Search PubMed⌕ Search

Biomedical subjects

D Marić

Publications and source records attributed to D Marić.

At least 19 recordsLinked to original sources

Secondary electron emission of carbonaceous dust particles.

In this paper we present measurements of the secondary electron emission yield (gamma) of a carbonaceous dust particle material, which was grown in argon diluted acetylene plasmas. One aim was to reach a better understanding of charging and discharging processes of dust particles in complex plasmas due to secondary electron emission and consequently to try to explain the anomalous behavior of electron density observed in afterglows of pulsed rf plasmas. We compared the results of a simple model and of a Monte Carlo simulation to the previously measured time dependence of the electron density in complex plasma afterglow. It was found that the value of the intrinsic secondary electron yield from the carbonaceous dust material is too low to explain the increase of electron density in the afterglow. It is, however, possible that the electrons charging the particles are weakly attached so that they may be released with high efficiency by ion bombardment due to field induced emission or by other mechanisms.

Journal Article↗

[Overuse injury syndromes in the shoulder area].

The shoulder is the most movable and the most unstable joint in a human body. The glenohumeral joint is particularly vulnerable because overhead activities put tremendous stress on its static stabilizers (ligamentous labral complex) and the dynamic stabilizers (rotator cuff muscles). Overhead activities may stretch or injure the static stabilizers. Minor aberrations in mechanisms controlling stability have a significant and cumulative effect on the shoulder biomechanics, and increase the risk of injury. Impingement syndrome and glenohumeral instability are predominant injuries affecting the shoulder.

Biomechanical Phenomena↗

The involvement of nitric oxide in stress-impaired testicular steroidogenesis.

The participation of the nitric oxide (NO) pathway in downregulation of testicular steroidogenesis in normal and stressed rats was investigated both in vivo and in vitro. In Leydig cells from normal animals, isosorbide dinitrate, an NO donor, decreased the human chorionic gonadotropin (CG)-stimulated and progesterone-derived androgen production. Also, the intratesticular injection of a precursor of NO, arginine (10 mg/testis), transiently decreased serum androgen levels and inhibited human CG-stimulated androgen production in acute testicular cultures. These effects were eliminated in rats cotreated with Nomega-nitro-L-arginine methyl ester (L-NAME) (2 X 600 microg/each testis). Acute immobilization stress (2 h) decreased serum androgen levels and inhibited human CG-stimulated androgen production in vitro. These effects were accompanied by a significant increase in nitrite, a stable oxidation product of NO, in testicular cultures. Bilateral intratesticular injection of L-NAME prevented the stress-induced decrease of human CG-stimulated androgen production, and significantly reduced the nitrite levels. These results implicate NO in normal and stress-impaired testicular steroidogenesis.

Animals↗

The effect of acute stress and opioid antagonist on the activity of NADPH-P450 reductase in rat Leydig cells.

Previous studies indicate that acute immobilization stress (IMO; 2 h) impaired testicular steroidogenesis primarily at the testicular level decreasing the activity of certain steroidogenic enzymes. In the present study unstressed rats as well as IMO rats (2 h) were treated by intratesticular injection of naltrexone methobromide (NMB; peripheral opioid receptor antagonist; 36 microg/testis) or vehicle at the beginning of and at 1 h of the IMO period. In IMO rats the activity of P450c17 was significantly reduced as well as the activity of NADPH-P450 reductase (which catalyzes the transfer of electrons from NADPH to cytochrome P450), while the activity of NADH-b5 reductase was not affected. Present data confirmed previous results that acute IMO reduced testicular P450c17 activity and implicate that decreased activity of NADPH-P450 reductase could be responsible for the inhibition of P450c17 under IMO conditions, while NADH-b5 reductase is probably not involved. NMB treatment antagonized the inhibitory effect of IMO on P450c17 and NADPH-P450 reductase activities. Such results put forward the implication that endogenous opioid peptides are involved in mediating the inhibitory effect of IMO on testicular steroidogenesis, and allow the speculation that NADPH-P450 reductase could be a possible site of such an inhibition.

