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Biomedical subjects

E Biró

Publications and source records attributed to E Biró.

At least 19 recordsLinked to original sources

The phospholipid composition and cholesterol content of platelet-derived microparticles: a comparison with platelet membrane fractions.

BACKGROUND: The processes that govern the distribution of molecules between platelets and the microparticles (MP) they release are unknown. Certain proteins are sorted selectively into MP, but lipid sorting has not been studied. OBJECTIVES: To compare the phospholipid composition and cholesterol content of platelet-derived MP obtained with various stimuli with that of isolated platelet membrane fractions. METHODS: Washed platelets from venous blood of healthy individuals (n = 6) were stimulated with collagen, thrombin, collagen plus thrombin, or A23187. Platelet activation, MP release and antigen exposure were assessed by flow cytometry. MPs were isolated by differential centrifugation. Platelet plasma-, granule- and intracellular membranes were isolated from platelet concentrates (n = 3; 10 donors each) by pressure homogenization and Percoll density gradient fractionation. The phospholipid composition and cholesterol content of MPs and membrane fractions were analyzed by high performance thin layer chromatography. RESULTS: The phospholipid composition of MPs was intermediate compared with that of platelet plasma- and granule membranes, and differed significantly from that of intracellular membranes. There were small but significant differences in phospholipid composition between the MPs produced by the various agonists, which paralleled differences in P-selectin exposure in case of the physiological agonists collagen, thrombin, or collagen plus thrombin. The cholesterol content of MPs tended to be higher than that of the three-platelet membrane fractions. CONCLUSIONS: Regarding its phospholipid content, the MP membrane is a composite of the platelet plasma- and granule membranes, showing subtle differences depending on the platelet agonist. The higher cholesterol content of MPs suggests their enrichment in lipid rafts.

Blood Platelets↗

Human cell-derived microparticles promote thrombus formation in vivo in a tissue factor-dependent manner.

BACKGROUND: Circulating microparticles of various cell types are present in healthy individuals and, in varying numbers and antigenic composition, in various disease states. To what extent these microparticles contribute to coagulation in vivo is unknown. OBJECTIVES: To examine the in vivo thrombogenicity of human microparticles. METHODS: Microparticles were isolated from pericardial blood of cardiac surgery patients and venous blood of healthy individuals. Their numbers, cellular source, and tissue factor (TF) exposure were determined using flow cytometry. Their in vitro procoagulant properties were studied in a fibrin generation test, and their in vivo thrombogenicity in a rat model. RESULTS: The total number of microparticles did not differ between pericardial samples and samples from healthy individuals (P = 0.786). In both groups, microparticles from platelets, erythrocytes, and granulocytes exposed TF. Microparticle-exposed TF antigen levels were higher in pericardial compared with healthy individual samples (P = 0.036). Pericardial microparticles were strongly procoagulant in vitro and highly thrombogenic in a venous stasis thrombosis model in rats, whereas microparticles from healthy individuals were not [thrombus weights 24.8 (12.2-41.3) mg vs. 0 (0-24.3) mg median and range; P < 0.001]. Preincubation of pericardial microparticles with an inhibitory antibody against human TF abolished their thrombogenicity [0 (0-4.4) mg; P < 0.01], while a control antibody had no effect [19.6 (12.6-53.7) mg; P > 0.05]. The thrombogenicity of the microparticles correlated strongly with their TF exposure (r = 0.9524, P = 0.001). CONCLUSIONS: Human cell-derived microparticles promote thrombus formation in vivo in a TF-dependent manner. They might be the direct cause of an increased thromboembolic tendency in various patient groups.

Adult↗

Involvement of endogenous corticotropin-releasing factor in mediation of neuroendocrine and behavioral effects to alpha-melanocyte-stimulating hormone.

The present work was to study if the alpha-melanocyte-stimulating hormone (alpha-MSH) was involved in activation of the pituitary-adrenal axis (PAA) in rats. The hormone increased plasma corticosterone (CORT) level, and induced an anxiogenic response as indicated by results from the elevated plus-maze test. Intracerebroventricular administration of corticotropin-releasing factor (CRF) antiserum (1:10, 1:20 and 1:100 dilutions in 1microl volume), overcame both the anxiogenic response and the PAA activating effect induced by alpha-MSH (50 microg s.c.) in a concentration-dependent manner. CRF antibody at the doses applied did not modify either the elevated plus-maze responses or CORT level by itself. Our results reveal that both the anxiogenic and the PAA activating effects of alpha-MSH are mediated by CRF.

Adrenal Glands↗

Mean corpuscular volume is not a reliable marker of red cell age in case of anisocytosis.

The present study was designed to determine the effect of anisocytosis on the association of MCV values with HbA1c and reticulocyte counts as markers of red cell age. Normo-, micro- and macrocytic samples, fractionated by counterflow centrifugal elutriation were studied. The previously described correlation between MCV and HbA1c was only observed in normal samples and in the middle fractions of samples with anisocytosis. At both extremes of the elutriation profile, curves for HbA1c content and reticulocyte count levelled out. Furthermore, in fractions containing the largest red cells of the microcytic series and the smallest red cells of normo- and macrocytic samples, reticulocyte count decreased while HbA1c content increased with increasing MCV. From these data it is concluded that MCV is not an absolute determinant of red cell age in case of anisocytosis.

