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Biomedical subjects

I Hajdu

Publications and source records attributed to I Hajdu.

At least 19 recordsLinked to original sources
PubMed2006

Ghrelin-induced sleep responses in ad libitum fed and food-restricted rats.

Ghrelin is an endogenous ligand for the growth hormone secretagogue receptor and a well-characterized food intake regulatory peptide. Hypothalamic ghrelin-, neuropeptide Y (NPY)-, and orexin-containing neurons form a feeding regulatory circuit. Orexins and NPY are also implicated in sleep-wake regulation. Sleep responses and motor activity after central administration of 0.2, 1, or 5 microg ghrelin in free-feeding rats as well as in feeding-restricted rats (1 microg dose) were determined. Food and water intake and behavioral responses after the light onset injection of saline or 1 microg ghrelin were also recorded. Light onset injection of ghrelin suppressed non-rapid-eye-movement sleep (NREMS) and rapid-eye-movement sleep (REMS) for 2 h. In the first hour, ghrelin induced increases in behavioral activity including feeding, exploring, and grooming and stimulated food and water intake. Ghrelin administration at dark onset also elicited NREMS and REMS suppression in hours 1 and 2, but the effect was not as marked as that, which occurred in the light period. In hours 3-12, a secondary NREMS increase was observed after some doses of ghrelin. In the feeding-restricted rats, ghrelin suppressed NREMS in hours 1 and 2 and REMS in hours 3-12. Data are consistent with the notion that ghrelin has a role in the integration of feeding, metabolism, and sleep regulation.

Analysis of Variance↗
PubMed2004

Fos-immunoreactivity in the hypothalamus: dependency on the diurnal rhythm, sleep, gender, and estrogen.

Diurnal variations and sleep deprivation-induced changes in the number of Fos-immunoreactive (Fos-IR) neurons in various hypothalamic/preoptic nuclei were studied in the rat. The nuclei implicated in sleep regulation, the ventrolateral preoptic (VLPO), median preoptic (MnPO), and suprachiasmatic (SCN, dorsomedial subdivision) nuclei, displayed maximum c-fos expression in the rest (light) period. Sleep deprivation (S.D.) suppressed Fos-IR in the dorsomedial subdivision of SCN but failed to alter Fos in the VLPO. Fos-IR increased in the VLPO during recovery after S.D. A nocturnal rise in Fos expression was detected in the arcuate (ARC), anterodorsal preoptic (ADP) and anteroventral periventricular (AVPV) nuclei whereas the lateroanterior hypothalamic nucleus (LA) and the ventrolateral subdivision of SCN did not display diurnal variations. S.D. stimulated Fos expression in the ARC, ADP, and LA. Statistically significant, albeit modest, differences were noted in the number of Fos-IR cells between males and cycling female (estrus/diestrus) in the VLPO, MnPO, ARC, LA, and AVPV, and the female ADP did not display diurnal variations. Ovariectomy (OVX) was followed by marked reduction in Fos expression in the VLPO, SCN, and AVPV, and the diurnal rhythm decreased in the VLPO, and vanished in the dorsomedial SCN, and AVP. Estrogen administration to OVX female rats stimulated Fos expression in most nuclei, and the lost diurnal variations reoccurred. In contrast, castration of male rats had little effect on Fos expression (slight rises in diurnal Fos in the ARC and ventrolateral SCN). The results suggest that Fos expression is highly estrogen-dependent in many hypothalamic nuclei including those that have been implicated in sleep regulation.

Animals↗
PubMed2004

Rhythms of ghrelin, leptin, and sleep in rats: effects of the normal diurnal cycle, restricted feeding, and sleep deprivation.

