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Biomedical subjects

L A Pálos

Publications and source records attributed to L A Pálos.

17 recordsLinked to original sources
PubMed1980

[Cholesterol deficiency. A pathogenetic factor in chronic anemias? Preliminary report of a study in three states (author's transl)].

It has been shown in several studies that there is a statistically confirmed connection between cholesterol and Hb levels in the sense that hypocholesterolemia and anemia occur together particular frequently. This was demonstrated in an epidemiological cross-section study of 3958 patient data, and also that in a retrospective case control study of 159 anemias there was a concurrent hypocholesterolemia. It is postulated that a causal connection exists which is explained by the fact that cholesterol deficiency leads to rigidity of the erythrocytes.

Adult↗
PubMed1979

Effect of hypoxia on the development of Drosophila melanogaster (Meigen).

Specimens of Oregon-R Drosophila melanogaster (Meigen) were bred in a defined sexual ratio in test chambers under different partial pressures of O2. In the gas mixture of 5--7% O2 plus 93--95% N2, the number of ovules dropped to nearly half even in the first generation, the time period of each development stage was considerably extended, and the size of the larvae decreased to a fraction of that of the controls. In the groups kept in a mixture of 10--12% O2 plus 88--90% N2, the same changes took place at a much slower rate, through several generations.

Aerospace Medicine↗
PubMed1979

The effect of some pyrimido-pyrimidine derivatives on blood coagulation and platelet aggregation.

Two pyrimido-pyrimidine derivatives, Chinoin 105 and Chinoin 123, respectively, were investigated with respect to the inhibition potency on platelet aggregation. It was shown that Chinoin 105 is a powerful inhibitor of aggregation of thrombocytes without effect on routine coagulation parameters in vitro. Chinoin 123 has a moderately inhibitory effect on the investigated reactions. An additive effect of Chinoin 105 to the inhibitory potential of PGE1 on platelet aggregation was proven.

Adenosine Diphosphate↗
PubMed1978

[Cholesterol deficiency. A pathogenetic factor in chronic anemias? Preliminary report of a study in three states (author's transl)].

It has been shown in several studies that there is a statistically confirmed connection between cholesterol and Hb levels in the sense that hypocholesterolemia and anemia occur together particularly frequently. This was demonstrated in an epidemiological cross-section study of 3958 patient data, and also that in a retrospective case control study of 159 anemias there wasa concurrent hypocholesterolemia. It is explained by the fact that cholesterol deficiency leads to rigidity of the erythrocytes.

Aged↗
PubMed1978

Disseminated intravascular coagulation developed in hyperbaric oxygen.

Male rats of 260 g were exposed to hyperbaric conditions of oxygen with different partial pressures and the changes of the haemostasis were studied. In 100% oxygen at 2 ATA, the animals died within 48 h. In 100% oxygen at 1 ATA, death occurred only after 3 d; however, in 24-48 h there developed disseminated intravascular coagulation (DIC). At the same time uncompensated acidosis of 7.34 +/- 0.02 was measured. Perivascular bleeding could be histologically demonstrated in different organs. The mixture of 60% oxygen and 40% nitrogen caused only a minimal DIC while a mixture of 40% oxygen and 60% nitrogen caused no changes in the haemostasis. Volunteer young males exposed to the mixture of 60% oxygen and 40% nitrogen, developed the beginning symptoms of DIC, which made it necessary to stop the experiments.

Animals↗
PubMed1978

Air reoxidation and reactivation of reduced thrombin.

About 80% of thrombin was inactivated after 50 minutes chemical reduction at 22 degrees C in a reaction mixture containing o.1 M mercaptoethanol and 2.6 M urea. The reduced protein was spontaneously reoxidated in air at 22 degrees C in 30--60 minutes. The reoxidation of disulphide bonds in thrombin led to partial reactivation of the enzyme. Recovery of thrombin activity after oxidation ranged from 0 to 60% according to the conditions of reoxidation in air. Heparin and copper ion increased the rate of reactivation, whereas in the presence of 10 mM iodoacetamide there was no reactivation.

Air↗
PubMed1977

Effect of collagen on thrombin inactivation by antithrombin-III and heparin.

Thrombin inactivation by antithrombin-III and heparin has been found to decrease in the presence of collagen, whereas thrombin activity and the rate of thrombin inactivation by antithrombin-III alone are not affected. Albumin, at the same concentration as collagen, does not influence either thrombin activity or thrombin inactivation by antithrombin-III or by antithrombin-III plus heparin.

Animals↗
PubMed1977

Some properties of human progressive antithrombin.

The effect of some mono- and divalent cations was examined on thrombin--antithrombin reaction in vitro. It was found that 0--0.1 M sodium- or potassium chloride did not affect either thrombin or antithrombin activity; at higher concentrations thrombin activity decreased. Calcium chloride as well as magnesium chloride at concentrations from 0 to 0.5 M increased enzyme activity, whereas at higher concentrations the activity decreased. Thrombin inactivation by antithrombin was also accelerated at calcium or magnesium chloride concentrations above 0.04 M. Antithrombin was inactivated at pH 7.3 at 65 degrees C in some minutes and heparin failed to protect it against heat denaturation. Thrombin inactivation by antithrombin did not proceed at 0 degrees C in 60 min, but the interaction between thrombin and antithrombin was facilitated in the presence of heparin.

Antithrombin III↗
PubMed1975

Action of heparin on thrombin-antithrombin reaction.

Thrombin partially purified from bovine plasma can be inactivated at 60 degress C. In the presence of 10 units of heparin the extent of inactivation decreases. When thrombin and heparin are mixed and incubated for 5 min at 0 degrees C before gel filtration on Sephadex G-200, thrombin with heparin is eluted prior to either thrombin or heparin laone. These data suggest a complex formation between thrombin and heparin. Immobilized heparin binds thrombin. The enzyme can be eluted with 0.05 M Tris-HCl buffer, pH 7.3, containing an ion mixture of Na+, K+ and Ca2+ at 73, 3 and 11 mM, respectively, at 0 degrees C and with 0.05 M Tris-HCl buffer, pH 7.3, containing 0.5 M NaCl at 20 degrees C. During the same chromatographic procedure, antithrombin-III (heparin cofactor) partially purified from human plasma is eluted with 0.05 M Tris-HCl buffer, pH 7.3, at 0 degrees C as well as 20 degrees C. Although, as described in the literature, heparin binds to antithrombin, our findings suggest another possibility, i.e. that the binding of heparin to thrombin induces a conformational change in the enzyme facilitating a complex formation between thrombin and antithrombin-III.

Antithrombin III↗
PubMed1974

Abnormal antithrombin III (antithrombin III "Budapest") as a cause of a familial thrombophilia.

A family with a high incidence of spontaneous thromboembolism has been investigated and those members affected were found to have significantly depressed levels of plasma and serum heparin cofactor activity; i.e., antithrombin III and anti-Xa activity. Further studies revealed that despite a marked diminution of antithrombin III activity in these patients measurement of antithrombin III by immunological techniques showed the levels to be normal. It is concluded that this anomaly represents a defect in the synthesis of the antithrombin III molecule. The abnormality appeared to be inherited but the mode of inheritance could not be determined with the available data.

Adsorption↗