情况有差异,结防机构医生追踪到位情况最好,到位率为74.2%。追踪未到位原因主要是报告卡姓名或地址等信息有误和患者住院治疗;④实施医疗机构与结防机构间合作措施后,被调查地区结防机构的就诊人数和发现的活动性肺结核患者数均较去年同期增加。结论医疗机构与结防机构间合作实施结核病控制,可提高肺结核病患者发现数量和治疗管理质量。     

大鼠腹裂模型肠管损伤的研究

目的研究先天性腹裂的肠管受损害情况，探讨该病术后并发症的原因。方法利用大鼠腹裂模型，运用组织学、生化学和免疫组织化学方法，分析腹裂胎鼠肠管的组织结构，DNA和蛋白质，细胞增生和凋亡等方面的改变。结果共获得腹裂胎鼠16只，对照胎鼠21只。与对照组相比，腹裂鼠肠管变短、充血水肿、粘连，肠壁表面纤维覆盖，壁内胶原沉积，DNA总量下降，蛋白质总量基本不变，细胞增生率下降，凋亡率上升。结论腹裂的肠管损伤是多方面的，是术后肠管运动和吸收功能异常的原因，大鼠的腹裂模型是对先天性腹裂的病因、病理等方面研究的合适工具。     

Differential roles of NMDA and non-NMDA receptor activation in induction and maintenance of thermal hyperalgesia in rats with painful peripheral mononeuropathy

Central activation of excitatory amino acid receptors has been implicated in neuropathic pain following nerve injury. In a rat model of painful peripheral mononeuropathy, we compared the effects of non-competitive NMDA receptor antagonists (MK 801 and HA966) and a non-NMDA receptor antagonist (CNQX) on induction and maintenance of thermal hyperalgesia induced by chronic constrictive injury (CCI) of the rat common sciatic nerve. Thermal hyperalgesia to radiant heat was assessed by using a foot-withdrawal test and NMDA/non-NMDA receptor antagonists were administered intrathecally onto the lumbar spinal cord before and after nerve injury. Four daily single treatments with 20 nmol HA966 or CNQX beginning 15 min prior to nerve ligation (pre-injury treatment), reliably reduced thermal hyperalgesia in CCI rats on days 3, 5, 7 and 10 after nerve ligation. Thermal hyperalgesia was also reduced in CCI rats receiving a single post-injury treatment with HA966 (20 or 80 nmol) or MK 801 (5 or 20 nmol) on day 3 after nerve ligation when thermal hyperalgesia was well developed. In contrast, a single post-injury CNQX (20 or 80 nmol) treatment failed to reduce thermal hyperalgesia or to potentiate effects of HA966 or MK 801 (5 or 20 nmol) on thermal hyperalgesia in CCI rats. Moreover, multiple post-injury CNQX treatments utilizing the same dose regime as employed for the pre-injury treatment attenuated thermal hyperalgesia but only when the treatment began 1 or 24 h (but not 72 h) after nerve ligation.(ABSTRACT TRUNCATED AT 250 WORDS)