普洛托品对正常大鼠学习能力及海马、大脑皮层乙酰胆碱酯酶活性的影响

目的：观察普洛托品（protopine,Pro)对正常大鼠学习能力及海马、大脑皮层乙酰胆碱酯酶活性的影响。方法：大鼠每天Pro 0.5mg/kg灌胃，28d后三等分Y迷宫测定大鼠学习成绩，并测定海马及大脑皮层乙酰胆碱酯酶活性。结果：Pro组大鼠达到学会标准所需的训练次数明显减少，与对照组比较差异有极显著性（P＜0．01），Pro组大鼠海马及大脑皮层乙酰胆碱酯酶活性亦明显降低，与对照组比较差异有显著性（P＜0．01，P＜0．05），结论：Pro可提高正常大鼠学习能力，并降低海马及大脑皮层乙酰胆碱酯酶活性。     

Slowly progressive hemiparesis in childhood as a consequence of Rasmussen encephalitis without or with delayed-onset seizures

Five young children developed slowly progressive hemiparesis as the initial manifestation of Rasmussen encephalitis (RE). Three have remained seizure free over an observational period of 1.3–1.9 years. In the remaining two patients, seizures occurred after 0.5 and 0.6 years respectively. We suggest that RE might be presently underdiagnosed and should be suspected in cases of new onset hemiparesis. In this series, three out of five patients showed oligoclonal bands on examination of cerebrospinal fluid (CSF) which represented additional diagnostic hints towards an immune-mediated condition. According to recently published formal diagnostic criteria, evidence of progressive cerebral hemiatrophy or bioptic identification of RE-typical inflammation confirms the diagnosis in such cases. Long-term immunotherapy is recommended in order to prevent further tissue loss and functional decline.     

间接免疫荧光法检测特异性IgG抗体对流行性出血热诊断意义

本文报告用间接免疫荧光法检测特异性IgG抗体对流行性出血热的诊断意义。53例不同病期的出血热患者的血清,其间接荧光抗体的阳性率为49/53(占92.45％)。有77.36％的患者血清,检出IgG抗体的时间是在发病后的1～2周。血清中IgG的滴度与疾病的严重性无密切相关。另25例非EHF患者,其血清特异性IgG抗体均为阴性。可见检测特异性IgG抗体对EHF的诊断颇为有用。     

采用DSA设备评价吞咽功能的初步探讨

目的:探讨运用DSA设备作吞咽功能检查的价值。材料和方法:用DSA设备对正常组24例,咽异感症患者32例,做上至颅底、下达第七颈椎平面的正侧位动态采集,了解吞咽状况,并行咽传输时间测定,进行对照研究。结果:正常对照组咽传输时间为1.441±0.302s,咽异感症患者咽传输时间为1.367±0.409s,两组结果相比统计学上无显著差异,但后者较易发生咽部钡剂滞留等改变。结论:DSA机由于采集速度快,不但在心血管检查及介入治疗方面有重要意义,而且在非血管性脏器的动力学检查中也起着一定的作用。由于能完整记录钡剂通过咽部的全过程,故此方法是吞咽功能检查的良好方法之一。     

T-2 toxin induces apoptosis, and selenium partly blocks, T-2 toxin induced apoptosis in chondrocytes through modulation of the Bax/Bcl-2 ratio.

T-2 toxin is one of the mycotoxins, a group of type A trichothecenes produced by several fungal genera including Fusarium species. In the present study, we have investigated the apoptotic effects of T-2 toxin on chondrocytes and the relationship between T-2 toxin induced chondrocyte apoptosis and its influence on Bcl-2/Bax protein and mRNA expression. We have also examined the inhibitory effects of selenium on chondrocyte apoptosis induced by T-2 toxin. We have combined morphological and biological techniques to establish the relevance of apoptosis in human chondrocyte death induced by T-2 toxin. Treatment with T-2 toxin caused accelerated apoptosis in a concentration dependent manner. The apoptosis induced by T-2 toxin involved an increased Bax/Bcl-2 ratio. Bcl-2 mRNA expression remained unchanged in chondrocyte apoptosis induced by T-2 toxin treatment, while Bax mRNA expression increased following treatment with T-2 toxin. Selenium could partly block the apoptosis of chondrocytes induced by T-2 toxin through decreasing the Bax/Bcl-2 ratio. These results suggest that, under our experimental conditions, apoptosis of chondrocytes can be induced by T-2 toxin (1-20ng/mL) via the Bcl-2 and Bax proteins, and the Bax/Bcl-2 ratio may play a critical role in governing the susceptibility to apoptosis induced by T-2 toxin in human chondrocytes.     

纳洛酮合参麦治疗慢性阻塞性肺病合并Ⅱ型呼吸衰竭34例

目的观察纳洛酮合参麦注射液治疗慢性阻塞性肺病合并Ⅱ型呼吸衰竭的效果。方法在常规治疗基础上,治疗组用纳洛酮、参麦注射液治疗本病34例,并设对照组对比。结果治疗组、对照组总有效率分别为85.3%、70.6%,治疗组优于对照组(P<0.05)。治疗组在治疗后各项指标比较均优于对照组(P<0.01或P<0.05)。结论本方法对本病有改善症状,缩短病程的功效。     

后循环缺血与眩晕

后循环又称椎基底动脉系统，由椎动脉、基底动脉和大脑后动脉（posterior cerebral artery，PCA）组成，主要向脑干、小脑、丘脑、枕叶、部分颞叶等结构供血。后循环缺血（posterior circulation ischemia,PCI）是常见的缺血性脑血管病。与前循环缺血一样，PCI也可按缺血程度和持续时间的不同分为短暂性脑缺血发作（transient ischemic attack,TIA）和脑梗死。其同义词包括椎基底动脉系统缺血、后循环TIA和脑梗死、椎基底动脉疾病、椎基底动脉血栓栓塞性疾病。     

Characterization of bortezomib-adapted I-45 mesothelioma cells

Background  

Bortezomib, a proteasome-specific inhibitor, has emerged as a promising cancer therapeutic agent. However, development of resistance to bortezomib may pose a challenge to effective anticancer therapy. Therefore, characterization of cellular mechanisms involved in bortezomib resistance and development of effective strategies to overcome this resistance represent important steps in the advancement of bortezomib-mediated cancer therapy.