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

A 73-year-old woman was admitted to the hospital for severe persistent vomiting with fever, drowsiness, and weight loss. Elevated serum levels of thyroid hormones and the presence of a consciousness disorder with fever and vomiting led to the diagnosis of thyroid storm. A low normal concentration of serum cortisol, urinary 17-hydroxycorticosteroids and an elevated plasma level of corticotropin suggest that an inadequate adrenal reserve have been involved in the pathogenesis of the thyroid storm in this patient. She responded to the administration of intravenous methimazole and oral supersaturated potassium iodide solution.
 ...
PMID:Thyroid storm associated with probable subclinical hypoadrenocorticism in an elderly woman. 133 85

To explore 5-HT1A receptor responsivity in panic disorder (PD), hypothermic, neuroendocrine and behavioral responses to the selective partial 5-HT1A receptor agonist ipsapirone (IPS) were investigated in patients with primary PD and healthy controls. Fourteen patients and matched controls received a single oral dose of 0.3 mg/kg IPS or placebo under double-blind, random-assignment conditions. IPS induced hypothermia and corticotropin (ACTH)/cortisol release but had only minimal effects on behavior. Compared with controls, the patients with PD exhibited significantly attenuated thermoregulatory and neuroendocrine responses to IPS. Although the healthy subjects reported increased drowsiness and the PD patients rated themselves more nervous and less calm following administration of IPS, no consistent changes in ratings of anxiety or panic symptoms were recorded. The impaired hypothermic and ACTH/cortisol responses following 5-HT1A receptor activation reflects subsensitivity of both the pre- and post-synaptic 5-HT1A receptor-effector system, thus supporting the hypothesis that a 5-HT1A receptor-related serotonergic dysfunction may be linked to the pathophysiology of PD. Future studies of 5-HT1A receptor-effector complex function in conjunction with assessment of the responsivity of other subtypes (e.g. 5-HT2, 5-HT3) should promote the evaluation of 5-HT system integrity in anxiety disorders and its involvement in anxiolytic drug effects.
 ...
PMID:5-HT1A receptor-effector system responsivity in panic disorder. 134 19

The effects of smoking normal-nicotine-delivery cigarettes on serum cortisol, plasma beta-endorphin (BE), and mood were measured in 8 male and 8 female smokers; 8 male and 8 female nonsmokers served as sham-smoking controls. Smoking five cigarettes of the smokers' usual type after overnight deprivation, either ad lib or via a quantified smoke delivery system, produced small but reliable elevations in serum cortisol concentrations; BE was elevated somewhat after two, but not after four or five cigarettes. Smoking-induced elevations in serum cortisol were correlated with decreases in self-reported drowsiness after two and five cigarettes. Additionally, female smokers reported more drowsiness at baseline and after smoking nicotine-free cigarettes than did male smokers or female nonsmokers. Results suggest that smoking-induced elevations in serum cortisol, which persist for at least the first five cigarettes of the day, may modulate the arousing effects of smoking under conditions of low arousal. Also, nicotine-deprived female smokers may experience subnormal arousal compared to male smokers or female nonsmokers.
 ...
PMID:Hormonal and subjective effects of smoking the first five cigarettes of the day: a comparison in males and females. 180 26

The effects of the selective 5-HT1A receptor agonist gepirone (10 and 20 mg orally) on neuroendocrine function and temperature were assessed using a single-blind cross-over design in 12 healthy male volunteers. Gepirone significantly increased plasma levels of ACTH, beta-endorphin, cortisol, prolactin and growth hormone. Following gepirone there was a significant decrease in body temperature and moderate increases in subjective reports of light-headedness, nausea and drowsiness. Our results are consistent with studies in rodents suggesting that 5-HT1A receptor agonists increase ACTH and prolactin secretion and decrease body temperature. Further investigations are needed to determine if the neuroendocrine and temperature effects of gepirone in humans are mediated by 5-HT1A receptors.
 ...
PMID:The effects of gepirone on neuroendocrine function and temperature in humans. 215 31

