Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In chicks with cannulae chronically implanted into the III cerebral ventricle, the effects of a single dose (10 micrograms) of beta-endorphin on GABA and free glutamic acid content, GAD and GABA-T activities in the diencephalon, brain-stem and brain hemispheres were studied at the time of maximal behavioural stuporous state and analgesia. A significant decrease in GABA concentration both in the diencephalon and brain-stem, accompanied by a significant increase in GABA-T activity in the same areas, was shown to occur. No changes were observed in GAD activity and in glutamic acid content in the studied areas of the brain. In conclusion, present experiments suggest that some central effects of a beta-endorphin may be due to an interference with GABA-ergic transmission.
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PMID:Effects of intraventricular beta-endorphin on GABA system in some areas of chick brain. 52 83

Various classes of antidepressant drugs with distinct pharmacologic actions are differentially effective in the treatment of classic melancholic depression--characterized by pathological hyperarousal and atypical depression--associated with lethargy, hypersomnia, and hyperphagia. All antidepressant agents exert their therapeutic efficacy only after prolonged administration. In situ hybridization histochemistry was used to examine in rats the effects of short-term (2 weeks) and long-term (8 weeks) administration of 3 different classes of activating antidepressant drugs which tend to be preferentially effective in treating atypical depressions, on the expression of central nervous system genes thought to be dysregulated in major depression. Daily administration (5 mg/kg, i.p.) of the selective 5-hydroxytryptophan (5-HT) reuptake inhibitor fluoxetine, the selective alpha 2-adrenergic receptor antagonist idazoxan, and the nonspecific monoamine oxidase A and B inhibitor phenelzine increased tyrosine hydroxylase mRNA levels by 70-150% in the locus coeruleus after 2 weeks of drug and by 71-115% after 8 weeks. The 3 drugs decreased corticotropin-releasing hormone mRNA levels by 30-48% in the paraventricular nucleus of the hypothalamus. The decreases occurred at 8 weeks but not at 2 weeks. No consistent change in steroid hormone receptor mRNA levels was seen in the hippocampus with the 3 drugs, but fluoxetine and idazoxan increased the level of mineralocorticoid receptor (MR) and glucocorticoid receptor (GR) mRNA, respectively, after 8 weeks of drug administration. Proopiomelanocortin (POMC) mRNA levels in the anterior pituitary and plasma adrenocorticotropic-hormone (ACTH) levels were not altered after 2 or 8 weeks of drug treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The antidepressants fluoxetine, idazoxan and phenelzine alter corticotropin-releasing hormone and tyrosine hydroxylase mRNA levels in rat brain: therapeutic implications. 135 83

Primary hypoadrenocorticism was diagnosed in ten young to middle-aged cats of mixed breeding. Five of the cats were male, and five were female. Historic signs included lethargy (n = 10), anorexia (n = 10), weight loss (n = 9), vomiting (n = 4), and polyuria (n = 3). Dehydration (n = 9), hypothermia (n = 8), prolonged capillary refill time (n = 5), weak pulse (n = 5), collapse (n = 3), and sinus bradycardia (n = 2) were found on physical examination. Results of initial laboratory tests revealed anemia (n = 3), absolute lymphocytosis (n = 2), absolute eosinophilia (n = 1), and azotemia and hyperphosphatemia (n = 10). Serum electrolyte changes included hyponatremia (n = 10), hyperkalemia (n = 9), hypochloremia (n = 9), and hypercalcemia (n = 1). The diagnosis of primary adrenocortical insufficiency was established on the basis of results of adrenocorticotropic hormone (ACTH) stimulation tests (n = 10) and endogenous plasma ACTH determinations (n = 7). Initial therapy for hypoadrenocorticism included intravenous administration of 0.9% saline and dexamethasone and intramuscular administration of desoxycorticosterone acetate in oil. Three cats were euthanatized shortly after diagnosis because of poor clinical response. Results of necropsy examination were unremarkable except for complete destruction of both adrenal cortices. Seven cats were treated chronically with oral prednisone or intramuscular methylprednisolone acetate for glucocorticoid supplementation and with oral fludrocortisone acetate or intramuscular injections of repository desoxycorticosterone pivalate for mineralocorticoid replacement. One cat died after 47 days of therapy from unknown causes; the other six cats are still alive and well after 3 to 70 months of treatment.
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PMID:Primary hypoadrenocorticism in ten cats. 246 93

