‘Ischemic tolerance’ phenomenon detected in various brain regions

We investigated the effects of mild and non-lethal ischemic insult on neuronal death following subsequent lethal ischemic stress in various brain regions, using a gerbil model of bilateral cerebral ischemia. Single 10-min ischemia consistently caused neuronal damage in the hippocampal CA1, CA2, CA3 and CA4, layer III/IV of the cerebral cortex, dorsolateral part of the caudoputamen and ventrolateral part of the thalamus. On the other hand, in double ischemia groups, 2-min ischemic insult 2 days before 10-min ischemia exhibited significant protection in the CA1 and CA3 of the hippocampus, the cerebral cortex, the caudoputamen and the thalamus. Five-min ischemic insult 2 days before 10-min ischemia also showed protective effect in the same areas as those of 2-min ischemia except for the CA1 region of the hippocampus, while 1-min ischemic insult exhibited no protective effect in any brain regions. In the immunoblot analysis, both 2- and 5-min ischemia caused increased synthesis of heat shock protein 72 (HSP 72) in the hippocampus, but 1-min ischemia did not. The present study demonstrated that the ‘ischemic tolerance’ phenomenon was widely found in the brain and also suggested that ischemic treatment severe enough to cause HSP 72 synthesis might be needed for induction of ‘ischemic tolerance’.     

Immunohistochemical analysis of inducible nitric oxide synthase (iNOS) and heat shock proteins (HSPs) in ameloblastomas

BACKGROUND: To clarify the possible role of nitric oxide (NO) and stress proteins in oncogenesis and cytodifferentiation of odontogenic epithelium. Inducible NO synthase (iNOS) and heat shock proteins (HSPs) were analyzed in ameloblastomas as well as in tooth germs. METHODS: Specimens of seven tooth germs, 36 benign ameloblastomas and five malignant ameloblastomas were examined by immunohistochemistry using antibodies against iNOS and 27-, 60- and 70-kDa HSPs (HSP27, HSP60 and HSP70). RESULTS: Immunoreactivity for iNOS was detected in normal and neoplastic odontogenic epithelial cells and was higher in malignant ameloblastomas than in tooth germs and benign ameloblastomas. HSP27 was expressed constitutively in all odontogenic epithelial cells in tooth germs and benign and malignant ameloblastomas. Expression of HSP60 and HSP70 was detected in normal and neoplastic odontogenic epithelial cells and was prominent in cells neighboring the basement membrane. HSP60 reactivity showed no apparent difference between normal and neoplastic odontogenic epithelium, whereas HSP70 expression was slightly higher in benign and malignant ameloblastomas than in tooth germs. CONCLUSIONS: Activation of iNOS might be associated with malignant potential of epithelial odontogenic tumors. Elevated expression of HSP70 is considered to be involved in neoplastic transformation of odontogenic epithelial cells.     

NE系列两种常用冲击波源碎石机治疗输尿管结石的疗效分析

目的分析并比较NE系列的两种冲击波源碎石机治疗输尿管结石的疗效、碎石时的疼痛程度、碎石时间及副作用。方法回顾性分析应用NE-IV型液电冲击波源碎石机治疗输尿管结石患者1290例及应用NE-VB型电磁冲击波源碎石机治疗输尿管结石患者1196例的临床资料,并进行疗效、碎石时间、碎石时的疼痛程度及副作用的比较。结果应用电磁冲击波源碎石机治疗输尿管上段结石患者的总有效率为85.4%,治疗时间23~60min,平均(35.3±5.7)min;输尿管下段结石患者的总有效率为94.6%,治疗时间3~60min,平均(30.5±6.1)min。碎石时患者的疼痛感觉轻。液电冲击波源碎石机治疗的输尿管上段结石患者的总有效率为75.7%,治疗时间25~110min,平均(38.0±9.8)min;输尿管下段结石为85.7%,治疗时间4~90min,平均(35.8±7.7)min。碎石时患者的疼痛感觉明显。此外,肾绞痛、血尿、恶心、呕吐、皮肤瘀斑等副作用明显高于电磁冲击波源碎石机治疗组。结论电磁冲击波源碎石机治疗输尿管结石疗效优于液电冲击波源碎石机,而且更安全、有效、痛苦小。     

复式脉冲低能量ESWL治疗肾结石769例报告

目的探讨复式脉冲HB-V型低能量体外冲击波碎石机治疗肾结石的治疗效果.方法采用复式脉冲HB-ESWL-VG型低能量碎石机治疗直径<2.0 cm的各类肾结石769例，治疗工作电压3～9 kV，平均冲击次数2 300次.结果肾盏结石总粉碎率为97.4%，其中上中盏结石复打率为13.1%，术后3个月排净率为89.4%，下盏结石复打率为17.3%，排净率为81.5%；肾盂结石粉碎率为98.3%，复打率为6.1%，术后3个月排净率为93.0%.结论复式脉冲低能量ESWL治疗肾结石具有治疗成功率高、复打率低、无严重并发症、副作用少之优点.     

