立体定向放射治疗非小细胞肺癌疗效观察

目的 研究立体定向放射治疗非小细胞肺癌的疗效.方法 107例非小细胞肺癌由立体定向治疗计划系统设计放射治疗计划,剂量体积直方图（DVH）评价和优化放射治疗计划,计划照射剂量为60～75 Gy（中位剂量68 Gy）,每次2.2～3.0 Gy,每天1次,每周5 d,由美国瓦里安CL2100加速器照射,射野为固定野和非共面野或者大旋转弧.按照美国放射治疗协作组（RTOG）和WHO标准观察急性放射反应和疗效.结果 疗效（CR＋PR）为88%（94/107）,（NC＋PD）即无效病例为12%（13/107）.1～3年生存率分别为85.78%、49.02%、23.88%.结论 立体定向放射治疗采用大弧旋转＋固定野照射,方法可行,有较好的疗效,早期并发症较低,能为患者耐受.     

邵东县中学生艾滋病知识调查分析

艾滋病 (AIDS)是一种病死率极高的传染病 ,在一些国家和地区已成为一种可影响国民经济发展及民族兴亡的严重社会问题。当前 ,艾滋病发病率在我国正处于快速增长时期 ,青少年是艾滋病传播的易感人群。为此 ,做好青少年预防艾滋病的工作 ,让青少年彻底摒弃造成艾滋病传播的各种危险行为 ,免遭艾滋病威胁尤为重要。为了解青少年对AIDS基本知识的掌握程度、态度及获得这些知识的途径 ,并为进一步开展青少年预防AIDS知识的宣传教育提供依据 ,于2 0 0 3年底对邵东县某中学 70 8名在校高中生进行了调查。1　材料和方法1 1　调查对象　　采取整…     

煤工尘肺患者下呼吸道产金属内酰胺酶铜绿假单胞菌感染状况

目的了解煤工尘肺患者下呼吸道产金属内酰胺酶的铜绿假单胞菌(PA)的感染状况及其耐药特性。方法分离下呼吸道感染的煤工尘肺患者痰液标本中的PA，根据药敏试验，筛选可疑产金属内酰胺酶PA，最后依据2-巯基丙酸双纸片法鉴定产金属内酰胺酶PA。结果40株PA中共筛选出10株可疑PA，最终确定产金属内酰胺酶PA6株。这些菌株均有很强的耐药性，对亚胺培南、头孢菌素、含酶抑制剂类抗菌药物全部耐药；对阿米卡星、环丙沙星、左氧氟沙星、庆大霉素等药物部分耐药。产金属内酰胺酶PA的耐药性远强于不产金属内酰胺酶的PA。结论产金属内酰胺酶PA的耐药性很强，应加强煤工尘肺患者产金属内酰胺酶PA的检测，以利于指导治疗和控制感染。     

GLP实验室资料档案的管理

原始资料系指记载研究工作的原始观察记录和有关文书材料,包括工作记录、各种照片、缩微胶片、缩微复制品、计算机打印资料、磁性载体和自动化仪器记录材料等.档案是指非临床安全性评价研究机构在从事非临床研究以及其它各项活动时直接形成的对机构和社会具有保存价值的各种文字、图表、声像等不同形式的历史记录.档案是安全性评价实践活动的真实记录,是社会的宝贵财富,应由资料档案室集中统一保管.档案工作是非临床安全性评价研究机构管理工作的组成部分,是反映和追溯安全性评价工作真实历史面貌的一项重要工作,是做好非临床研究的重要基础工作之一.     

我对SCSI的认识

简要地描述了SCSI的性能、用途以及使用的注意事项     

流媒体技术在中医药教学中的应用

进入21世纪,我校的在校学生已达1万多人,繁重的教学任务迫切需要我们利用现代教育技术来提高教学水平.     

