神经系统与内分泌系统的相互影响与协同作用

在人体内,神经系统和内分泌系统紧密联系,协调配合,相互作用。它们的基本功能都是信息传递,在此功能之上,两大系统几乎调控着机体全部的代谢活动。将以综述的形式,介绍神经内分泌系统的结构基础,神经系统与内分泌系统的相互作用,以及两大系统共同发挥作用的主要领域。     

土壤生物与土壤污染研究前沿与展望

随着社会经济发展,人类生产活动对自然环境产生越来越广泛深刻的影响,土壤污染已成为危及生态系统稳定、农产品质量安全和人体健康的突出环境问题之一。重金属、有机污染化合物、病原菌及抗性基因等各类污染物大量进入土壤后,对土壤生物系统造成毒害作用,影响到土壤生态功能;另一方面,土壤生物如细菌、真菌、土壤动物等在一定程度上能够适应土壤污染,深刻影响着污染物在土壤中的迁移转化过程,在土壤污染修复中具有潜在重要作用。从土壤污染的生态毒理效应、土壤生物对土壤污染的响应与适应机制、污染土壤修复原理与技术等三方面综述了土壤生物与土壤污染相关研究前沿,展望了重点研究方向。     

留学生组织学与胚胎学教学特点与经验

我室已承担留学生组织学与胚胎学教学7届,在课程内容设置和时间安排、教材选用、任课教师遴选、教学方法和教学手段以及考试与成绩评定方面积累了一些经验,了解了留学生教学的特点,同时在教学中仍然存在一些不足。需要在实践中不断找出存在的问题并及时解决,使留学生教学质量稳步上升。     

制药设备与工程设计课程教学改革与实践

制药设备与工程设计是制药工程专业一门工程素质培养核心课程,作者结合实践,就课程内容建设、教学方法及实践教学环节3个方面,对该课程的教学提出一些个人看法,以期形成工科专业制药设备与工程设计独特的教学体系。     

谈动脉血与静脉血的概念与教学

通过对血液循环系统和呼吸系统的动脉和静脉血管、体循环和肺循环、肺泡气血交换和组织换气、动脉血和静脉血等问题的讨论,比较和探讨中学生物学与大学医学本科教育中关于动脉血和静脉血等相关内容的教学重点。     

整合素与肿瘤的转移与血管生成

整合素是一类介导细胞与细胞外基质及细胞与细胞间黏附的细胞黏附分子受体,肿瘤细胞与胞外基质的相互作用对肿瘤的生成及转移有着重要的影响,整合素在肿瘤的生成、侵袭、转移以及肿瘤血管的生成过程中起着重要的作用。本文对整合素的结构、功能,以及它在肿瘤的血管生成过程中的作用,它与细胞外基质间的相互关系做了介绍。     

立克次体与立克次体病的检测与鉴定

立克次体是一类严格细胞内寄生的原核细胞型微生物,已被列入生物战剂名录。立克次体病是一类严重威胁人类健康的人兽共患的自然疫源性疾病。立克次体严格的细胞寄生性决定了立克次体病的诊断不同于传统方法,需根据流行病学资料、临床症状和体征及实验室检测进行综合判断,通常实验室检测是明确诊断的主要依据。从病原体的分离和培养到目前的基因水平比对,立克次体的检测技术虽发展了100多年,但人类尚未实现早期快速诊断立克次体病的目标。本文主要综述了立克次体与立克次体病检测与鉴定的研究进展。     

军事医学科学院放射与辐射剂量学研究进展与展望

本文系统介绍了60年来军事医学科学院放射与辐射医学研究所从防原医学至放射与辐射医学研究各个阶段辐射剂量学研究的主要情况,包括核试验剂量保证、生物效应照射实验条件及剂量学方法的建立、事故照射剂量重建技术、辐射防护学及其剂量评价、医疗和诊断剂量学、辐射加工剂量及辐照工艺、辐射剂量测量技术、核设施事故剂量学、辐射剂量标准、微波剂量学等所获得的成果和经验,在此基础上,对该所辐射剂量学发展方向和研究重点进行了分析和论述.     

