亚砷酸间接失活牙髓的临床体会

<正> 1998～2001年间,对麻醉效果欠佳或有牙科畏惧症的患者应用亚砷酸间接失活192颗牙,效果满意,现报道如下。1 材料和方法1.1 一般资料 来本院门诊就诊的慢性牙髓炎且根尖孔已形成的磨牙,共计182例患者,患牙192颗,其中男88例,92颗,女94例,100颗,年龄21～72岁。     

补体及其抑制剂与心肌缺血/再灌注损伤

心肌缺血／再灌注可诱发导致心肌损伤的炎症状态。由于在临床上抗氧自由基和中性粒细胞激活治疗效果的不尽如人意，人们又把目光转向其他在临床上对心肌缺血／再灌注损伤可能更重要的致病因素，如补体、氧化剂和凋亡等。目前，补体系统已被证实在心肌缺血／再灌注损伤中起重要作用，并成为实验缺血／再灌注损伤的一个主要治疗靶点。在过去的十余年中，已经有几个补体抑制剂从实验室进入临床试验，并取得了一定成果。近几年，随着对补体与心肌缺血／再灌注损伤研究的不断深入，又有了一些新的发现。本文主要就补体及其抑制剂在心肌缺血／再灌注损伤中的研究及目前的新发现做一综述。     

炎症时血清淀粉样蛋白A和C反应蛋白的变化

血清淀粉样蛋白A(SAA)是组织淀粉样A蛋白的前体,它由淀粉样原纤维组成,与继发性淀粉样变性发病有关.SAA和C反应蛋白(CRP)均为主要的急性时相反应蛋白,临床上可用于监测急性期反应.CRP对细菌感染是一敏感指标,但对病毒感染因其浓度变化幅度小而敏感性较低.本文比较了SAA和CRP在病毒性感染和细菌感染时的变化,认为SAA对急性病毒性感染是一灵敏的监测指标.     

脉冲振荡法在慢性咳嗽临床应用中的探讨

目的 观察本院门诊就诊的慢性咳嗽患者的肺通气功能及气道阻力变化情况.方法 设立实验组和健康对照组,采用普通肺功能及脉冲振荡法检查,比较两组75%最大呼气流量(MEF75)、50%最大呼气流量(MEF50)、25%最大呼气流量(MEF25)以及脉冲振荡法之呼吸总阻抗(Z5)、总气道阻力(R5)、中心气道阻力(R20)及周边弹性阻力(X5)各项指标的数值变化.实验组行支气管扩张剂治疗14 d,再观察上述指标.结果 治疗前实验组同健康组比较,各项指标差异有统计学意义.实验组治疗前后比较,各项指标差异有统计学意义.治疗后实验组与对照组比较,各项指标差异无统计学意义.结论 总气道阻力、小气道阻力及周边弹性阻力增加,大气道阻力未增加.支气管扩张剂治疗慢性咳嗽有效.     

细胞蜡块在诊断棘球蚴病中的应用北大核心CSCD

棘球蚴病又名包虫病,是细粒棘球绦虫幼虫（棘球蚴）寄生于家畜等多种食草动物和人的组织器官内的人兽共患寄生虫病,多发于世界各地牧区。以往该病的诊断是基于普通细胞学,如今,随着细胞蜡块技术的不断发展,大大拓展了细胞病理学诊断的实用范围和能力。     

肿瘤微环境分析技术的研究进展

摘 要：肿瘤微环境与肿瘤的形成、增殖及转移方面关系密切,越来越多的观点认为对肿瘤微环境的调控可以干预肿瘤进程,但受限于肿瘤微环境的复杂性,目前对其认识非常有限。全文就目前常用的单细胞测序技术、多标记免疫荧光技术、多分子成像技术、转录组测序技术和质谱流式细胞技术在肿瘤微环境中的应用分析情况进行总结分析。     