17-alpha-Hydroxyprogesterone↗

The effect of opioid antagonists in local regulation of testicular response to acute stress in adult rats.

The present study examined the effects of naloxone (N) and naltrexone-methobromide (NMB; an opioid receptor antagonist that does not cross the blood-brain barrier) on testicular steroidogenesis during acute immobilization stress (IMO; 2 h) in adult rats. Unstressed rats as well as IMO rats were treated by unilateral intratesticular injection of N (20 micrograms/testis), NMB (36 micrograms/testis), or vehicle at the beginning of and at 1 h of the IMO period. In IMO rats serum T levels were significantly reduced, while serum luteinizing hormone levels were not affected. N and NMB normalized serum T levels in IMO rats and had no effects in controls. In IMO rats the activities of 3 beta-hydroxysteroid dehydrogenase (HSD) and P450(17 alpha, lyase) were significantly reduced, while the activity of 17 beta-HSD was not affected. N and NMB antagonized the inhibitory effect of IMO on 3 beta-HSD and P450(17 alpha, lyase) but did not alter enzyme activity in freely moving rats. Acute IMO decreased basal and human chorionic gonadotropin-stimulated androgen production by hemitestis preparation, but N (10(-4) M) added directly to the incubation medium blocked the decrease and had no effect on testes from freely moving control rats. These results support the conclusion that endogenous opioid peptides are potentially important paracrine regulators of testicular steroidogenesis under stress conditions.

3-Hydroxysteroid Dehydrogenases↗

Effects of acute and chronic immobilization stress on rat Leydig cell steroidogenesis.

In rats, acute immobilization (IMO) stress (2 h) induced a fall in the serum androgen concentrations (T+DHT) without detectable changes in serum luteinizing hormone (LH) values. In vitro studies, using a suspension of Leydig cells from adult rat testis, demonstrated that acute stress inhibited conversion of progesterone (P) or 17hydroxyprogesterone (17OHP) to T while conversion of androstendione (delta 4 A) was not affected. Acute IMO reduced activity of 3 beta-hydroxysteroid dehydrogenase (3 beta-HSD) and decreased basal and hCG-stimulated progesterone and androgen production. Chronic IMO stress (2 h daily for 10 days) induced a decrease in serum androgen level with decline in serum LH values. In vitro, hCG-stimulated progesterone and androgen production by suspension of Leydig cells, as well as conversion of P and 17OHP to T were not significantly altered. Our data demonstrates that acute IMO stress impaired testicular steroidogenesis primarily at the testicular level (decreasing the activity of certain enzymes), while chronic IMO stress exerts the effect mainly on the hypothalamic-pituitary axis; reduced serum LH levels elicit a decrease in serum androgen levels.

Animals↗

Enkephalin-induced stimulation of humoral and cellular immune reactions in aged rats.

Twenty-month-old Wistar rats received intraperitoneal injections of the opioid pentapeptide, methionine-enkephalin (Met-Enk) in periods before and after immunization with cellular and soluble antigens. Animals were treated with 0.2 mg of Met-Enk/kg b.w., a dose previously found to increase immune capacity in young adult rats. Saline-treated 20-month-old, and Met-Enk-treated rats and saline-treated 8-week-old controls were set up for each experimental group. Immune performance was evaluated by plaque-forming cell response, antibody production and various immunoinflammatory reactions. At autopsy, thymus and spleen were weighed and processed for histological examination. The results showed that 0.2 mg dose of Met-Enk produced significant enhancement of both humoral and cellular immune responses in senescent rats. Methionine-enkephalin treatment also induced a significant increase in thymus and spleen weights in these animals. Analysis of the cellular make up of these organs revealed the enlargement of cortical and medullary areas, and pronounced pyroninophilia in the subcortical zone of the thymus and thymus-dependent areas of the spleen. The results suggest that Met-Enk exerts an immunorestorative activity in aged animals, and that changes in the opioid system may play an important role in the maintenance of immune functions during senescence.

