开口箭对小鼠5-羟色胺分泌的影响

目的:采用灌胃、石蜡切片、免疫组化染色和ELISA等方法,探讨开口箭对小鼠5-羟色胺(5-HT)分泌的影响.方法选取20²2g健康昆明小鼠20只,均分成A,B,C,D 4组,分别以蒸馏水和0.25、0.50、1.00mg/mL的开口箭灌胃,0.20mL/次/d,连续灌胃7d.第8d对全部小鼠摘眼球取血,ELISA检测血清5-HT质量浓度;取血后立即处死小鼠,取十二指肠,4%甲醛固定,石蜡切片,免疫组化染色,镜下统计5-HT阳性细胞数量.结果与A组相比,B,C,D组小鼠血液5-HT质量浓度逐渐降低,十二指肠肠壁组织中5-HT阳性细胞数也明显减少.结论开口箭会下调小鼠5-HT的分泌.     

Genetic enhancement of learning and memory in mice.

Hebb's rule (1949) states that learning and memory are based on modifications of synaptic strength among neurons that are simultaneously active. This implies that enhanced synaptic coincidence detection would lead to better learning and memory. If the NMDA (N-methyl-D-aspartate) receptor, a synaptic coincidence detector, acts as a graded switch for memory formation, enhanced signal detection by NMDA receptors should enhance learning and memory. Here we show that overexpression of NMDA receptor 2B (NR2B) in the forebrains of transgenic mice leads to enhanced activation of NMDA receptors, facilitating synaptic potentiation in response to stimulation at 10-100 Hz. These mice exhibit superior ability in learning and memory in various behavioural tasks, showing that NR2B is critical in gating the age-dependent threshold for plasticity and memory formation. NMDA-receptor-dependent modifications of synaptic efficacy, therefore, represent a unifying mechanism for associative learning and memory. Our results suggest that genetic enhancement of mental and cognitive attributes such as intelligence and memory in mammals is feasible.     

Genetic hypertension in rats is accompanied by a defect in renal prostaglandin catabolism.

Noradrenaline releases prostaglandins in the kidney, and in rats these augment rather than reduce vasoconstriction produced by the amine. Homogenates of kidneys of New Zealand rats inbred for hypertension exhibit lower prostaglandin inactivation by 15-hydroxydehydrogenase than controls. At the same time, augmentation of noradrenaline vasoconstriction by the released prostaglandin is exaggerated. This biochemical defect could be the inherited abnormality primarily responsible for the development of hypertension in these animals.     

Genetic analysis of autoimmune type 1 diabetes mellitus in mice.

Two genes, Idd-3 and Idd-4, that influence the onset of autoimmune type 1 diabetes in the nonobese diabetic mouse have been located on chromosomes 3 and 11, outside the chromosome 17 major histocompatibility complex. A genetic map of the mouse genome, analysed using the polymerase chain reaction, has been assembled specifically for the study. On the basis of comparative maps of the mouse and human genomes, the homologue of Idd-3 may reside on human chromosomes 1 or 4 and Idd-4 on chromosome 17.     

The structure of complement C3b provides insights into complement activation and regulation

The human complement system is an important component of innate immunity. Complement-derived products mediate functions contributing to pathogen killing and elimination. However, inappropriate activation of the system contributes to the pathogenesis of immunological and inflammatory diseases. Complement component 3 (C3) occupies a central position because of the manifold biological activities of its activation fragments, including the major fragment, C3b, which anchors the assembly of convertases effecting C3 and C5 activation. C3 is converted to C3b by proteolysis of its anaphylatoxin domain, by either of two C3 convertases. This activates a stable thioester bond, leading to the covalent attachment of C3b to cell-surface or protein-surface hydroxyl groups through transesterification. The cleavage and activation of C3 exposes binding sites for factors B, H and I, properdin, decay accelerating factor (DAF, CD55), membrane cofactor protein (MCP, CD46), complement receptor 1 (CR1, CD35) and viral molecules such as vaccinia virus complement-control protein. C3b associates with these molecules in different configurations and forms complexes mediating the activation, amplification and regulation of the complement response. Structures of C3 and C3c, a fragment derived from the proteolysis of C3b, have revealed a domain configuration, including six macroglobulin domains (MG1-MG6; nomenclature follows ref. 5) arranged in a ring, termed the beta-ring. However, because neither C3 nor C3c is active in complement activation and regulation, questions about function can be answered only through direct observations on C3b. Here we present a structure of C3b that reveals a marked loss of secondary structure in the CUB (for 'complement C1r/C1s, Uegf, Bmp1') domain, which together with the resulting translocation of the thioester domain provides a molecular basis for conformational changes accompanying the conversion of C3 to C3b. The total conformational changes make many proposed ligand-binding sites more accessible and create a cavity that shields target peptide bonds from access by factor I. A covalently bound N-acetyl-l-threonine residue demonstrates the geometry of C3b attachment to surface hydroxyl groups.     

DL-5型移动式整定大直流发生器的研制

采用分体移动、组装使用的结构而设计的DL-5型移动式整定大直流发生器,解决了低压大直流发生器主变压器中磁感应强度不均匀问题,并且验证了有脉动低压大直流对“直流快速开关”整定的误差公式。     

Genetic selection for reproductive photoresponsiveness in deer mice

Seasonal breeding is common in mammals, particularly in habitats outside the tropics. Climate and availability of food are the ultimate factors that usually dictate the optimal time of year for a mammal to breed; however, day length (photoperiod) often serves as the proximal cue to signal the onset or cessation of seasonal reproduction. Some individuals in some populations of deer mice are reproductively responsive to photoperiod, while other individuals in the same population are not. As shown here, selection can dramatically alter the frequency of photoresponsiveness in a laboratory population in only two generations. To our knowledge this is the first demonstration of selection for reproductive photoresponsiveness in any mammal. By implication, some wild populations of deer mice must use multiple, genetic-based reproductive strategies, and the degree to which each such strategy is exhibited must be subject to rapid change in response to both seasonally and momentarily changing climatic and dietary conditions.     

The scid mutation in mice causes a general defect in DNA repair

Mice homozygous for the scid mutation on chromosome 16 have a severe combined immune deficiency as a result of their inability to correctly rearrange their immunoglobulin and T-cell receptor genes. In scid mice, when precursors for B and T lymphocytes reach the stage of development requiring expression of these surface receptors, a defective recombinase system aberrantly cuts and rejoins the receptor gene segments greatly reducing the efficiency of producing functional receptors. As a result, most scid mice have no detectable B or T lymphocytes. We have demonstrated that the scid defect is not specific to lymphocyte development. Myeloid cells and fibroblasts from scid mice show a marked increase in sensitivity to ionizing radiation, indicating that the scid mutation leads to an inability to repair DNA damage induced by ionizing radiation as well as interfering with rearrangement of the immunoglobulin and T-cell receptor genes.     

遗传标记在甜瓜遗传育种中的应用

综述了遗传标记在研究甜瓜起源地、分类、遗传多样性、图谱构建及分子辅助育种等方面的应用。