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Annichino-Bizzacchi, Joyce Maria 1957. "Avaliação de alguns parametros da coagulação sanguinea e fibrinolise em pacientes com mieloma multiplo." [s.n.], 1989. http://repositorio.unicamp.br/jspui/handle/REPOSIP/308731.
Full textAbstract:
Orientador : Claudio A. M. SampaioTese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas
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Resumo: O mieloma múltiplo é uma doença neoplásica caracterizada pela proliferação de um clone anormal de plasmócitos, que geralmente sintetizam quantidades anormais' de paraproteína monoclonal. A presença da paraproteína pode interferir com a hemostasia por alterações na função plaquetária, pela infiltração do tecido conectivo impedindo a exposição do cOlageno, pela formação de inibidores ou de complexos inespecíficos com os fatores de coagulação...Observação: O resumo, na integra, podera ser visualizado no texto completo da tese digital
Abstract: Multiple mieloma is a neoplastic disease caracterized by the proliferation of an abnormal cIone of pIasmoc~tes, which enerall synthesize abnormal omounts of monoclonal immunoglobulin. Presence of paraprotein can modif~ the hemostasis through alteration in the pIatelet function, infiltration of the connective tissue interfering with the collagen e~position, formation of specific inhibitors or unespecific comple~es with coagulation factors...Note: The complete abstract is available with the full electronic digital thesis or dissertations
Doutorado
Doutor em Medicina
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Crescencio, Amanda Paulino. "Relação entre as concentrações plasmáticas e peritoneais de dímeros-D e as variáveis clínicas e laboratoriais de equinos com síndrome cólica." Botucatu, 2017. http://hdl.handle.net/11449/152230.
Full textAbstract:
Orientador: Marcos Jun WatanabeCoorientador: Carlos Alberto Husnni
Banca: Juliana de Moura Alonso
Banca: Paula Alessandra Di Filippo
Resumo: Nos equinos, os distúrbios gastrointestinais (GI) são as causas mais comuns de problemas de coagulação, podendo gerar complicações fatais. Atualmente, uma das ferramentas mais sensíveis para avaliação da hipercoagulabilidade e hiperfibrinólise em cavalos é a determinação das concentrações de dímeros-D. Dessa forma, objetivou-se relacionar as concentrações plasmáticas e peritoneais de dímeros-D com as variáveis clínicas (frequência cardíaca, frequência respiratória, cor das membranas mucosas, tempo de preenchimento capilar, temperatura retal, grau de dor e tempo de evolução do quadro) e laboratoriais (hematócrito, proteína plasmática total, plaquetas, fibrinogênio e leucócitos sanguíneos, além de proteína, fibrinogênio, células nucleadas, bactérias e glicose no líquido peritoneal) de equinos com síndrome cólica e com o diagnóstico e prognóstico desses casos. Foram utilizados 86 equinos com idade mediana de 6,5 anos e com peso mediano de 400 Kg. Os animais foram submetidos ao exame clínico e coleta de amostras de sangue e líquido peritoneal (LP) na admissão. As concentrações plasmáticas e peritoneais de dímeros-D foram avaliadas através de um ensaio semiquantitativo de aglutinação em látex. Apesar das concentrações plasmáticas e peritoneais de dímeros-D terem demonstrado um sentido biológico relacionado à gravidade dos casos de cólica na análise descritiva, isso não foi comprovado estatisticamente através da análise multivariada. Portanto, concluímos que a determinação das conc... (Resumo completo, clicar acesso eletrônico abaixo)
Abstract: In horses, gastrointestinal (GI) disorders are the most common cause of coagulation problems, which can lead to fatal complications. One of the most sensitive tools for assessing hypercoagulability and hyperfibrinolysis in horses is the determination of D-dimer concentrations. The aim of this study was to correlate the plasma and peritoneal D-dimer concentrations with the clinical variables (heart rate, respiratory rate, mucous membranes color, capillary filling time, rectal temperature, pain degree, and time frame evolution) (hematocrit, total plasma protein, platelets, fibrinogen and blood leukocytes, as well as protein, fibrinogen, nucleated cells, bacteria and glucose in the peritoneal fluid) of horses with colic syndrome and with the diagnosis and prognosis of these cases. A total of 86 horses with a median age of 6.5 years and with a median weight of 400 kg were used. The animals were submitted to clinical examination and collection of blood and peritoneal fluid (LP) samples at admission. Plasma and peritoneal concentrations of D-dimers were evaluated by a semi-quantitative latex agglutination assay. Although plasma and peritoneal concentrations of D-dimers demonstrated a biological significance related to the severity of colic cases in the descriptive analysis, this was not statistically demonstrated through multivariate analysis. Therefore, we concluded that the determination of plasma and peritoneal concentrations of D-dimers using semi-quantitative latex agglutinati... (Complete abstract click electronic access below)
Mestre
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Alonso, Juliana de Moura [UNESP]. "Avaliação da reatividade peritoneal de equinos submetidos à enterotomia de cólon menor e tratados com heparina pela via subcutânea." Universidade Estadual Paulista (UNESP), 2013. http://hdl.handle.net/11449/89147.
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000760136.pdf: 3009097 bytes, checksum: ab6e7c1fbf6f7224e3b942dec747e608 (MD5)As afecções do cólon menor são causas frequentes de síndrome cólica, sendo a enterotomia rotineiramente empregada para a remoção de fecalitos, enterólitos e corpos estranhos. O trauma cirúrgico resulta em inflamação difusa e ocorrência de peritonite asséptica devido à manipulação e ao acesso cirúrgico. Objetivou-se estudar a reatividade peritoneal após a realização de enterotomia e abrasão do cólon menor em equinos tratados ou não com heparina sistêmica. Foram utilizados dez equinos com idade média de 9 ± 3,87anos e 358 ± 30,28 Kg de massa corporal, divididos em dois grupos de cinco animais, sendo um grupo o controle (GC) e o outro tratado (GT). Ambos os grupos foram submetidos à laparotomia e enterotomia de cólon menor através da via paralombar direita em posição quadrupedal e receberam flunixin meglumine, gentamicina e associação de penicilinas. Ao GT, acrescentou-se heparina (150 UI/Kg SC, BID, 5 dias). Os animais foram avaliados quanto ao exame físico; hemograma; fibrinogênio; coagulograma; proteínas de fase aguda, séricas e peritoneais; características macroscópicas, físico-químicas e citológicas do líquido peritoneal; concentrações peritoneais do ativador e inibidor do plasminogênio tecidual e dímero D. Para tanto, pradonizaram-se os seguintes momentos de avaliação: M0-prévio à enterotomia; M1-12 horas; M2 - 1dia, M3- 2dias, M4- 4dias e M5- 6 dias; M6- 10 dias e M7- 14 dias após a enterotomia. Observou-se que a heparina resultou em anemia e diminuição da contagem de plaquetas, aumento do tempo de tromboplastina parcial ativada e aumento nas concentrações séricas e peritoneais das proteínas de fase aguda, entretanto diminuiu a formação de dímeros D, sugerindo diminuição da formação de coágulos de fibrina. Após 15 dias da enterotomia, realizou-se o exame laparoscópico, que não demonstrou diferença na deposição de fibrina entre os grupos, entretanto...
