Proceedings of the Association of American Physicians最新文献_第4页

Angiotensin II induces alpha3(IV) collagen expression in cultured murine proximal tubular cells. 血管紧张素II诱导小鼠近端小管细胞中α 3(IV)胶原蛋白的表达。

Proceedings of the Association of American Physicians Pub Date : 1999-07-01 DOI: 10.1046/j.1525-1381.1999.99117.x

G Wolf, R Kalluri, F N Ziyadeh, E G Neilson, R A Stahl

{"title":"Angiotensin II induces alpha3(IV) collagen expression in cultured murine proximal tubular cells.","authors":"G Wolf, R Kalluri, F N Ziyadeh, E G Neilson, R A Stahl","doi":"10.1046/j.1525-1381.1999.99117.x","DOIUrl":"https://doi.org/10.1046/j.1525-1381.1999.99117.x","url":null,"abstract":"Angiotensin II (ANG II) induces cellular hypertrophy of cultured proximal tubular cells from various species. This hypertrophic response is associated with an increase in synthesis of basement membrane-associated collagen type IV. Previous investigations by our group have shown that ANG II stimulates mRNA and protein expression of the \"classic\" alpha1 and alpha2(IV) chains in cultured murine proximal tubular cells (murine cortical tubules [MCT cells]). Since it is clearer today that kidney basement membranes also contain heterotrimers of novel type IV collagens, the aim of the present study was to evaluate whether ANG II may influence the expression of alpha3 and alpha5(IV) collagen chains in MCT cells. A single dose of 10-8-10-6 M ANG II stimulated mRNA expression of alpha3(IV), but not of alpha5(IV), in MCT cells cultured in serum-free media. This response was mediated through AT1-receptors because losartan, but not an AT2-receptor antagonist, abolished the ANG II-induced expression of alpha3(IV) transcripts. Transient transfection of MCT cells with transforming growth factor-beta1 (TGF-beta1) antisense phosphorothioate-modified oligonucleotides partly abolished the ANG II-induced alpha3(IV) mRNA expression. Furthermore, Western blots of cellular lysates incubated with polyclonal antibodies generated against the recombinant collagen chains revealed that ANG II stimulated alpha3(IV) but not alpha5(IV) protein expression. This stimulation was partly prevented by co-incubation with a neutralizing anti-TGF-beta1-3 antibody. In summary, our data indicate that ANG II stimulates expression of the alpha3(IV) collagen chain in cultured MCT cells, due in part to TGF-beta1 activation.","PeriodicalId":20612,"journal":{"name":"Proceedings of the Association of American Physicians","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1999-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21284762","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 35

Abner McGehee harvey 1911-1998 Abner McGehee harvey 1911-1998

Proceedings of the Association of American Physicians Pub Date : 1999-07-01 DOI: 10.1046/J.1525-1381.1999.99001.X

McKusick

引用次数: 2

The potential influence of insulin and plasminogen activator inhibitor type 1 on the formation of vulnerable atherosclerotic plaques associated with type 2 diabetes. 胰岛素和1型纤溶酶原激活物抑制剂对2型糖尿病相关易损动脉粥样硬化斑块形成的潜在影响

Proceedings of the Association of American Physicians Pub Date : 1999-07-01 DOI: 10.1046/j.1525-1381.1999.99231.x

B E Sobel

{"title":"The potential influence of insulin and plasminogen activator inhibitor type 1 on the formation of vulnerable atherosclerotic plaques associated with type 2 diabetes.","authors":"B E Sobel","doi":"10.1046/j.1525-1381.1999.99231.x","DOIUrl":"https://doi.org/10.1046/j.1525-1381.1999.99231.x","url":null,"abstract":"Insulin-resistant states, including type 2 diabetes mellitus, are associated with increased concentrations of plasminogen activator inhibitor type 1 (PAI-1) in blood and in extracted coronary atheroma, as well as with an increased incidence of acute coronary syndromes, known to be precipitated by the rupture of vulnerable atherosclerotic plaques. However, plaque rupture is potentiated by proteolysis. Accordingly, the parallel relationship between augmentation of concentrations of an inhibitor of proteolysis and plaque vulnerability appears to be paradoxical. The following resolution is proposed. Reduced cellularity of plaques may result when high concentrations of PAI-1 in early atheroma inhibit the migration of vascular smooth muscle cells into the neointima. Such migrating cells subsequently proliferate. If their total number is reduced, the composition of plaques may be altered throughout development with the reduction of vascular smooth muscle cell content and consequent additional changes. In aggregate, such changes may render mature, complex plaques vulnerable to rupture mediated by proteolysis responsible for the degradation of thin fibrous caps on relatively acellular, lipid-laden plaques.","PeriodicalId":20612,"journal":{"name":"Proceedings of the Association of American Physicians","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1999-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21284754","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 50

