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1. |
The Birth of Endothelium: Journal of Endothelial Cell Research |
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Endothelium,
Volume 1,
Issue 1,
1993,
Page 1-3
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ISSN:1062-3329
DOI:10.3109/10623329309100950
出版商:Taylor&Francis
年代:1993
数据来源: Taylor
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2. |
Restenosis after Coronary Angioplasty: Pathogenesis of Neointimal Thickening Initiated by Endothelial Loss |
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Endothelium,
Volume 1,
Issue 1,
1993,
Page 5-22
ShirotaniManabu,
YuiYoshiki,
KawaiChuichi,
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ISSN:1062-3329
DOI:10.3109/10623329309100951
出版商:Taylor&Francis
年代:1993
数据来源: Taylor
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3. |
Ultrastructural Localization of Nitric Oxide Synthase in Intima of Rabbit Aorta |
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Endothelium,
Volume 1,
Issue 1,
1993,
Page 23-29
LoeschAndrzej,
BurnstockGeoffrey,
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摘要:
The localization of nitric oxide synthase (NOS) in rabbit aorta was investigated by electron-immunocytochemistry. Using the pre-embedding peroxidase-antiperoxidase technique, a neuronal isoform (type I) of NOS was localized in a small subpopulation of endothelial cells (approximately 5–6% of all observed cell profiles). This finding indicates that the endothelium of rabbit aorta is heterogeneous. Together with the post-embedding immuno-gold technique the results showed that the immunolabelling was predominantly in the cytoplasm of endothelial cells. In particular, a relation of gold particles with ribosomes was evident but no labelling in cytoplasmic vesicles was observed. Immunoreactivity for NOS was also localized extracellularly between the endothelial cells and the inner muscle layers.
ISSN:1062-3329
DOI:10.3109/10623329309100952
出版商:Taylor&Francis
年代:1993
数据来源: Taylor
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4. |
S-Nitroso-N-acetylpenicillamine is a Potent Inhibitor of Neutrophil-Endothelial Interaction |
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Endothelium,
Volume 1,
Issue 1,
1993,
Page 31-39
LiangXin,
LeferAllan M.,
ZipkinRobert E.,
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摘要:
Inhibition of polymorphonuclear (PMN) leukocytes' adherence to the endothelium and their consequent activation represents a novel approach to the treatment of those diseases in which PMNs play an important role. In this study, we observed the effects ofS-nitroso-N-acetylpenicillamine (SNAP), a nitrosothiol nitric oxide (NO) donor, on cat PMN adherence to autologous coronary vascular endothelium and activated PMN-induced vasocontraction with accompanying endothelial dysfunction. SNAP, at concentrations between 2.5 nM to 250 nM, dilated cat coronary artery rings in a concentration-dependent manner with peak vasodilator responses occurring at 50 nM. Addition of 1 nM SNAP, a concentration at which no significant vasorelaxation occurred, significantly inhibited leukotriene B4(LTB4activated PMN adherence to normal endothelium (p<0.05). Inhibition of endothelial NO formation by N -nitro-L-arginine methyl ester induced a two- to three-fold increase of PMN adherence to the endothelium, which was almost completely prevented by 1 nM-SNAP (p<0.001). Moreover, addition of InM-SNAP also significantly decreased LTB4activated PMN-induced vasocontraction and prevented endothelial dysfunction. These results indicate that SNAP has significant anti-PMN effects, and may have particular utility in preventing tissue injury associated with myocardial ischemia and reperfusion.
ISSN:1062-3329
DOI:10.3109/10623329309100953
出版商:Taylor&Francis
年代:1993
数据来源: Taylor
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5. |
Enhanced Adhesion of Colon Carcinoma Cells to Thrombin Stimulated Endothelial Cells |
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Endothelium,
Volume 1,
Issue 1,
1993,
Page 41-45
MartìnInés,
MetzelaarMarcel J.,
MenardSylvie,
MantovaniAlberto,
DejanaElisabetta,
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摘要:
Treatment of cultured human umbilical vein endothelial cells (EC) with thrombin caused a significant increase in their adhesivity to three human colon carcinoma cell lines (CC). Thrombin effect was directed to EC and was both concentration and time dependent. Treatment of EC with antibodies to P-selectin or CC with antibodies to Lewis X and Lewis a sugar groups inhibited thrombin effect. This newly described thrombin activity might play, a role in tumor cell lodgement in target organs during metastatic spread.