Small colon affections are frequent causes of abdominal pain, and enterotomy is routinely employed for removal of fecalith, enteroliths and foreign bodies. Surgical trauma results in diffuse inflammation and aseptic peritonitis occurrence due to handling and surgical access. The aim of this study was to evaluate peritoneal reactivity after small colon enterotomy and abrasion in horses treated or not with systemic heparin. Were used ten horses with a mean age of 9 ± 3.87 years and 358 ± 30,28 body weight, divided into two groups of five animals: one control group (CG) and the other treated (TG). Both groups underwent laparotomy and small colon enterotomy via right paralumbar flank in standing position and received flunixin meglumine, gentamicin and penicillin association. TG received also heparin (150 IU / kg SC BID, 5 days). Animals were evaluated for physiological parameters, hemogram, fibrinogen, coagulation markers, serum and peritoneal acute phase proteins, peritoneal fluid macroscopic, physico-chemical and cytological characteristics, peritoneal concentrations of tissue plasminogen activator and inhibitor and d-dimer. Assessments were performed prior to enterotomy-M0, M1-12 hours after enterotomy; M2 - 1 day, M3 - 2days; M4 - 4days; M5 - 6 days; M6-10 days and M7 - 14 days after the enterotomy. Heparin resulted in anemia and decreased platelet counts, increased in partial thromboplastin activated time and increased serum and peritoneal acute phase proteins, however, resulted in decreased formation of fibrin clots and d dimer formation. After 15 days of enterotomy, laparoscopic examination showed no difference in fibrin deposition between the groups, and a slight diffuse peritoneal reactivity higher to treated group. So, heparin showed as negative effect the development of anemia, significant decrease in platelet count and acting as a proinflammatory agent, however shown to reduce fibrin deposition and formation ...
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Alonso, Juliana de Moura. "Avaliação da reatividade peritoneal de equinos submetidos à enterotomia de cólon menor e tratados com heparina pela via subcutânea /." Botucatu, 2013. http://hdl.handle.net/11449/89147.
Full textAbstract:
Orientador: Carloa Alberto HussniBanca: Armen Thomassian
Banca: Luis Cláudio Lopes Corrêa da Silva
Resumo: As afecções do cólon menor são causas frequentes de síndrome cólica, sendo a enterotomia rotineiramente empregada para a remoção de fecalitos, enterólitos e corpos estranhos. O trauma cirúrgico resulta em inflamação difusa e ocorrência de peritonite asséptica devido à manipulação e ao acesso cirúrgico. Objetivou-se estudar a reatividade peritoneal após a realização de enterotomia e abrasão do cólon menor em equinos tratados ou não com heparina sistêmica. Foram utilizados dez equinos com idade média de 9 ± 3,87anos e 358 ± 30,28 Kg de massa corporal, divididos em dois grupos de cinco animais, sendo um grupo o controle (GC) e o outro tratado (GT). Ambos os grupos foram submetidos à laparotomia e enterotomia de cólon menor através da via paralombar direita em posição quadrupedal e receberam flunixin meglumine, gentamicina e associação de penicilinas. Ao GT, acrescentou-se heparina (150 UI/Kg SC, BID, 5 dias). Os animais foram avaliados quanto ao exame físico; hemograma; fibrinogênio; coagulograma; proteínas de fase aguda, séricas e peritoneais; características macroscópicas, físico-químicas e citológicas do líquido peritoneal; concentrações peritoneais do ativador e inibidor do plasminogênio tecidual e dímero D. Para tanto, pradonizaram-se os seguintes momentos de avaliação: M0-prévio à enterotomia; M1-12 horas; M2 - 1dia, M3- 2dias, M4- 4dias e M5- 6 dias; M6- 10 dias e M7- 14 dias após a enterotomia. Observou-se que a heparina resultou em anemia e diminuição da contagem de plaquetas, aumento do tempo de tromboplastina parcial ativada e aumento nas concentrações séricas e peritoneais das proteínas de fase aguda, entretanto diminuiu a formação de dímeros D, sugerindo diminuição da formação de coágulos de fibrina. Após 15 dias da enterotomia, realizou-se o exame laparoscópico, que não demonstrou diferença na deposição de fibrina entre os grupos, entretanto ...
Abstract: Small colon affections are frequent causes of abdominal pain, and enterotomy is routinely employed for removal of fecalith, enteroliths and foreign bodies. Surgical trauma results in diffuse inflammation and aseptic peritonitis occurrence due to handling and surgical access. The aim of this study was to evaluate peritoneal reactivity after small colon enterotomy and abrasion in horses treated or not with systemic heparin. Were used ten horses with a mean age of 9 ± 3.87 years and 358 ± 30,28 body weight, divided into two groups of five animals: one control group (CG) and the other treated (TG). Both groups underwent laparotomy and small colon enterotomy via right paralumbar flank in standing position and received flunixin meglumine, gentamicin and penicillin association. TG received also heparin (150 IU / kg SC BID, 5 days). Animals were evaluated for physiological parameters, hemogram, fibrinogen, coagulation markers, serum and peritoneal acute phase proteins, peritoneal fluid macroscopic, physico-chemical and cytological characteristics, peritoneal concentrations of tissue plasminogen activator and inhibitor and d-dimer. Assessments were performed prior to enterotomy-M0, M1-12 hours after enterotomy; M2 - 1 day, M3 - 2days; M4 - 4days; M5 - 6 days; M6-10 days and M7 - 14 days after the enterotomy. Heparin resulted in anemia and decreased platelet counts, increased in partial thromboplastin activated time and increased serum and peritoneal acute phase proteins, however, resulted in decreased formation of fibrin clots and d dimer formation. After 15 days of enterotomy, laparoscopic examination showed no difference in fibrin deposition between the groups, and a slight diffuse peritoneal reactivity higher to treated group. So, heparin showed as negative effect the development of anemia, significant decrease in platelet count and acting as a proinflammatory agent, however shown to reduce fibrin deposition and formation ...
Mestre
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Araujo, Graziela Silveira. "Avaliação de alguns parametros da fibrinolise e do fator XIII em pacientes com trombose venosa profunda espontanea e doença hemorragica." [s.n.], 2008. http://repositorio.unicamp.br/jspui/handle/REPOSIP/310159.
Full textAbstract:
Orientador: Joyce Maria Annichino-BizzacchiDissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas
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Resumo: Em uma parcela de pacientes com quadro clínico hemorrágico ou trombótico, nenhum diagnóstico etiológico é estabelecido. Os pacientes com doença hemorrágica, muitas vezes importante, podem apresentar todos os exames de triagem e dosagem específica de fatores da coagulação dentro dos valores da normalidade. OBS.: O resumo na integra poderá ser visualizado no link ou texto completo da tese digital
Abstract: In a parcel of patients with hemorrhagic or thrombotic clinical picture, none etiologic diagnosis is established. The patients with hemorrhagic desorder, many times important, can present all inside the screening tests and specific dosage of factors of the coagulation of the values of normality. Note: the complete abstract is avaiable with the link or full eletronic digital theses or dissertations
Mestrado
Biologia Estrutural, Celular, Molecular e do Desenvolvimento
Mestre em Fisiopatologia Médica
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De, Lange Zelda. "Global fibrinolytic potential of black South Africans in the North West Province / Z. de Lange." Thesis, North-West University, 2013. http://hdl.handle.net/10394/9645.
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INTRODUCTION AND AIM
The prevalence of cardiovascular disease (CVD) has increased significantly in the black South African population in recent years. Early in the development of CVD, atherosclerotic plaques form in the vessel wall. When this plaque becomes unstable and ruptures, the coagulation cascade is activated and a blood clot forms. The function of this clot is to stop bleeding. However, it cannot remain in the vasculature indefinitely and has to be lysed again. The ability of the body to lyse clots can be measured with global fibrinolytic potential (GFP) assays and expressed as lysis time. Increased clot lysis time (CLT) has been shown to be significantly associated with various CVD risk factors and CVD events in Caucasian populations while very little information is available for other ethnicities. In this study we investigated plasma GFP and its relation to CVD risk factors in a large black African population. We also determined the effect of three polymorphisms in the promoter area of the plasminogen activator inhibitor-1 (PAI-1) gene on PAI-1act (activity) levels (a main determinant of CLT) and CLT, together with gene-environment interactions and the effect of urbanisation on these interactions.