A case of a huge inoperable adrenocortical carcinoma which secreted testosterone without characteristic symptoms was treated with o,p'-DDD (2,2-bis(2-chlorophenyl-4 cholorophenyl) 1,1-dichloroethane). With this therapy, the tumor decreased in size which was confirmed by the computed tomography (CT). Eighteen months later, however, lethargy and logopathy appeared and the tumor grew again rapidly with the withdrawal of o,p'-DDD performed for the evaluation of these mental disturbances. The tumor then diminished gradually in size soon after the treatment was resumed and the above unfavorable symptoms were not developed again with the combined administration of a central nervous stimulant. During o,p'-DDD treatment, plasma testosterone and estrogen decreased, and plasma aldosterone also decreased but within the normal range. Plasma cortisol also tended to decrease despite hydrocortisone was administered. Plasma adrenocorticotropic hormone (ACTH) was maintained within the normal range for the first six months but then increased gradually. It decreased and became normal with the additional administration of hydrocortisone. The patient's normal menstruation at the preadministrative stage changed to oligomenorrhea, then amenorrhea after the treatment, but no endocrinological sign except for the menses was observed during the treatment.
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PMID:Adrenocortical carcinoma responded to treatment with o,p'-DDD--a case report. 609 39

Blood samples were analyzed for beta-endorphin from 43 non-torpid black bear (Ursus americanus), 8 torpid black bear, 3 non-torpid brown bear (Ursus arctos), 14 moose (Alces alces), 6 mountain goats (Oreamnus americanus) and 30 Steller sea lions (Eumetopias jubatus). Beta-endorphin levels were detected in all species sampled and there were no significant differences in levels among non-torpid black bear, brown bear and sea lions. Also, no differences were detected between moose and mountain goats, but all other comparisons were significantly different (P less than 0.001). Torpid black bear had higher levels than all other groups. Moose and mountain goats had the lowest levels. The possibility of beta-endorphin influencing behavior and physiology of mammals is discussed.
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PMID:Beta-endorphin levels in blood from selected Alaskan mammals. 627 90

A male infant with secondary hypothyroidism is described. Within the first month after birth, the patient manifested feeding difficulties, lethargy, persistent jaundice, umbilical hernia, and large anterior and open posterior fontanels. The roentgenogram of the knee joints at 27 days showed absence of the distal femoral epiphyses. His serum thyroid-stimulating hormone (TSH) level was low despite decreased levels of triiodothyronine (T3) and tetraiodothyronine (T4) in serum. Assessment of the hypothalamic-pituitary hormone (TRH) nor growth hormone (GH) responses to L-arginine and insulin, while responses of both luteinizing hormone (LH) and follicle-stimulating hormone (FSH) to luteinizing hormone-releasing hormone (LH-RH) and adrenocorticotropic hormone (ACTH) to insulin were within normal limits. The malady of the patient in this case was not detected by newborn screening for congenital hypothyroidism due to the fact that in the Aomori district of Japan thyroid screening involves only the measurement of TSH. Such measurement cannot detect cases of secondary or tertiary hypothyroidism such as our patient. Replacement therapy was initiated at 58 days and his physical and mental development has been regarded as normal since treatment.
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PMID:Congenital secondary hypothyroidism with low serum GH and prolactin levels in a 27-day-old male infant. 628 48

