The release, distribution, and clearance of human β-thromboglobulin and platelet factor 4

Dawes, J.; Smith, R. C.; Pepper, Duncan S.

doi:10.1016/0049-3848(78)90279-7

Cited by 298 publications

(112 citation statements)

References 10 publications

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“…The persistence of slightly elevated (3TG levels in plasma at 180 min may be simply explained by the plasma half-life of 0TG, which is equal to approximately 100 min. 20 Although the precise mechanisms cannot be discussed further from the present results, it appears that in vivo platelet activation is triggered by insulin-induced hypoglycemia. One should therefore recommend that hypoglycemic episodes be avoided or at least maintained within reasonable limits in all insulin-treated diabetic patients, even in those who are submitted to intensified insulin therapies with pumps.…”

mentioning

confidence: 52%

Plasma β-Thromboglobulin Response to Insulin-induced Hypoglycemia in Type I Diabetic Patients

et al. 1984

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SUMMARYThe effect of an insulin-induced hypoglycemia was examined in 14 type I diabetic patients. After an overnight blood glucose normalization, each patient received an additional intravenous bolus of 3 U regular insulin at 0900 h (time 0). Blood glucose was continuously recorded up to 180 min. Plasma samples were assayed for p-thromboglobulin ((5TG, ng/ml), pancreatic glucagon (pg/ml), cortisol (|xg/dl), and growth hormone (ng/ml) 30 min before the insulin stress, at time 0, at blood glucose nadir, and at 180 min. The blood glucose fell from a baseline level of 85.0 ± 3.2 mg/dl to a nadir value of 39.2 ± 1 . 9 mg/dl (P < 0.001) reached at an average time of 41.4 ± 4.9 min. Plasma PTG increased significantly (P < 0.05) during the insulin stress: 93.4 ± 23.7 ng/ml at nadir versus 42.5 ± 5.9 at time 0. Plasma cortisol and growth hormone were significantly increased (P < 0.02 and P < 0.01) at nadir compared with time 0 values. Plasma pancreatic glucagon was higher at nadir than at time 0, but the difference was not significant. The present results indicate that in vivo platelet activation can be triggered by hypoglycemic episodes in insulin-treated diabetic patients. DIABETES 1984; 33:907-909. N ear-normal circadian blood glucose, metabolic, and hormonal profiles can be achieved in insulindependent diabetic patients by either continuous subcutaneous insulin infusion or intensified conventional insulin therapy, 13 but such treatments do not result in a total eradication of the hypoglycemic risk. 45 Although it has been reported that severe hypoglycemia can occur during continuous subcutaneous insulin infusion, 4 it seems that the hypoglycemic episodes usually remain moderate or asymptomatic 5 provided that the patients have no defect in

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confidence: 52%

Plasma β-Thromboglobulin Response to Insulin-induced Hypoglycemia in Type I Diabetic Patients

et al. 1984

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“…Since then, a number of other proteins have been discovered, usually incidentally, to increase in the plasma after intravenous heparin administration. The known heparin-releasable proteins are lipoprotein lipase, 1 hepatic triglyceride lipase, 2 platelet factor 4, 3 tissue factor pathway inhibitor, 4 extracellular superoxide dismutase, 5 diamine oxidase (histaminase), 6 and tumor necrosis factor-binding protein-1. 7 Tissue-type plasminogen activator may also be heparin releasable after its secretion from endothelial cells.…”

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confidence: 99%

Identification of novel heparin-releasable proteins, as well as the cytokines midkine and pleiotrophin, in human postheparin plasma.