To determine the relationships among plasma ghrelin and leptin concentrations and hypothalamic ghrelin contents, and sleep, cortical brain temperature (Tcrt), and feeding, we determined these parameters in rats in three experimental conditions: in free-feeding rats with normal diurnal rhythms, in rats with feeding restricted to the 12-h light period (RF), and in rats subjected to 5-h of sleep deprivation (SD) at the beginning of the light cycle. Plasma ghrelin and leptin displayed diurnal rhythms with the ghrelin peak preceding and the leptin peak following the major daily feeding peak in hour 1 after dark onset. RF reversed the diurnal rhythm of these hormones and the rhythm of rapid-eye-movement sleep (REMS) and significantly altered the rhythm of Tcrt. In contrast, the duration and intensity of non-REMS (NREMS) were hardly responsive to RF. SD failed to change leptin concentrations, but it promptly stimulated plasma ghrelin and induced eating. SD elicited biphasic variations in the hypothalamic ghrelin contents. SD increased plasma corticosterone, but corticosterone did not seem to influence either leptin or ghrelin. The results suggest a strong relationship between feeding and the diurnal rhythm of leptin and that feeding also fundamentally modulates the diurnal rhythm of ghrelin. The variations in hypothalamic ghrelin contents might be associated with sleep-wake activity in rats, but, unlike the previous observations in humans, obvious links could not be detected between sleep and the diurnal rhythms of plasma concentrations of either ghrelin or leptin in the rat.

Animals↗
PubMed2002

Sleep of transgenic mice producing excess rat growth hormone.

The effects of chronic excess of growth hormone (GH) on sleep-wake activity was determined in giant transgenic mice in which the metallothionein-1 promoter stimulates the expression of rat GH (MT-rGH mice) and in their normal littermates. In the MT-rGH mice, the time spent in spontaneous non-rapid eye movement sleep (NREMS) was enhanced moderately, and rapid eye movement sleep (REMS) time increased greatly during the light period. After a 12-h sleep deprivation, the MT-rGH mice continued to sleep more than the normal mice, but there were no differences in the increments in NREMS, REMS, and electroencephalogram (EEG) slow-wave activity (SWA) during NREMS between the two groups. Injection of the somatostatin analog octreotide elicited a prompt sleep suppression followed by increases in SWA during NREMS in normal mice. These changes were attenuated in the MT-rGH mice. The decreased responsiveness to octreotide is explained by a chronic suppression of hypothalamic GH-releasing hormone in the MT-rGH mice. Enhancements in spontaneous REMS are attributed to the REMS-promoting activity of GH. The increases in spontaneous NREMS are, however, not consistent with our current understanding of the role of somatotropic hormones in sleep regulation. Metabolic, neurotransmitter, or hormonal changes associated with chronic GH excess may indirectly influence sleep.

Animals↗
PubMed2001

The somatostatin analog, octreotide, causes accumulation of growth hormone-releasing hormone and depletion of angiotensin in the rat hypothalamus.

Rats were injected intracerebroventricularly with the somatostatin analog, octreotide (OCT; 0.1 microg) or vehicle, and hypothalamic contents of growth hormone-releasing hormone (GHRH), angiotensin II, and vasopressin were determined 10 min, 1, 3 and 6 h post-injection. OCT elicited an immediate release of angiotensin II (10 min) and a rise in GHRH content (1 h) followed by gradual (1-6 h) depletion of accumulated GHRH. Hypothalamic vasopressin was not altered but decreases in pituitary vasopressin occurred 10 min post-injection. The OCT-induced alterations in GHRH may explain previously reported changes in sleep whereas angiotensin may mediate OCT-induced drinking, vasopressin secretion and rises in blood pressure via sst2 somatostatin receptors.

Angiotensin II↗
PubMed2000

Octreotide-induced drinking, vasopressin, and pressure responses: role of central angiotensin and ACh.

The involvement of central angiotensinergic and cholinergic mechanisms in the effects of the intracerebroventricularly injected somatostatin analog octreotide (Oct) on drinking, blood pressure, and vasopressin secretion in the rat was investigated. Intracerebroventricular Oct elicited prompt drinking lasting for 10 min. Water consumption depended on the dose of Oct (0.01, 0.1, and 0. 4 microgram). The drinking response to Oct was inhibited by pretreatments with the intracerebroventricularly injected angiotensin-converting enzyme inhibitor captopril, the AT(1)/AT(2) angiotensin receptor antagonist saralasin, the selective AT(1) receptor antagonist losartan, or the muscarinic cholinergic receptor antagonist atropine. The dipsogenic effect of Oct was not altered by prior subcutaneous injection of naloxone. Oct stimulated vasopressin secretion and enhanced blood pressure. These responses were also blocked by pretreatments with captopril or atropine. Previous reports indicate that the central angiotensinergic and cholinergic mechanisms stimulate drinking and vasopressin secretion independently. We suggest that somatostatin acting on sst2 or sst5 receptors modulates central angiotensinergic and cholinergic mechanisms involved in the regulation of fluid balance.

