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Biomedical subjects

M Balaskó

Publications and source records attributed to M Balaskó.

12 recordsLinked to original sources

Neutron imaging of Zr-1%Nb fuel cladding material containing hydrogen.

Hydrogen distribution and hydride phases were analyzed in reactor fuel cladding pressure tube Zr-1%Nb material up to 13,300 ppm. From neutron diffraction measurements, formation of cubic delta-ZrH2 and a small amount of tetragonal gamma-ZrH was established. Texture effects were analyzed by imaging plate technique. From neutron radiography images a linear model was set up that adequately described the relationship between gray levels and nominal H-concentrations. The H-distribution was unveiled by 3D intensity histograms and fractal analysis of multilevel-segmented neutron radiography images.

Journal Article↗

Semi-simultaneous application of neutron and X-ray radiography in revealing the defects in an Al casting.

A semi-simultaneous application of neutron and X-ray radiography (NR, XR) respectively, was applied to an Al casting. The experiments were performed at the 10MW VVR-SM research reactor in Budapest (Hungary). The aim was to reveal, identify and parameterize the hidden defects in the Al casting. The joint application of NR and XR revealed hidden defects located in the Al casting. Image analysis of the NR and XR images unveiled a cone-like dimensionality of the defects. The spectral density analysis of the images showed a distinctly different character for the hidden defect region of Al casting in comparison with that of the defect-free one.

Journal Article↗

Analyzing of segregation in mixtures of 3-methylpyridine and heavy water by dynamic neutron radiography.

The closed-loop phase diagram of 3-methylpyridine-heavy water mixture was studied, to our best knowledge, for the first time with dynamic neutron radiography (DNR) at the 10MW VVR-SM Research Reactor in Budapest (Hungary). Visualized were the (i) lower temperature non-segregated states (below 38 degrees C), (ii) transition (40-43 degrees C), (iii) segregated states (46-128 degrees C), (iv) higher temperature transition (110-128 degrees C) and (v) higher temperature non-segregated states. The non-segregated state belonging to 141 degrees C, was found to be definitely dissimilar from the lower temperature state. Existence of a solid-like structure at the liquid-liquid interface was indicated.

Journal Article↗

Multiple neural mechanisms of fever.

In rats, fevers induced by moderate-to-high doses of intravenous lipopolysaccharide consist of three phases (phases 1, 2 and 3) with body temperature peaks at approximately 1, 2, and 5 h postinjection, respectively. In this study, the effects of bilateral truncal subdiaphragmatic vagotomy and intraperitoneal capsaicin desensitization on febrile phases 1-3 were assessed in adult Wistar rats. Surgical vagotomy was performed approximately 30 d before the experiment; this procedure interrupts both afferent and efferent vagal fibers. Capsaicin was administered intraperitoneally in two consecutive injections (2 and 3 mg/kg, 3 h apart) 1 week prior to the experiment; this procedure desensitizes afferent fibers, primarily within the abdominal cavity, and does not lead to the known thermal effects of systemic capsaicin desensitization. At a neutral ambient temperature, the rats were given Escherichia coli lipopolysaccharide (10 microg/kg) through a preimplanted jugular catheter, and their colonic temperature wes measured by thermocouples for 7 h. The control rats exhibited the typical triphasic febrile responses. Confirming our earlier studies, subdiaphragmatic vagotomy did not affect phases 1 and 2; it did, however, result in a 2.5-fold reduction of phase 3. Capsaicin desensitization modified the febrile response differently: phases 2 and 3 were unaffected, but phase 1 disappeared. We suggest that neural afferent fibers (nonvagal but perhaps vagal as well) play an important role in the early febrile response (phase 1) by transducing peripheral pyrogenic signals to the brain. We also suggest that vagal efferent fibers are likely to participate in the later febrile response (phase 3) via an unknown mechanism.

Animals↗

Central thermoregulatory effects of neuropeptide Y and orexin A in rats.

Orexin A and neuropeptide Y that are known to induce a feeding response when applied centrally, in the present studies also caused hypothermia. Neuropeptide Y elicited hypothermia by depressing metabolic rate (without affecting heat loss mechanisms), while orexin A acted through enhancing peripheral heat loss (without affecting metabolic rate). Neither peptide induced coordinated thermoregulatory changes, both of them appeared to influence thermoregulation via different effector mechanisms.

Adaptation, Physiological↗

Hyperphagia in cold-adapted rats: a possible role for neuropeptide Y.

The feeding response to intracerebroventricular injection of neuropeptide Y or to starvation is greater in cold-adapted than in non-adapted rats, suggesting that with cold-adaptation the central sensitivity to this peptide is increased. Hypometabolism and hypothermia (which usually follow the administration of neuropeptide Y) cannot, however, be demonstrated in the course of cold-adaptation per se.

Adaptation, Physiological↗

Grammatical choice and affective experience in a second-language test.

This study measured the affective experience of 12 subjects reading grammatically correct and incorrect versions of 50 sentences, Questionnaire I, in their second language (French). This was followed by a multiple choice grammar test, Questionnaire II, using the same 50 sentences and offering the correct and incorrect answers. Subjects tended to choose correct as well as incorrect responses corresponding to their highest affective rating within each entry. In all cases the subjects' behavior was higher than chance level and thus followed a trend to maximize pleasure. This result supports the hypothesis according to which the key to decision-making lies in the affective dimension of conscious experience.

Adult↗

Cholecystokinin participates in the mediation of fever.

Cholecystokinin of the central nervous system participates in the pathogenesis of lipopolysaccharide-induced fever in rats, contributing mainly to the first phase rise of this fever. The mediatory role is connected to type-B receptors of cholecystokinin.

Animals↗