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Biomedical subjects

E Stark

Publications and source records attributed to E Stark.

At least 55 records · Page 3Linked to original sources

Immunocytochemical demonstration of human immunodeficiency virus infected cells in the cerebrospinal fluid.

Although involvement of the central nervous system represents one of the most common manifestations of the acquired immunodeficiency syndrome (AIDS), a standard diagnostic test for this condition has not yet been established. At necropsy human immunodeficiency virus (HIV) has been demonstrated in brain macrophages in such patients. HIV antigen was detected in CSF macrophages by immunocytochemistry in six out of 11 HIV infected patients. In addition to the detection of intrathecal synthesis of anti-HIV antibodies this method may be suitable for early diagnosis of CNS involvement in AIDS patients.

Acquired Immunodeficiency Syndrome↗

Prolactin release induced by opiate agonists, effect of glucocorticoid pretreatment in intact and adrenalectomized rats.

Cortisol administered at a dose of 25 mg/kg 24 h before measurements decreased the prolactin secretion induced by intraventricularly given opioids (dynorphin, beta-endorphin, Met-enkephalin or D-Met-Pro-enkephalinamide). The effect of cortisol was depressed by actinomycin D pretreatment. The cortisol-induced inhibition of the action of morphine was facilitated in adrenalectomized animals; measuring the effects of increasing doses of cortisol a maximal inhibition was obtained at a dose of 5 mg/kg. The opioid-induced corticosterone secretion was not affected 24 h after a single administration of cortisol. The present results show that the cortisol-induced inhibition of opioid-induced prolactin secretion is dependent on protein synthesis and independent of changes in drug metabolism, and of the type of opiate receptor preferentially affected by the opiate agonists employed.

Adrenalectomy↗

Consistency of repeated flow-volume parameters in airway challenge studies.

A maximal lung inflation is known to alter airway tone in man. Recent investigations, examining how this phenomenon relates to bronchial provocation testing, suggest that a deep inspiration will decrease airway resistance and underestimate the subsequent decrement in lung function following airway challenge. Because the recovery of baseline tone is rapid following a deep inspiration, we evaluated the consistency of three consecutive partial and maximal expiratory flow-volume maneuvers performed at approximately 45- to 60-second intervals. Functional parameters including the forced expiratory volume in 1 s and the maximal expiratory flow at 60% of the vital capacity below total lung capacity on the partial curve (MEF40%P) were constant at each measurement point following induced bronchoconstriction or bronchodilation in both healthy and asthmatic subjects. We suggest that with 45 s between maneuvers, repeatable parameters can be attained from three consecutive flow-volume curves.

Airway Resistance↗

Women and children at risk: a feminist perspective on child abuse.

Viewing child abuse through the prism of woman battering reveals that both problems originate in conflicts over gender identity and male authority. Data indicate that men, not women, typically commit serious child abuse. A study of the mothers of child abuse victims shows that battering is the most common context for child abuse, that the battering male is the typical child abuser, that the battered mothers have no distinctive pathology in their backgrounds, and that clinicians respond punitively to the battered mothers. The child abuse establishment assigns responsibility for abuse to mothers regardless of who assaults the child, and responds punitively to women, withholding vital resources and often removing the child to foster care, if women are battered or otherwise fail to meet expectations of "good mothering." The combination of male control, misleading psychological knowledge about women's propensity for "bonding," and sanctions used to enforce gender stereotypes of motherhood combine to increase the entrapment and inequality from which battering and child abuse originate, a process termed "patriarchal mothering." The best way to prevent child abuse is through "female empowerment."

Child↗

Mollaret's meningitis: CSF-immunocytological examinations.

Mollaret's meningitis is a rare clinical entity consisting of recurrent attacks of meningeal irritation, which, after a sudden onset, last for a few days. The prognosis appears to be excellent, although the aetiology has not been established. In the CSF so-called endothelial cells are a typical finding, but their classification is not yet clear. In the present case immunocytological examination of CSF cells revealed that the so-called Mollaret cells are monocytes. The time course of changes in helper/suppressor ratio is similar to that in other infectious diseases of the central nervous system.

Antibodies, Monoclonal↗

Polyneuropathy in Waldenström's macroglobulinaemia. Passive transfer from man to mouse.

To support the hypothesis of an immunopathogenesis of polyneuropathy in Waldenström's macroglobulinaemia (MW), serum IgM fractions of MW patients were applied intraperitoneally to mice for 17 days. Sections of liver, kidney, M. glutaeus maximus, central nervous system (CNS) and both Nn. ischiadici were examined for IgM, IgG, C3 and as control IgD with PAP-immunostaining. IgM deposits were found in every organ except the CNS. In peripheral nerves larger amounts were visualized in perineurium and endoneural space, whereas myelin lamellae and periaxon did not stain. Therefore, perhaps our investigation reveals a greater permeability of the blood-nerve barrier (BNB) compared with the blood-brain barrier (BBB). The involvement of the monoclonal IgM of MW, which has been shown to react in vitro with peripheral nerve constituents, appears possible in the pathogenesis of polyneuropathy.

