Intra-arterial administration of cell-based biological agents for ischemic stroke therapy

Introduction: Ischemic stroke is becoming a primary cause of disability and death worldwide. To date, therapeutic options remain limited focusing on mechanical thrombolysis or administration of thrombolytic agents. However, these therapies do not promote neuroprotection and neuro-restoration of the ischemic area of the brain.

Areas covered: This review highlights the option of minimal invasive, intra-arterial, administration of biological agents for stroke therapy. The authors provide an update of all available studies, discuss issues that influence outcomes and describe future perspectives which aim to improve clinical outcomes. New therapeutic options based on cellular and molecular interactions following an ischemic brain event, will be highlighted.

Expert opinion: Intra-arterial administration of biological agents during trans-catheter thrombolysis or thrombectomy could limit neuronal cell death and facilitate regeneration or neurogenesis following ischemic brain injury. Despite the initial progress, further meticulous studies are needed in order to establish the clinical use of stem cell-induced neuroprotection and neuroregeneration.     

Tumor induction by ras and myc oncogenes in fetal and neonatal brain: modulating effects of developmental stage and retroviral dose

Introduction into fetal rat brain cells of a replication-defective retroviral vector harboring v-Ha-ras and v-gag-myc rapidly causes the induction of highly malignant undifferentiated neuroectodermal tumors following transplantation into the brains of syngeneic hosts [Wiestler, et al. (1992) Cancer Res. 52: 3760–3767]. In the present study, we have investigated the modulating effect of the developmental stage of neural target cells and of the dose of the retroviral vector used in the grafting experiments. Exposure of fetal cells from embryonic day (E)12 or E14 produced a 100% incidence of malignant neuroectodermal tumors which led to the death of recipient animals after a median latency period of 32 days. A 100-fold reduction of the virus dose from 2.062×10⁶ to 2.062×10⁴ focus-forming units/ml resulted in a lower tumor incidence of 25%. Of six neural grafts exposed to v-Ha-ras and v-myc at E16, only one showed evidence of tumorigenesis (low-grade astrocytoma and hemangioma). All other transplants were morphologically normal for observation periods of 26 weeks, indicating a marked loss of transforming activity of ras and myc in more advanced stages of brain development. In retrovirus-exposed donor cells which caused the development of neural tumors in recipient rats, malignant transformation was also evident during culture in vitro, usually after 9–12 days. Oncogene complementation was also studied in the newborn rat brain. After microinjection of the retroviral vector into the brain at postnatal day (P)0, P1 and P3, 5 out of 20 animals (25%) developed a total of seven brain tumors. Histopathologically, three of these neoplasms were malignant neuroectodermal tumors which, in contrast to those induced in fetal brain transplants showed evidence of focal glial and/or neuronal differentiation. In addition, we observed one oligodendroglioma, two hemangiomas and a malignant hemangioendothelioma. These data indicate that neural precursor cells and endothelia of the rat brain represent the major target cells for the complementary action of ras and myc and that the use of target cells from later developmental stages (E16 and postnatal) leads to the induction of both primitive and more differentiated neoplasms.These studies were supported by the Fonds zur Förderung der wissenschaftlichen Forschung in Österreich (Erwin Schrödinger fellowship, JO501-MED), by the Swiss National Science Foundation and by the Cancer League of the Kanton of Zürich     

Multiple spike-train analysis using mutual interval matrix

The principal-component approach is applied to the analysis of sequences of neuronal action potentials (spike trains). Multiple spike trains are represented as a sequence of vectors of mutual interspike intervals and are considered to be part of the trajectory of a dynamic system. The trajectory matrix is decomposed into a number of ‘basic spike patterns’ and their relative magnitudes by singular-value decomposition. The representation provides a convenient framework for analysis of dynamic relations and cooperation between neurons in an observed network. Examples of applications to simulated and cerebellar data are presented.     

