具有可测系数的非线性抛物型方程的初混边值问题(英文)

ＩＮＩＴＩＡＬ┐ＭＩＸＥＤＢＯＵＮＤＡＲＹＶＡＬＵＥＰＲＯＢＬＥＭＦＯＲＮＯＮＬＩＮＥＡＲＰＡＲＡＢＯＬＩＣＥＱＵＡＴＩＯＮＳＷＩＴＨＭＥＡＳＵＲＡＢＬＥＣＯＥＦＦＩＣＩＥＮＴＳ＊ＸｕＫｅｍｉｎｇＦｅｎｇＬｉｂｏＤｅｐａｒｔｍｅｎｔｏｆＦｕｎｄａｍｅ...     

MAGNETIC RELAXATION AT EARLY TIMES AND FLUX DIFFUSION BARRIER V（J，B，T） FOR Ti－1223 DOPED WITH Pb AND Ba BY COMPLEX AC SUSCEPTIBILITY MEASUREMENTS

ＭＡＧＮＥＴＩＣＲＥＬＡＸＡＴＩＯＮＡＴＥＡＲＬＹＴＩＭＥＳＡＮＤＦＬＵＸＤＩＦＦＵＳＩＯＮＢＡＲＲＩＥＲＶ（Ｊ，Ｂ，Ｔ）ＦＯＲＴｉ－１２２３ＤＯＰＥＤＷＩＴＨＰｂＡＮＤＢａＢＹＣＯＭＰＬＥＸＡＣＳＵＳＣＥＰＴＩＢＩＬＩＴＹＭＥＡＳＵＲＥＭＥＮＴＳＤ...     

INSITUCOMBINEDTEMPERATUREPROGRAMMEDREDUCTION─MOSSBAUERSPECTROSCOPICTECHNIQUESTUDYOFTHEINTERMEDIATESF

ＩＮＳＩＴＵＣＯＭＢＩＮＥＤＴＥＭＰＥＲＡＴＵＲＥＰＲＯＧＲＡＭＭＥＤＲＥＤＵＣＴＩＯＮ┐ＭＯＳＳＢＡＵＥＲＳＰＥＣＴＲＯＳＣＯＰＩＣＴＥＣＨＮＩＱＵＥＳＴＵＤＹＯＦＴＨＥＩＮＴＥＲＭＥＤＩＡＴＥＳＦＯＲＭＥＤＤＵＲＩＮＧＴＨＥＲＥＤＵＣＴＩＯＮＯＦ...     

BIOGENESIS OF THYLAKOID MEMBRANES WITH RECONSTRUCTION OF CHLOROPHYLL-PROTEIN COMPLEXES IN DELETION-MUTANT OF ORF469 IN BLUE-GREEN ALGA

ＢＩＯＧＥＮＥＳＩＳＯＦＴＨＹＬＡＫＯＩＤＭＥＭＢＲＡＮＥＳＷＩＴＨＲＥＣＯＮＳＴＲＵＣＴＩＯＮＯＦＣＨＬＯＲＯＰＨＹＬＬ－ＰＲＯＴＥＩＮＣＯＭＰＬＥＸＥＳＩＮＤＥＬＥＴＩＯＮ－ＭＵＴＡＮＴＯＦＯＲＦ４６９ＩＮＢＬＵＥ－ＧＲＥＥＮＡＬＧＡＷｕＱｉｎ...     

ON THE EXPONENT SET OF PRIMITIVE LOCALLY SEMICOMPLETE DIGRAPHS

ＯＮＴＨＥＥＸＰＯＮＥＮＴＳＥＴＯＦＰＲＩＭＩＴＩＶＥＬＯＣＡＬＬＹＳＥＭＩＣＯＭＰＬＥＴＥＤＩＧＲＡＰＨＳ￥ＺｈａｎｇＫｅｍｉｎｇ１）；ＢｕＹｕｅｈｕａ２）（１）ＤｅｐａｒｔｍｅｎｔｏｆＭａｔｈｃｍａｔｉｅｓ，ＮａｎｊｉｎｇＵｎｉｖｅｒｓｉｔｙ，Ｎ...     