ISSN:1062-3329
DOI:10.3109/10623329309100954
出版商:Taylor&Francis
年代:1993
数据来源: Taylor
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6. |
TNFαInduces E-Selectin Expression and PECAM-1 (CD31) Redistribution in Extracutaneous Tissues |
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Endothelium,
Volume 1,
Issue 1,
1993,
Page 47-54
IoffredaM. D.,
AlbeldaS. M.,
ElderD. E.,
RaduA.,
LeventhalL. C.,
ZweimanB.,
MurphyG. F.,
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摘要:
We evaluated the experimental utility of short-term organ culture to assess cytokine-dependent endothelial activation in extracutaneous tissues. Effects of tumor necrosis factor-alpha (TNFα) on E-selectin and platelet-endothelial cell adhesion molecule-1 (PECAM-1) were assessed immunocytochemically in tissue derived from human gastrointestinal tract, female genital tract, breast, lung, kidney, and skin. Normal vessels in control explants from these sites did not stain for E-selectin and expressed PECAM-1 uniformly along plasma membranes of lumenal endothelial cells. Cytokine-stimulated vessels in explants exposed to TNFa for 6 hours revealed marked induction of E-selectin and redistribution of PECAM-1 to interendothelial junctions. PECAM-1 redistribution was also confirmed in situ using Type I skin allergic reactions in which mast cell TNF is presumably released. As in cytokine-stimulated skin, E-selectin expression in extracutaneous tissues was restricted to postcapillary venules, although anastomotic junctions between capillaries and venules were more clearly defined at extracutaneous sites. These data establish short-term organ culture as a potentially useful means of assessing endothelial activation in extracutaneous tissues.
ISSN:1062-3329
DOI:10.3109/10623329309100955
出版商:Taylor&Francis
年代:1993
数据来源: Taylor
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7. |
Effect of the Endothelin ETAReceptor Antagonist, BQ-123, on Pressor Responses to Endothelin Family Peptides |
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Endothelium,
Volume 1,
Issue 1,
1993,
Page 55-59
PollockDavid M.,
DivishBarbara J.,
PolakowskiJames S.,
OpgenorthTerry J.,
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摘要:
Experiments were conducted to determine the ability of the newly discovered ETAreceptor antagonist, BQ-123, to inhibit the pressor responses to several members of the human endothelin peptide family in anesthetized rats. Big ET-1 produced a greater increase in mean arterial pressure compared to ET-1 (67±10% vs. 44±4%, p<0.05; both at 1 nmol/kg i.v.). Prior administration of BQ-123 (10 mg/kg i.v.) was more effective at inhibiting the response to Big ET-1 compared to ET-1. Following ETAreceptor blockade, ET-1 produced a small, but significant, increase in mean arterial pressure (15±2%) while Big ET-1 had no effect (5±2%). Big ET-3 and ET-3 at 1 nmol/kg i.v. produced similar increases in mean arterial pressure, although less than that produced by either Big ET-1 or ET-1 (p<0.05). ETAreceptor antagonism blocked 64% of the pressor response to both Big ET-3 and ET-3. We conclude that blockade of pressor responses to each of the endothelin peptides suggests that the increases in arterial pressure are primarily mediated by ETAreceptor activation with the exception of a small component of the response to ET-1. ET-3-induced activation of ETAreceptors occursin vivodespite the observation that ET-3 is known to have relatively low affinity for the ETAreceptor.
ISSN:1062-3329
DOI:10.3109/10623329309100956
出版商:Taylor&Francis
年代:1993
数据来源: Taylor
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8. |
Intravenous Immune Globulin Reduces the IgG Antiendothelial Cell Antibody Response in Kawasaki Disease |
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Endothelium,
Volume 1,
Issue 1,
1993,
Page 61-66
SaloE.,
WangelA. G.,
PelkonenP.,
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摘要:
IgG class antiendothelial cell antibodies were sought by a cellular ELISA in 350 samples from 118 patients with Kawasaki disease. They were found in 62 of the patients (52%); including 12 of 18 patients with a coronary artery lesion and 34 of 67 in whom such a lesion was not detected. Their frequency was similar in patients who had received intravenous immune globulin (18 of 40) and in those who had not (43 of 78). However, the mean antibody levels rose significantly in patients who were not treated with intravenous immune globulin but no such rise occurred in treated patients whose mean and peak antibody levels remained significantly lower than those of untreated patients. These results suggest that intravenous immune globulin reduces the magnitude of the antiendothelial cell antibody response in patients with Kawasaki disease.
ISSN:1062-3329
DOI:10.3109/10623329309100957
出版商:Taylor&Francis
年代:1993
数据来源: Taylor
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9. |
Perspectives in Endothelial Cell Research over the Next Decade |
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Endothelium,
Volume 1,
Issue 1,
1993,
Page 67-68
VadasM. A.,
AngusJ. A.,
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摘要:
The understanding of endothelial biology has exploded over the last decade. In spite of excellent progress in a number of areas, for example, mechanism of cellular adhesion and regulation of vascular tone, fundamental aspects of endothelial biology remain to be explored. We have highlighted specific areas in which there should be solid progress over the next ten years and which we believe should be strongly promoted by the new journalEndothelium.
ISSN:1062-3329
DOI:10.3109/10623329309100958
出版商:Taylor&Francis
年代:1993
数据来源: Taylor
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10. |
Conference Report: Endothelial Cell Heterogeneity and Organ Specificity |
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Endothelium,
Volume 1,
Issue 1,
1993,
Page 69-70
LelkesPeter I.,
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PDF (212KB)
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ISSN:1062-3329
DOI:10.3109/10623329309100959
出版商:Taylor&Francis
年代:1993
数据来源: Taylor
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