PARTICIPANTS AND METHODS
Apparently healthy men and women between the ages of 35 and 65 years were recruited to take part in the South African arm of the Prospective Urban and Rural Epidemiology (PURE) study. Approximately 1000 rural and 1000 urban black African individuals participated. Data and samples were collected during a 12-week collection period in 2005 for cross-sectional analysis.
RESULTS
Increased PAI-1act levels, body mass index (BMI), glycosylated haemoglobin (HbA1c), triglycerides, fibrinogen concentration, C-reactive protein, female sex, positive HIV-status and the metabolic syndrome were all associated with prolonged CLTs, while increased habitual alcohol consumption was associated with shorter iv
CLTs. Urban-rural differences for CLT existed in women only. This is likely due to the larger extent of rural-urban differences in other CVD risk factors observed in women compared to what was observed in men. Of the CVD risk factors measured, PAI-1 explained the largest proportion of the variance in CLT (27%). Owing to the important role PAI-1act plays in CLT, we investigated three polymorphisms in the PAI-1 gene promoter area (the 4G/5G polymorphism, the novel SNP C428T and SNP G429A (previously identified)), and the influence of these polymorphisms on PAI-1act levels and CLT. The frequency of the 5G allele was high (0.85) in comparison with previously reported literature. PAI-1act increased significantly across genotypes in the urban (5G/5G: 3.84 U/ml; 4G/5G: 4.85 U/ml; 4G/4G: 5.96 U/ml p=0.009) but not the rural subgroup, while CLT did not differ. We found significant interactions between the 4G/5G polymorphism and BMI, waist circumference and triglycerides in determining PAI-1act, and between the 4G/5G polymorphism and fibrinogen and fibrinogen gamma prime in determining CLT. Direct relationships with PAI-1act or CLT were not found for the C428T and G429A polymorphisms; they did, however, influence associations of other environmental factors with PAI-1act and CLT. Several of these interactions differed significantly between rural and urban subgroups, particularly in individuals harbouring the mutant alleles.
CONCLUSION
CLT associated with many of the same CVD risk factors described in the literature for Caucasian populations, but also with other risk factors. Rural-urban differences in CLT are dependent on the association of CLT with other CVD risk factors in the rural-urban setting. Genetic polymorphisms of the PAI-1 gene did not directly influence CLT, despite influencing PAI-1act. The main contributor to PAI-1act variance, however, was (central) obesity. The effect of the 4G/5G polymorphism on PAI-1act, as well as gene–environment interactions for the C428T and G429A genotypes in determining PAI-1act and CLT, were significantly influenced by urbanisation.Thesis (PhD (Nutrition))--North-West University, Potchefstroom Campus, 2013.
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Santos, Izabela Ribeiro. "Avaliação dos níveis de TAFI (inibidor da fibrinolise ativado pela trombina), do PAI-1 (inibidor do ativador do plasminogênio tipo 1) e frequência de seus polimorfismos na dislipidemia." Universidade Federal de Minas Gerais, 2013. http://hdl.handle.net/1843/BUOS-9C6GDL.
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Cardiovascular diseases are a public health concern with high morbidity and mortality, affected by risk factors such as diabetes mellitus, smoking, physical inactivity, hypertension, obesity and dyslipidemia. Dyslipidemia is defined as alterations in lipid metabolism that change the levels of lipoproteins, constituting a major risk factor for atherosclerosis and its complications. Moreover, it affects the haemostatic system, especially in the fibrinolysis. Several proteins comprising the fibrinolytic system regulates fibrinolysis by acting indirectly on the degradation of the fibrin clot, specially the inhibitor by Thrombin Activatable Fibrinolysis Inhibitor (TAFI) and Plasminogen Activator Inhibitor type 1 (PAI-1). Increased levels of TAFI have been associated with cardiovascular events, as well as increased serum PAI-1, which is already considered as a risk factor for such events. This study evaluated the association of acquired risk factors, the polymorphisms Thr325Ile, Ala147Thr and +1542C/G in the TAFI gene and 4G/5G in the PAI-1 gene and its plasma levels with dyslipidemia through the investigation of 109 dyslipidemic and 105 normolipemic individuals. We conducted analyses of biochemical and lipidic profile, as well as hemostatic parameters (TAFI and PAI-1 by ELISA) and molecular analysis using Polymerase Chain Reaction (PCR) to verify the genotypic and allelic frequencies for the polymorphisms studied. It was observed that hypertension, increased body mass index and menopause are more common in dyslipidemic individuals and they have higher TAFI levels. The alleles 325Ile, Ala147 and C showed association with lower TAFI levels. Ala147Thr and Thr325Ile polymorphisms are independently associated with dyslipidemia in males. The 4G/5G polymorphism and PAI-1 levels were not related with the disease. The results suggest that only TAFI may be independently associated with dyslipidemia.As doenças cardiovasculares constituem um problema de saúde pública, com morbidade e mortalidade elevadas, afetadas por fatores de risco associados, como o diabetes mellitus, tabagismo, sedentarismo, hipertensão arterial, obesidade e as dislipidemias. Estas se definem como alterações do metabolismo lipídico que modificam os níveis das lipoproteínas, constituindo um dos principais fatores de risco para a aterosclerose e suas complicações. A dislipidemia influencia o sistema hemostático, especialmente na redução da fibrinólise. Várias proteínas compõem o sistema fibrinolítico e regulam a fibrinólise ao atuarem indiretamente na degradação do coágulo de fibrina, em especial o Inibidor da Fibrinólise Ativado pela Trombina (TAFI) e o Inibidor do Ativador do Plasminogênio Tipo 1 (PAI-1). Níveis aumentados de TAFI têm sido associados aos eventos cardiovasculares, assim como o aumento da concentração plasmática de PAI-1, o qual já é considerado, na literatura, como um fator de risco para estes eventos. Este estudo avaliou a associação de fatores de risco adquiridos, dos polimorfismos Thr325Ile, Ala147Thr e +1542C/G no gene TAFI e 4G/5G no gene PAI-1 e seus níveis plasmáticos com a dislipidemia investigando 109 indivíduos dislipidêmicos e 105 normolipêmicos. Foram realizadas análises bioquímicas do perfil lipídico e análises hemostáticas dos parâmetros TAFI e PAI-1 pelo método de ELISA, bem como análises moleculares, pela técnica de Reação em Cadeia da Polimerase (PCR), para verificar as frequências genotípicas e alélicas para os polimorfismos estudados. Foi observado que, dentre os fatores de risco, a hipertensão, o aumento do índice de massa corporal e a menopausa são mais frequentes em indivíduos dislipidêmicos e estes possuem maiores níveis de TAFI. Os alelos 325Ile, Ala147 e C foram associados a menores níveis plasmáticos da proteína. Os polimorfismos Thr325Ile e Ala147Thr demonstraram associação independente com a dislipidemia em indivíduos do sexo masculino. Para o polimorfismo 4G/5G e os níveis de PAI-1 não foi encontrada a mesma relação com a doença. Os resultados sugerem que apenas o TAFI está associado independente à dislipidemia.
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Moraes, Samira Lauar de. "Estudo de alguns parametros da coagulação e fibrinolise no hipertireoidismo e hipotireoidismo : avaliação da importancia da via beta adrenergico nas alterações dos fatores VIII e de von Willebrand em modelos experimentais." [s.n.], 1996. http://repositorio.unicamp.br/jspui/handle/REPOSIP/310162.
