湖泊水库结构生态动态模型

综述了湖泊水库结构生态动态模型的研究进展及其在湖泊水库环境生态模拟中的应用。结果表明,热力学理论为获取湖泊水库生态系统的特性提供了一条整体性的途径,热力学概念“Ｙｏｎｇ”可将生态学理论（达尔文理论）和热力学理论（最大Ｙｏｎｇ原理）很好地联系起来。引入Ｙｏｎｇ后,许多重要模型参数的目标函数可根据最大Ｙｏｎｇ原理获得,达尔文“达者生存”理论可被定量为一个生态约束条件用于发展湖泊水库结构生态结构模型,从     

广西猕猴桃发展的策略分析

分析了广西猕猴桃发展的有利条件和现状, 并提出了相应的发展策略, 可供各级领导和有关生产单位参考, 对促进广西猕猴桃进一步发展具有指导意义。     

广东内伶仃岛猕猴食性及食源植物分析

论文对内伶仃岛猕猴(Macaca mulatta)的植物食性进行了全面调查,并测定了食源植物适食部分的比重。研究结果表明:(1)猕猴食源植物约200种,以叶食性、果食性最为丰富;(2)猕猴的活动区域以阔叶林、灌木林等植被类型为主;(3)食源植物以热带亚热带成分为主,与栖息地植被组成特征相适应;(4)内伶仃岛猕猴种群发展的容纳量最适为820～1640只(平均1230只),而以743～1485只(平均1114只)最为合适,其总食量约相当于适食性优质植物资源总蕴藏量的10%～20%。     

限气贮藏猕猴桃果实伤害产生机制的研究

采用ＰＥ袋方法于常温一藏秦猕猴桃,贮藏期间袋内ＣＯ２浓度高于６％时果实会产生伤害贮藏前期,果实的果肉和果心硬度均很高,这与两部位淀粉酶和多聚半乳糖醛酸酶活性严重被抑制淀粉和果胶物质水解被抑制有关。贮藏中期,果肉出现水浸状,到贮藏末期,果心和照相机人均很快腐烂,这主要与Ｖｃ含量明显降低,导致膜脂过氧化加剧有关。而与ＳＯＤ活性变化关系不大。而贮藏期间,果心硬度明显高于果肉,这与果心淀粉酶和多聚半乳醛酸     

Sauromatum gaoligongense(Araceae), a New Species from Gaoligong Mountains

本文描述了天南星科斑龙芋属一个新种,高黎贡山斑龙芋Sauromatum gaoligongense Z.L.Wang et H.Li,其显著特点是叶柄下部具3～5枚株芽。     

ANTIPYRETIC ACTION OF DEXAMETHASONE ON EGTAZIC ACIDINDUCED FEVER IN RABBITS

本文用脑室灌注和Ｆｕｒａ２测定细胞内游离钙技术观察了地塞米松（ｄｅｘａｍｅｔｈａｓｏｎｅ,ＤＥＸ）对家兔乙二醇双（２氨基乙醚）四乙酸性发热效应和下丘脑细胞内游离钙浓度（［Ｃａ２＋］ｉ）的影响,借此深入探讨地塞米松解热作用的中枢机制。结果发现：脑室灌注乙二醇双（２氨基乙醚）四乙酸（０６ｎｍｏｌ）引起家兔结肠温度明显升高,静脉注射地塞米松（５ｍｇ／ｋｇ）显著抑制家兔乙二醇双（２氨基乙醚）四乙酸性发热,地塞米松（６０～１２０μｍｏｌ／Ｌ）并不影响下丘脑细胞内［Ｃａ２＋］ｉ,而事先脑室灌注抑制基因转录的放线菌素Ｄ（３ｎｍｏｌ）则完全取消了地塞米松对乙二醇双（２氨基乙醚）四乙酸性发热的解热作用。这些结果提示：地塞米松显著抑制家兔乙二醇双（２氨基乙醚）四乙酸性发热,其机制与地塞米松激活脑内某些基因的表达有关,而与下丘脑神经细胞跨膜钙离子流无关。     

Tropomyosin is localized in the nuclear matrix and chromosome scaffold of physarum polycephalum