Aging↗

Immunostimulatory activity of prothymosin-alpha in senescence.

In this study we evaluated the immunorestorative activity of prothymosin-alpha (ProT-alpha) in senescence. Aged rats were repeatedly injected with ProT-alpha after antigen challenge. Both humoral and cell-mediated immune reactions were tested. The results show that ProT-alpha exerted a marked immunopotentiating effect in aged rats. Moreover, ProT-alpha induced enhancement of PFC response, and skin hypersensitivity reactions were more pronounced in senescent rats than in young adult controls. ProT-alpha treatment increased thymus and spleen weights in aged rats, and induced qualitative and quantitative improvements of the cellular make-up of the thymus and thymus-dependent areas of the spleen. The results imply that "restoring" thymus endocrine function by exogenous administration of ProT-alpha may improve immune system homeostasis in senescence.

Aging↗

Magnetic fields, brain and immunity: effect on humoral and cell-mediated immune responses.

Magnetic fields (MF) can influence biological systems in a wide range of animal species and humans. We report here on the influence of static MF, locally applied to the brain area, on immune system performances in the rat. In the first series of experiments two AKMA micromagnets (M) with the influx density of 600 Gauss were bilaterally implanted (with "N" polarity facing the cranial bones) and fixed to the skull posterior to the fronto-parietal suture (parietal brain exposure). Rats implanted with iron beads (I) and sham-operated (SO) rats served as controls. Animals were exposed to MF or I during different periods of time before and after immunization with several soluble or cellular antigens. We report here on the in vivo immunoregulating effects of centrally applied MF on plaque-forming cell (PFC) response, local hypersensitivity skin reactions and experimental allergic encephalomyelitis. The selective influence of MF applied to different brain regions on PFC response was evaluated, as well. For this purpose, two M were bilaterally implanted in the area of (a) frontal, (b) parietal and (c) occipital brain regions. Rats were under the influence of MF for 20 days before and 4 days after immunization with sheep red blood cells. Groups of nonimmunized rats were exposed for 14, 24 and 34 days to parietally implanted M or I, and the number of peripheral blood CD4+ and CD8+ cells determined by mouse anti-rat W3/25 and MRC OX 8 monoclonal antibodies. The results show an overall in vivo immunopotentiation of humoral and cell-mediated immune responses in rats exposed to MF. Furthermore, these immunomodulating effects of centrally applied MF depend on at least two basic parameters, time of exposure and brain region exposed. The highest immune performance was obtained after exposure of the occipital brain region for a total period of 24 days. The results provide further evidence of the complex interrelationship between the environment, the central nervous system and the immune system.

Animals↗

Enkephalinase-inhibitors modulate immune responses.

Exogenous opioid peptides, and enkephalins in particular, modulate a variety of immune performances in vivo and in vitro. In this study, the immunomodulatory role of endogenous opioids was investigated by means of central and peripheral administration of four peptidase inhibitors in the rat. Animals sensitized with sheep red blood cells (SRBC) were daily treated intraperitoneally (i.p.) with 0.2 mg/kg or 1 mg/kg of each inhibitor, or intracerebroventricularly (i.c.v.) with 0.02 mg/kg and 0.2 mg/kg of bestatin, des-tyrosine-methionine-enkephalin, (Des-Tyr1)Met-Enk; and actinonin, and 0.005 and 0.5 mg/kg of N-Carboxymethyl-phenilalanine-leucine,(N-C)Phe-Leu. Controls were injected i.p. and i.c.v. with saline. The results revealed that in animals treated i.p. with 0.2 mg/kg of bestatin and (N-C)Phe-Leu potentiated the plaque-forming cell (PFC) response and hemagglutinin production. In contrast, these immune responses were suppressed by 1 mg/kg. On the other hand, i.p. doses of 0.2 and 1 mg/kg of actinonin and (Des-Tyr1)Met-Enk potentiated humoral immune responses. When given i.c.v., all of the inhibitors used exerted clear dose-dependent immunomodulatory effects, i.e. increase in the PFC response and hemagglutinin production when given at lower doses (0.005-0.02 mg/kg), and decrease when injected with higher doses (0.2-0.5 mg/kg). These effects of enkephalin-related peptidase inhibitors, applied i.p. and i.c.v., suggest the involvement of endogenous enkephalins in immune mechanisms.