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Orientador: Joyce Maria Annichino BizzacchiDissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
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Resumo: Não informado
Abstract: Although clinically important abnormalities of hemostasis are unusual in patients with thyroid disease, coagulation and fibrinolytic systems are, nonetheless affected by hormone alterations. Patients with hypothyroidism may present abnormal bleeding. The precise nature of the "ohemostatic defect was explained by a decrease in several coagulation factors, an increase in fibrinolytic activity and an abnormal platelet adhesiveness. If the hypercoagulable state contributes to increase the risk of thromboembolic complications in hypothyroid patients, the relatively increased fibrinolytic activity in such patients probably has a protective role. Although precise statistics are not available, thromboembolic disorders do not seem to be common in patients with hyperthyroidism. These' patients showed a specific elevation of the factors VIII and von Willebrand and a reduction in plasma fibrinolytic activity. Maybe, hyperdynamic circulation may counterbalance these potential hypercoagulable changes. One of the hypothesis for elevated anti-hemophilic factor activity in hyperthyroidism is based on the fact that epinephrine infusion in normal subjects is followed by elevated levels of hemostasis changes that have been reported and not yet adequately explained. The aim of this study was to evaluate components of contact phase, coagulation, natural factor VIII activity, and hyperthyroid subjects which have an increased sensitivity to the etfects of cathecolamines. An experimental model with dogs before and after hypothyroidism induction was performed in order to study the importance of the f3 adrenergic receptors in levels of factor VIII and von Willebrand. During the clinic phase ofthis study, we analyzed 33 untreated hyperthyroid patients (mean age 39:!:13 years old), 20 hypothyroid patients (mean age 23:t6 years). Ali patients were female. Twenty nine female euthyroid subjects (mean age 48:!:18 years) were the control Group. The following was analyzed: activated Partial Thromboplastin Time (APTT), Prothrombin Time (TP), Thrombin Time (TT), Factors V, Vil, VIll , XI and XII, Fibrinogen, Protein C (PC), Protein S (PS), Cl-inhibitor (C 1), alpha 2-macroglobulin (alpha-2), prealbumin and von Willebrand factor, Plasmatic prekallikrein (PK), triiodothyronine (T3 ), tetraiodothyronine (T 4) total and tree, TSH and TSHus. Only ~actor XII and the a. 2-macroglobulin were decreased during the contact phase in hypothyroid patients. We do not believe that tlfts decrease in factor XII levels is due to the reduction on protein synthesis. We have determined other coagulation factors; they are more sensitive to alterations in hepatic proteins synthesis, like factor Vil and PK. They were not altered in hypothyroid patients. The decrease of a. 2 macroglobulin in hypothyroid patients could represent a regulatory mechanism against fybrinolysis. Both factor VIII and von Willebrand were increased in hyperthyroid patients. These factors were similar in the hypothyroid and the control group. Final common pathway parameters and fibrinogen did not show a significant difference between the three groups...Note: The complete abstract is available with the full electronic digital thesis or dissertations
Mestrado
Clinica Medica
Mestre em Medicina
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Tremblay, Isabelle. "Érythropoïétine et fibrinolyse intrarénale /." Thèse, Trois-Rivières : Université du Québec à Trois-Rivières, 1999. http://www.uqtr.ca/biblio/notice/resume/03-2200554R.html.
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Tremblay, Isabelle. "Érythropoïétine et fibrinolyse intrarénale." Thèse, Université du Québec à Trois-Rivières, 1999. http://depot-e.uqtr.ca/3585/1/000658989.pdf.
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Siguret, Virginie. "Fibrinolyse et maladie de Buerger : à propos de 16 cas." Paris 5, 1990. http://www.theses.fr/1990PA05P209.
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Leithäuser, Renate. "Blutgerinnung und Fibrinolyse bei hochintensiver Kurzzeitbelastung." [S.l.] : [s.n.], 2003. http://www.diss.fu-berlin.de/2003/267/index.html.
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LAURENCE, MICHEL. "Etude de la fibrinolyse dans les hyperlipoproteinemies." Aix-Marseille 2, 1989. http://www.theses.fr/1989AIX20359.
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Lormeau, Boris. "Fibrinolyse et diabete sucre : role de l'hyperinsulinisme." Amiens, 1991. http://www.theses.fr/1991AMIEM053.
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Frossard, Marie Carole Mougel Eric. "Prise en charge des accidents vasculaires cérébraux aux urgences de l'hôpital de Remiremont étude sur 50 cas /." [S.l.] : [s.n.], 2008. http://www.scd.uhp-nancy.fr/docnum/SCDMED_T_2008_FROSSARD_MARIE_CAROLE.pdf.
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Willich, Tobias R. "Entwicklung und Evaluation eines Fibrinolyse-Globaltestes "Fibrinolytische Kapazität"." [S.l.] : [s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=975008331.
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Willich, Tobias R. "Entwicklung und Evaluation eines Fibrinolyse-Globaltestes "Fibrinolytische Kapazität"." Doctoral thesis, Humboldt-Universität zu Berlin, Medizinische Fakultät - Universitätsklinikum Charité, 2005. http://dx.doi.org/10.18452/15251.
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Es wurde ein zweistufiger, indirekter enzymatischer Assay (Fibrinolytische-Kapazität, FC) in zwei Varianten (basal, aktiviert) vorgestellt, der summarisch Störungen der Fibrinolyse erfasst, da in ihn die Gesamtaktivität der Aktivatoren und Inhibitoren des Plasmas einfließt. In der ersten Stufe wird Plasma Urokinase zugeführt, welche mit Plasminogenaktivatorinhibitoren interagiert. Die noch freie Urokinase aktiviert Plasminogen zu Plasmin. Die plasmatischen Antiplasmine, hauptsächlich alpha 2-Antiplasmin, werden oxidativ mit Taurin-Chloramin inaktiviert. Schließlich wird die resultierende Plasminmenge mit einem chromogenen Substrat quantifiziert. In einer zweiten Variante wird die kontaktphasenabhängige Fibrinolyse vorher sehr potent mit Dextransulfat stimuliert. Zur Validierung wurde der Einfluss von PAI-1, Fibrinogen und Plasminogen untersucht. Störgrößen wie Antioxidantien, parenterale Antikoagulantien, Phenprocoumon, Aprotinin, Tranexamsäure, Thrombozyten und Bilirubin wurden ebenfalls untersucht. Zusätzlich wurde der Test anhand eines Normal-, Thrombose- und Schwangerenkollektives sowie zweier kleiner Kollektive (Schwangere und Patienten unter oraler Antikoagulation) im Zeitverlauf untersucht. Beide FC-Varianten bilden dabei die prothrombotischen Faktoren unterschiedlich ab. In der Regressionsanalyse reagiert die basale FC eher auf Veränderungen der PAI-1- und Plasminogenkonzentrationen, die aktivierte FC eher auf Plasminogen und Thrombose. Thrombose wird durch die aktivierte FC besser als durch die basale FC diagnostiziert (beta-Koeffizienten für Thrombose -0,12 vs. -0,26, Zusammenhangsmaß Eta² von FC und Thrombose 5,6% vs. 9,9%, Entscheidungsgrenze (Cut-Off) für Thrombose 33,0% vs. 66,2% für basale bzw. aktivierte FC). Beide FC-Varianten besitzen ähnliche Sensitivität, Spezifität, prädiktive Werte und relative Risikos für Thrombose bei FC-Werten unterhalb der Entscheidungsgrenze. Die Thromboseerkennbarkeit ist für beide Varianten gleichwertig bei einer Übereinstimmung untereinander von 61,3% (Cohen-Kappa-Koeffizient). Bei der Abklärung einer akuten Thrombose ist dieser Fibrinolyse-Globaltest in der Lage, Ursachen innerhalb des fibrinolytischen Systems zu erkennen.A two-step indirect enzymatic assay (fibrinolytic capacity, FC) was presented in two variations (basal, activated) detecting the total fibrinolytic disturbances by its ability to assess the entire plasmatic activity of activators and inhibitors. In the first step urokinase is added to plasma, which interacts with plasminogen-activator-inhibitors. The remaining urokinase activated plasminogen to plasmin. The plasmatic antiplasmines, mainly alpha 2-antiplasmine were oxidative inhibited with taurine-chloramine. Finally the resulting amount of plasmin was quantified using a chromogenic substrate. In a second variation the contact-phase fibrinolysis was highly stimulated with dextran-sulfate. The influence of PAI-1, fibrinogen and plasminogen were analysed including disturbing substances such as antioxidants, parenteral anticoagulants, phenprocoumon, aprotinine, tranexamic acid, platelets and bilirubine. In addition, validation was performed including healthy individuals, patients with thrombosis and pregnant women and two small cohorts (pregnant women and patients under oral anticoagulation) over time. The prothrombotic factors were differently represented by the two FC-variations. In the regression analysis the basal FC reacted predominantly to alterations in the concentration of PAI-1 and plasminogen. In contrast the activated FC was more likely affected by plasminogen and thrombosis. The activated FC was more sensitive in the detection of thrombosis than the basal FC (with a beta-coefficient for thrombosis -0,12 vs. -0,26, a coefficient of strength of association eta² from FC with thrombosis 5,6% vs. 9,9% and a cut-off for thrombosis 33,0% vs. 66,2% for basal and activated FC respectively). Below these cut-offs both FC-variations had equal sensitivity, specificity, predictive values and relative risks in the detection of thrombosis by FC-values. The ability to detect thrombosis were equally with a correspondence of 61,3% (Cohen-Kappa-coefficient). This fibrinolytic global-test is able to identify the underlying cause within the fibrinolytic system for the a clarification of acute thrombosis.
