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991.
玉米幼苗萎蔫过程中某些理化性质变化的研究   总被引:7,自引:2,他引:7  
玉米幼苗在暂时性萎蔫期间失水速率相对较慢,可溶性糖,脯氨酸等渗透调度物质的积累较多,SOD活性增加,而在永久性萎缩期间失水速率较快,渗透调节物质减少,SOD活性下降,在玉米幼苗萎蔫的全过程中,叶绿素,蛋白质含量及CAT,POD活性等迅速下降,质膜透性增大,膜脂过氧化加剧。  相似文献   
992.
Modulators of cadherin function are of great interest given that the cadherin complex actively contributes to the morphogenesis of virtually all tissues. The catenin p120(ctn) (formerly p120cas) was first identified as a src- and receptor-protein tyrosine kinase substrate and later shown to interact directly with cadherins. In common with beta-catenin and plakoglobin (gamma-catenin), p120(ctn) contains a central Armadillo repeat region by which it binds cadherin cytoplasmic domains. However, little is known about the function of p120(ctn) within the cadherin complex. We examined the role of p120(ctn)1A in early vertebrate development via its exogenous expression in Xenopus. Ventral overexpression of p120(ctn)1A, in contrast to beta-catenin, did not induce the formation of duplicate axial structures resulting from the activation of the Wnt signaling pathway, nor did p120(ctn) affect mesoderm induction. Rather, dorsal misexpression of p120(ctn) specifically perturbed gastrulation. Lineage tracing of cells expressing exogenous p120(ctn) indicated that cell movements were disrupted, while in vitro studies suggested that this may have been a consequence of reduced adhesion between blastomeres. Thus, while cadherin-binding proteins beta-catenin, plakoglobin, and p120(ctn) are members of the Armadillo protein family, it is clear that these proteins have distinct biological functions in early vertebrate development. This work indicates that p120(ctn) has a role in cadherin function and that heightened expression of p120(ctn) interferes with appropriate cell-cell interactions necessary for morphogenesis.  相似文献   
993.
小麦—中间偃麦草抗条锈衍生系的分子细胞遗传学研究   总被引:10,自引:1,他引:10  
应用缺体回交法,以部分阿勃缺体为母本,中4为父本,培育出1个对目前条锈病优势小种和新小种高抗至免疫的小麦--中间偃麦草衍生系N9025-3-3-2-1-1。研究表明,该选系在形态学和细胞学上已经基本稳定,染色体构型为2n=42=21“,抗病性来自中间偃麦草(Thinopyron intermedium)。以中间偃麦草DNA为探针,对N9025-3-3-2-1-1进行基因组原位杂交分析结果证明,它为小麦-中间偃麦草异代换-易位系。  相似文献   
994.
995.
通过田间试验对两种磷处理的274个大豆基因型叶片酸性磷酸酶活性进行筛选,并将其中8个进行营养液栽培试验以研究磷胁迫对其叶片酸性磷酸酶同工酶表达的影响.结果表明,大豆叶片酸性磷酸酶活性存在着明显的基因型差异,不施磷处理提高了大部分(约60%)供试基因型叶片酸性磷酸酶的活性.营养液栽培试验表明,低磷处理普遍提高了所有8个供试大豆基因型叶片酸性磷酸酶的活性.等电聚焦电泳结果表明,供试大豆基因型的老叶和新叶中均有6条酸性磷酸酶的同工酶带.低磷处理显著增加了叶片酸性磷酸酶酶带的活性,但是没有诱导新的酸性磷酸酶酶带产生.研究发现叶片酸性磷酸酶活性可作为反映大豆磷胁迫的酶学指标;磷胁迫诱导大豆叶片酸性磷酸酶活性的增加是由于已有同工酶活性的提高而不是由于特异性酶带的产生.  相似文献   
996.
Dai J  Li Y  Ji C  Jin F  Zheng Z  Wang X  Sun X  Xu X  Gu S  Xie Y  Mao Y 《Cytogenetic and genome research》2003,103(1-2):74-78
This study reports the cloning and characterization of two novel human zinc finger protein cDNAs (ZNF460 and ZNF461) from a fetal brain cDNA library. The ZNF460 cDNA is 3,135 bp in length encoding a 562-amino-acid polypeptide and the ZNF461 cDNA is 2,548 bp encoding a 563-amino-acid protein. Both of the proteins contain a KRAB A+B box and eleven C2H2 type zinc finger motifs. ZNF461 shows high similarity with the rat GIOT-1 gene (GIOT1). The ZNF460 gene mapped to 19q13.4 with 3 exons, and ZNF461 mapped to 19q13.1 with 6 exons. Both of the two genes are ubiquitously expressed in normal human tissues and the abundance of the ZNF460 mRNA is relatively low.  相似文献   
997.
998.
Fibrinolysis is a process responsible for the dissolution of formed thrombi to re‐establish blood flow after thrombus formation. Plasminogen activator inhibitor‐1 (PAI‐1) inhibits urokinase‐type and tissue‐type plasminogen activator (uPA and tPA) and is the major negative regulator of fibrinolysis. Inhibition of PAI‐1 activity prevents thrombosis and accelerates fibrinolysis. However, a specific antagonist of PAI‐1 is currently unavailable for therapeutic use. We screened a panel of uPA variants with mutations at and near the active site to maximize their binding to PAI‐1 and identified a potent PAI‐1 antagonist, PAItrap. PAItrap is the serine protease domain of urokinase containing active‐site mutation (S195A) and four additional mutations (G37bR–R217L–C122A–N145Q). PAItrap inhibits human recombinant PAI‐1 with high potency (Kd = 0.15 nM) and high specificity. In vitro using human plasma, PAItrap showed significant thrombolytic activity by inhibiting endogenous PAI‐1. In addition, PAItrap inhibits both human and murine PAI‐1, allowing the evaluation in murine models. In vivo, using a laser‐induced thrombosis mouse model in which thrombus formation and fibrinolysis are monitored by intravital microscopy, PAItrap reduced fibrin generation and inhibited platelet accumulation following vascular injury. Therefore, this work demonstrates the feasibility to generate PAI‐1 inhibitors using inactivated urokinase.  相似文献   
999.