Novotny

Maffi

Mehta

et al. 1993

Arterioscler Thromb

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The heparin-releasable proteins are a group of proteins that are targeted to the endothelial surface by attachment to glycosaminoglycans and may have functions specific to the endothelium-blood interface. In this study, heparin-affinity chromatography of human postheparin plasma was used as a method to identify and study novel heparin-releasable proteins. Six proteins seen on sodium dodecyl sulfatepolyacrylamide gel electrophoresis gels have increased levels in plasma after intravenous heparin. The six proteins are platelet factor 4, midkine, pleiotrophin, and several novel proteins. Midkine and pleiotrophin are related cytokines that are developmentally regulated, neurotrophic, and mitogenic. Additional studies show that levels of midkine and pleiotrophin peak at 10 to 30 minutes after injection of heparin. Heparin-releasable midkine and pleiotrophin do not originate from blood cells or the kidney. Heparinreleasable midkine may originate from endothelial cells. Soft agar culture of an adenocarcinoma cell line (SW-13) demonstrates growth-stimulating activity similar to that described for pleiotrophin in the heparin-agarose eluate of postheparin plasma but not in the heparin-agarose eluate of preheparin plasma. It is concluded there are more heparin-releasable proteins than previously identified, including midkine and pleiotrophin, and that heparin-affinity chromatography of postheparin plasma is a useful technique for identifying novel heparin-releasable proteins.

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“…O fator 4 plaquetário foi descrito em 1969 por Niewiaroswski e Thomas. É uma proteína de 70 aminoácidos secretada como um complexo de 2 tetrâmeros (68)(69)(70) . Age por interferência na ação da heparina e, portanto, promove a coagulação.…”

Section: Marcadores De Ativação Plaquetáriaunclassified

Ativação plaquetária na esclerose sistêmica e alternativas metodológicas para sua avaliação

Massabki¹,

Lourenço²,

Andrade³

2004

Rev. Bras. Reumatol.

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A esclerose sistêmica (ES) é uma doença sistêmica caracterizada por microangiopatia, exuberante atividade do fibroblasto e anormalidades imunológicas. A faceta microangiopática é responsável pela maioria das complicações com potencial mortalidade. A interação entre o endotélio e as plaquetas desempenha um papel importante na fisiopatologia da ES. Evidências de ativação plaquetária na ES incluem níveis séricos elevados de substâncias derivadas das plaquetas (fator 4 plaquetário, fator de Von Willenbrand, tromboxane A2 e ß-tromboglobulina), agregados plaquetários circulantes, anormalidades ultraestruturais nas plaquetas e a presença de plaquetas aderidas ao endotélio. A presente revisão aborda de forma crítica os princípios e problemas potenciais dos principais métodos de avaliação da função e ativação plaquetárias. A avaliação da capacidade de agregação das plaquetas é feita com e sem a adição de agonistas (adenosina difosfato, colágeno e adrenalina). A ativação plaquetária pode ser avaliada de duas formas: pela dosagem da concentração plasmática de substâncias que são liberadas pela ativação plaquetária (ex., tromboxane, fator 4 plaquetário) e pela mensuração da expressão em membrana plaquetária de moléculas que são transportadas para a membrana plaquetária durante o processo de ativação das plaquetas (ex., GMP-140 e glicoproteína IIb/IIIa). Uma contribuição recente para este campo foi dada pela demonstração de que a enolase específica de neurônios (NSE) é liberada das plaquetas para o plasma em pacientes com ES em atividade. Assim, a dosagem da NSE, que é um exame disponível nos principais laboratórios com ênfase na dosagem de marcadores tumorais, pode se tornar um marcador de atividade plaquetária de grande utilidade em diversas condições clínicas.Palavras-chave: esclerose sistêmica, agregação plaquetária, ativação plaquetária.

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The release, distribution, and clearance of human β-thromboglobulin and platelet factor 4

Cited by 298 publications

References 10 publications

Plasma β-Thromboglobulin Response to Insulin-induced Hypoglycemia in Type I Diabetic Patients

Plasma β-Thromboglobulin Response to Insulin-induced Hypoglycemia in Type I Diabetic Patients

Identification of novel heparin-releasable proteins, as well as the cytokines midkine and pleiotrophin, in human postheparin plasma.

Ativação plaquetária na esclerose sistêmica e alternativas metodológicas para sua avaliação

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