生态环境用水研究现状、问题分析与基本构架探索

生态学与水文学交叉研究是目前国际上前沿研究领域之一,生态环境用水研究则是连接生态过程与水文过程、刻画生态演化与水资源相互关系的核心问题。对生态、环境用水产生与发展的基本过程进行了回顾,并根据对已有成果的综合分析提出了目前研究中存在的5方面主要问题。首先,生态用水尚需理论上的进一步升华,这一点突出体现在生态用水的概念与内涵表述上;其次,在生态用水研究中,缺乏合理的生态保护目标的建立,因而影响到了研究成果的实际应用价值;第三,目前的研究均是针对较大尺度所作的,不能在生态机理与物理机制上揭示生态用水规律,因此,不适于具体问题的深入分析,个别实验在由“点“尺度向生态用水计算的“面“尺度转换时缺乏基础,从而严重影响了研究成果的精度;第四,生态用水机理是生态用水研究中至为关键的工作,以往研究主要依据野外宏观观测资料来探讨,缺乏直接的实验依据;第五,没有涉及生态用水对生态系统稳定性、生态用水满足程度及其波动性对生态系统影响等方面,从而也使得研究成果的科学性受到影响。同时作者认为,中国工程院“中国可持续发展水资源研究报告“中的生态环境用水概念对我国地大物博,地质地貌与气候类型多样的特点给给予了更多的关注,故可以确定为全国性的生态环境用水概念。最后文章认为应当将生态用水与环境用水分别予以考虑,并给出了其新的概念构架。     

石河子莫索湾垦区绿洲景观格局变化分析

以新疆石河子１５０团场为例,从景观多样性、优势度、均匀度、分离度、分维数、嵌块体伸长指数、聚集度、嵌块体数目破碎化指数、嵌块体形状碎化指数等９个方面,对其景观格局进行了分析,结果表明：随着干扰时间的延长,整个景观的多样性和均匀度下降,而优势度聚集度指数值增加,这说明,该团场绿洲愈来愈由少数嵌块体类型所控制,嵌块体伸长度指数的增加与分维数的下降则说明,该团场绿洲嵌块体形状有愈加规则、愈趋简单势。而嵌块体形状破碎化指标数、数目破碎化指数、分离度指数的变化情况显示,１５０团场绿洲景观的破碎化程度在逐渐增加,其中以自然和半自然嵌块体的影响最大,对于人工景观而言,这意味着人类活动对１５０团绿洲施加的直接影响在逐渐减弱、而间接影响在增强。     

鄂尔多斯高原北缘水分梯度下天然植被分布格局初探

以鄂尔多斯高原杭锦旗北部独贵塔拉镇的过渡带为研究对象,通过样线调查,研究了水分梯度下天然植被的空间分布规律.TWINSPAN的分类结果表明,群落以中生和旱生为主,一些耐盐的植物散布其中;相邻样方间相似性指数的变化反映了不同类型群落在研究区内的镶嵌分布,从而形成了该区域内群落的多样性和复杂性.对植被样方与地形地貌因子的CCA排序结果显示,植被群落空间格局的形成更多地取决于区域内的水分变化梯度.在本文的研究尺度上,这种水分变化梯度主要由微地形地貌的变化来决定,而不是由与黄河的距离因子来决定.因此,在本区域的土地开发利用过程中,应充分考虑目前已经形成的相对稳定的地形地貌单元特点,在缺乏完善的风沙防护措施和排水除盐措施的情况下,不宜采取大规模平整土地进行综合开发.     

New insights into the physiology of natural foraging

The purpose of this symposium was to examine how foraging physiology is studied in the field across a diversity of species and habitats. While field studies are constrained by the relatively poor ability to control the experiment, the natural variability in both the environment and animal behavior provides insights into adaptation to change that are usually not tested in the laboratory. Talks in this session examined how foraging energy (both costs and gains) is partitioned over time. "Time," in this case, ranged from evolutionary time (how different animals are designed to most efficiently forage), to long, lifetime periods (development of foraging ability and growth), to short-duration feeding bouts, and ultimately to the minutes to hours following ingestion (metabolic and biochemical changes). From this diversity, two core themes emerged: that foraging strategies and behaviors are limited by physiology and biochemical processes and that time plays a central role in the organization of foraging behaviors and the physiological processes that underlie those behaviors.     

