The release of a human platelet specific protein measured by a radioimmunoassay

Ludlam, C. A.; Moore, Stephen; Bolton, A.E.; Pepper, Duncan S.; Cash, J. D.

doi:10.1016/0049-3848(75)90066-3

Cited by 280 publications

(70 citation statements)

References 5 publications

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“…The role of platelets during the antigen induced asthmatic attack has also been investigated by monitoring circulating platelet numbers and plasma levels of the platelet specific protein ,Bthromboglobulin (,TBG) released from the a granule of the platelet following platelet lysis (Ludlam et al, 1975). The effect of indomethacin pretreatment on the nature of the antigen induced asthmatic attack, and on these arachidonic acid metabolites as well as platelet involvement has been investigated.…”

Section: Introductionmentioning

confidence: 99%

Lung function and plasma levels of thromboxane B2, 6‐ketoprostaglandin F1 alpha and beta‐thromboglobulin in antigen‐induced asthma before and after indomethacin pretreatment.

Shephard¹,

Malan²,

Macfarlane³

et al. 1985

Brit J Clinical Pharma

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1 The effect of specific antigen challenge on the lung function of eight allergic asthmatic patients after placebo and indomethacin pretreatment has been investigated. 2 Plasma levels of thromboxane B2(TxB2), metabolite of thromboxane A2, 6-ketoPGFia, metabolite of epoprostenol, (prostacyclin, PGI2) and ,-thromboglobulin (,TBG) following antigen challenge in these eight patients have also been measured after placebo and indomethacin pretreatment. 3 Each patient underwent two antigen inhalations 1 week apart. One challenge took place after 4 days pretreatment with indomethacin capsules 25 mg four times daily, and the other took place following 4 days placebo pretreatment, one matched capsule four times daily. The order of administration was random but balanced and blind with respect to the patient. 4 Following placebo pretreatment two patients presented with an early antigen response only, four presented with a biphasic antigen response and two presented with a delayed antigen response only. The asthmatic response for each patient was consistent on reexposure. 5 Indomethacin pretreatment suppressed the delayed antigen induced asthmatic response. This suppression was reproducible. 6 There was a rise in plasma TxB2 levels on antigen challenge following placebo pretreatment but not following indomethacin pretreatment, whereas there was a rise in 6-keto-PGF1I after antigen challenge following indomethacin but not placebo pretreatment.7 No significant change in plasma ,BTBG or platelet counts from control values was observed following antigen challenge with either placebo or indomethacin pretreatment. 8 It is suggested that the production of PGI2 and suppression of TxA2 by indomethacin pretreatment contribute to the suppression of the delayed antigen induced asthmatic response and that platelets play a minimal role in this process.Keywords thromboxane B2 6-keto-prostaglandin Fla P-thromboglobulin platelets indomethacin antigen-induced asthma

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Section: Introductionmentioning

confidence: 99%

Lung function and plasma levels of thromboxane B2, 6‐ketoprostaglandin F1 alpha and beta‐thromboglobulin in antigen‐induced asthma before and after indomethacin pretreatment.

Shephard¹,

Malan²,

Macfarlane³

et al. 1985

Brit J Clinical Pharma

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“…The patients involved in this study had all been scheduled for abortion and had provided informed consent to participate in the study. The patients' ages ranged from 19 to 41 yr with a mean of 22 yr and the estimated duration of gestation ranged from 10 to 18 wk with a mean of 16 wk. 200 ml of sterile sodium chloride (20%) was injected into the uterine cavity over a 2-to 3-min period by the patient's obstetrician.…”

Section: Introductionmentioning

confidence: 99%

“…These proteins are platelet factor 4 (PF4) and beta thromboglobulin (,TG). Specific assays applicable to clinical blood samples have been developed for FPA (12), PF4 (13)(14)(15), and ,3TG (15,16). An assay for FPB (3) in vitro has also been developed and this paper describes the use of this assay to identify a plasminproduced peptide, which includes FPB and is derived from the NH2-terminal end of the B,3 chain.…”

Section: Introductionmentioning

confidence: 99%

Sequence of Fibrinogen Proteolysis and Platelet Release after Intrauterine Infusion of Hypertonic Saline

Nossel¹,

Wasser²,

Kaplan³

et al. 1979

J. Clin. Invest.

109

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A B S T R A C T Plasma fibrinopeptide B (B,81-14 or FPB) immunoreactivity was studied by radioimmunoassay in patients who received intrauterine infusion of hypertonic saline to terminate pregnancy. FPB immunoreactivity increased with thrombin treatment (TIFPB) suggesting the presence of a larger FPBcontaining peptide, since purified FPB is not altered by thrombin, whereas thrombin increases the immunoreactivity of B,B1-42 (which includes FPB) 10-fold. TIFPB immunoreactivity in plasma, drawn 4 h after hypertonic saline infusion eluted from Sephadex G-50 similarly to isolated B,p1-42. Streptokinase, incubated with normal plasma progressively generated TIFPB immunoreactivity, which showed a major component which eluted from Sephadex G-50 similarly to B,B1-42. Streptokinase generated TIFPB much more rapidly in reptilase-treated plasma that contains fibrin I, (which still includes FPB), indicating that fibrin I is preferred over fibrinogen as a substrate for plasmin cleavage of arginine (B,842)-alanine (B,843). Serial studies were then made in 10 patients receiving intrauterine hypertonic saline. Fibrinopeptide A (FPA) levels rose immediately, reached a peak between 1 and 2 h, were declining at4 h, and were normal at24 and 48 h. TIFPB levels rose slightly in the 1st h, reached a peak at 4 h, and had returned to base-line values at 24 h. Serum fibrinogen degradation product levels were unchanged at 1 h, reached their highest level at 4 h, and were still markedly elevated at 24 and 48 h. Fibrinogen levels dropped slightly being lowest at 4 and 24 h. Platelet counts declined in parallel with the fibrinogen levels over the first 4 h, but continued to decrease through 48 h. Beta thromboglobulin (,fTG) levels generally paralleled FPA levels whereas platelet factor 4 (PF4) levels showed only slight changes. The data indicate that immediately after intrauterine hypertonic saline Dr. Kaplan is a Senior Investigator of the New York Heart Association.

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“…O fator 4 plaquetário e a beta-tromboglobulina diferem apenas em sua porção amino-terminal 4, o que lhes confere similaridade química e imunológica (72) , embora tenham funções inteiramente distintas. Ambas as proteínas podem ser medidas de maneira eficaz tanto por radioimunoensaio quanto por enzimaimunoensaio (39)(40)(41)56,(73)(74)(75)(76) .…”

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 of a human platelet specific protein measured by a radioimmunoassay

Cited by 280 publications

References 5 publications

Lung function and plasma levels of thromboxane B2, 6‐ketoprostaglandin F1 alpha and beta‐thromboglobulin in antigen‐induced asthma before and after indomethacin pretreatment.

Lung function and plasma levels of thromboxane B2, 6‐ketoprostaglandin F1 alpha and beta‐thromboglobulin in antigen‐induced asthma before and after indomethacin pretreatment.

Sequence of Fibrinogen Proteolysis and Platelet Release after Intrauterine Infusion of Hypertonic Saline

Ativação plaquetária na esclerose sistêmica e alternativas metodológicas para sua avaliação

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