Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 2 de 2
Filtrar
Mais filtros










Base de dados
Tipo de estudo
Intervalo de ano de publicação
1.
Dis Markers ; 19(6): 251-8, 2003.
Artigo em Inglês | MEDLINE | ID: mdl-15258325

RESUMO

UNLABELLED: Diabetes mellitus is associated with disturbances in haemostasis that could contribute to the development of thrombotic complications.The present study was undertaken to determine the behavior of coagulation variables and fibrinolytic system in diabetes mellitus. Forty five diabetic patients and forty five matched controls were evaluated by doing the following haemostatic parameter, prothrombin time, partial thromboplastin time, thrombin time, coagulation factors assay II, VII, IX, & plasma fibrinogen, ADP-induced platelet aggregation, protein C, alpha2- antiplasmin, PAI and FDPs. Generally diabetic patients have high levels of fibrinogen, alpha2- antiplasmin, & PAI and lower level of protein C. Other haemostatic parameters did not show statistically significant difference between diabetic patients and control group. Significantly elevated levels of PAI, alpha2- antiplasmin together with low protein C level in diabetic patients may result in the disturbance of haemostatic balance favoring thrombotic events. CONCLUSION: High levels of plasma fibrinogen, alpha2A- antiplasmin with low plasma protein C activity could lead to a prothrombotic tendency in insulin dependent diabetic patients. Moreover, in non-insulin dependent diabetic patients, the above mentioned parameters together with high levels of ADP-induced platelet aggregation and plasminogen activator inhibitor may increase the risk of thrombotic complications. Obesity can be considered as an additional risk factor for development of thrombosis in diabetic patients.


Assuntos
Diabetes Mellitus/sangue , Hemostasia , Fibrinogênio/análise , Humanos , Inibidor 1 de Ativador de Plasminogênio/genética , Agregação Plaquetária , Proteína C/análise
2.
Tumori ; 88(6): 513-21, 2002.
Artigo em Inglês | MEDLINE | ID: mdl-12597149

RESUMO

In the present study the chemopreventive activities of DFMO, the irreversible inhibitor of ornithine decarboxylase, and finasteride, the inhibitor of prostatic 5a-reductase, against the development of chemically induced prostate adenocarcinoma by methylnitrosourea/testosterone propionate in male Wistar rats were investigated. According to histological examination, oral administration of DFMO and finasteride, either alone or combined, for two months to MNU/TP-inoculated rats reduced the tumor incidence to 11.11%, 10% and 10%, respectively, compared to tumored controls (64.3%). DFMO and/or finasteride treatment resulted in significant reductions in the wet weight of the prostate gland and seminal vesicles and its ratio relative to the total body weight, as well as the levels of prostate total protein, DNA, RNA and DNA/RNA ratio, compared to tumored controls. However, the effect of the combined treatment was of no statistical significance compared to single DFMO or finasteride treatment, as demonstrated by the non-significant differences between the mean values of most of the studied parameters. The tumor chemopreventive activity and the prostate growth inhibitory effect of DFMO and finasteride were due to suppression of prostate polyamine synthesis. ANOVA test revealed that the relative weight of the prostate as well as blood and tissue polyamine levels could be used as significant endpoint biomarkers for DFMO and finasteride as cancer chemopreventive agents.


Assuntos
Adenocarcinoma/prevenção & controle , Anticarcinógenos/uso terapêutico , Poliaminas Biogênicas/metabolismo , Biomarcadores Tumorais/metabolismo , Eflornitina/uso terapêutico , Inibidores Enzimáticos/uso terapêutico , Finasterida/uso terapêutico , Neoplasias da Próstata/prevenção & controle , Adenocarcinoma/induzido quimicamente , Adenocarcinoma/metabolismo , Análise de Variância , Animais , Antineoplásicos/uso terapêutico , Poliaminas Biogênicas/sangue , Biomarcadores Tumorais/sangue , Biomarcadores Tumorais/genética , DNA de Neoplasias/metabolismo , Masculino , Neoplasias da Próstata/induzido quimicamente , Neoplasias da Próstata/metabolismo , RNA Neoplásico/metabolismo , Ratos , Ratos Wistar
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA
...