C/EBPα基因与肿瘤

C/EBPα基因是抑癌基因,有抑制增殖、促进分化和调节DNA损伤反应等作用。各种机制如对抗性的蛋白质-蛋白质相互作用、基因突变和翻译后修饰等导致C/EBPα转录抑制或活性丧失,可能诱发肿瘤。本文结合国内外研究现状,介绍C/EBPα基因的结构、功能及与肿瘤的诊断、治疗和预后的关系。     

Role of tumor cell glycoproteins immunologically related to glycoproteins Ib and IIb/IIIa in tumor cell-platelet and tumor cell-matrix interactions

A panel of monoclonal and polyclonal antibodies raised against human platelet GpIb or the GpIIb/IIIa complex were used to detect immunologically related molecules on two cell lines derived from human solid tumors. Human cervical carcinoma (MS751) and human colon carcinoma (clone A) expressed molecules immunologically related to platelet GpIb and GpIIb/IIIa complex. These molecules were localized to their plasma membranes by immunofluorescence and immunocytochemistry. The immunologically related GpIb was evenly distributed on the tumor cell membrane with occasional areas of aggregates, whereas the immunologically related GpIIb/IIIa had a pronounced punctate distribution of aggregates in prefixed cells. When MS751 or clone A cells were pretreated with antibodies against platelet GpIb and/or the GpIIb/IIIa complex, their ability to induce platelet aggregation was significantly inhibited. In addition, when tumor cells were pretreated with antibodies against the platelet IIb/IIIa complex, adherence to fibronectin-coated plates was also significantly inhibited. These results suggest a role for these immunologically related tumor cell glycoproteins in tumor cell-host cell (i.e., platelet, endothelial cells) interactions, tumor cell interactions with components of the subendothelial matrix, and subsequent tumor metastasis.     

Role of tumor necrosis factor in monocyte/macrophage tumor cytotoxicity in vitro

The ability of activated monocytes/macrophages to exert cytotoxic effects in vitro which are preferentially manifest on target cells displaying a transformed phenotype has elicited intense efforts aimed at a molecular characterization of the underlying mechanism. This multistep reaction is typified by an apparently stringent requirement for conjugation between the effector and target to facilitate cytotoxicity, which has therefore long caused bias against the role of soluble effector molecules in mediating target cell damage. However, several laboratories have recently demonstrated a compelling role for at least one such mediator, tumor necrosis factor (TNF), in cell-mediated cytotoxicity exerted against certain target cells; these studies indicated that specific anti-TNF antibodies could block direct monocyte/macrophage-mediated cytotoxicity of TNF-sensitive targets. More recently we have shown that some targets which are completely resistant to soluble or fluid-phase TNF are effectively lysed by a TNF-dependent mechanism upon coculture with activated macrophages under conditions in which conjugation is facilitated. Furthermore, macrophage-mediated cytolysis of both TNF-sensitive and TNF-resistant targets occurs independently of the action of secreted TNF via this mechanism. The purpose of this review is to consider the implications of distinct modes of effector cell delivery of TNF to the target for molecular characterization of the target injury phase of macrophage-mediated tumor cytotoxicity.     

Anticachectin/tumor necrosis factor-alpha antibodies attenuate development of cachexia in tumor models

C57BL/6 mice bearing either a transplantable methylcholanthrene-induced sarcoma or Lewis lung adenocarcinoma were passively immunized every other day with a rabbit immunoglobulin fraction raised against murine cachectin/tumor necrosis factor-alpha. Mice bearing methylcholanthrene-induced sarcoma developed tumor-associated hypophagia that was attenuated by anticachectin immunoglobulin treatment. In the same tumor-bearing animals, anticachectin treatment also significantly reduced the extent of carcass protein and fat loss, and reduced tumor weight. Mice bearing Lewis lung adenocarcinoma did not develop significant anorexia or carcass lean tissue depletion as tumor growth progressed, but they lost carcass lipid. Treatment of Lewis lung adenocarcinoma bearing mice with anticachectin antibodies diminished the degree of carcass lipid depletion and prevented plasma hypertriglyceridemia. However, in both tumor models, anticachectin treatment did not affect either the development of anemia, hypoalbuminemia or the increase in serum amyloid P concentrations seen with increasing tumor burden. We conclude that an endogenous cachectin response, inhibitable by exogenously administered antibody, contributes to anorexia and to changes in body fat and protein metabolism in these tumor-bearing animals. Neutralizing endogenous cachectin production with antibodies offers the potential to reduce tissue wasting that is frequently associated with neoplastic disease, but it does not appear to affect all of the hematologic and acute phase responses in these murine tumor models.     

