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.     

西安市2～3岁儿童的气质结构探讨

本文采用幼儿气质问卷(TTS)对233名2～3岁入托儿童的气质结构进行了研究。结果显示:该年龄组不同性别儿童的气质结构无明显差异;本组儿童的主要气质类型为中间偏易型(I一E),其次为容易抚育型(E);同西方(美国纽约)儿童比较,我国儿童的气质结构有一定特征。     

免疫荧光法与 Giemsa 氏法检测沙眼衣原体的比较

本文用免疫荧光法与 Giemsa 氏法检测明显沙眼患者,两法阳性率相差无几。但在临床肉眼观察认为正常时,其阳性率分别为24.77%及11.58%(P<0.05),差异有显著意义,表明免疫荧光法检测早期沙眼较 Giemsa 氏法敏感。临床认为正常眼,经实验室检查25.56%为阳性,说明开展沙眼的实验室诊断是必要的。     

少数民族女大学生生理卫生常识和艾滋病相关知识调查

为了解少数民族女大学生对生理卫生常识及艾滋病(AIDS)相关知识的掌握情况,中央民委于2007年3月对所属7大民族院校的2006级新生(女)进行了问卷调查,为探索少数民族院校健康教育模式提供科学依据,现报告如下。1对象与方法1.1对象2007年3月调查中南民族大学2006级(新生)女大学生2     

Biologic effects of hyperthermia and radiation on gastric cancer cells (SGC-7901) in vitro. II. Ultrastructural changes of cells

Different characteristic damages of the SGC-7901 gastric adenocarcinoma cells were studied by electron microscopy 1, 36, 72, 96 and 120 hours after heating and radiation in vitro. The visible damages, such as the enlarged mitochondria, increase of lysosomes and perichromatin granules could be shown 1 hour after heating (43 degrees C for 30 min) but no visible damages of the cells were shown until 36 hours following radiation (500 rad). In order to study the ultrastructural changes of the gastric cancer cells in mitosis after heating and radiation, we have used the new method of ultrastructural research in selecting and observing the M cell in vitro and found loosened structure of chromosome and disappearance of microtubules 1 hour following hyperthermia. At the same time, no apparent abnormalities of the mitotic cells were observed after radiation. It is the chief cause of division delay in heat injured cells. However, the chromosomes and microtubules of the new mitotic cells could recover 36 hours after heating (43 degrees C for 30 min). After radiation, the giant cells and abnormal morphologic changes of cells gradually increase and the living cells decrease. Unexpectedly, the division of a few giant cells is observed 72 hours after heating and radiation.     

脑健冲剂对AD大鼠5-HT和 MAO影响的实验研究

目的:采用脑健冲剂治疗AD,观察脑健冲剂对AD大鼠海马区5-羟色胺和MAO的影响.方法:本实验采用D-半乳糖拟衰老,Aβ1-40损害联合所致AD模型,用脑健冲剂治疗.结果:脑健冲剂可提高海马5-羟色胺含量和降低MAO的水平.结论:脑健冲剂可治疗AD.     

A PRELIMINARY STUDY OF THE ACTION OF MALE HOR MONE ON HIGH DENSITY LIPOPROTEIN-CHOLESTEROL

Plasma testosterone and estradiol are determined in 72 patients with abnormal high density lipoprotein. cholesterol (HDL-C) and high density lipoprotein cholesterol/total cholesterol (H/T) ratio values, and in 72 randomly chosen males with normal HDLC and H/T values. The results showed that plasma testosterone levels in the groups with abnormal HDL-C and H/T were obviously lower than those in the controls. Statistically significant differences were found in all the abnormal groups in comparison with the controls (P0.20). Testosterone levels lowered further with increasing age in the groups with abnormal HDL-C and H/T., the most obvious drops were in the groups around 56 years of age (P<0.005). The data indicate that male hormone deficiency may reduce HDL-C and H.'T and facilitate the process of atherosclero_is. Therefore, it seems rational to treat such patients with male sex hormone preparations or to use the traditional Chinese medicines which strengthen Yang (maleness) in a new attempt to treat and prevent CHD.     

Adeno-associated virus vector-mediated systemic delivery of IFN-beta combined with low-dose cyclophosphamide affects tumor regression in murine neuroblastoma models.

PURPOSE: Type I IFNs (IFN-alpha/beta) have shown significant antitumor activity in preclinical models but limited efficacy and significant toxicity in clinical trials. We hypothesized that the antitumor activity of type I IFNs could be enhanced by chronic, low-dose systemic delivery and sought to test this in murine neuroblastoma models. EXPERIMENTAL DESIGN: Continuous liver-generated expression of human IFN-beta (hINF-beta) was achieved through a gene therapy-mediated approach using adeno-associated virus vectors encoding hIFN-beta (AAV hINF-beta). Orthotopic localized retroperitoneal and disseminated models of neuroblastoma were established using three different xenografts. Immunohistochemical analysis and ELISA were used to evaluate the antiangiogenic effect of therapy. RESULTS: The development of both localized orthotopic (retroperitoneal) and disseminated neuroblastoma was prevented in all mice expressing hINF-beta. Continued growth of established retroperitoneal tumors, treated with AAV hINF-beta as monotherapy, was significantly restricted, and survival for mice with established, disseminated disease was significantly prolonged following administration of AAV hINF-beta. Analysis of treated tumors revealed a significant antiangiogenic effect. Mean intratumoral vessel density was diminished and expression of the angiogenic factors vascular endothelial growth factor and basic fibroblast growth factor were both decreased. Finally, combination therapy in which AAV hIFN-beta was used together with low-dose cyclophosphamide resulted in regression of both established retroperitoneal and disseminated disease. CONCLUSIONS: AAV-mediated delivery of hIFN-beta when used as monotherapy was able to restrict neuroblastoma growth due in part to inhibition of angiogenesis. When used in combination with conventional chemotherapy, AAV hIFN-beta was able to effect complete tumor regression.