浅谈社会主义市场经济条件下的高校后勤队伍建设与管理

浅谈社会主义市场经济条件下的高校后勤队伍建设与管理ＡＮＥＬＥＭＥＮＴＡＲＹＤＩＳＣＵＳＳＩＯＮＯＮＴＨＥＥＳＴＡＢＬＩＳＨＭＥＮＴ＆ＭＡＮＡＧＭＥＮＴＯＦＴＨＥＲＥＡＲＳＥＲＶＩＣＥＳＯＦＵＮＩＶＥＲＳＩＴＩＥＳＵＮＤＥＲＴＨＥＣＯＮＤＩＴＩＯＮＯＦ...     

REGULARIZING OPERATOR ALGORITHM FOR INVERSION OF PARTICLE SIZEDISTRIBUTION FROM LIGHT SCATTERING SPECTRUM

ＲＥＧＵＬＡＲＩＺＩＮＧＯＰＥＲＡＴＯＲＡＬＧＯＲＩＴＨＭＦＯＲＩＮＶＥＲＳＩＯＮＯＦＰＡＲＴＩＣＬＥＳＩＺＥＤＩＳＴＲＩＢＵＴＩＯＮＦＲＯＭＬＩＧＨＴＳＣＡＴＴＥＲＩＮＧＳＰＥＣＴＲＵＭ￥ＨｅＪｉｎｇ；ＷａｎｇＳｈｉｍｉｎ；ＣｈｅｎｇＪｉａｎｃｈｕ...     

THE OPTICAL OBSERVATION OF THE COLLISTIONS OF COMET SHOEMAKER－LEVY 9 WITH JUPITER

ＴＨＥＯＰＴＩＣＡＬＯＢＳＥＲＶＡＴＩＯＮＯＦＴＨＥＣＯＬＬＩＳＴＩＯＮＳＯＦＣＯＭＥＴＳＨＯＥＭＡＫＥＲ－ＬＥＶＹ９ＷＩＴＨＪＵＰＩＴＥＲ￥ＺｈｏｕＨｏｎｇｎａｎ（ＤｅｐａｒｔｍｅｎｔｏｆＡｓｔｒｏｎｏｍｙ，ＮａｎｊｉｎｇＵｎｉｖｅｒｓｉｔｙ，２１...     

ACOUSTIC NONLINEARITY PARAMETER TOMOGRAPHY WITH FINITE AMPLITUDE SOUND WAVE

ＡＣＯＵＳＴＩＣＮＯＮＬＩＮＥＡＲＩＴＹＰＡＲＡＭＥＴＥＲＴＯＭＯＧＲＡＰＨＹＷＩＴＨＦＩＮＩＴＥＡＭＰＬＩＴＵＤＥＳＯＵＮＤＷＡＶＥＺｈａｎｇＤｏｎｇ；ＧｏｎｇＸｉｕｆｅｎ；ＹｅＳｈｉｇｏｎｇ（ＩｎｓｔｉｔｕｔｅｏｆＡｃｏｕｓｔｉｃｓ，ＫｅｙＬａｂ...     

浅谈高校人事档案收集渠道和方式

浅谈高校人事档案收集渠道和方式ＡＢＲＩＥＦＤＩＳＣＵＳＳＩＯＩＮＯＮＭＥＤＩＵＭＳＡＮＤＳＴＹＬＥＳＯＦＴＨＥＰＥＲＯＳＮＮＥＬＡＲＣＨＩＶＥＳＣＯＬＬＥＣＴＩＯＮＯＦＣＯＬＬＥＧＥＳ／ＵＮＩＶＥＲＳＩＴＩＥＳ翁巧英ＷｅｎＱｉａｏｙｉｎｇ（浙江水产学...     

尿激酶原激活是其催化纤溶酶原激活的限速步骤

尿激酶原催化纤溶酶原的激活包括3个反应：（1）尿激酶原内在酶活性催化纤溶酶原转化为纤溶酶；（2）纤溶酶激活尿激酶原变成尿激酶；（3）尿激酶激活纤溶酶原，所以一直以来人们对尿激酶原激活纤溶酶原的过程知之甚少．研究发现EACA可以抑制尿激酶原催化的纤溶酶原激活。通过EACA对上述3个反应的影响进行逐个分析，观察到在EACA浓度为2．0mmol／L时，尿激酶原内在酶活性催化纤溶酶原激活的反应速度提高了4．5倍，尿激酶激活纤溶酶原的反应速度提高了6倍．相反地，纤溶酶激活尿激酶原变成尿激酶的反直被抑制了50％，此反应决定了EACA对尿激酶原催化纤溶酶原激活反应的抑制作用．该结果提示尿激酶原催化纤溶酶原激活反应的限速步骤是纤溶酶激活尿激酶原变成尿激酶，缘于纤溶酶和尿激酶原的赖氨酸结合位点的相互作用．     