试论磁场治疗恶性肿瘤中的三对矛盾凋亡与增殖免疫与肿瘤阻塞与供给

脉冲梯度磁场(峰值磁场0.2~2.0T,梯度10~100T.M-1,脉冲宽度20~200ms,重复频率0.16~1.34HZ)抑制鼠恶性肿瘤的细胞增殖和诱导细胞凋亡,提高宿主细胞免疫功能和抑制肿瘤生长,阻塞供给肿瘤生长的新生血管。虽然进一步的清晰的机理研究是非常需要的,但是上面的发现能够成为治疗恶性肿瘤的一种新方法。     

PI3K/Akt信号传导通路与肿瘤

信号转导通路的异常激活是肿瘤细胞的发生、发展重要步骤,PI3K/Akt 信号通路在人类绝大多数恶性肿瘤中被异常激活,其在肿瘤的增殖、存活、细胞运动、抵抗凋亡、血管发生和转移以及对化疗耐药、放疗抗拒中发挥了重要作用.因此,通过对PI3K/Akt 通路的研究进一步了解肿瘤的发生、发展机制,并寻求抗肿瘤药物的新靶点,本文就 PI3K/Akt 信号转导通路的结构特点、与肿瘤发生、发展的关系及其时放化疗的影响作一综述.     

Vaccination with metastasis-related tumor associated antigen TPD52 and CpG/ODN induces protective tumor immunity

Tumor protein D52 (TPD52) is involved in transformation and metastasis and has been shown to be over-expressed in tumor cells compared to normal cells and tissues. Murine TPD52 (mD52) shares 86% protein identity with the human TPD52 orthologue (hD52). To study TPD52 protein as a target for active vaccination recombinant, mD52 was administered as a protein-based vaccine. Naïve mice were immunized with either mD52 protein and CpG/ODN as a molecular adjuvant or CpG/ODN alone. Two weeks following the final immunization, mice were challenged s.c. with syngeneic tumor cells that over-express mD52. Two distinct murine tumor cell lines were used for challenge in this model, mKSA and 3T3.mD52. Half of the mice immunized with mD52 and CpG/ODN rejected or delayed onset of mKSA s.c. tumor cell growth, and 40% of mice challenged with 3T3.mD52 rejected s.c. tumor growth, as well as the formation of spontaneous lethal lung metastases. Mice immunized with mD52 and CpG/ODN generated detectable mD52-specific IgG antibody responses indicating that mD52 protein vaccination induced an adaptive immune response. In addition, mice that rejected tumor challenge generated tumor-specific cytotoxic T lymphocytes’ responses. Importantly, microscopic and gross evaluation of organs from mD52 immunized mice revealed no evidence of autoimmunity as assessed by absence of T cell infiltration and absence of microscopic pathology. Together, these data demonstrate that mD52 vaccination induces an immune response that is capable of rejecting tumors that over-express mD52 without the induction of harmful autoimmunity.     

HGF／SF-Met signaling in tumor progression

Tumor progression is a multi-step process that requires a sequential selection of specific malignant phenotypes. Met activation may induce different phenotypes depending on tumor stage: inducing proliferation and angiogenesis in primary tumors, stimulating motility to form micrometastases, and regaining the proliferation phenotype to form overt metastases. To study how HGF/SF-induced proliferative phenotypes switch to the invasive phenotype is important for understanding the mechanism of tumor progression and will provide an attractive target for cancer intervention and therapy.     

The zebrafish/tumor xenograft angiogenesis assay

Here we describe a method to study tumor angiogenesis in zebrafish (Danio rerio) based on the injection of proangiogenic mammalian tumor cells into the perivitelline space of zebrafish embryos at 48 h post-fertilization. Within 24-48 h, proangiogenic tumor grafts induce a neovascular response originating from the developing subintestinal vessels. This can be observed at macroscopic and microscopic levels after whole-mount alkaline phosphatase staining of wild-type zebrafish embryos, or by fluorescence microscopy in transgenic VEGFR2:G-RCFP embryos in which endothelial cells express the green fluorescent protein under the control of the VEGFR2/KDR promoter. Angiogenesis inhibitors added to the injected cell suspension or to the fish water prevent tumor-induced neovascularization. The assay is rapid and inexpensive, representing a novel tool for investigating tumor angiogenesis and for antiangiogenic drug discovery. Also, gene inactivation by antisense morpholino oligonucleotides injection in zebrafish embryos may allow the identification of genes involved in tumor angiogenesis.