Correlation between high-resolution computed tomographic, magnetic resonance and pathological findings in cases with non-cancerous but suspicious lung nodules

Computed tomography scans, including thin-section high-resolution computed tomography (HRCT), occasionally fail to differentiate between small non-cancerous nodules from lung cancers. We describe nine such lesions ( < 20 mm in diameter) initially identified through our screening program for lung cancer using CT scanning. Pathological diagnoses included nodular fibrosis (n = 4), granuloma (n = 1), cryptococcoma (n = 1), localised organising pneumonia (n = 1), inflammatory pseudo-tumour (n = 1) and sclerosing haemangioma (n = 1). High-resolution CT findings, together with MRI findings with contrast-enhanced dynamic studies, were retrospectively evaluated. Additional cases should be identified and radiologically characterised in order to reduce the number of non-cancerous tumours that are treated by unnecessary surgery. Received: 28 February 2000; Accepted: 29 February 2000     

Molecular serotonergic mechanisms appear to mediate genetic sensitivity to cocaine-induced convulsions

Cocaine-induced convulsions appear to be mediated by serotonin (5-HT) neurotransmission, acting primarily at 5-HT(2) receptors. However, this effect of cocaine is attenuated by cocaine binding at sigma and muscarinic M(1) and M(2) sites. This study examined whether the aforementioned neural sites mediate the nearly two-fold difference in sensitivity to cocaine-induced convulsions across C57BL/6J (6J) and C57BL/6ByJ (6ByJ) mice. Experiment 1 compared 5-HT transporter densities across several brain regions of 6J and 6ByJ mice and cocaine-induced convulsions following pretreatment with the 5-HT reuptake inhibitor fluoxetine. Experiment 2 compared 5-HT(2) receptor densities across these mice and cocaine-induced convulsions following pretreatment with the 5-HT(2) antagonist cinanserin. There were no differences in 5-HT transporter densities, however, fluoxetine produced a greater facilitation of cocaine-induced convulsions in 6ByJ relative to 6J mice, suggesting that sensitivity to convulsions is mediated postsynaptically. Indeed, 5-HT(2) density was higher in 6ByJ relative to 6J mice in the amygdaloid ridge, hypothalamus, and midbrain. In addition, cinanserin attenuated convulsions more potently in 6J relative to 6ByJ mice. There were no differences in the densities or affinities of 5-HT(1), muscarinic, or sigma receptors across these strains, suggesting that density of these latter sites does not mediate genetic sensitivity to cocaine-induced convulsions. Since 6ByJ mice are less sensitive to convulsions despite the fact that they have more 5-HT(2) receptors, we hypothesized that these mice may exhibit a weaker linkage of 5-HT(2) sites to their second-messenger system relative to 6J mice. However, in experiment 3 we demonstrated that 5-HT(2)-receptor mediated phosphoinositide hydrolysis was higher in 6ByJ relative to 6J mice in the same regions also displaying higher 5-HT(2) densities. This study suggests that 5-HT(2) receptors mediate genetic sensitivity to cocaine-induced convulsions, further supporting the role of these sites in mediating this toxic effect of cocaine.     

CoQ10 fails to protect brain against focal and global ischemia in rats

OBJECTIVE: Release of oxygen free radicals occurs following cerebral ischemia. Studies show that oxygen free radicals mediate ischemic brain injury. CoQ10 is a potent free radical scavenger and may offset brain injury associated with reperfusion. We tested exogeneous CoQ10 as a neuroprotectant in rats following both global and focal ischemic insults. METHODS: Rats were subjected to either 4-vessel occlusion ischemia (4-VO, 10 min occlusion, 7-day survival) or middle cerebral artery occlusion (MCAO, 120 min-occlusion, 22.5 h survival). Regional cerebral blood flows (rCBF) and physiological variables such as blood pressure, pO2, pCO2, plasma glucose and hematocrit were monitored and measured in focal ischemia. The animals were randomized to receive treatments of either phosphate buffered saline (PBS) vehicle or CoQ10 following global or focal ischemia. Injection times were at the end of ischemia and 3 h later for both models of ischemia. Histological outcomes are expressed as a percentage of hippocampal CA(1) cell injury in global ischemia or percentage of cortical infarct over that of non-ischemic hemisphere in focal ischemia. RESULTS: In global ischemia, animals treated with PBS vehicle and CoQ10 had 86+/-5% (n=8) and 83+/-10% (n=8), respectively, of hippocampal CA(1) cell injury (P>0.05). The percentage of infarct volumes in animals following focal ischemia were 23+/-9% (control, n=10) and 25+/-9% (CoQ10, n=10). There were no temperature or physiological differences between the two treatment groups. CONCLUSION: Acute treatment with CoQ10 via intraperitoneal injection does not prevent neuronal injuries following global and focal ischemia.