沙市城区连续10年应用微生物制剂控制蚊虫的效果评价

目的：观察10年来主要应用苏云金杆菌以色列变种地方株（B．t－187）控制蚊虫的效果。方法：按WHO推荐的方法，在实验室进行生物测定，以确定B．t－187乳剂使用浓度，然后进行现场灭蚊效果观察。结果：使用效价为380～460国际单位，剂量为1～2ml／m2的B．t－187乳剂能有效控制蚊约和成蚊密度，成蚊平均相对叮咬密度比处理前下降89．4％，并降低了蚊虫的季节性高峰。结论：该生物制剂对按蚊、库蚊、伊蚊幼虫的毒杀效果颇佳，蚊幼尚无产生抗性的迹象。     

东南亚及西太平洋区的丝虫病

淋巴丝虫病为东南亚、西太平洋及南太平洋的重要公共卫生问题。此为慢性病，丝虫之成虫寄生于淋巴管或淋巴结，长达10－18年之久，致淋巴循环受阻塞而形成象皮病。根据微丝蚴在人体末梢血液之出现时间，分为日间和夜间之周期型与亚周期型。媒介多达40余种。防治方法主要赖药物治疗，世界卫生组织预期以现有的药物可于2020年消灭全球之淋巴丝虫病。本将班氏丝虫、马未丝虫及旁汶丝虫发现之经过，微丝蚴定期性，病媒蚊种及防治原则，作了相当完整的综述。笔曾在中所提及的多数国家实地防治丝虫病。     

遥感技术在蚊虫孳生地监测中的应用

遥感技术作为一种快速、有效的监测工具,目前在国外已越来越多地应用于蚊虫调查和防治研究中。本文就遥感技术的原理、方法、以及在蚊虫研究中的应用作一概述,并对遥感在我国蚊虫研究的应用前景予以展望。     

长效驱避剂的初步筛选研究

目的　研究一种对人有效保护时间 >8h ,且安全经济的长效驱避剂配方。方法　采用实验室 (GB T173 2 2 .10 -1998)和现场的药效测试方法对所配制的驱避剂配方进行效果测试。结果　实验室试验表明 ,以 2 0 %IR3 5 3 5配制 10、12、13、14号驱避剂配方在实验室内对白纹伊蚊的有效防护时间可达 8h以上 ;现场试验表明 ,10、12、13、14号驱避剂配方对人有效防止丘陵地区伊蚊的叮咬时间达 9h ,有效防止稻田地区中华按蚊的叮咬时间达 8h。结论以 2 0 %IR3 5 3 5与纤维素配制的驱避剂对人的有效保护时间可达 8h。纤维素对IR3 5 3 5有一定延长有效保护时间的缓释作用。实验所用配方对人的皮肤无不良反应 ,可作为户外活动人群防止蚊虫刺叮的驱避剂。     

波纹龙虱捕食蚊幼功能反应研究

作者于1991年7～9月,对波纹龙虱捕食淡色库蚊幼虫功能反应进行了研究。结果表明。在实验室条件下,波纹龙虱的捕食量随着蚊幼密度的增加而增大,其曲线符合Holling Ⅱ型功能反应,即其捕食量与猎物密度呈负加速曲线型。并根据Holling圆盘方程,建立了波纹龙虱捕食功能反应数学模型。波纹龙虱的寻找效应随着猜物密度的增加而降低。     

利用T7和PR双启动子的新型表达载体的构建及其应用

构建具有λＰＲ与Ｔ７双启动动子的新型原核表达载体ｐＤＯＧ，以便使用同一载体研究不同诱导条件下，重组蛋白在大肠杆菌中表达，降解以及折叠的情况，从而选择最佳的诱导条件。方法采用ｐＢＶ２２０与ＰＥＴ－３表达载体作为原始材料，将ＰＥＴ－３上包括Ｔ７启动子与Ｔ７ｇ－１０释译起始序列的一段序列克隆到     

巨噬细胞炎性蛋白4的突变和原核表达

目的 探索如何抑制嗜酸细胞的趋化作用，选择β-趋化因子巨噬细胞炎性蛋白4（MIP4）的突变性（Met-MIP4)作为趋化因子受体3的拮抗剂，将Met-MIP4基因在原核细胞中进行表达。方法 设计MIP4基因的PCR引物并进行氨基酸突变，将MIP4N末端的丙氨酸突变为蛋氨酸，以正常人肺酸突变，将MIP4N末端的丙氨酸突变为蛋氨酸。以正常人肺cDNA文库为模板，PCR方法获取Met-MIP4基因，克隆入载体pUC19，测序验证序列已得到突变，将正确的基因插入到GST融合表达载体pGEX-4T中，以IPTG诱导表达。结果 PCR产物为220bp左右的片段，连接入pUC19质粒后测序验证获得正确突变，构建的pGEX-4T融合表达载体在大肠杆菌中表达，经SDS-PAGE凝胶电泳显示有大小约34kU的新生融合蛋白表达。结论 成功突变并克隆了β-趋化因子MIP4基因，SDS-PAGE表明，与GST融合的Met-MIP4突变体已得到表达，为进一步研究其生物学活性奠定了基础。