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.     

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)     

肱骨远端全骺分离骨折(附12例报告)

肱骨远端全骺分离骨折为儿童肘部损伤中少见损伤,常与肱骨髁上骨折和婴幼儿的肘关节脱位相混淆。本文报告12例,占同期肱骨远端骨骺损伤的7.1%。12例中骨骺内移9例、外科3例。根据X线片和手术发现,属Salter-Harris Ⅰ型8例、Ⅱ型3例、Ⅴ型1例。骨骺碎裂为2块或3块者4例,其中1例兼有压缩。手法复位5例,手法整复失败或陈旧损伤,行切开复位7例。结果6例满意、3例较好,3例肘关节活动受限明显。12例中肘内翻5°～14°者4例,前臂无不稳现象。本文还就病因、损伤机理、诊断和鉴别诊断等问题进行了讨论。     

病案质量整体管理的做法

病案质量是衡量临床工作质量的重要标志。目前，因重效益轻质量、重科研轻临床现象突出，致病案质量有所下降。因此，应加强病案质量整体管理，建立医院、科室、个人三级病案质量控制体系；以病案内涵质量为核心内容，制定完善科学的病案质量评价标准；加强岗前培训，抓人员素质的提高；强化病案过程质量管理和终末质量管理，重视病案质量信息反馈作用。     

离子色谱法测定硫酸软骨素的含量

建立了用离子色谱法测定硫酸软骨素的方法。在６ｍｏｌ／Ｌ盐酸介质中将硫酸软骨素水解生成等摩尔的硫酸根离子，然后用ＡｎｉｏｎＨＣ离子色谱柱进行分离，以硼酸钠／葡萄糖酸钠淋洗液为流动相，流速１．５ｍｌ／ｍｉｎ，电导检测器检测。硫酸根离子在０．００１～０．０８０ｍｇ／ｍｌ浓度范围内线性关系良好，相关系数为０．９９９４，最低检测浓度为０．０００６ｍｇ／ｍｌ。样品中硫酸根离子的加样回收率为９８．５１％～９９．５２％，硫酸软骨素原料药和注射液及鲨鱼软骨粉胶囊中硫酸软骨素测定的相对标准偏差分别为０．２５％，１．０６％和１．９６％。该方法已应用于多种硫酸软骨素制剂中硫酸软骨素的含量测定     

丁胱亚磺酰亚胺排空组织谷胱甘肽对大鼠心肌谷胱甘肽系统的影响

目的:观察采用谷氨酰半胱氨酸合成酶抑制剂--丁胱亚磺酰亚胺(BSO)排空大鼠心肌谷胱甘肽(GSH)是否影响大鼠心肌组织GSH的稳态,以及是否对GSH代谢相关酶活性及mRNA表达产生影响.方法:采用长时间力竭运动、注射BSO排空GSH两种实验模型,比较对照组与注射BSO组SD大鼠心肌在静息状态和长时间力竭运动后GSH状态及其代谢变化.结果:注射BSO 8天后,大鼠心脏GSH含量分别为对照组?%,且GSH的下降伴随着氧化型谷胱甘肽(GSSG)的下降,GSH/GSSG的比值无显著变化.GSH排空导致GSH代谢酶活性发生适应性变化,注射BSO后心肌中谷胱甘肽过氧化物酶(GPX)活性与对照组相比显著下降(P < 0.001).注射BSO组与对照组相比,心肌谷氨酰转肽酶(GGT)活性显著增加(P < 0.05).注射BSO力竭组与注射BSO组相比,心肌GGT活性显著增加(P < 0.001),心肌注射BSO抑制γ-谷氨酰半胱酸合成酶(GCS)活性,注射BSO力竭组大鼠心肌GCS mRNA表达量高于注射BSO组,表明极度排空谷胱甘肽后,GCS mRNA表达量的增加可能是机体产生的应激反应.