Opioid agonists were used to investigate the modulation of seizures mediated by mu, kappa and delta opiate receptors in the seizure-sensitive Mongolian gerbil. Morphine (1.0-25 mg/kg, s.c.) were used as prototypic agonists for mu, kappa and delta opiate receptors. Each opioid decreased the incidence and severity of the seizure as compared to control values. The anticonvulsant effects of morphine (10 mg/kg, s.c.) and ketocyclazocine (0.5 mg/kg, s.c.) were reversed by naloxone (1.0 mg/kg, s.c.), while the anticonvulsant effects of N-allylnormetazocine (2 mg/kg, s.c.) were not significantly changed by naloxone. Additionally, abnormal behavior was observed following administration of the opioids. Morphine (10 mg/kg, s.c.) produced excitation and hyperresponsiveness with intermittent cataleptic-like states. Ketocyclazocine (10 mg/kg, s.c.) predominantly produced a stuporous, immobile state, accompanied by some loss of posture. N-allylnormetazocine (10 mg/kg, s.c.) produced ataxia and stereotypic side-to-side head nodding . Naloxone was able to reverse the behavioral effects produced by morphine and ketocyclazocine but not those produced by N-allylnormetazocine. The data presented are consistent with earlier studies which demonstrated the anticonvulsant effects of beta-endorphin in the gerbil. This study further suggests that opioids have a protective role against seizure activity in the gerbil and the opioid anticonvulsant effect is not specific to one type of opioid agonist.
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PMID:Similar anticonvulsant, but unique, behavioural effects of opioid agonists in the seizure-sensitive Mongolian gerbil. 633 Jun 6

In chicks (Gallus domesticus) the effects of beta-endorphin and D-Ala-2-methionine-enkephalinamide given into the third cerebral ventricle on behaviour, electrocortical activity and body temperature were studied. Dose-dependent behavioural stuporous state, decrease in painful stimuli and hypothermic effects were observed after both peptides. Electrocortical high-amplitude slow frequency waves occurred during behavioural sedation and stupor. Spectrum power analysis has allowed to quantify the ECoG activity and has revealed an increase in total voltage output with a predominant increase within the lower spectrum frequencies. The hypothermic effects were significantly more marked when chicks were kept at ambient temperature below their thermoneutral range. Behavioural, electrocortical and body temperature effects were rapidly reversed by naloxone showing that these effects are mediated through an activation of specific opioid receptors.
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PMID:Effects of intraventricular beta-endorphin and D-ALA2-methionine-enkephalinamide on behaviour, spectrum power of electrocortical activity and body temperature in chicks. 739 25

To determine whether childhood intestinal intussusception is associated with elevated plasma beta-endorphin levels, a series of patients was studied prospectively. Fourteen patients (age range between 3 months and 7 years) presented to two university pediatric emergency departments in Chicago with clinical symptoms and signs of intussusception. Venous blood (2cc) was withdrawn for plasma beta-endorphin determination, followed by barium enema. Plasma beta-endorphin levels were measured by radioimmunoassay. The mean beta-endorphin level of the 8 patients with barium enema proven intussusception was 14.1 +/- 12.0 pg/ml. Two of these patients presented with marked lethargy and had beta-endorphin levels of 7.5 and 21.2 pg/ml. The mean plasma beta-endorphin level of the 5 patients with negative barium enema studies was 18.1 +/- 10.0 pg/ml (P = 0.56). A sixth control patient had a plasma beta-endorphin level of 1569 pg/ml. In conclusion, childhood intestinal intussusception is not associated with elevated plasma beta-endorphin levels.
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PMID:Plasma beta-endorphin levels and childhood intussusception. 788 94

We present two patients with manifest acquired immunodeficiency syndrome (AIDS) suffering from a generalized cytomegalovirus (CMV) infection. Over the course of several weeks they had developed a state of increasing lethargy and fatigue and one patient had noticed a darkening of his skin. These and other symptoms (vomiting, diarrhoea, hypotension) were suggestive of adrenal insufficiency. Laboratory findings included an increase of serum potassium levels, a decrease of serum sodium concentrations and elevated levels of the adrenocorticotropic hormone (ACTH). These findings, as well as the prompt therapeutic response to hydrocortisone established the diagnosis of adrenal insufficiency. Although definitive proof is lacking, generalised CMV infection is the most likely cause of our patients' symptoms. For the early initiation of appropriate substitution therapy, persons infected with the human immunodeficiency virus (HIV) with signs of CMV infection should be carefully and repeatedly monitored for clinical and laboratory signs of adrenal insufficiency.
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PMID:Primary adrenal insufficiency in two patients with the acquired immunodeficiency syndrome associated with disseminated cytomegaloviral infection. 940 82


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