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GABRIEL, ANDRE. "Fibrinolyse in situ dans les thromboses arterielles peripheriques." Clermont-Ferrand 1, 1990. http://www.theses.fr/1990CLF13818.
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Brun, Cécile. "Etude de la fibrinolyse chez le sujet âgé." Paris 5, 1993. http://www.theses.fr/1993PA05P245.
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DESDAMES, ARIANE. "Fibrinolyse et grossesse : a propos de 3 observations." Lille 2, 1989. http://www.theses.fr/1989LIL2M133.
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Bastard, Christophe Gacem Karim. "La fibrinolyse intrapéricardique présentation d'un cas clinique et revue de la littérature /." [S.l.] : [s.n.], 2005. http://theses.univ-nantes.fr/thesemed/bastardMED05.pdf.
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MONTAIGNE, ANNE. "Traitement fibrinolytique chez le sujet age : a propos de 10 observations de patients ages de 75 ans et plus." Lille 2, 1989. http://www.theses.fr/1989LIL2M054.
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Gaussem, Pascale. "L'inhibiteur spécifique de l'activateur tissulaire du plasminogène : aspects biochimiques, biologiques et cliniques." Paris 13, 1991. http://www.theses.fr/1991PA132005.
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L'activateur tissulaire du plasminogène (t-pa) est le principal activateur du systeme fibrinolytique. Le t-pa est synthétisé par la cellule endothéliale et libère sous l'action de divers stimulus. Il possède une forte affinité pour la fibrine qui lui permet de transformer in situ le plasminogène en plasmine, enzyme fibrinolytique active. En revanche, libéré dans la circulation, le t-pa est immédiatement neutralise en formant un complexe stable avec son inhibiteur spécifique, le pai-1. Le pai-1 plasmatique est décrit sous deux formes biologiques: une forme active et une forme latente activable par le sds. Nous avons étudié les interactions entre ces protéines et le sds. Nos résultats ont montre que le pai-1 traite par le sds n'est pas active mais dénaturé comme le prouve son incapacité à former des complexes avec le t-pa. Par ailleurs, les complexes t-pa-pai-1 sont dissocies après traitement par le sds, ce qui suggère l'absence de liaison de covalence dans le complexe. Nous avons ensuite développé une méthode de dosage du pai-1 plasmatique adaptable au diagnostic biologique des états d'hypofibrinolyse. Dans un deuxième temps, nous avons mis au point une méthode globale d'exploration de la fibrinolyse basée sur la mesure de la lyse d'un caillot plasmatique, que nous avons appliquée à l'exploration de patients ayant une pathologie thromboembolique
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Cointe, Sylvie. "Microparticules : activité fibrinolytique dans le choc septique et approche innovante de standardisation." Thesis, Aix-Marseille, 2015. http://www.theses.fr/2015AIXM5504.
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Les microparticules sont des vésicules extracellulaires qui résultent du remodelage des phospholipides membranaires en réponse à une activation ou une apoptose. La vision initiale leur attribuant une activité uniquement procoagulante s’avère plus complexe, par la mise en évidence d'une activité plasminogénolytique portée par les MPs endothéliales, tumorales et leucocytaires (MPLs). Au cours de ce travail, nous avons démontré un nouveau mécanisme impliquant les MPLs comme des vecteurs d’une activité fibrinolytique capable de lyser un thrombus fibrino-plaquettaire en fonction de leur activité de génération de plasmine. Cette activité s’intègre dans un rôle protecteur des MPs capable de contrebalancer le risque de microthromboses associé au choc septique. Cette activité fibrinolytique identifie les MPs comme des biomarqueurs déterminants pour le pronostic vital mais aussi comme des cibles thérapeutiques potentielles, pouvant être à l’origine de biothérapies vésiculaires basées sur la génération de MPs fibrinolytiques de grade clinique. L’évaluation du bénéfice apporté par les MPs est actuellement limitée par un manque de standardisation. Dans une seconde partie de ce travail, nous avons proposé une nouvelle stratégie de standardisation de la cytométrie en flux. Cette stratégie a été évaluée dans le cadre d'une étude multicentrique internationale qui a montré pour la première fois l’absence de différence significative des numérations des MPs entre des instruments de configuration optique différente. Maitriser des protocoles standardisés est une étape indispensable pour accélérer le transfert de ces innovations diagnostiques et thérapeutiques au lit du patientThe microparticles are extracellular vesicles resulting from the remodeling of membrane phospholipids in response to activation or apoptosis. The initial vision only assigning a procoagulant activity is more complex, by highlighting a range plasminogenolytic activity by endothelial, tumor and leukocyte (MPLS) MPs. In this work, we demonstrated a novel mechanism involving MPLS as vectors fibrinolytic activity able to lyse a fibrin-platelet thrombus on the basis of generation of plasmin activity. This activity is part of a protective role of MPs which may counterbalance the risk of microthromboses associated with septic shock. This fibrinolytic activity identifies MPs as key biomarkers for prognosis but also as potential therapeutic targets that can be the source of vesicular biotherapies based on generation of fibrinolytic MPs of clinical grade. The evaluation of the benefit provided by MPs is currently limited by a lack of standardization. In the second part of this work, we proposed a new strategy for standardization of flow cytometry. This strategy was evaluated in a multicenter international study that showed for the first time no significant difference in MPs counts between different optical configuration tools. To master standardized protocols is a necessary step to improve the transfer of these diagnostic and therapeutic innovations to the patient
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Mombelli, Giorgio. "Aktivierung der Gerinnung und Fibrinolyse bei nicht thromboembolischen Krankheiten /." [Bern] : [Universität Bern], 2000. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.