Adjuvants, Immunologic↗

Changes of experimental allergic encephalomyelitis by methionine-enkephalin injected into lateral ventricles of the rat brain.

Our previous investigations have shown that the opioid peptide methionine-enkephalin (Met-Enk) modulates in vivo a variety of humoral and cell-mediated immune performances. In this study, rats bearing polyethylene cannulae permanently inserted into the lateral ventricles of the brain were used. Experimental allergic encephalomyelitis (EAE) was induced with guinea pig spinal cord in complete Freund's adjuvant injected into the left hind foot pad. The following groups of cannulated rats were tested: nontreated with Met-Enk or saline, intracerebroventricularly (i.c.v.) injected with saline, and i.c.v. treated with low (1 microgram/kg) dose of Met-Enk and high (1 mg/kg) dose of Met-Enk. Intact noncannulated rats sensitized for EAE served as an additional control. The results showed that i.c.v. treatment with 1 microgram/kg of Met-Enk significantly increased the incidence and severity of EAE. In contrast, injections of 1 mg/kg of Met-Enk produced a moderate decline of clinical EAE, but marked diminution of inflammatory lesions in the brain. Interestingly, histopathology of EAE was more pronounced in control rats treated i.c.v. with saline. On the other hand, control cannulated rats noninjected with saline exhibited a striking decrease of neurological and histopathological signs of the disease, thus indicating a suppressive effect of stress (surgical procedure) on EAE. In conclusion, the present study showing the central effect of Met-Enk on EAE when peptide was applied in the cerebral cavity, and earlier studies which revealed the peripheral effect on EAE when Met-Enk was administered intraperitoneally, suggests that Met-Enk exerts its immunomodulatory action both centrally and peripherally.

Animals↗

In vivo effect of prothymosin-alpha 1 on humoral and cell-mediated immune responses in the young rat.

There is a large body of evidence for the role of thymosin peptides in immunogenesis and immunity. In this paper we report on the influence of prothymosin alpha 1 (ProT-alpha 1), a hormone-like peptide derived from the calf thymus, on humoral and cellular immune reactions in the rat. Young adults received intraperitoneal injections of ProT-alpha 1 in the periods before and after immunization with cellular and soluble antigens. ProT-alpha-treatment produced a dose-dependent increase of both humoral and cell-mediated immune responses. The thymus weight increased but not that of spleen. Treatment of nonimmunized rats with this polypeptide significantly elevated the number of CD4+ and decreased the number of CD8+ cells in the peripheral blood. The results suggest a potent immunostimulatory activity of ProT-alpha 1 and imply direct action of this polypeptide on T lymphocytes.

Adjuvants, Immunologic↗

Euthyroid sick syndrome in children with acute viral hepatitis A.

According to the clinical findings, the activity of serum asparate aminotransferase (EC 2.6.1.1), alanine aminotransferase (EC 2.6.1.2) and the level of total bilirubin, 45 children with acute viral hepatitis A were divided into two groups: with mild and moderately severe degree of disease. By determining the products of the peripheral thyroxine metabolism-T3 and rT3, as well as the other thyroid parameters (T4, FT4, TSH and TBG) we have found significantly lower T3 level and significantly higher T4 and TBG levels in both groups of patients in comparison with control group. At the same time, the level of biologically less active rT3 was increased in patients with moderately severe form of disease, while no differences were found in the values of TSH between the ill and control patients. TRH induced TSH release was normal in all patients. The results of this study point to the development of euthyroid sick syndrome or low T3 syndrome in children with viral hepatitis A.

Acute Disease↗