Animals↗

Diurnal variation in prolactin, adrenocorticotropin and corticosterone release induced by opiate agonists in intact and adrenalectomized rats.

Diurnal variations of the effectivity of beta-endorphin (beta-End), dynorphin (DYN), Met-enkephalin (Met-Enk), D-Met2-Pro5-enkephalinamide (D-Met-Pro-Enk) and morphine to induce prolactin (PRL) and adrenocorticotropin (ACTH)/corticosterone (CS) release in intact and adrenalectomized rats have been examined. The response to morphine (10 mg/kg s.c.), Met-Enk (200 micrograms/rat i.c.v.) and D-Met-Pro-Enk (0.5 microgram/rat i.c.v.) did not change with different times of the day, while that to beta-End (0.5 microgram/rat i.c.v.), DYN (1 microgram/rat i.c.v.) and U50-488H, a selective kappa agonist (10 mg/kg s.c.), showed a circadian rhythm in stimulating PRL release, with a higher increase in the afternoon (16.00-17.00 h) than in the morning (08.00-09.00 h). In adrenalectomized rats the loss of this circadian rhythm was shown. The CS release evoked by morphine, D-Met-Pro-Enk, Met-Enk and DYN was demonstrable only in the morning when the basal CS level was significantly lower than in the afternoon. The afternoon release of ACTH by morphine was higher than in the morning in adrenalectomized rats. beta-End and U50-488H were equally active in the morning and in the afternoon in increasing CS secretion. The present results suggest that the diurnal rhythm in the response of CS and PRL release to opioids is in relation with the glucocorticoid secretion.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗

Increase of progesterone production in human and rat luteal cells by beta-adrenergic stimulation.

The effects of the beta 2-adrenergic agonist hexoprenaline were studied on the progesterone production of rat and human corpora lutea and compared to hCG-induced hormone production. Human corpora lutea were obtained from healthy patients, rat corpora lutea were harvested on day 6 of pseudopregnancy. Corpora lutea were digested by trypsin and homogeneous luteal cell suspension (6 X 10(5) cells/ml) was incubated for 2 h. Hexoprenaline and hCG were added to the medium and progesterone production was measured by RIA. Hexoprenaline or hCG dose-dependently increased the progesterone production of rat luteal cells and of human cells in mid- and late luteal phase. Moreover, hexoprenaline further increased the hCG-induced hormone production. The stimulatory effect of hexoprenaline could be prevented by propranolol. It is supposed that beta 2-adrenergic stimulation induces an increase in progesterone production of luteal cells and potentiates the effects of gonadotropic hormones.

Animals↗

Primary germinoma of the brain. Immunocytochemical demonstration of tumour cells in the cerebrospinal fluid.

A patient is presented, who developed a suprasellar tumour. Stereotactical biopsy of the tumour revealed the diagnosis of a dysgerminoma. Immunocytochemical examination of the CSF showed neoplastic cells staining for human chorionic gonadotropin and for alpha-fetoprotein. The authors stress the possibility to diagnose primary intracranial germ cell tumours without operation.

Adolescent↗

Stimulation of progesterone production by adrenocorticotropic hormone and prostaglandin E2 in rat luteal cells.

The effects of adrenocorticotropic hormone (ACTH), human chorionic gonadotropin (hCG) and prostaglandin E2 (PGE2) on the progesterone secretion of luteal cells from rats were studied. Corpora lutea were harvested on Day 6 of pseudopregnancy and digested by trypsin. Homogeneous suspensions of luteal cells were used for short-term incubation. ACTH, PGE2, and hCG were added to the medium and the changes in progesterone production were measured by radioimmunoassay (RIA). Furthermore, specific ACTH-binding sites of the luteal cell membrane were studied by Scatchard analysis. ACTH, PGE2 and hCG increased synthesis of progesterone, and the combination of hCG with ACTH or PGE2 further increased production of the hormone. The effect of ACTH could be prevented by indomethacin. These effect of ACTH seem to be connected with specific ACTH-binding sites of the luteal cell membrane and with increased production of PGE2.

Adrenocorticotropic Hormone↗

Long-term effects of hypothalamic paraventricular lesion on CRF content and stimulated ACTH secretion.

