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。     

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。     

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。     

草鱼与鲢鱼肥胖基因克隆与序列分析

肥胖基因产物leptin是调节哺乳动物摄食、能量代谢等生命活动的重要细胞因子。 应用RT-PCR和RACE法获得了草鱼(Ctenopharyngodon idellus)和鲢鱼(Hypophthalmichthys molitrix) leptin基因的全长cDNA序列分别为1 096 bp和1 176 bp,编码173和172个氨基酸。氨基酸序列同源性分析表明,草鱼和鲢鱼的leptin序列与其它鲤科鱼类leptin的同源性较高,而与其他鱼类的leptin同源性很低,但所有鱼类的leptin均含有用于形成二硫键的高度保守的半胱氨酸。系统进化树分析显示,草鱼和鲢鱼leptin与其他鱼类leptin聚于一进化分支。应用PCR和Genome Walker方法,进一步获得了草鱼和鲢鱼leptin基因的内含子和5′侧翼区序列。结果表明,获得的草鱼和鲢鱼leptin基因长度分别为2 129 bp和2 192 bp,含有与其他脊椎动物leptin相似的基因结构（含三个外显子和两个内含子）。本研究为深入研究鱼类肥胖基因结构功能关系与鱼类抗肥胖品系定向遗传选育奠定了良好的基础。     

微生物遗传学与育种课程教学改革与探索

微生物遗传学与育种是“生物工程专业卓越人才实验班”和“生物工程国际留学生班”的必修课程。然而,传统授课模式在内容选择、教学方法及手段和考核形式等方面均存在诸多不足。为了提高教学质量和效果,促进天津科技大学微生物学教学领域的进步和发展,更加高效地培养国家需要、满足国际需求的创新领军人才,文中对微生物遗传学与育种的教学内容、教学方法及手段、课程考核方式进行了改革与探索。借助最新科研进展、课前预习体系、视频展示、考核方式多样化等形式对授课模式进行创新性改革。不仅使学生掌握了微生物遗传学与育种的相关专业知识,更加锻炼了学生的主观能动性、团队合作意识和专业外语表达水平,培养了学生对微生物遗传学相关科学知识的兴趣。     

综合利用与加工 怎样采集与加工薇菜

薇菜,学名叫做紫其(Osmunda japonica),以往误称“薇”,视为巢蕨的一种。蕨类植物,紫其科。多年生草本,由于幼株披有黄色细纤绒毛,所以长白山区俗称“牛毛广”、“牛毛蕨”。我国东北、陕甘等地山区,以及日本、朝鲜等均有分布。生于溪边、林下沼泽,喜湿。嫩叶可供食用,富含多种人体必需氨基酸、维生素、纤维素、鞣酸和铁、钙等矿物元     

糖生物学与糖工程的兴起与前景

糖生物学与糖工程的兴起与前景金城,张树政（中国科学院微生物研究所,北京１０００８０）一、糖生物学与糖工程的兴起近年来糖的研究在国际引起了日益广泛的重视,对糖及糖缀合物的研究已逐渐成为生物学研究领域中的新的热点,一些发达国家尤其重视这一研究。英国牛津大...     

高职生物化学与分子生物学课程教学改革与实践

针对高职生物化学与分子生物学课程理论内容多、错综复杂、抽象难懂,实践性强、涉及技术面广,学生学习起来感到难以理清头绪,学到的知识不容易形成体系,师生普遍反映该课程教学难度大,学习效果差的实际情况。为此在生物化学与分子生物学教学中,以生物化学与分子生物学岗位工作任务为引领,以强化技能训练为主导,将生物化学与分子生物学抽象的理论知识融合于岗位工作任务之中,构建了项目化课程体系,教学方法改革创新、多措并举,考核方式多元化。结果表明:通过课程改革与实践,提高学生对课程学习的学习兴趣和参与度,培养了学生的动手操作能力、创新思维能力创和团队合作能力,取得了显著教学效果,促进教学相长。     

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.