神经妥乐平对误诊误治的交感神经链综合征疗效观察

目的观察神经妥乐平对误诊误治交感神经链综合征的疗效。方法交感神经链综合征患者60例。应用神经妥乐平注射液6 ml静脉滴注,1次/d,14 d为1个疗程,治疗后进行疗效评估。结果应用神经妥乐平后,总有效率为83.33%。与治疗前比较,差异有统计学意义(P<0.05)。结论交感神经链综合征诊断时易误诊,症状多种多样,可表现为复杂而带有情感色彩的内脏不适感。神经妥乐平注射液药理作用较广泛,具有多部位、多环节、多靶点的作用特点,对交感神经链综合征疗效显著。     

金纳多注射液治疗急性缺血性脑卒中疗效观察

目的：观察金纳多注射液治疗急性缺血性脑卒中的治疗效果。方法100例急性缺血性脑卒中患者随机分成对照组和治疗组,各50例。对照组给予血塞通注射液治疗,治疗组给予金纳多注射液治疗,疗程均为14 d。比较两组治疗前后的神经功能缺损评分变化及临床疗效。结果治疗组有效率为86%,对照组有效率为54%,两组有效率比较,差异有统计学意义(P<0.05)。对照组及治疗组治疗后14 d神经功能缺损评分分别为(27.6±2.01)分和(16.8±6.73)分,两组比较差异有统计学意义(P<0.05)。结论金纳多注射液可以促进损伤神经功能恢复,有效地降低致残率,提高患者的生活质量,在急性缺血性脑卒中的治疗中临床疗效较好。     

地塞米松对脑损伤大鼠核转录因子-κB水平的影响

Objective To explore the effects of dexamethasone on nuclear factor-kB (NF-κB) expression in brain tissue after traumatic brain injury (TBI). Methods Forty rats were randomly divided into two groups: dexamethasone treatment and no treatment, and severe brain injury was produced by gas percussion in both groups. At 0, 6, 24, 72 and 120 hours after injury, 5 rats of each group were executed and the histopathological changes in brain tissue in rats were observed by hematoxylin-eosin (HE) stain. The expression of NF-κB in brain tissue of rats was detected by immunohistochemical method. Results NF-κB expression was significantly up-regulated at 6 hours in brain tissue of rats after TBI (P<0.05), reaching the highest level at 24 hours (P<0. 01). It showed a tendency to lower, but was still high at 120 hours after TBI (P<0. 05 or P<0. 01). After treatment with dexamethasone, NF-κB level was lowered at 6, 24 and 72 hours (all P<0. 01). Conclusion NF-κB expression is up-regulated in brain tissue in early period after TBI, and keeps on a high level, thus inducing inflammatory response to produce secondary injury to brain tissue. Dexamethasone shows protective effects by regulating the levels of NF-κB and prevents secondary injury which is caused by the inflammatory cytokines in rat brain tissue after TBI.     

地塞米松对脑损伤大鼠核转录因子-κB水平的影响

Objective To explore the effects of dexamethasone on nuclear factor-kB (NF-κB) expression in brain tissue after traumatic brain injury (TBI). Methods Forty rats were randomly divided into two groups: dexamethasone treatment and no treatment, and severe brain injury was produced by gas percussion in both groups. At 0, 6, 24, 72 and 120 hours after injury, 5 rats of each group were executed and the histopathological changes in brain tissue in rats were observed by hematoxylin-eosin (HE) stain. The expression of NF-κB in brain tissue of rats was detected by immunohistochemical method. Results NF-κB expression was significantly up-regulated at 6 hours in brain tissue of rats after TBI (P<0.05), reaching the highest level at 24 hours (P<0. 01). It showed a tendency to lower, but was still high at 120 hours after TBI (P<0. 05 or P<0. 01). After treatment with dexamethasone, NF-κB level was lowered at 6, 24 and 72 hours (all P<0. 01). Conclusion NF-κB expression is up-regulated in brain tissue in early period after TBI, and keeps on a high level, thus inducing inflammatory response to produce secondary injury to brain tissue. Dexamethasone shows protective effects by regulating the levels of NF-κB and prevents secondary injury which is caused by the inflammatory cytokines in rat brain tissue after TBI.