Experiments were conducted on 90 non-strain male albino rats to study the possibility of compensating food intake and the functions related to its activity in disturbances caused by damage to the arcuate region of the hypothalamus. Neuropeptides beta-lipotropin (beta-LTP) and beta-endorphin were chosen as the compensation factors. The registered parameters were as follows: the volume of food and water intake, feeding and drinking behaviors, orientating-exploratory activity, comforting behavior, and the duration of sleep and drowsiness. It was established that destruction of the hypothalamic arcuate zone is attended by the formation of a specific syndrome including disorders of food and water intake and other forms of behavior. Intraventricular injections of beta-LPT and beta-endorphin under such conditions was conductive to the restoration of the disturbed functions and compensated for food intake and other related functions.
 ...
PMID:[Beta-lipotropin and beta-endorphin in the hypothalamic syndrome]. 229 71

The efficacy of naloxone in reducing the incidence of side effects after intrathecal injection of morphine and the effects of maternal naloxone administration on the condition of the newborn were evaluated in 40 patients. Patients in labor were given a 1-mg intrathecal injection of morphine and, 1 hr later, either a 0.4-mg bolus of naloxone, followed by a 0.4-0.6 mg/hr intravenous infusion of naloxone, or an intravenous bolus of saline, followed by an intravenous infusion of saline. Intrathecal morphine provided at least 50% pain relief in 78% of patients given naloxone, and in 82% given saline. Intravenous naloxone significantly decreased the incidence of pruritus during labor and delivery. There was no significant decrease in the incidence of nausea, vomiting, somnolence, dizziness, or urinary retention in patients given naloxone. Despite placental transfer of naloxone, neonatal outcome was not adversely affected. For both groups, maternal beta-endorphin levels decreased significantly with the onset of analgesia and returned to control levels at delivery. We conclude that intravenous infusion of naloxone reduced pruritus after intrathecal injection of 1 mg of morphine for labor pain without lessening analgesia or adversely affecting maternal or neonatal status.
 ...
PMID:The effects of naloxone associated with the intrathecal use of morphine in labor. 316 Feb 59

Eight psychiatric patients with tardive dyskinesia (TD) were treated with single doses of the synthetic met-enkephalin analogue FK 33-824 (1, 2, and 3 mg IM) morphine (10 mg SC) and naloxone, an opiate receptor antagonist (0.8 mg IM). The drug effects were assessed by blind evaluation of randomly sequenced videotapes made before and during treatment. FK 33-824 (1, 2, and 3 mg IM) slightly reduced TD (P < 0.05) and increased preexisting bradykinesia. The effect on TD, however, was pronounced only in patients concurrently treated with neuroleptics in relatively high doses. Morphine had a similar although weaker antihyperkinetic effect, whereas naloxone had no effect. Side effects of FK 33-824 included dizziness, heaviness in the extremities, slurred speech, and dryness of mouth. Morphine caused drowsiness, dizziness, ataxia, and nausea, and naloxone had no side effects. The results do not point to a primary role of enkephalin in the pathophysiology of TD, but enkephalin may interact with dopamine functions and potentiate some of the effects of neuroleptic drugs.
 ...
PMID:Enkephalin, morphine, and naloxone in tardive dyskinesia. 677 5

Corticotropin releasing hormone (CRH) is the primary modulator of ACTH release from the pituitary, and a neuromodulator in limbic and autonomic brain regions. Dysfunction of CRH-mediated neurotransmission is emerging as a critical mechanism in several disorders. Therefore, modulation of CRH availability at receptor sites is a potentially powerful therapeutic tool. Inhibitory analogues of CRH have been tested in rodents and primates, but their safety and hormonal effects in humans are unknown. We administered a CRH-antagonist, alpha-helical-CRH-(9-41) to six individuals. Each received two intravenous infusions: 50 micrograms kg-1 on day 1, and 100 micrograms kg-1 on the following morning. These doses block both endocrine and central effects of CRH in experimental animals. ACTH, cortisol, electrolytes, glucose and autonomic parameters were monitored in comparison with control values. Infusion of CRH antagonist did not alter heart rate, blood pressure, temperature or plasma electrolytes and glucose. Pre-infusion plasma ACTH levels averaged 26.8 +/- 6.7 pg ml-1 on day 1, and 29.0 +/- 5.8 pg ml-1 on day 2. Post-infusion values were 11.8 +/- 2 and 11.5 +/- 2.4 pg ml-1, significantly lower than pre-infusion levels. Plasma cortisol levels, which averaged 21.4 +/- 4 micrograms dl-1 on the first morning and 22.9 +/- 4.2 on the second, also decreased significantly after CRH antagonist infusions (to 14.0 +/- 2.9 micrograms dl-1 on day 1, and 13.9 +/- 3.0 micrograms dl-1 on day 2). Hormonal changes were transient, and circadian rhythm was not affected. Though not measured formally, euphoria, anxiety or somnolence were not observed. In conclusion, CRH antagonist administration to adults reduces hormonal secretion by pituitary corticotrophs, with resulting decrease in plasma ACTH and cortisol.
 ...
PMID:Inhibition of pituitary-adrenal secretion by a corticotropin releasing hormone antagonist in humans. 911 58

