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G Molaro

Publications and source records attributed to G Molaro.

At least 19 recordsLinked to original sources
PubMed1987

Ha-ras-1 restriction fragment length polymorphism and susceptibility to colon adenocarcinoma.

It is not yet clear whether some polymorphic variants of the Ha-ras-1 gene confer genetic predisposition to cancer. However, recent data on myelodysplasia and lung cancer are controversial. To clarify this point, 62 colorectal adenocarcinoma patients were examined for the Ha-ras-1 gene restriction fragment length polymorphism and results were compared with those of 108 healthy blood donors. No Ha-ras-1 polymorphic variants specifically associated with the cancer patients were detected. However, a specific genotype was significantly more frequent in the healthy donors than in the cancer patients (16% versus 5%), suggesting an interaction between the two alleles of the gene.

Adenocarcinoma↗
PubMed1987

[Fibrinolysis and hemorrhage after streptokinase in acute myocardial infarct].

The purpose of this study is to analyze the relationship between occurrence of hemorrhagic complications, kinetic of fibrinogen degradation-regeneration and the changes of prothrombin time (PT), partial thromboplastin time (PTT), after intravenous administration of Streptokinase (SK), 1.500.000 U., in acute myocardial infarction. 45 selected patients with acute myocardial infarction had pretreatment analysis and serial post-SK measurement of fibrinogen levels, PT, PTT (for 48 hours). Basal fibrinogen levels were 3.2 g/l and displayed significant depression for 18 hours (0.30-0.46 g/l) and normalization after 30 hours from SK infusion. Similar behaviour showed PT and PTT. Minor bleeding was identified in 25 patients. In bleeders mean fibrinogen levels, PT, PTT before and maximum changes after SK were not significantly different compared with non bleeders. We conclude that SK infusion produces important and prolonged changes of fibrinogen levels, PT, PTT; hemorrhagic risk is not related, however, to the extent of lytic state, but probably to pre-existent vascular derangement, predisposing to bleeding complications during fibrinolytic therapy. Therefore we believe to be prudent to delay the infusion of heparin for 12-18 hours after SK administration, when fibrinogen levels are beginning to increase.

Female↗
PubMed1986

OKT4+ chronic lymphocytic leukaemia cells display different reactivity with selected monoclonal antibody combinations.

Four cases of chronic T lymphocytic leukaemia are characterized by selected monoclonal antibody combinations and double-fluorescence studies. We found 3 possible combinations: OKT4++ Leu8++ Leu9+, OKT4++ Leu8+ Leu9- and the OKT4++ Leu9++ Leu8- phenotypes are correlated with different biological aspects of the disease. No markers of T cell activation were found, and serological examinations did not reveal anti-HTLV-I antibodies. In considering a larger number of patients, multiparametric analysis could be useful to better classify this heterogeneous type of leukaemia.

Aged↗
PubMed1980

Normal platelet adhesiveness and aggregation in congenital PTA or Hageman factor deficiency.

Platelet adhesiveness and aggregation were studied in two patients with congenital factor XI deficiency and in a patient with congenital factor XII deficiency. A normal aggregation pattern was observed in every instance, regardless of the aggregating agent. The same was true for platelet adhesiveness. It is concluded that factor XI and factor XII play no role in platelet aggregation and adhesiveness.

Bleeding Time↗
PubMed1977

The effect of heparin on the interaction of factor VIII and human platelets in vitro.

Heparin was found to inhibit the interaction between human factor VIII and platelets. This was noted in two different systems, namely, platelet aggregation induced by neuraminidase-treated human cryoprecipitate and platelet aggregation induced by ristocetin-human factor VIII complex. Heparin appeared to have an inhibitory effect on the above systems similar to that reported on bovine factor VIII-induced platelet aggregation.

Blood Platelets↗
PubMed1975

Factor X Friuli coagulation disorder. The demise of the index patient.

The up-dated case history of the index patient with the factor X Friuli coagulation disorder is reported. The patient, aged 72, died of irreversible shock after progressive jaundice with symptoms of renal, cardiac and hepatic failure. The autopsy showed carcinoma of the head of the pancreas, diffuse petecchial hemorrhages, massive adrenal gland hemorrhage and minimal athero-arteriosclerotic lesions of all arteries. The significance of minimal athero-arteriosclerotic changes in a patient with a congenital coagulation defect is discussed.

Aged↗
PubMedDate not supplied

Combined factor VIII and factor XI congenital deficiency: a case report.

Combined congenital defect involving both Factor VIII and XI is a very rare disorder. We describe a case of combined Factor VIII and XI deficiency in which the propositus has a mild hemophilia A and inherited a Factor XI deficiency from the father. Moreover, we report on the benefit of DDAVP administration to the patient during a bleeding episode.

Adult↗