Kunitz抑制剂家族成员抑肽酶对纤溶酶原活化的抑制作用

抑肽酶属Kunitz抑制剂家族成员，能够抑制激肽释放酶、纤溶酶及胰蛋白酶的蛋白水解活性．研究表明，抑肽酶能够抑制尿激酶型-纤溶酶原激活刹（u—PA）和组织型纤溶酶原激活剂（t—PA）对纤溶酶原的激活，但不影响u—PA和t—PA对小分子底物的酰胺水解活性．用u—PA研究了上述作用的机制，发现抑肽酶与u—PA的丝氨酸蛋白酶功能区特异性结合，而与纤溶酶原没有相互作用．抑肽酶与uPA的结合并不阻断u—PA的活性位点，因为u—PA对小分子底物的水解活性仍然保持．上述发现提示抑肽酶可能存在另一种抑制作用模式，该模式不同于以前报道的关于Kunitz抑制剂或纤溶酶原激活酶抑制剂的作用．由于人体内的Kunitz抑制剂与抑肽酶在结构上非常相似，根据研究结果，推测体内纤溶酶原的激活作用并非仅受丝氨酸蛋白酶抑制剂的控制。     

大批量制备人血浆纤维蛋白溶酶原

血浆经大豆胰蛋白酶抑制物、苯甲基磺酰氟和苯甲脒预处理,保持低温操作,以及赖氨酸—Sepharose 4B 亲和载体合成手续的改进,可以从近千毫升血浆中以140mg/L 血浆的产率制得低纤维蛋白溶解酶活性的纤维蛋白溶酶原制剂。     

溶栓剂蛋白质工程的新进展

介绍了国内外溶栓剂蛋白质工程方面的新进展,主要涉及了组织型纤溶酶原激活剂(t-PA)、尿激酶型纤溶酶原激活剂(u-PA)、链激酶(SK)、葡萄球菌激酶(SAK)、DSPA及TSV-PA的研究进展。一些PA突变体及新型溶栓剂,如K2P、TNK-PA和STAR等的临床实验结果表明它们在延长体内半寿期、增强对血纤维蛋白选择性和溶栓效率等方面有较大的改进。但溶栓治疗造成的颅内出血等局部性出血问题仍是目前的难题之一,说明新型溶栓剂的研制有很大潜力。     

酰化纤溶酶原-链激酶 (APSAC)的制备和生物学性质

建立在Lys-Sepharose4B柱上用人纤溶酶原(HPg),链激酶(SK)和对氨基苯甲酸对脒基苯酚酯合成新型溶栓药物酰化纤溶酶原-链激酶(APSAC)的一种新方法,该法使APSAC的纯度和收率大为提高,分子量为130000,体外有明显溶栓效果,在兔体内半衰期8.8h.用同方法制备的未经修饰的纤溶酶原-链激酶复合物(PSAC)在兔血浆内半衰期仅为12min.     

Serpin-resistant mutants of human tissue-type plasminogen activator

Tissue-type plasminogen activator (t-PA) converts the inactive zymogen, plasminogen, into the powerful protease, plasmin, which then degrades the fibrin meshwork of thrombi. To prevent systemic activation of plasminogen, plasma contains several inhibitors of t-PA, the most important of which is plasminogen activator inhibitor-1 (PAI-1), a member of the serpin superfamily. As the ability to produce serpin-resistant variants of t-PA could increase the potential of this enzyme as a thrombolytic agent, we have used the known three-dimensional structure of the complex between trypsin and bovine pancreatic trypsin inhibitor (BPTI) to model the interactions between the active site of human t-PA and PAI-1. On the basis of this model we then altered by site-directed mutagenesis those amino acids of t-PA predicted to make contact with PAI-1 but not with the substrate plasminogen. We report here that although the resulting mutants have enzymatic properties similar to those of wild-type t-PA, they display significant resistance to inhibition by PAI-1. For example, following incubation with an amount of the serpin that completely inhibits the wild-type enzyme, one variant retains 95% of its initial activity. This mutant is also resistant to inhibition by the complex mixture of serpins present in human plasma.     