The Nramp1 protein and its role in resistance to infection and macrophage function. Nramp1蛋白及其在抗感染和巨噬细胞功能中的作用。

Proceedings of the Association of American Physicians Pub Date : 1999-07-01 DOI: 10.1046/j.1525-1381.1999.99236.x

F Canonne-Hergaux, S Gruenheid, G Govoni, P Gros

{"title":"The Nramp1 protein and its role in resistance to infection and macrophage function.","authors":"F Canonne-Hergaux, S Gruenheid, G Govoni, P Gros","doi":"10.1046/j.1525-1381.1999.99236.x","DOIUrl":"https://doi.org/10.1046/j.1525-1381.1999.99236.x","url":null,"abstract":"Susceptibility to infectious diseases is under genetic control in humans. Animal models provide an ideal tool to study the genetic component of susceptibility and to identify candidate genes that can then be tested for association or linkage studies in human populations from endemic areas of disease. The Nramp1 gene was isolated by positional cloning the host resistance locus Bcg/Ity/Lsh, and mutations at this locus impair the resistance of mice to infections with intracellular parasites, such as Salmonella, Leishmania, and Mycobacterium. Allelic variants at the human Nramp1 homologue have recently been found to be associated with susceptibility to tuberculosis and leprosy in humans. The Nramp1 protein is an integral membrane protein expressed exclusively in the lysosomal compartment of monocytes and macrophages. After phagocytosis, Nramp1 is targeted to the membrane of the microbe-containing phagosome, where it may modify the intraphagosomal milieu to affect microbial replication. Although the biochemical mechanism of action of Nramp1 at that site remains unknown, Nramp homologues have been identified in many other animal species and actually define a protein family conserved from bacteria to humans. Some of these homologues have been shown to be divalent cation transporters. Recently, a second member of the mammalian Nramp family, Nramp2, was discovered and shown to be mutated in animal models of iron deficiency. The Nramp2 protein was subsequently shown to be the major transferrin-independent iron uptake system of the intestine. Together, these results suggest that Nramp1 may control intracellular microbial replication by actively removing iron or other divalent cations from the phagosomal space.","PeriodicalId":20612,"journal":{"name":"Proceedings of the Association of American Physicians","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1999-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21284155","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 164

Genetic determinants of HIV-1 infection and its manifestations. HIV-1感染的遗传决定因素及其表现。

Proceedings of the Association of American Physicians Pub Date : 1999-07-01 DOI: 10.1046/j.1525-1381.1999.99238.x