West syndrome (WS) is an age dependent epileptic syndrome caused by various brain disorders. WS has been frequently classified in two groups, cryptogenic and symptomatic. As symptomatic WS consists of patients with numerous types of brain lesions, the prognosis and evolutional changes may be different among the types of brain lesions. WS is resistant to treatment to most conventional antiepileptic drugs, and only valproic acid, benzodiazepines, adrenocorticotropic hormone (ACTH), corticosteroids and vigabatrin have been found efficacious. Benzodiazepine, notably nitrazepam, and less clonazepam had been effective in bringing spasms under control but emerging tolerance and significant side effects (hypotonia and drowsiness) precluded its wider use. ACTH has been the treatment of choice for infantile spasms ever since Sorel and Dusaucy-Bouloye described its effectiveness in 1958. Despite the empirical approach steroids were capable of controlling the spasms and normalizing EEG in about 60% of cases. Corticotropin (ACTH) was used in doses from 5 to 180 I.U. daily, prednizolone 2-10 mg/kg daily, hydrocortisone 5-10 mg/kg daily and dexamethason 0.3-0.5 mg/kg. However, poor consensus was defined regarding the best steroid molecule to use, the dosage, and the duration of treatment. Also frequent and sometimes serious side effects have occurred during ACTH therapy, notably serious infections and hypertension that promoted continuous search for alternative and safer drugs tolerated outpatient treatment, good tolerance and minor side effects. Recently a specific visual field loss has been reported in treated adults that raised concern about safety of vigabatrin. New reports in children claim that vigabatrin treatment of children and adolescents has a lower risk for visual field defect than in adults, because of reported reversibility. Vigabatrin paediatric advisory group recommend the trial of vigabatrin for 12-14 days as first treatment for WS and in the case of good clinical response continuation of therapy for six months. Other new antiepileptic drugs (lamotrigine, topiramate, felbamate and zonisamide) have shown significant efficacy in the treatment of resistant WS to previous medication. The current task is to determine risk/benefit ratios of these two drugs (vigabatine, ACTH) and to delineate the group of patients with WS where their use would be optimal.
 ...
PMID:[West syndrome--new therapeutic approach]. 1563 97

A 44-year-old woman reported several weeks of fatigue, somnolence, pain in the large joints, nausea, and decreased appetite. She had also noted an unintentional 11-kg weight loss over a period of 6 months. She had a remote history of amenorrhea, but she was presently menstruating regularly. She was taking no medications, with the exception of acetaminophen as needed for knee pain. The diagnosis of adrenal insufficiency (AI) was considered. Serum cortisol level after adrenocorticotropin hormone (ACTH) stimulation was abnormal. Because her plasma ACTH level was not increased, a diagnosis of secondary AI (due to deficiency in ACTH) was made. Magnetic resonance imaging of the brain performed to exclude the presence of a sellar or suprasellar mass showed reduction in size of the pituitary gland and an increased cerebrospinal fluid content within the sella, consistent with a partially empty sella. The patient's symptoms improved rapidly with hydrocortisone therapy but during follow-up, the dose of hydrocortisone was found to be excessive. Important differences exist between primary and secondary AI, and the diagnosis of secondary AI may be challenging. The therapy of AI should be carefully tailored to the requirements of the individual patient.
 ...
PMID:Adrenal insufficiency. 1652 31


1 2 Next >>