Objective

Sarcopenia might be associated with bone fragility in elderly individuals. This study aimed to investigate the prevalence of sarcopenia and its association with fragility fracture sites in elderly Chinese patients.

Methods

Patients (322 men and 435 women) aged 65–94 years and with a history of fragility fractures in the ankle, wrist, vertebrae or hip, and healthy men (n = 1263) and women (n = 1057) aged 65–92 years without a history of fractures were enrolled. Whole-body dual energy X-ray absorptiometry was used to analyze skeletal muscle mass index (SMI), fat mass and bone mineral density. Sarcopenia was defined as SMI less than two standard deviations below the mean of a young reference group.

Results

Sarcopenia occurrence varied with fracture location. Sarcopenia was more common in females with vertebral and hip fractures and in men with hip and ankle fractures than in the non-fracture group). Sarcopenia was significantly more prevalent in men with wrist, hip and ankle fractures than in women. SMI was correlated with BMD in different fracture groups. Logistic regression analyses revealed that lower SMI was associated with an increased risk of hip fracture both in men and women and ankle fracture in men.

Discussion

Sarcopenia may be an independent risk factor for hip and ankle fractures in men, and for hip fractures in women.  相似文献   
1000.
The delivery of Ca2+ into cells by CaV channels provides the trigger for many cellular actions, such as cardiac muscle contraction and neurotransmitter release. Thus, a full understanding of Ca2+ permeation through these channels is critical. Using whole-cell voltage-clamp recordings, we recently demonstrated that voltage modulates the apparent affinity of N-type (CaV2.2) channels for permeating Ca2+ and Ba2+ ions. While we took many steps to ensure the high fidelity of our recordings, problems can occur when CaV currents become large and fast, or when currents run down. Thus, we use here single channel recordings to further test the hypothesis that permeating ions interact with N-type channels in a voltage-dependent manner. We also examined L-type (CaV1.2) channels to determine if these channels also exhibit voltage-dependent permeation. Like our whole-cell data, we find that voltage modulates N-channel affinity for Ba2+ at voltages > 0 mV, but has little or no effect at voltages < 0 mV. Furthermore, we demonstrate that permeation through L-channel is also modulated by voltage. Thus, voltage-dependence may be a common feature of divalent cation permeation through CaV1 and CaV2 channels (i.e. high-voltage activated CaV channels). The voltage dependence of CaV1 channel permeation is likely a mechanism mediating sustained Ca2+ influx during the plateau phase of the cardiac action potential.  相似文献   
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