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)

Trichosanthin was administered intramuscularly into mature male ICR mice at a dosage of 0.2mg/25g, daily for three days. The mice were sacrificed four hours after the last injection. Their brains were dissected out and divided into three regions: A(thalamus and hypothalamus), B(cerebral cortex) and C(cerebellum and brainstem). Their pituitaries were also removed. The pituitaries and the various brain regions were extracted with hot 1M acetic acid. The extracts were lyophilized and reconstituted in radioimmunoassay (RIA) buffer before assay for beta-endorphin by RIA. It was found that there was a significant elevation of beta-endorphin concentration after trichosanthin treatment only in brain region A. The data suggest that trichosanthin does not adversely affect the brain.
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PMID:Trichosanthin, a ribosome inactivating and anti-HIV protein, does not alter the concentration of beta-endorphin in the mouse brain. 819 93

The present work describes time-dependent changes in the content of corticotropin-releasing hormone (CRH), adrenocorticotropin (ACTH), and beta-endorphin (beta-EP) in the hypothalamus (HT) and anterior pituitary (AP) and in the concentration of ACTH and beta-EP in the plasma during the 17 beta estradiol (E2) benzoate (E2B)-induced luteinizing hormone (LH) surge in ovariectomized cynomolgus monkeys. Monkeys were euthanized at 0, 30, 48, 72, and 96 hr post-E2B. HT and AP were rapidly dissected, extracted in 2 N acetic acid containing 1 mM phenylmethane sulfonyl fluoride at 4 degrees C, and centrifuged at 18,000g for 30 min. Peptide concentrations were measured in the supernatant by specific radioimmunoassays (RIAs). In the HT, there were significant (P < 0.05) decreases in ACTH and beta-EP content by 30 hr post-E2B and a significant (P < 0.05) decrease in HT CRH content 48 hr post-E2B. Thereafter, CRH, ACTH, and beta-EP content increased up to 72 hr post-E2B. In the AP, there was an almost linear decrease in the CRH content through 48 hr post-E2B followed by a marked 20-fold (P < 0.01) increase in the AP CRH content at 72 hr post-E2B, which corresponds to the time of the descending arm of the LH surge. The patterns of ACTH and beta-EP content were very similar in the AP, while that of CRH differed markedly. In contrast, in the HT CRH, ACTH, and beta-EP profiles were very similar. Significant (P < 0.05) increases in circulating levels of ACTH, beta-EP, and cortisol were evident at 30 hr (all 3 hormones), 48 hr (beta-EP and cortisol), and 72 hr (cortisol) post-E2B, which corresponds with the time of decreased hypothalamic content of CRH, ACTH, and beta-EP. These results suggest that there maybe a marked activation of the hypothalamo-anterior pituitary-adrenal axis during the negative and positive feedback phases of the E2B-induced LH surge in the ovariectomized monkey.
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PMID:Activation of the hypothalamo-anterior pituitary corticotropin-releasing hormone, adrenocorticotropin hormone and beta-endorphin systems during the estradiol 17 beta-induced plasma LH surge in the ovariectomized monkey. 856 23

Increased levels of 5-hydroxyindole acetic acid (5-HIAA) were found in a patient with a tumor arising in the middle ear. Iodine-123-metaiodobenzylguanidine ([123I]MIBG) scintigraphy and biochemical analysis showed evidence of serotonin production by the tumor. Immunohistochemistry of the tumor showed reactivity with antibodies directed against serotonin, chromogranin, leu-7 and neuron-specific enolase; S-100, met-enkephalin, leu-enkephalin and glial fibrillary acid protein were negative. This case suggests a close relationship between functioning paragangliomas and carcinoid tumors because a strong clinical and endocrinological resemblance exists. The hormonal activity found is discussed in relation to extra-adrenal paragangliomas. We recommend urinary screening not only for detection of increased levels of catecholamines, but also of 5-HIAA in all patients with paragangliomas of the head and neck. When elevated levels are found, [123I]MIBG scintigraphy should be performed to localize the areas of increased uptake in or outside the head and neck region.
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PMID:Carcinoid tumor of the jugulo-tympanic region. 866 59

A 75-year-old female presented with a suprasellar granular cell tumor. Computed tomography (CT) revealed a high dense suprasellar mass with strong postcontrast enhancement. Magnetic resonance imaging showed a round suprasellar mass, which was hyperintense on the T1-weighted images with nonhomogeneous enhancement after the administration of gadolinium-diethylenetriaminepenta- acetic acid, and hypointense on the T2-weighted images. Cerebral angiography demonstrated no abnormal findings. The tumor was partially removed via a right frontotemporal craniotomy. The histological diagnosis was suprasellar granular cell tumor. Her postoperative course was uneventful other than mild and transient diabetes insipidus. She has remained asymptomatic without CT evidence of tumor regrowth for 20 months after the surgery. Immunohistochemical studies showed positive reaction for S-100 protein in the tumor cell nuclei, but no reaction for glial fibrillary acidic protein, neurofilament protein, Leu-7, oxytocin, beta-endorphin, adrenocorticotropic hormone, and vimentin. This case provides additional evidence for the astrocytic origin of suprasellar granular cell tumor.
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PMID:Suprasellar granular cell tumor. 874 Dec 54