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Hanss, Michel. "Recherche d'anomalies de la fibrinolyse chez l'homme et applications." Lyon 1, 2002. http://www.theses.fr/2002LYO1T185.
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La 4e de couverture indique : "La fibrinolyse permet entre autre la destruction du thrombus. Son dérèglement contribue à la survenue de pathologies thrombotiques et hémorragiques. Nous avons mis en place une exploration de la fibrinolyse plasmatique chez l'homme. La nature moléculaire d'un déficit familial en antiplasmine est différente des 5 cas décrits dans la littérature. Ces mutations privées nécessitent donc d'être identifiées et caractérisées pour préciser l'hétérogénéité d'expression clinique. Cependant la mesure de cet inhibiteur doit répondre à des critères élémentaires de qualité comme nous l'avons proposé au cours du travail collaboratif effectué sous l'égide de la Société Internationale de Thrombose et d'Hémostase. Au cours de l'insuffisance hépatique, les anomalies biologiques attendues nous ont conduit à proposer une limitation du risque hémorragique par des techniques anatomiquement moins invasives que celles habituellement utilisées. Au cours des thrombopénies, une augmentation de la fibrinolyse a été notée, qui peut correspondre à une réactivité endothéliale exacerbée ou à un déficit acquis en inhibiteur, et justifie un traitement préventif par antifibrinolytique. Au contraire, l'hypofibrinolyse trouvée au cours des fécondations in vitro peut participer à l'augmentation du risque thrombotique chez ces patientes et être suivi à titre préventif. La valeur diagnostique de l'urokinase trouvée en pathologie hépatique carcinomateuse a été confirmé par les études ultérieures. Certains variants humains du fibrinogène affectant plus particulièrement la fibrinolyse, le recensement permanent de ces anomalies sous forme d'une base de données à vocation et à portée internationales permet de grouper les cas similaires afin d'appréhender le risque encouru en termes de thrombose ou d'hémorragie, risque non systématique et nécessitant des abords thérapeutiques opposés pour une maladie d'apparence monomorphe. "
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Zöllner, Sabine. "Das fibrinolytische System bei Niereninsuffizienz möglicher Mediator vaskulärer Erkrankungen." Bochum Paragon-Verl, 2008. http://d-nb.info/989384209/04.
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Daumüller, Tobias. "Lokale Katheterlyse bei submassiver Lungenembolie unter besonderer Berücksichtigung des Fountain-Katheter-Systems - Akut- und Langzeitverlauf." [S.l. : s.n.], 2008. http://nbn-resolving.de/urn:nbn:de:bsz:289-vts-63465.
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Fille, Alexandre. "Activite fibrinolytique du plasma chez le sujet masculin hypogonadique : interet d'un traitement par androgenes." Toulouse 3, 1991. http://www.theses.fr/1991TOU31516.
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KOUCHOUK, ALAIN. "La coagulation post-morten : revue bibliographique." Lille 2, 1989. http://www.theses.fr/1989LIL2M284.
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Hourdin, Séverine. "Propriétés fibrinolytiques des carbones après traitement biologique et électrochimique." Cergy-Pontoise, 2002. http://www.theses.fr/2002CERG0171.
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L'utilisation de matériaux en contact avec le sang est souvent limitée par la formation d'un thrombus suite à l'adsorption rapide des protéines plasmatiques. Une des stratégies développée pour diminuer le caractère thrombogène des matériaux consiste à élaborer une surface adsorbant préférentiellement le plasminogène, principal zymogène de la fibrinolyse. L'objectif de ce travail est d'améliorer les propriétés fibrinolytiques du carbone par traitements biologique et électrochimique. Cet objectif implique de mieux connaître la stabilité thermique de la plasmine (forme active du plasminogène) adsorbée spontanément sur des surfaces de carbone en présence d'un substrat chromogène (S-2251). Les modifications consistent à adsorber spontanément une couche de fibrinogène, oxydé électrochimiquement ou non, ainsi qu'à déposer des films de Langmuir-Blodgett hydrophiles ou hydrophobes de natures différentes. Nous avons mis en évidence une transition cinétique du 1er ordre de l'activité amidolytique de la plasmine adsorbée. Nous avons ensuite étudié l'effet de l'application d'un potentiel électrique sur du graphite supportant à la fois du fibrinogène et de la plasmine. Les résultats montrent que la présence de fibrinogène favorise l'activité amidolytique de la plasmine adsorbée lorsqu'elle a été soumise à des potentiels anodiques. Pour étudier les propriétés fibrinolytiques de ces surfaces, nous avons vérifié que le plasminogène adsorbé conservait sa capacité à se convertir en plasmine en présence de t-PA (principal activateur physiologique du plasminogène). Dans ce but, la surface de graphite modifiée par adsorption de fibrinogène a été exposé à du plasma puis placée en présence de t-PA, de fibrinogène et d'un substrat chromogène plus sensible (S-2403). Les expériences montrent que l'application de potentiels électriques à la sous-couche de fibrinogène est susceptible d'intervenir indirectement sur les propriétés fibrinolytiques du matériauThe use of material in contact with blood is limited primarily because of rapid adsorption of plasma proteins followed by thrombus formation. One strategy for decreasing the thrombogenicity of the implant is to develop a material which preferentially adsorbs plasminogen, principal zymogen of the fibrinolytic pathway. The aim of this work is to improve the fibrinolytic properties of carbon by different biological and electrochemical treatments. To document this aspect, the thermal behavior of plasmin (the active form of plasminogen) following its spontaneous adsorption onto bare and modified graphite and glassy carbons was studied in the presence of a chromogenic substrate (S-2251). Surfaces were modified with a coating of fibrinogen either electrochemically oxidized or not. Deposition of Langmuir-Blodgett films onto the former surfaces was also performed, thus leading to either hydrophobic or hydrophilic surfaces. In all cases, results show the occurrence of a first order kinetic transition of the adsorbed plasmin. The effect of the application of electrical potentials on graphite modified by fibrinogen and plasmin was also studied. Results show that fibrinogen favors the catalytic activity of plasmin when anodic potentials are applied. To study the fibrinolytic properties of these surfaces, we verified that the adsorbed plasminogen could always convert to plasmin in the presence of t-PA (the principal physiological activator of plasminogen). In this purpose, fibrinogen-modified graphite surface was exposed to plasma and then placed in the presence of t-PA, fibrinogen and a more sensible chromogenic substrate (S-2403). Experiments demonstrate that the application of electrical potentials to the fibrinogen coating can indirectly affect the fibrinolytic properties of the material. Especially in the case of anodic potentials, the amidolytic activity of the generated plasmin is significantly enhanced. This activity is ten times higher at a particular potential value
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Gautier-Morel, Sophie. "Complications hémorragiques induites au cours de la fibrinolyse par rtPA : mécanismes physiopathologiques et approches pharmacologiques." Lille 2, 2005. http://www.theses.fr/2005LIL2S005.