R A Kaslow, J M McNicholl

{"title":"Genetic determinants of HIV-1 infection and its manifestations.","authors":"R A Kaslow, J M McNicholl","doi":"10.1046/j.1525-1381.1999.99238.x","DOIUrl":"https://doi.org/10.1046/j.1525-1381.1999.99238.x","url":null,"abstract":"The human immunodeficiency virus type 1 (HIV-1), which has become pandemic within a single generation, has encountered an immune system in which genetically encoded elements have evolved gradually under different environmental pressures in diverse populations. Important heritable differences in genes that alter susceptibility to HIV-1 infection or the rate of deterioration of immunity, or both, have been discovered in cohorts carefully defined for intensity of exposure to the virus, viral subtype characteristics, and onset and course of infection. For the highly polymorphic human leukocyte antigen (HLA) antigen processing and presenting system, the principle that small contributions of multiple interactive HLA marker combinations (primarily in the class I pathway) significantly modulate the course of HIV-1 infection has now been confirmed in several independently evaluated groups of patients. Variants of HLA genes probably also play some role in the acquisition of infection by the various routes of transmission. Genes for an elaborate set of circulating chemokine molecules and their cell-surface receptors clearly regulate cell attachment and penetration of HIV. Certain allelic forms of one, the CCR5 gene, alter susceptibility to infection and the rate of progression of disease; in the homozygous state, a deleted form (Delta32 CCR5) strongly protects against infection, and in infected heterozygotes, it slows the disease process somewhat. Mutants in genes of other chemokine system components further differentiate the response to infection, and frequencies of these forms vary between and within races. Work relating additional genetic markers to HIV infection or disease is at earlier stages. Dissecting the effects of multiple variants in complex gene systems will clearly require organized comprehensive approaches in considerably larger populations than have typically been assembled.","PeriodicalId":20612,"journal":{"name":"Proceedings of the Association of American Physicians","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1999-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21284753","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 35

Enterococci: new aspects of an old organism. 肠球菌:一种古老生物体的新面貌。

Proceedings of the Association of American Physicians Pub Date : 1999-07-01 DOI: 10.1046/j.1525-1381.1999.99241.x

B E Murray, G M Weinstock

引用次数: 74

Novel mechanisms of calcium handling by the osteoclast: A review-hypothesis. 破骨细胞处理钙的新机制:一个假设综述。

Proceedings of the Association of American Physicians Pub Date : 1999-07-01 DOI: 10.1046/j.1525-1381.1999.99233.x

M Zaidi, B S Moonga, O A Adebanjo

{"title":"Novel mechanisms of calcium handling by the osteoclast: A review-hypothesis.","authors":"M Zaidi, B S Moonga, O A Adebanjo","doi":"10.1046/j.1525-1381.1999.99233.x","DOIUrl":"https://doi.org/10.1046/j.1525-1381.1999.99233.x","url":null,"abstract":"The osteoclast is a cell that is unique in its ability to resorb bone and, in doing so, becomes exposed to unusually high millimolar Ca2+ concentrations. It is generally accepted that, during resorption, osteoclasts can \"sense\" changes in their ambient Ca2+ concentration. This triggers a sharp cytosolic Ca2+ increase through both Ca2+ release and Ca2+ influx. The change in cytosolic Ca2+ is transduced finally into inhibition of bone resorption. It has been shown that a type 2 ryanodine receptor isoform, expressed uniquely in the plasma membrane, functions as a Ca2+ influx channel and possibly as a Ca2+ sensor. Ryanodine receptors are ordinarily Ca2+ release channels that have a microsomal membrane location in a wide variety of eukaryotic cells, including the osteoclasts. However, only recently has it become obvious that ryanodine receptors are also expressed in osteoclast nuclear membranes, at which site they probably gate nucleoplasmic Ca2+ influx. Nucleoplasmic Ca2+ in turn regulates key nuclear processes, including gene expression and apoptosis. Here, we review the potential mechanisms underlying the recognition, movement, and effects of Ca2+ in the osteoclast. We will also speculate on the general biological significance of the unique processes used by the osteoclast to handle high Ca2+ loads during bone resorption.","PeriodicalId":20612,"journal":{"name":"Proceedings of the Association of American Physicians","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1999-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21284761","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 34

Abner McGehee harvey 1911-1998 Abner McGehee harvey 1911-1998

Proceedings of the Association of American Physicians Pub Date : 1999-07-01

McKusick

引用次数: 0

Thematic review series VII: genetic variability in response to infection introduction 专题审查系列七:应对感染引入的遗传变异

Proceedings of the Association of American Physicians Pub Date : 1999-07-01 DOI: 10.1046/j.1525-1381.1999.99003.x

Weatherall

引用次数: 1

The immunogenetics of resistance to malaria. 抗疟疾的免疫遗传学。

Proceedings of the Association of American Physicians Pub Date : 1999-07-01 DOI: 10.1046/j.1525-1381.1999.99234.x

A V Hill

引用次数: 56