Acetylcholine↗
PubMed1999

Central administration of the somatostatin analog octreotide induces captopril-insensitive sleep responses.

The effects of intracerebroventricular injections of the long-lasting somatostatin analog octreotide (Oct) were studied on sleep and behavior in rats. Pyrogen-free physiological saline and Oct (0.001, 0.01, 0.1 microgram) or vehicle were administered at light onset, and the electroencephalogram (EEG), motor activity, and cortical brain temperature were recorded during the 12-h light period. Plasma growth hormone (GH) concentrations were measured in samples taken at 30-min intervals after Oct. Oct (0.01 and 0.1 microgram) suppressed non-rapid eye movement sleep (NREMS) for 1-2 h. NREMS intensity (delta EEG activity during NREMS) dose dependently increased in hour 3 postinjection and thereafter (0.1 microgram). Plasma GH concentrations were suppressed after Oct (0.01 and 0.1 microgram), but pulses of GH secretions occurred 90-120 min postinjection in each rat. Oct (0.1 microgram) enhanced behavioral activity, including prompt drinking followed by grooming, scratching, and feeding. Intracerebroventricular injection of the angiotensin-converting enzyme inhibitor captopril (30 microgram, 10 min before Oct), blocked these behavioral responses but not the Oct-induced sleep alterations. The changes in sleep after intracerebroventricular Oct suggest an intracerebral action site and might result from Oct-induced variations in the sleep-promoting activity of GH-releasing hormone.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1994

A unique association of renal carcinoma with sarcoid reaction in the kidney.

Sarcoid reactions have been described in association with lymphomas and rarely with other solid tumors. We describe a patient with renal papillary adenocarcinoma and prominent sarcoid-like granulomatous infiltration of the ipsilateral and most likely the contralateral kidney. There was no evidence of extrarenal granulomas. This is the first description of impairment in renal function in a patient with renal carcinoma and with sarcoid reaction to this tumor isolated in the kidney.

Adenocarcinoma, Papillary↗
PubMed1990

Association of intracranial meningioma with arteriovenous malformation.

Simultaneous occurrence of a cerebral arteriovenous malformation and a primary brain tumor is rare. A case of a left occipital meningioma and a right parietotemporal arteriovenous malformation is reported. Clinical, radiological, and postmortem findings are described. Thirty previous reports of arteriovenous malformations associated with primary brain tumors are reviewed. In 18 cases the two lesions were intermixed or in close proximity. This spatial relationship between the lesions suggests more than a coincidental association. Several hypotheses are proposed to explain common causal connections.

Aged↗
PubMed1988

The role of H-2 in apoferritin-induced murine immune complex glomerulonephritis.

The role of the major histocompatibility complex in the development of apoferritin induced immune complex glomerulonephritis was studied in H-2 congenic B10 mice. The glomerular lesions varied strikingly among the three different strains studied. The B10 (H-2b) mice had minimal mesangial expansion or no lesions at all. The B10.BR (H-2k) mice had mesangial expansion and proliferative glomerulonephritis without crescents or interstitial mononuclear cell infiltration. In contrast, the B10.D2 (H-2d) mice had necrotizing glomerulonephritis with crescents and an interstitial mononuclear cell infiltrate. Immunofluorescence and electron microscopy demonstrated only minimal mesangial deposits in B10 (H-2b) mice, predominantly mesangial deposition in the B10.BR (H-2k) mice, and mesangial and subepithelial immune complex deposits in B10.D2 (H-2d) mice. These morphologic differences correlated with functional abnormalities. Only the B10.D2 (H-2d) mice developed proteinuria, hematuria, and elevated blood urea nitrogen. They also had the most elevated antiapoferritin IgG levels. These experiments demonstrate that differences in the pathologic lesions and susceptibility to immune complex glomerulonephritis can be seen in animals that differ only at the H-2 locus. This model will lend itself to the study of the mechanisms by which the major histocompatibility complex influences the development of immune complex glomerulonephritis.