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Le mécanisme des complications hémorragiques cérébrales induites lors de l’utilisation du rtPA, activateur du plasminogène dans les accidents ischémiques cérébraux, est mal élucidé. En utilisant un modèle d’ischémie cérébrale par occlusion intraluminale de l’artère cérébrale moyenne, notre objectif a été d’étudier l’implication du thrombus, de la paroi vasculaire et de l’ischémie dans la physiopathologie de ces complications. Dans un deuxième temps, les potentielles cibles pharmacologiques pour leur prévention ont été étudiées. Nos données suggèrent que le traitement par rtPA conduit à la survenue de complications hémorragiques, et que la présence de produits de thrombolyse, en particulier de plasmine, majore la sévérité de ces complications, en parallèle d’une augmentation du volume d’infarctus, d’une majoration des altérations de la fonction endothéliale vasculaire et d’une augmentation dela perméabilité de la barrière hémato-encéphalique. Cette modification de la perméabilité est associée à une modification de l’expression des metalloproteases, enzymes impliquées dans la dégradation de la matrice extracellulaire des vaisseaux, et conduit à une modification de l’infiltration des polynucléaires neutrophiles. En ce qui concerne les cibles pharmacologiques potentielles, deux voies ont été explorées : (i) l’induction d’une neutropénie par la vinblastine prévient les altérations endothéliales vasculaires post-ischémiques et protége de la survenue des complications hémorragiques de la fibrinolyse en association avec une diminution du volume d’infarctus (ii) le fénofibrate, agoniste des récepteurs PPARs, protège des altérations endothéliales vasculaires post-ischémiques, en parallèle d’une diminution des lésions ischémiques et d’une diminution de l’apparition des complications hémorragiques. En conclusion, la protection du vaisseau lors de la fibrinolyse semble être une cible pharmacologique pertinente pour prévenir le risque de complicationshémorragiques induites par le rtPAThe use of rtPA (tissue-plasminogen recombinant activator) in stroke is associated with a risk of cerebral hemorrhagic complications, whom physiopathological mechanisms are not fully elucidated. Using a model of cerebral ischaemia by middle cerebral artery occlusion (MCAO), our objective was to firstly study the respective implication of thrombus, vascular wall and ischaemia in the physiopathology of rtPA-induced hemorrhages. Secondly, potential pharmacological targets for their prevention were studied. Our data confirmed that the treatment by rtPA led to hemorrhagic complications and suggested the role of thrombolysis products, in particular of plasmine, in the severity of these complications. In parallel, we observed an increase in the infarct volume, an increase in the vascular endothelial post-ischemic alterations and an increase in the blood-brain barrier (BBB) permeability. Th e modification of the BBB permeability was associated with an activation of metalloproteinase-9, enzyme implied in the matrix extracellular degradation, and contributed to the polymorphonuclear infiltration. Concerning the potential pharmacological targets, two pathways were explored : (i) the induction of a neutropenia by vinblastine prevented from post-ischaemic vascular alterations and limited the risk of rtPA-induced hemorrhagic complications in parallel to a reduction in the infarct volume (ii) the use of fenofibrate, agonist of the PPAR alpha receptors, protected from post-iscaemic vascular alterations in parallel with a reduction in the ischaemic lesions. Preliminary results suggested that the use of fenofibrate was also associated with a reduction of rtPA-induced hemorrhagic complications. In conclusion, the protection of vessels during the fibrinolysis seems to be a relevant pharmacological target to prevent the risk of rtPA-induced hemorrhagic complications
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Lequitte, Philippe. "Thrombose et fibrinolyse au cours du syndrome néphrotique de l'enfant." Paris 5, 1996. http://www.theses.fr/1996PA05P042.
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Ragonnet, Delphine. "Thrombose de prothese mecanique en position mitrale traitee par fibrinolyse." Reims, 1993. http://www.theses.fr/1993REIMM070.
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MIRSHAHI, BIBI SHAH SOLTAN. "Fibrinolyse associee aux cellules : implication dans les cancers de l'ovaire." Paris 7, 1993. http://www.theses.fr/1993PA077082.
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Notre travail a consiste a analyser les relations entre urokinase et cellules dans le processus tumoral. Nous avons etudie essentiellement les cancers de l'ovaire par des investigations biologiques chez les malades et par des etudes fondamentales sur les cellules isolees. Nous avons montre qu'au niveau des cellules tumorales, l'urokinase mais egalement son inhibiteur le pal-1 etaient des facteurs d'invasivite tumorale. Cette production par les cellules tumorales se traduit par une augmentation des produits de degradation de la fibrine qui diffusent dans le sang circulant. Pendant la chimiotherapie, l'activation de la fibrinolyse au niveau des monocytes par certaines drogues utilisees comme l'adriamycine ou l'interferon gamma pourrait au contraire favoriser la defense de l'hote contre les cellules tumorales, en augmentant la migration des cellules dans la matrice extracellulaire et en degradant la fibrine peritumorale. Toutefois, a cote de cette action interessante dans la lutte antitumorale exercee par les monocytes actives par la chimiotherapie, l'activation conduit egalement a une augmentation de synthese du fibrinogene par les hepatocytes, ce qui constitue un facteur de risque vasculaire qui est essentiellement lie a la production de lif. Cette augmentation de production du fibrinogene liee a l'activation des monocytes actives peut etre efficacement inhibee par la pentoxifylline. Un travail de biologie cellulaire sur les cellules isolees de cancer de l'ovaire nous a permis d'isoler un clone de cellules mutantes qui perd sa capacite de synthetiser l'urokinase mais conserve son recepteur. Ceci va nous permettre d'envisager la cooperation des cellules stromales productrices d'urokinase et des cellules cancereuses qui possedent le recepteur dans l'invasivite tumorale
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MARTIMORT, SYLVIE. "La fibrinolyse intra-cerebrale dans les accidents vasculaires cerebraux ischemiques." Lille 2, 1991. http://www.theses.fr/1991LIL2M309.
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Brummer, Astrid Bettina. "Der Effekt von Abciximab auf die Hämostase, Fibrinolyse sowie die Veränderungen von inflammatorischen Parametern und Adhäsionsmolekülen bei Patienten mit Akutem Koronarsyndrom und PTCA." [S.l. : s.n.], 2006.
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Frère, Corinne. "Thrombin-Activatable Fibrinolysis Inhibitor : étude de la relation génotype-phénotype." Aix Marseille 2, 2006. http://www.theses.fr/2006AIX20695.
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Le Thrombin-Activatable Fibrinolysis Inhibitor (TAFI) est un inhibiteur de la fibrinolyse. Les taux plasmatiques de TAFI Ag présentent une forte variabilité interindividuelle faiblement expliquée par les facteurs environnementaux. Nous avons évalué la contribution des polymorphismes du gène à la variabilité des taux de TAFI Ag. Deux polymorphismes (T+1583A et -2345 2G/1G) ont un effet additif expliquant 25 % de la variabilité des taux. Nous avons ensuite étudié le lien entre polymorphismes du gène du TAFI et risque de maladie coronaire. L’allèle Thr147 est un facteur de risque de survenue d’infarctus du myocarde. Nous avons enfin mesuré les variations des taux plasmatiques de TAFI Ag chez des patients durant l’infarctus du myocarde et la thrombolyse. Ce travail a permis d’objectiver le rôle de la plasmine comme activateur du TAFI in vivo. L’utilisation d’inhibiteurs du TAFI comme traitement adjuvant au cours de la thrombolyse semble une perspective thérapeutique intéressanteThe Thrombin-Activatable Fibrinolysis Inhibitor (TAFI) is a fibrinolysis inhibitor. A great interindividual variability in TAFI Ag levels has been described. In this work, we have demonstrated that TAFI gene polymorphisms explain 25% of TAFI level variability. This effect seems to be the consequence of the action of 2 polymorphisms. A trans-ethnic study enabled us to identify the T+1583A and -2345 2G/1G polymorphisms as potently QTNs. We have further studied the association between TAFI polymorphisms and coronary heart disease and demonstrated that the Thr147 allele is a risk factor for coronary heart disease. Finally, we have studied TAFI levels during myocardial infarction and thrombolysis
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BOLZONELLA, PENE CAROLINE. "Steroides sexuels, lipoproteines et activite fibrinolytique du plasma chez 46 patients eugonadiques." Toulouse 3, 1990. http://www.theses.fr/1990TOU31557.