Erythrocyte Aging↗

Role of different neurotransmitter systems in the cholecystokinin octapeptide-induced anxiogenic response in rats.

The possible involvement of different neurotransmitter systems in the anxiogenic action of cholecystokinin octapeptide sulphate ester (CCK-8) was investigated in rats. Intracerebroventricularly (i.c.v.) administered CCK-8 induced an anxiogenic response in an elevated plus-maze test. Pretreatment with dopaminergic, muscarinergic acetylcholine receptor blockers and an opiate receptor antagonist blocked the anxiogenic response to CCK-8. The alpha and beta adrenoreceptor, the GABA receptor and the 5-hydroxytryptamine (5-HT) receptor blockers were not able to modulate the 'anxiogenic-like' effect of CCK-8. The results suggest that the anxiogenic effects of CCK-8 are mediated via different neurotransmitters and the anxiogenic action can be prevented by receptor blockers to these transmitters.

Adrenergic alpha-Antagonists↗

The effects of atrial natriuretic peptide (ANP1-28) on corticotropin releasing factor in brain of rats.

We have shown that ANP has anxiolytic-like effects in behavioral studies. Since CRF is thought to be involved in emotional state of the brain, the present study was undertaken to follow the possible alterations in corticotropin-releasing factor-like immunoreactivity (CRF-LI) in different regions of the brain in rats following ANP treatment. CRF-LI immunoreactivity was determined in hypothalamic and extrahypothalamic brain areas after central injection of atrial natriuretic peptide 1-28 (ANP1-28) in rats. After various doses of ANP1-28 administration the CRF-LI significantly increased in the hypothalamus, the hippocampus and the frontal cortex. In the amygdala, ANP caused a marked but nonsignificant CRF-LI enhancement. In the basal forebrain, the CRF-LI decreased. These results suggest that ANP1-28 may moderate activation of the CRF-ergic system in the brain which could be related to the neuroendocrine and behavioral action.

Animals↗

Role of endogenous CRF in the mediation of neuroendocrine and behavioral responses to calcitonin gene-related peptide in rats.

In the present study, the possible role of cortocotropin-releasing hormone (CRF) in the action of calcitonin gene-related peptide (CGRP) on the pituitary-adrenal axis and open-field activity of rats was tested. CGRP administered into the lateral brain ventricle led to a dose-dependent increase in plasma corticosterone level, which could be blocked by pretreatment with CRF antiserum. CGRP injected into the lateral brain ventricle increased the grooming and rearing activity and decreased the locomotor activity in an open field. On pretreatment with CRF antiserum, the action of CGRP on grooming was blocked, while the action on locomotion and rearing activity was unchanged. The results suggest that the CGRP-induced action on pituitary-adrenal activation is mediated by CRF. The action of CGRP on grooming in an open field is related to the pituitary-adrenal activation, and either CRF or adrenocorticotropic hormone or both may be involved in mediating the action of CGRP. The action of CGRP on rearing and locomotion is not affected by CRF antiserum, indicating that the two behavioral actions are regulated by different mechanisms.

Animals↗

Role of endogenous corticotropin-releasing factor in mediation of neuroendocrine and behavioral responses to cholecystokinin octapeptide sulfate ester in rats.

The possible involvement of endogenous corticotropin-releasing factor (CRF) in the anxiogenic and pituitary-adrenal-axis-activating effects of cholecystokinin octapeptide sulfate ester (CCK 8) was investigated in rats. Intracerebroventricularly (i.c.v.) administered CCK 8 induced an anxiogenic response in an elevated plus-maze test, and enhanced the plasma corticosterone level. Pretreatment with different dilutions (1:10, 1:20 and 1:100, i.c.v.) of CRF antiserum and different doses of a CRF receptor antagonist, alpha-helical CRF (ahCRF, 0.001-1.0 microgram, i.c.v.) prevented the anxiogenic response to CCK 8 in a dose-dependent manner. None of the doses of CRF antiserum or ahCRF alone produced any alteration in either the elevated plus-maze paradigm or corticosterone level in saline-treated control rats. The results strongly suggest that the anxiogenic and hypothalamo-pituitary-adrenal-activating effects of CCK 8 are mediated via CRF.

Animals↗

Light- and electron microscopic studies of the liver in "bronze baby" syndrome.

The light- and electron-microscopic changes of the hepatic tissue of a case with the "bronze baby" syndrome were described. The light-microscopic examinations revealed intrahepatic cholestasis of the hepatocanalicular type associated with portal inflammation. The electron-microscopic examinations showed dense deposits in the hepatic cells, Kupffer cells and in the bile canaliculi. The bile canaliculi were distended, the canalicular membrane severely destructed. The patient included in the study has been free of symptoms for 2 years.

Biopsy↗