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Phenotypes vascular

The categories for outcomes of DIVI are used to group phenotypic vascular findings according to histomorphologic similarities and candidate sensitive and specific biomarker response independent of etiology, mechanisms, and sites of injury (Zhang et al., 2012 Bendjama et al., 2014). [Pg.398]

EDI), and water to produce a group of biodegradable PU foams. The interconnected pores varied in size from 10 to 2 mm in diameter. Rabbit bone-marrow stromal cells cultured on the materials for up to 30 days formed multilayers of confluent cells and were phenotypically similar to those grown on tissue culture PS. It supported the adherence and proliferation of both bone-marrow stromal cells and chondrocytes in vitro. In subdermal implants the investigators found that the material showed infiltration of both vascular cells and connective tissue. [Pg.237]

Aghi M, Cohen KS, Klein RJ, Scadden DT, Chiocca EA (2006) Tumor stromal-derived factor-1 recruits vascular progenitors to mitotic neovasculature, where microenvironment influences their differentiated phenotypes. Cancer Res 66 9054-9064... [Pg.266]

Ragolia, L., et al. (2003). Prostaglandin D2 synthase inhibits the exaggerated growth phenotype of spontaneously hypertensive rat vascular smooth muscle cells. J. Biol. Chem. 278, 22175-81. [Pg.384]

Song J, Wan Y, Rolfe BE, Campbell JH, Campbell GR (1998) Effect of estrogen on vascular smooth muscle cells is dependent upon cellular phenotype. Atherosclerosis 140 97-104... [Pg.245]

Normally, quiescent platelets freely circulate through the vasculature, reflective of the hemocompatible character of the vascular endothelium and the anti-thrombotic nature of healthy human blood vessels. Traumatic vascular damage incites a spatially and temporally coordinated platelet transformation encompassing several major, sequential phenotypic changes platelet adhesion to subendothelial matrix components... [Pg.300]

Vascular plants are known to induce a variety of phenotypic changes in response to damage, including changes in secondary metabolite concentrations. Induced plant responses may lead to increased resistance toward future herbivory if changes have... [Pg.151]

Atypical dysbetalipoproteinemia, associated with the APOE-313 phenotype rather than the classic APOE-212 phenotype, is characterized by severe hypercholesterolemia and hypertriglyceridemia, xanthomatosis, premature vascular disease, and a preponderance of 3-VLDL. Subjects with atypical dysbetalipoproteinemia are homozygous for an amino acid substitution in APOE at residue 158 (495). In AD, APOE-4 carriers show lower levels of APOE in the CSF compared to controls (496). [Pg.297]

Cacabelos, R., Fernandez-Novoa, L., Corzo, L., et al. (2004) Phenotypic profiles and functional genomics in dementia with a vascular component. Neurol. Res., 26, 459-480. [Pg.327]

Activation of endothelial cells leads to changes in endothehal ceU properties such as loss of vascular integrity, expression of adhesion molecules, antithrombotic to prothrombotic phenotype changes, cytokine production and the upregulation of HLA molecules. All these diverse effects can be attributed to the activation of transcription factors [44]. Of the presently known transcription factors, NFkB is believed to be one of the most important in the regulation of endothehal cell activation. After a stimulus at the cell surface which is caused by e.g. [Pg.177]

Finally, we consider physiological expression or suppression, and the long latent period between carcinogen treatment and tumor appearance. While it makes sense to think in terms of phenotypic lag, clonal growth, vascularization, immuno-suppression, and other phenomena, we just do not know enough today to define clear-cut experimental approaches. However, at the human level, the undesirable endpoints of this series of processes are clear teratologic syndromes, cancer, and heritable birth defects. [Pg.16]

Reddy, M.A., Villeneuve, L.M., Wang, M., Lanting, L. and Natarajan, R. (2008) Role of the lysine-spedfic demefhylase 1 in the proinfiammatory phenotype of vascular smooth muscle cells of diabetic mice. Circulation Research, 103, 615-623. [Pg.285]

Silva GV, Litovsky S, Assad JA, Sousa AL, Martin BJ, Vela D, Coulter SC, Lin J, Ober J, Vaughn WK, Branco RV, Oliveira EM, He R, Geng YJ, Willerson JT, Perin EC. Mesenchymal stem cells differentiate into an endothelial phenotype, enhance vascular density, and improve heart function in a canine chronic ischemia model. Circulation 2005 111 150-156. [Pg.124]

Rennick RE, Connat JL, Burnstock G, Rothery S, Severs NJ, Green CR Expression of connexin 43 gap junctions between cultured vascular smooth muscle cells is dependent upon phenotype. Cell Tissue Res 1993 271 323-332. [Pg.134]

Investigating the phenotype of BrdU+ in PHR we did not observe differences between control and postischemic brains. A proportion of BrdU+ cells (up to 15%) expressed the phenotype of either microglia or astroglia (Fig. 30A), and some vascular cells incorporated BrdU as well. BrdU+ oligodendrocytes or cells with a neuronal phenotype were not observed (Fig. 30B). Thus, over 75% of the BrdU+ cells in the PHR were of an unknown phenotype. [Pg.49]


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See also in sourсe #XX -- [ Pg.213 , Pg.214 , Pg.215 , Pg.216 , Pg.217 , Pg.218 , Pg.219 ]




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