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Biomedical subjects

U Armani

Publications and source records attributed to U Armani.

At least 37 records · Page 2Linked to original sources
PubMed1985

Lactate overproduction in platelets of subjects affected with myeloproliferative disorders.

In platelets of patients affected with myeloproliferative disorders, glycolytic and glycogenolytic flux have been examined. Results of studies on glucose uptake, glycogen breakdown and lactate formation have been reported. No difference in glucose uptake between controls and patients was observed, but in patients a higher lactate formation was always noted in the presence or absence of exogenous glucose, in correlation with a higher glycogen breakdown rate. Results could be explained by modified regulation mechanisms on glycogen phosphorylase.

Adult↗
PubMed1984

Some aspects of platelet glucose metabolism in thrombocytosis due to myeloproliferative disorders.

Some aspects of the glucose metabolism were investigated in platelets of 11 healthy donors and 11 patients suffering from thrombocytosis due to myeloproliferative disorders. Out of all the glycolytic compounds measured in resting platelets, dihydroxyacetonephosphate and fructose 1,6 bisphosphate were significantly higher in cells of subjects with thrombocytosis. No difference was observed in the basic net flux of glucose through the hexose monophosphate shunt. Addition of arachidonic acid to platelets of patients with thrombocytosis had a very poor effect in stimulation of the hexose monophosphate shunt, whereas high values of activation were obtained in control platelets. Lactate production determined by collagen was found significantly higher in all patients. These data observed in platelets of patients could be explained by a decreased pool of metabolic adenine nucleotides.

Adult↗
PubMed1984

Platelet membrane fatty acids in thrombocytosis due to myeloproliferative disorders.

The fatty acid composition of platelet membranes has been analysed in patients with thrombocytosis due to myeloproliferative disorders, who had not taken any drugs. A significant increase in palmitic and oleic acid, together with a decrease in stearic, linoleic and arachidonic acids was observed. The fatty acid pattern of platelet membranes was also analysed in patients during treatment with ASA (acetylsalicylic acid). ASA ingestion completely normalizes the platelet content of palmitic acid and partially that of stearic and arachidonic acid, whereas it has no effect on the level of linoleic acid and raises that of oleic acid. The altered pattern of fatty acids observed in patients may interfere with platelet function by decreasing membrane fluidity. Treatment of patients with ASA seems to act on platelet membranes by partially normalizing the fatty acid composition.

Adult↗
PubMed1984

Platelet glyoxalases in thrombocytosis.

In platelets of patients suffering from thrombocytosis due to myeloproliferative disorders, glyoxalase I activity is significantly higher than in controls (P less than 0.01), while glyoxalase II levels are the same (P less than 0.3). The cellular concentration of glutathione is also increased in patients. Km values for methylglyoxal (glyoxalase I) and S-lactoylglutathione (glyoxalase II) are identical both in normal and pathological subjects, as are the thermostability of the two enzymes. The higher activity observed for glyoxalase I in patients could be related to a specific role of this enzyme in platelets.

Adult↗
PubMed1984

Platelet lysosomal enzymes are normal in myeloproliferative disorders.

In platelets of subjects affected with myeloproliferative disorders the following lysosomal enzymes were studied: alpha-mannosidase, alpha-fucosidase, beta-galactosidase, beta-glucosidase, beta-glucuronidase, beta-N-acetylglucosaminidase and acid phosphatase. For each enzyme the specific activity, the optimum of pH and buffer, Km and saturating substrate concentrations, as well as thermostability were determined. Control and patient enzymes showed no difference.

Blood Platelets↗
PubMed1983

[A method for erythrocyte filtration].

Erythrocyte deformability is one of the most important factors on determining blood viscosity. Many microcirculation damages are caused by alteration of viscosity. We propose a method for evaluate erythrocyte filtration using Nucleopore membranes, to study erythrocyte deformability. Normal ranges are calculated in young healthy subjects. Mean filtration time is determined on 5 filtrations for every subject. Filtration rate is expressed by sec/ml and correlated whit haematocrit. The method is not easily utilizable, but it can be useful in the knowledge of the role of the erythrocyte deformability in the altered microcirculation.

Blood Viscosity↗
PubMed1983

[A method for the assay of fibrinopeptide in plasma].

Fibrinopeptide A (FPA) levels have been assayed in 10 normal subjects using a radioimmunoassay (RIA-mat FPA Mallinckrodt). Mean values were 0,97 +/- 0,46 ng/ml. The variation coefficient of the test was 4,82%. The method is well standardized and seems to be useful in the diagnosis of venous thrombosis and in the control of heparin treatment. It seems to be also useful in the evidentiation of an activation af the coagulation system in some diseases (cardiovascular diseases, diabetes etc.)

Fibrinogen↗
PubMed1981

[Platelet function in the dog].

Platelet aggregation with Born test was performed in 9 normal dogs. ADP, Epinephrine and Collagen were employed to stimulate platelets. With ADP, canine platelet aggregation was lower than human platelet aggregation, while, with Epinephrine and Collagen, aggregation was similar to that obtained with human platelets. Therefore the dog might be a model to study pharmacological interactions on platelet function.

Adenosine Diphosphate↗
PubMed1979

[Changes induced with varying solutions of normal plasma on granulocyte capillary tube migration].

In the present work we have evaluated the effect of decreasing concentrations of normal plasma in TC 199 on leukocyte capillary migration. From the 1st to the 4th hour of migration, normal plasma at 100%-80%-60%-40% concentration, significantly inhibits leukocyte migration. The inhibitory effect is lost, only by a few plasmas, at 60% and 40% concentration, during the following migration hours. Normal plasma at 20% and 10% concentration doesn't show any inhibitory effect on leukocyte capillary migration. Therefore, for clinical studies on pathological plasmas we recommend the use o plasma at 20% or 10% concentration to avoid aspecific inhibition.

Cell Movement↗
PubMed1979

[Standardization of the method of granulocyte capillary tube migration].

In the present work a method is described to standardize each step of leukocyte capillary tube migration assay. The conclusions of our study are: natrium heparin can be used as anticoagulant; the use of calibrated microcapillaries is recommended; migration chambers must lay on a horizontal surface; results can be evaluated by a ocular for radial immunodiffusion from the 16th to 20th hour of migration.

Cell Movement↗