体外震波对骨和骨疾病的作用及其机制

体外震波（extracorporeal shock wave，ESW）于20世纪80年代中期开始用于骨科领域，目前，它作为一种非侵入性治疗方法用于治疗多种骨相关疾病。为指导其进一步用于临床治疗并提高疗效，了解它对正常骨组织的影响和对骨疾病的治疗作用及其机制非常重要。现已有不少学者对这些方面进行了相关的基础与临床研究，取得了明显进展。本文就体外震波对骨和骨疾病的作用及其机制综述如下。     

感染性休克早期目标指导性治疗方案的应用体会

目的 为加强外科围手术期处理，观察应用早期目标指导性治疗方案（early goal directed therapy，EGDT）对感染性休克患者的救治效果。方法 运用EGDT使入ICU8h内的感染性休克患者的中心静脉压（CVP）、平均动脉压（MAP）和上腔静脉血氧饱和度（ScvO2）达标。结果 本组20例感染性休克患者，在8h内CVP达标20例，MAP达标20例，ScvO2达标16例。结论 应用EDGT治疗感染性休克有较好的理论基础和实用性，在限定的时间内使所有的目标值达标存在一定的困难。     

非控制性出血性休克低压复苏治疗效果的研究

目的　应用大鼠脾损伤非控制性出血性休克模型探讨低压及低压扩容复苏治疗非控制性出血性休克的可行性。方法　雄性Wistar大鼠 5 0只 ,在大鼠脾损伤模型复制成功后随机等分为 5组 ,组 1 :假手术组 ;组 2 :休克未处理组 ;组 3:常压复苏组 (急救期控制MAP在 80mmHg以上 ) ;组 4 :低压复苏组 (急救期控制MAP在 6 0mmHg±5mmHg) ;组 5 :低压扩容复苏组 (急救期输入硝普钠 5 μg·kg- 1 ·min- 1 ,同时输液控制MAP在 6 0mmHg± 5mmHg)。结果　 1～ 5组平均存活时间 (min)分别为 1 80、73.5 0± 8.0 4、1 1 4 .30± 31 .33、1 4 6 .70± 2 8.0 7和 1 71 .6 0± 1 5 .74 ,除组1、组 5外 (P =0 .0 6 71 ) ,其余各组间比较均有统计学意义 (P <0 .0 5 ) ;2～ 5组的急救期出血量 (ml·kg- 1 )分别为 :3.79± 1 .39、1 7.4 1± 8.88、8.6 7± 4 .5 9、1 0 .33± 4 .31 ,其中组 3出血量明显高于其他各组 (P <0 .0 1 ) ;组 4、组 5与组 2比较出血量明显增多 (P <0 .0 5 )。结论　在非控制性出血性休克治疗中 ,低压及低压复合适量硝普钠扩容复苏方法可改善组织代谢 ,提高生存时间 ,是更为理想的复苏方法     

The peri‐microvascular edema in hippocampal CA1 area in a rat model of sepsis

Encephalopathy is a common complication of sepsis. However, little is known about the morphological changes that occur in the brain during sepsis. In this study, fecal peritonitis was induced in Wistar rats, which had been monitored for 4 h before their brains were removed and samples from the CA1 area taken. In addition to higher blood pressure with a decreasing pattern and a significant drop in rectal temperature, an increased heart rate and marked respiratory failure were observed. The tissue was investigated and compared with corresponding hippocampal samples taken from sham‐operated and not operated control groups. Significantly more peri‐microvascular edema was found in the hippocampal CA1 area in the septic group. The percentages of the peri‐microvascular edema were 158.57 ± 3.6%, 122.84 ± 1.5% and 120.24 ± 1.9% in the fecal peritonitis group, sham‐operated and not operated control groups, respectively. The results may suggest that the edema observed around the microvessels may participate in the pathogenesis of the septic encephalopathy probably by causing in the microvascular permeability characteristics.     

胆源性感染性休克兔血栓素、前列环素与血小板聚集率的变化

动态观察胆总管急性完全性梗阻并感染、继发休克兔的血浆血栓素(TXA_2)和前列环素(PGI_2)的稳定代谢产物 TXB_2和6-keto-PGF_(1α)含量及血小板聚集率的变化。结果,血浆 TXB_2呈进行性升高,20h 后(休克时)呈下降趋势,血浆6-keto-PGF_(1α)6h 升高,随后回降;血小板聚集率呈进行性下降。提示血栓素和前列环素、血小板聚集率的变化在重症急性胆管炎、胆源性感染性休克发病过程中起重要病理生理作用,与病情和预后转归有重要联系。     

The heat shock/oxidative stress connection

Involvement of free-radical oxidations in the aging process has been a topic of interest since Harman's original contribution. Because of the close association between aging and Alzheimer disease (AD) and the qualitative similarity in the neuropathology of both conditions, it has been proposed by many investigators that oxidative stress may be important in AD. If such modality of injury was indeed involved, one should expect to find markers of oxidation and heat shock (since free radicals are key mediators of heat-shock induction) in brains of patients with AD. In fact, several studies documented abnormal expression of antioxidant enzymes and heat-shock proteins (HSP) along with other markers of oxidation in AD brains. We showed that abnormally expressed antioxidant enzymes are topographically associated with senile plaques and neurofibrillary tangles, and that the activity of these enzymes is (contrary to what one would expect) markedly reduced. These findings have recently been confirmed by other investigators. Despite a large amount of evidence that suggests an association between oxidative stress and the pathogenesis of AD, it is not yet known whether oxidative stress is a cause or consequence of the disorder. Future research efforts regarding the oxidative stress hypothesis of AD should include attempts, at generating AD pathology by oxidative means in laboratory animals, determining the role and integrity of the heat-shock response in AD, as well as that of various antioxidant systems, growth factors, and hormones with antioxidant and neuroprotective properties.