Animals↗
PubMed1986

Peanut agglutinin binding as a histochemical tool for diagnosis of eosinophilic granuloma.

Histochemical detection of peanut agglutinin binding performed on tissue sections in 11 cases of eosinophilic granuloma of bone revealed simultaneous appearance of the reaction product both at the cell surface and within the cytoplasm (in the Golgi area) of a vast majority of Langerhans' cells. Based on this unique characteristic of Langerhans' cells, peanut agglutinin binding assay may represent a simple and inexpensive tool for morphologic differentiation of eosinophilic granuloma or other types of histiocytosis X from other monocytic and histiocytic lesions in equivocal cases.

Adolescent↗
PubMed1985

Choroid plexus as a barrier to immunoglobulin delivery into cerebrospinal fluid.

The concentration of gamma globulins is greatly increased in the cerebrospinal fluid (CSF) during inflammatory and degenerative disorders of the central nervous system (CNS). The mechanism by which immunoglobulins enter the CSF under normal conditions is unknown. The extent of participation of the blood-brain barrier in protein delivery to the CSF is unclear, although the choroid plexus is known to have primary responsibility for the formation and movement of certain proteins into the CSF. To investigate the role of the choroid plexus in immunoglobulin delivery to the CSF, the authors evaluated rat brain tissue by light and electron microscopic immunohistochemical technique using the peroxidase technique of immunoglobulin (Ig)G and IgA detection. Peanut agglutinin was used to identify macrophages, cells known to have important immune functions and which have been reported as a normal component of the choroid plexus. Antisera to IgG' and IgA demonstrated diffuse surface staining of the choroidal epithelial cells with light and electron microscopy; the cytoplasm and nuclei did not contain immunoglobulins. Macrophages were not present in the choroid plexus, in contrast to previous reports. The results demonstrate that immunoglobulins do not enter the CSF via the choroid plexus, unlike other proteins in similar concentrations in the CSF. In addition, macrophages are shown to be an insignificant component of the plexus, thereby further diminishing the likelihood of participation-of the choroid plexus in the regulation of immunoglobulin entry into the CNS under normal conditions.

Animals↗
PubMed1983

Ultrastructural studies of human lymphoid cells. mu and J chain expression as a function of B cell differentiation.

J chain expression was examined as a function of the stage in differentiation along the B cell axis in humans. Intracellular distribution of J and mu chains in leukemic HLA-DR+ null and pre-B cells, and in normal B cells stimulated with pokeweed mitogen (PWM) was determined by immunoelectron microscopy and radioimmunoassay (RIA). J chain was detected in leukemic null and pre-B cells on free and membrane-bound ribosomes in the cytoplasm, or on perinuclear cisternae. Mu chain was found on free ribosomes and ribosomal clusters in leukemic pre-B cells but was absent in the leukemic null cells. In pre-B cell lines, mu chain was seen within rough endoplasmic reticulum (RER) and the Golgi apparatus whereas J chain was not detected in these organelles. However, both mu and J chain were detected in RER and the Golgi apparatus of immature and mature plasma cells induced by PWM stimulation of normal peripheral blood lymphocytes. Low levels of J chain were also detected by RIA in lysates of leukemic null and pre-B cells. Most of the intracellular J chain became detectable after reduction and alkylation of cell lysates, and free J chain was not found in the culture supernatants. The amount of intracellular and secreted immunoglobulin-bound J chain increased dramatically after PWM stimulation of peripheral blood lymphocytes. The majority of J chain-positive cells seen over an 8 d culture interval were lymphocytes and lymphoblasts, while mu chain was found primarily in plasma cells. These results suggest that J chain expression precedes mu chain synthesis during B cell differentiation and that a combination of the two chains for secretion is not initiated until the onset of plasma cells maturation.