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Kouri, Dominique El. "Syndrome inflammatoire et parametres de l'hemostase a partir d'une etude de 4 facteurs determinants : ps, c4b-bp, pa1, f1+2." Nantes, 1994. http://www.theses.fr/1994NANT205M.
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Rouy, Didier. "L'impact dans la fibrinolyse des composants plasmatiques impliques dans les interactions entre les domaines kringles du plasminogene et la fibrine." Paris 7, 1991. http://www.theses.fr/1991PA077201.
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La fibrinolyse plasmatique est un mecanisme physiologique qui permet la dissolution des caillots dans la circulation. Cette reaction repose sur la transformation d'un pro-enzyme plasmatique, le plasminogene, en plasmine, l'enzyme fibrinolytique active. L'activation ne peut se produire qu'a la surface d'un caillot de fibrine sous l'action de l'activateur tissulaire du plasminogene. La regulation de la fixation et de l'activation du plasminogene repose sur l'alpha2-antiplasmine, la glycoproteine riche en histidine et la lipoproteine (a). Nous avons etudie in vitro par des methodes de biochimie analytique les possibles interactions entre ces facteurs en utilisant des proteines purifiees ou des plasmas sur un support mimant la surface d'un caillot de fibrine. La glycoproteine riche en histidine diminue la quantite de zymogene disponible pour la reaction. L'alpha2-antiplasmine, en inhibant la plasmine formee, empeche la formation de derives partiellement degrades du plasminogene et de la plasmine, et diminue la generation a la surface de la fibrine de nouveaux sites de liaison pour le plasminogene. Le lipoproteine (a) agit par un mecanisme d'inhibition non-competitive sur la quantite de plasminogene fixe par l'intermediaire de l'apoproteine (a), presentant une grande homologie avec le plasminogene. L'utilisation d'une forme recombinante d'apoproteine (a) a confirme ces resultats. La lipoproteine (a), particule atherogene, pourrait non seulement diminuer l'efficacite de la reaction fibrinolytique, mais aussi induire l'accumulation de cholesterol. Ces deux facteurs constitueraient le lien entre les mecanismes d'atherogenese et de thrombogenese, permettant d'expliquer le developpement de thromboses sur des plaques d'atherome
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Aubert, Hélène. "Mise en évidence du déterminisme génétique du taux plasmatique de TAFI : Etude de la contribution du TAFI au risque thrombotique artériel." Aix-Marseille 2, 2003. http://www.theses.fr/2003AIX22063.
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Sow, Christian. "Fibrinolyse et rhéologie de la grossesse : évolution au cours du temps et perturbations dans la pré-eclampsie." Bordeaux 2, 1988. http://www.theses.fr/1988BOR25124.
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Perdue-Legendre, Edouard. "La fibrinolyse préhospitalière : expérience du Samu de Bordeaux sur deux ans." Bordeaux 2, 1994. http://www.theses.fr/1994BOR2M042.
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Perez, Thierry. "Traitement fibrinolytique des thromboses de valves cardiaques mécaniques chez l'enfant." Bordeaux 2, 1998. http://www.theses.fr/1998BOR23092.
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Lacroix, Romaric. "Microparticules : de la génération de plasmine à la standardisation d'un biomarqueur émergeant." Thesis, Aix-Marseille 2, 2010. http://www.theses.fr/2010AIX22959/document.
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Les microparticules (MP) sont des vésicules qui résultent du bourgeonnement des membranesdes cellules activées ou apoptotiques. Leur capacité à vectoriser des systèmes fonctionnelsexprimés par leurs cellules d’origine nous a conduit à explorer, la génération de plasmine àleur surface. Dans un premier travail, nous montrons que les MP dérivées de cellulesendothéliales (MPE) sont des surfaces catalytiques capables d’activer le plasminogène par lesystème de l’urokinase et de son récepteur (uPA/uPAR). Les MPE agissent comme desvecteurs de plasmine constituant une nouvelle voie dans la régulation des activitésprotéolytiques de l’endothélium. Dans un second travail, nous avons montré que l’uPA portéepar les cellules ou par les MPE est spécifiquement impliquée dans un mécanismereconnaissance du plasminogène lié à une autre surface biologique générant de la plasmine insitu avec une grande efficacité. Dans un troisième travail, nous montrons que cette activitéfibrinolytique est détectable sur les MP extraites de la circulation sanguine, où elle est plusspécifiquement portée par les sous populations endothéliales et leucocytaires. Cette activitéqui est dépendante de l’uPA mais aussi de l’activateur tissulaire du plasminogène, estmodulée dans des pathologies cardiovasculaires et auto-immunes. Dans une seconde partie, lapertinence de la mesure des MP comme biomarqueur en pratique clinique nous a amené ànous focaliser sur leurs méthodes d’analyse. En effet, à l’heure actuelle, l’évaluation dubénéfice apporté par les MP est limitée par un manque de standardisation des méthodologies.Dans ce travail, nous présentons une nouvelle stratégie de standardisation de la cytométrie enflux (CMF) et son évaluation dans le cadre d’une étude multicentrique utilisant des microbillesfluorescentes calibrées en taille. Enfin, nous discutons dans une revue les limitesactuelles de la CMF et les stratégies ou améliorations technologiques permettant de lesdépasserMicroparticles (MP) are small vesicles resulting from the blebbing of cell membranes in response to activation or apoptosis. Because they express functional molecules from their parent cells, plasmin generation at their surface has been explored. First we have shown that endothelial derived MP (EMP) promote plasminogen activation at their surface in an urokinase and its receptor (uPA/uPAR) dependant manner. Thus, plasmin generation by EMP constitutes a new pathway for the regulation of the endothelium proteolytic activities. Second, we have shown that cellular or MP uPA is specifically involved in the recognition and effective activation of plasminogen bound to another biological surface. Third, we have demonstrated that circulating endothelial and leukocytes MP bear this plasminogenolytic activity which it not only uPA but also tissue-type plasminogen activator dependant and modulate in pathological settings such as cardiovascular and auto-immune diseases. Supported by this work, a patent on a method to measure MP plasmin activity has been filed. In a second part, we focused on analytical methods available to measure MP. Indeed, there is an increasing interest to measure MP as biomarker in clinical practice. However, the evaluation of their input for patients is impeding by methodological concerns and a lack of standardization so far. In this work, we present a new strategy based a size-calibrated fluorescent beads for the standardization of flow cytometry (FCM). This approach was evaluated in a multicentre study. Finally, we reviewed the present limitation of the FCM for MP measurement and the strategies or technological improvements to overcome them
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Losco, Patrice. "Comparaison des effets du thermalisme associé ou non à la Troxérutine sur les paramètres de la fibrinolyse et de la rhéologie chez l'insuffisant veineux chronique." Bordeaux 2, 1995. http://www.theses.fr/1995BOR23093.
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Desclaux, Caroline. "La thrombolyse après 70 ans dans l'infarctus du myocarde." Bordeaux 2, 1997. http://www.theses.fr/1997BOR2M016.
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Lu, He. "Effet de la plasmine sur les plaquettes : modifications structurales et fonctionnelles." Rouen, 1990. http://www.theses.fr/1990ROUE06TP.
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Besse, Patrick. "L'angioplastie associée à la fibrinolyse intra-coronarienne pour la recanalisation précoce de l'infarctus du myocarde." Bordeaux 2, 1988. http://www.theses.fr/1988BOR25002.
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