Lipoprotein(a) modulation of endothelial cell surface fibrinolysis and its potential role in atherosclerosis

Endothelial cells play a critical role in thromboregulation by virtue of a surface-connected fibrinolytic system. Cultured endothelial cells synthesize and secrete tissue-type plasminogen activator (t-PA) which can bind to at least two discrete sites on the cell surface. These binding sites preserve the catalytic activity of t-PA and protect it from its physiological inhibitor (PAI-1). N-terminal glutamic acid plasminogen (Glu-PLG), the main circulating fibrinolytic zymogen, also interacts specifically with the endothelial cell surface. Binding is associated with a 12-fold increase in catalytic efficiency of plasmin generation by t-PA which may reflect conversion of Glu-PLG to its plasmin-modified form, N-terminal lysine plasminogen (Lys-PLG). Lipoprotein(a) is an atherogenic lipoprotein particle which contains the plasminogen-like apolipoprotein(a) bound to low density lipoprotein. We report here that lipoprotein(a) interferes with endothelial cell fibrinolysis by inhibiting plasminogen binding and hence plasmin generation. In addition, we demonstrate lipoprotein(a) accumulation in atherosclerotic lesions. These findings may provide a link between impaired cell surface fibrinolysis and progressive atherosclerosis.     

Role of plasminogen activator and plasminogen activator inhibitor type-1 in luteolysis——a minireview

This minireview summarized our recent studies on the role of plasminogen activator (PA) and inhibitor type-1 (PAI-1) in luteolysis. We have demonstrated that (1) both tissue type and urokinase type plasminogen activators (tPA and uPA) and a plasminogen activator inhibitor type-1 (PAI-1) were present in the corpus luteum of rat and rhesus monkey; (2) decrease in progesterone production in corpus luteum was well correlated with a sharp increase in tPA (but not uPA) and PAI-1 secretion; (3) exogenous tPA decreased luteal progesterone synthesis while monoclonal antibodies increased progesterone production; (4) interferon y inhibited luteal progesterone synthesis and stimulated tPA production while LH plus pro-lactin increased progesterone production and decreased tPA (but not uPA) activity in cultured luteal cells; (5) increase in proteolysis in the corpus luteum was also correlated with decrease in progesterone production in mouse. These data suggest that local degradation of extracellular matrix controlled by plasminogen activator and inhibitor is involved in the processes of luteolysis.     

Role of plasminogen activator and plasminogen activator inhibitor type-1 in luteolysis—a minireview

This minireview summarized our recent studies on the role of plasminogen activator (PA) and inhibitor type-1 (PAI-1) in luteolysis. We have demonstrated that (1) both tissue type and urokinase type plasminogen activators (tPA and uPA) and a plasminogen activator inhibitor type-1 (PAI-1) were present in the corpus luteum of rat and rhesus monkey; (2) decrease in progesterone production in corpus luteum was well correlated with a sharp increase in tPA (but not uPA) and PAI-1 secretion; (3) exogenous tPA decreased luteal progesterone synthesis while monoclonal antibodies increased progesterone production; (4) interferony inhibited luteal progesterone synthesis and stimulated tPA production while LH plus prolactin increased progesterone production and decreased tPA (hut not uPA) activity in cultured luteal cells; (5) increase in proteolysis in the corpus luteum was also correlated with decrease in progesterone production in mouse. These data suggest that local degradation of extracellular matrix controlled by plasminogen activator and inhibitor is involved in the processes of luteolysis.     

A potential basis for the thrombotic risks associated with lipoprotein(a)

Lipoprotein(a) (Lp(a)) has been strongly linked with atherosclerosis and is an independent risk factor for myocardial infarction. Distinguishing Lp(a) from other low-density lipoprotein particles is its content of a unique apoprotein, apo(a). The recently described sequence of apo(a) indicates a remarkable homology with plasminogen, the zymogen of the primary thrombolytic enzyme, plasmin. Lp(a) may contain 37 or more disulphide-looped kringle structures, which are 75-85% identical to the fourth kringle of plasminogen. Plasminogen receptors are widely distributed on blood cells and are present at extremely high density on endothelial cells. These receptors promote thrombolysis by accelerating plasminogen activation and protecting plasmin from inhibition. If, by molecular mimicry, Lp(a) competes with plasminogen for receptors, then thrombolysis would be inhibited and thrombosis promoted. Here we provide support for such a mechanism being responsible for the thrombotic risks associated with elevated Lp(a) by demonstrating that Lp(a) inhibits plasminogen binding to cells.