The effect of short-term (1 wk) and long-term (6 wk) lesion of the paraventricular nucleus (PVN) on the hypothalamopituitary-adrenal axis was studied. Six weeks after PVN lesion there was no change in resting morning plasma ACTH and corticosterone levels. The increase of plasma ACTH levels that occurs 8 days after adrenalectomy was inhibited 6 wk after placing a lesion in the PVN. In contrast, 6 wk after PVN lesion the plasma ACTH response measured 3 min after laparatomy and intestinal traction under ether anesthesia was not significantly different from that in the controls. The responsiveness to corticotropin-releasing factor (CRF)-41 of anterior pituitary segments incubated in vitro increased slightly at 6 wk after PVN lesion. The amount of CRF-41-like immunoreactive material in the stalk-median eminence decreased to approximately 14% of the control, while that in neural lobe failed to change. We suggest that the ACTH hypersecretion after adrenalectomy is driven predominantly by CRF-and/or AVP-producing neurons in and around the PVN, whereas other sources of CRF-41, increased pituitary sensitivity or other hypothalamic factors, may restore stress-induced ACTH release in the absence of the region of the PVN.

Adrenalectomy↗

Central nervous system control of pituitary vasopressin receptors: evidence for involvement of multiple factors.

The regulation of pituitary vasopressin (VP) receptor concentration was investigated in rats with antero-lateral cuts (ALC) placed around the hypothalamus, as well as in Brattleboro homozygotes (HO) that genetically suffer from a lack of AVP. Hypothalamic ALCs caused a reduction in (3H)-AVP binding, while counteracting the dramatic fall in binding that normally occurs after adrenalectomy. Surprisingly, in HO rats, long-term adrenalectomy did cause pituitary AVP receptor number to decrease to an extent similar to that seen in normal rats. However, the receptor disappeared twice as rapidly in heterozygote controls than in HO animals, with calculated half-lives of 1.1 and 2.0 days, respectively. In HO, chronic administration of VP reduced receptor concentration by about 80%, while the same dose of oxytocin (OT) produced only a 20-30% reduction. Whereas dexamethasone injections did reverse the depressing effect of adrenalectomy on pituitary AVP receptors, they failed to enhance binding in sham-operated controls, treated or not with VP; thereby suggesting a central site of action of the steroid. In contrast, in rats with hypothalamic ALCs (i.e. with the pituitary lacking central control), corticosterone implants did antagonize the reduction in receptor density caused by adrenalectomy. We conclude that the pituitary AVP receptor system lies mainly under control of the central nervous system, through a mechanism of action that not only seems to imply AVP and OT, but probably also some other hypothalamic factor(s). Glucocorticoids appear to exert a dual effect, acting indirectly through negative feedback control of neuropeptide release and, possibly, also directly on the pituitary to regulate binding sites.

Adrenalectomy↗

Direct effects of ACTH on the ovary.

We have summarized the data of our former experiments which clearly demonstrate that ACTH increases ovarian blood flow in various mammals. Furthermore, when the ovary is primed with gonadotropic hormones it stimulates secretion of 17 beta-oestradiol and progesterone.

Adrenocorticotropic Hormone↗

[Asthma, eosinophilia and systemic vasculitis: Churg-Strauss syndrome].

In two female patients asthma, marked eosinophilia and symptoms of systemic vasculitis could be classified clinically or histologically as allergic angiitis and granulomatosis (Churg-Strauss syndrome). The course in one patient went back over 20 years, characterized by an asymptomatic interval of 16 years. It is to be assumed that the disease is more frequent than it is diagnosed. It has to be thought of when, in addition to asthma and eosinophilia, there is evidence of involvement of other organs.

Asthma↗

Reactivity of sera and isolated monoclonal IgM from patients with Waldenström's macroglobulinaemia with peripheral nerve myelin.

Sera of 23 patients with Waldenström's macroglobulinaemia and six monoclonal IgM paraproteins, which had been isolated from these sera, were examined for reactivity against peripheral nerve tissue. Of these 23 patients, 12 had clinical signs of peripheral polyneuropathy (PN). Using an indirect immunofluorescence method, all sera and monoclonal IgM preparations reacted with peripheral nerve structures, displaying a distinct granular fluorescence pattern with anti-IgM sera. The Waldenström sera reacted mainly with structures at the border of the myelin sheath, as well as between myelin and axon, and occasionally with the axon itself. There was no difference between sera of patients with PN and those without. Negative results were obtained in a complement fixation assay. Of the 23 sera, 15 reacted in an antibody-dependent lymphocyte-mediated cytotoxicity reaction (ADLC) with peripheral nerve myelin, and to a much lesser extent with myelin basic protein from CNS. Five of the six isolated monoclonal IgM preparations also gave positive ADLC reactions. These results constitute additional evidence for an immunological mechanism in the pathogenesis of PN in Waldenström's macroglobulinaemia.

Aged↗