B-Lymphocytes↗
PubMed1983

The immunohistochemical detection of J chain in lymphoid cells in tissue sections: the necessity of trypsin digestion.

The immunohistochemical detection of J chain in histological sections of tonsils was compared to that of immunoglobulin IgG, IgM, and IgA. Pretreatment of tissue sections with detergents (saponin and Triton X-100) and with proteolytic enzyme (trypsin) at different experimental conditions has shown (i) 0.1% trypsin digestion for 1 hr at room temperature increased dramatically both the number of J-chain-positive cells detected, and the intensity of the color reaction, while the detergents had no noticeable effect; (ii) under the same conditions, trypsin also improved the detection of immunoglobulins, but quantitatively and qualitatively far less effectively than for J chain. The effect of trypsin occurred after 30 min. These results indicate that in tissue sections, the antigenic determinants of J chain are "masked" in the molecule of immunoglobulin in such a manner that the use of trypsin hydrolysis may be important for its successful detection at the light microscopic level. In the case of intact immunoglobulins, this is less important.

Humans↗
PubMed1983

Lipid and blood pressure-lowering effect of mackerel diet in man.

Fifteen healthy volunteers were put on a mackerel and herring diet, consisting of a prescribed daily isocaloric regimen in a cross-over design, for 2 weeks. Eicosapentaenoic acid (EPA - C20:5, n-3) was predominantly incorporated into cholesterol esters, whereas docosahexaenoic acid (C22:6, n-3) appeared more in serum triglycerides, indicating that the function of the latter may be different from that of EPA. After mackerel ingestion, serum triglycerides, total cholesterol and lecithin cholesterol acyl transferase (LCAT) activity were significantly decreased, returning to basal levels 3 months later. Low density lipoprotein (LDL) cholesterol, high density lipoprotein (HDL) cholesterol and postheparin lipolytic activity (PHLA) remained unchanged at the end of the mackerel diet. Generally, after the herring diet the differences were minor, only LCAT activity being significantly decreased. A markedly lower systolic and diastolic blood pressure at the end of the mackerel period could be observed. After herring diet a slight diminution of blood pressure was not significant. Accordingly, plasma noradrenaline was only significantly decreased at the end of the mackerel period. Dopamine-beta-hydroxylase (DBH) activity in serum had no differences before, during and after the study. From the data presented it can be said that a mackerel diet exerts a beneficial influence on cardiovascular risk.

Adult↗
PubMed1983

Ultrastructural localization of the transferrin receptor and transferrin on marrow cell surfaces.

The monoclonal antibody OKT9 (a known transferrin receptor antibody) and a monoclonal antibody to transferrin (ATfn) were used to localize the transferrin receptor and transferrin on marrow cells. After incubation of cell suspensions with the antibody, the cells were reacted with an affinity purified Fab fragment of goat anti-mouse IgG conjugated to horseradish peroxidase (GAM-HRP), which was in turn visualized by reaction with 3,3'-diaminobenzidine (DAB). Erythroblast cell surfaces stained intensely with OKT9-GAM-HRP-DAB, weaker staining was observed on reticulocyte surfaces, whereas erythrocyte surfaces lacked staining. Staining was present on surface caveolae, which often contained endogenous ferritin particles. Moderate to strong OKT9 staining was observed on less than 10% of presumed lymphoid cells. Monocytes, macrophages, promyelocytes, granulocytes, megakaryocytes and platelets consistently lacked OKT9 staining. ATfn-GAM-HRP-DAB staining of erythroid cells was similar to that observed with OKT9 staining; however, in contrast to the latter staining, ATfn stained the surfaces of megakaryocytes, platelets, monocytes and most lymphocytes. Promyelocytes stained weakly, whereas late granulocytes lacked staining. These results indicate that the T9 transferrin receptor (1) is largely confined to erythroid cells in marrow, (2) is diffusely distributed on the surface of early erythroid cells, (3) decreases with cell maturation, and (4) is lost when haemoglobin synthesis is completed. Transferrin appears in a similar distribution on erythroid cell surfaces but also appears to bind to some cell surfaces lacking the T9 receptor.

Antibodies, Monoclonal↗