The cyclic GMP-dependent protein kinase EGL-4 regulates olfactory adaptation in C. elegans

Prolonged odor exposure causes a specific, reversible adaptation of olfactory responses. A genetic screen for negative regulators of olfaction uncovered mutations in the cGMP-dependent protein kinase EGL-4 that disrupt olfactory adaptation in C. elegans. G protein-coupled olfactory receptors within the AWC olfactory neuron signal through cGMP and a cGMP-gated channel. The cGMP-dependent kinase functions in AWC neurons during odor exposure to direct adaptation to AWC-sensed odors, suggesting that adaptation is a cell intrinsic process initiated by cGMP. A predicted phosphorylation site on the beta subunit of the cGMP-gated channel is required for adaptation after short odor exposure, suggesting that phosphorylation of signaling molecules generates adaptation at early time points. A predicted nuclear localization signal within EGL-4 is required for adaptation after longer odor exposure, suggesting that nuclear translocation of EGL-4 triggers late forms of adaptation.     

病毒融合蛋白的结构和功能

病毒融合蛋白可以分为三种类型,不同类型的病毒融合蛋白的结构差异很大,但是会采用相似的"发卡"构象实现融合.在一定条件下,病毒融合蛋白的疏水结构域,融合环或融合肽插入靶膜中,通过其自身折叠形成发卡使病毒和宿主的膜靠近.与此同时,融合蛋白构象变化会释放出足够的能量将双方膜打破并完成融合.本文中,我们总结了三种类型病毒融合蛋白的特征,并对其中央发卡三聚体结构域、跨膜结构域以及近膜结构域在融合过程中的作用进行了论述.     

Genes required for axon pathfinding and extension in the C. elegans nerve ring.

Over half of the neurons in Caenorhabditis elegans send axons to the nerve ring, a large neuropil in the head of the animal. Genetic screens in animals that express the green fluorescent protein in a subset of sensory neurons identified eight new sax genes that affect the morphology of nerve ring axons. sax-3/robo mutations disrupt axon guidance in the nerve ring, while sax-5, sax-9 and unc-44 disrupt both axon guidance and axon extension. Axon extension and guidance proceed normally in sax-1, sax-2, sax-6, sax-7 and sax-8 mutants, but these animals exhibit later defects in the maintenance of nerve ring structure. The functions of existing guidance genes in nerve ring development were also examined, revealing that SAX-3/Robo acts in parallel to the VAB-1/Eph receptor and the UNC-6/netrin, UNC-40/DCC guidance systems for ventral guidance of axons in the amphid commissure, a major route of axon entry into the nerve ring. In addition, SAX-3/Robo and the VAB-1/Eph receptor both function to prevent aberrant axon crossing at the ventral midline. Together, these genes define pathways required for axon growth, guidance and maintenance during nervous system development.     

Serine phosphorylation of the v-rel oncogene product/pp40 complex

The transforming protein encoded by the v-rel oncogene of reticuloendotheliosis virus has been purified from REV-T transformed lymphoid cells by sequential DEAE-Sepharose and immunoaffinity chromatography. The purified preparation consisted of pp59v-rel and the 40 kDa cellular protein which is complexed with the v-rel oncogene product in transformed cells as well as some minor proteins. Incubation of this purified preparation in the presence of Mg2+ and (gamma-32P)ATP resulted in phosphorylation of both pp59v-rel and the 40 kDa protein. This preparation was also able to phosphorylate casein on serine residues. Immunoprecipitates obtained from extracts of REV-T transformed lymphoid cells labeled with 32P-orthophosphate contained 59 and 40 kDa phosphoproteins. Both pp59v-rel and the 40 kDa protein were phosphorylated on serine residues in transformed cells.     

Multiple independent activations of the neu oncogene by a point mutation altering the transmembrane domain of p185

The neu oncogene, which is frequently activated in neuro- and glioblastomas of BDIX rats, was originally identified in the NIH 3T3 focus-forming assay. cDNA clones of the normal and transforming alleles of neu have been isolated. When these clones are inserted into the expression vector pSV2, they direct the synthesis of p185, the neu gene product. The transforming cDNA clone yields foci when transfected onto a NIH 3T3 monolayer, but the normal cDNA does not. The construction of in vitro recombinants between the normal and transforming cDNAs has allowed the determination of the mutation responsible for the activation of the neu proto-oncogene. A single point mutation changes a valine in the transmembrane domain of the predicted protein product insert to a glutamic acid. The DNAs from four independent cell lines containing activated neu oncogenes contain the identical mutation at this position.