The nuclei and chromosomes were isolated from plasmodia of Physarum polycephalum.The nuclear matrix and chromosome scaffold were obtained after the DNA and most of the proteins were extracted with DNase I and 2 M NaCl.SD-PAGE analyses revealed that the nuclear matrix and chromosome scaffold contained a 37 kD polypeptide which is equivalent to tropomyosin in molecular weight.Immunofluorescence observations upon slide preparations labeled with anti-tropomyosin antibody showed that the nuclear matrix and chromosome scaffold emanated bright fluorescence,suggesting the presence of the antigen in them.Immunodotting results confirmed the presence of tropomyosin in the nuclear matrix and chromosome scaffold.Immunoelectron microscopic observations further demonstrated that tropomyosin was dispersively distributed in the interphase nuclei and metaphase chromosomes.     

Anti-TCR antibody treatment activates a novel population of nonintestinal CD8 alpha alpha+ TCR alpha beta+ regulatory T cells and prevents experimental autoimmune encephalomyelitis

CD8alphaalpha+CD4-TCRalphabeta+ T cells are a special lineage of T cells found predominantly within the intestine as intraepithelial lymphocytes and have been shown to be involved in the maintenance of immune homeostasis. Although these cells are independent of classical MHC class I (class Ia) molecules, their origin and function in peripheral lymphoid tissues are unknown. We have recently identified a novel subset of nonintestinal CD8alphaalpha+CD4-TCRalphabeta+ regulatory T cells (CD8alphaalpha Tregs) that recognize a TCR peptide from the conserved CDR2 region of the TCR Vbeta8.2-chain in the context of a class Ib molecule, Qa-1a, and control- activated Vbeta8.2+ T cells mediating experimental autoimmune encephalomyelitis. Using flow cytometry, spectratyping, and real-time PCR analysis of T cell clones and short-term lines, we have determined the TCR repertoire of the CD8alphaalpha regulatory T cells (Tregs) and found that they predominantly use the TCR Vbeta6 gene segment. In vivo injection of anti-TCR Vbeta6 mAb results in activation of the CD8alphaalpha Tregs, inhibition of the Th1-like pathogenic response to the immunizing Ag, and protection from experimental autoimmune encephalomyelitis. These data suggest that activation of the CD8alphaalpha Tregs present in peripheral lymphoid organs other than the gut can be exploited for the control of T cell-mediated autoimmune diseases.     

The myocardial response to adrenomedullin involves increased cAMP generation as well as augmented Akt phosphorylation

In this work we aimed to observe (1) the changes in adrenomedullin (AM) and its receptor system - calcitonin receptor-like receptor (CRLR) and receptor activity modifying proteins (RAMPs) - in myocardial ischemic injury and (2) the response of injuried myocardia to AM and the phosphorylation of Akt to illustrate the protective mechanism of AM in ischemic myocardia. Male SD rats were subcutaneously injected with isoproterenol (ISO) to induce myocardial ischemia. The mRNA levels of AM, CRLR, RAMP1, RAMP2 and RAMP3 were determined by RT-PCR. Protein levels of Akt, phosphor-Akt, CRLR, RAMP1, RAMP2 and RAMP3 were assayed by Western blot. Results showed that, compared with that of the controls, ISO-treated rats showed lower cardiac function and myocardial injury. The mRNA relative amount of AM, CRLR, RAMP1, RAMP2 and RAMP3 in the myocardia of ISO-treated rats was increased. The elevated mRNA levels of CRLR, RAMP1, RAMP2 and RAMP3 were positively correlated with AM content in injured myocardia. The protein levels of CRLR, RAMP1, RAMP2 and RAMP3 in injured myocardia were increased compared with that of control myocardia. AM-stimulated cAMP generation in myocardia was elevated in the ISO group, and was antagonized by AM(22-52) and CGRP(8-37). Western blot analyses revealed that AM significantly enhanced Akt phosphorylation in injured myocardia, which was blocked by pretreatment with AM(22-52) or CGRP(8-37). Ischemia-injured myocardia hyper-expressed AM and its receptors - CRLR, RAMP1, RAMP2 and RAMP3 - and the response of ischemic myocardia to AM was potentiated, and the level of Akt phosphorylation was also increased, which suggests that changes in cardiac AM/AM receptor might play an important role in the pathogenesis of myocardial ischemic injury.