To obtain information on long-term circadian consequences of administering melatonin neonatally to rats, we assessed the 24-hour rhythms of 1) serum prolactin (PRL), luteinizing hormone (LH), and growth hormone (GH), and 2) medial basal hypothalamic dopamine (DA) and serotonin (5-HT) metabolism and corticotropin-releasing hormone (CRH) content in 60-day old male rats injected with 100 micrograms of melatonin on the 5th day of life. Controls receiving vehicle alone showed serum PRL concentration (when 60 days of age) attaining its maximum at the end of the light period (i.e., at 2000 hr), while in melatonin-injected rats high PRL values were found between 1200 and 2000 hr. Twenty-four hour changes in serum LH levels exhibited a maximum at noon, and to a similar extent in vehicle- and melatonin-treated rats. Neonatal melatonin injection did not affect serum GH concentration when the rats were adult. In the medial basal hypothalamus (MBH), the dihydroxyphenyl acetic acid (DOPAC)/ DA ratio attained a maximum at midnight, its amplitude being significantly higher in melatonin- than in vehicle-treated rats. Neonatally melatonin-injected rats also exhibited a second maximum in DOPAC/DA ratio at noon, coinciding with a minimum in DA levels of MBH. The 5-hydroxyindoleacetic acid (5-HIAA)/5-HT ratio in MBH showed significant diurnal variations in vehicle-injected controls with maxima at 1200 and 0400 hr, while in melatonin-treated rats a single maximum occurred at 2400 hr. These maximum correlated with minima in 5-HT content of MBH. Neonatal melatonin injection brought about a significant increase in the CRH content of MBH, as well as distortion of its diurnal rhythmicity, a maximum being found at noon in controls and at 1800 hr in melatonin-treated rats. The results indicate that exposure to melatonin early in life affects subsequent diurnal rhythmicity of PRL release, and of DA and 5-HT turnover and CRH content in the MBH of rats.
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PMID:Twenty-four hour rhythms of serum prolactin, growth hormone and luteinizing hormone levels, and of medial basal hypothalamic corticotropin-releasing hormone levels and dopamine and serotonin metabolism in rats neonatally administered melatonin. 906 71

We evaluated protocols for the extraction of calcitonin gene-related peptide, neuropeptide Y, substance P, peptide YY and beta-endorphin from rat lung tissue for subsequent radioimmunoassay. The effects of varying acidity of the extraction solution and repeating extraction on the recovery of peptide immunoreactivity and non-specific tracer-binding were compared by analysis of variance. Moreover, variability of immunoreactivity was quantified for comparison. Considering all three criteria, the optimal acidity for extraction was: 0.1 M or 1 M acetic acid for CGRP and beta-endorphin, 0.1 M acetic acid for NPY, 1 M acetic acid for substance P and phosphate buffer for peptide YY. Double or combined extraction unambiguously improved assay results only for substance P. Reversed-phase high-performance liquid chromatography of CGRP-, NPY- and SP-immunoreactivity obtained from selected extracts suggested that differences in recovery of these peptides are not explainable by differential peptide fragmentation during extraction.
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PMID:Analytical extraction of regulatory peptides from rat lung tissue. 943 21

Earlier studies indicate that nitrous oxide antinociception is mediated by opioid receptors, and we have hypothesized that nitrous oxide stimulates a neuronal release of an endogenous opioid peptide (EOP) that stimulates opioid receptors. To further test this hypothesis, male NIH Swiss mice were pretreated intracerebroventricularly with rabbit antisera to opioid peptides or with various inhibitors of peptidases involved in the degradation of EOPs. Mice were subsequently exposed to three different concentrations of nitrous oxide in oxygen, and their antinociceptive responsiveness was measured using the acetic acid abdominal constriction test. Nitrous oxide antinociception was significantly attenuated by 24-h pretreatment with antisera to various fragments of dynorphin (DYN) but not by antisera against methionine-enkephalin (ME) or beta-endorphin (beta-EP). In other experiments, nitrous oxide antinociception was significantly enhanced by 30-min pretreatment with phosphoramidon, an inhibitor of endopeptidase 24.11, which has been implicated in DYN degradation, but not bestatin or captopril, which inhibit aminopeptidase and angiotensin-converting enzyme, respectively. The latter enzymes have been implicated in degradation of certain EOPs albeit not DYN. These findings support the hypothesis that nitrous oxide antinociception in the mouse abdominal constriction test is mediated by endogenous DYN acting in the central nervous system.
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PMID:Role of brain dynorphin in nitrous oxide antinociception in mice. 1067 72

Human growth hormone was prepared from acetone-dried pituitary powder by hot glacial acetic acid extraction and subsequent precipitation by sodium chloride and cold acetone. The yield was 13 per cent and the preparation was called practical growth hormone in recognition of its complement of corticotropin. Treatment of two dwarfs with practical growth hormone in aqueous solution, 1 or 2 mg intramuscularly on alternate days, accelerated the growth rate and there were no physical signs or laboratory indications of adrenal stimulation or other adverse effects. The preparation is recommended for its safety, simplicity and relatively good yield.
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PMID:PRACTICAL HUMAN GROWTH HORMONE. PREPARATION AND CLINICAL USE. 1413 99

Previously we showed that peptides PGP, PG, GP and semax have protective anti-ulcer properties using different models of ulcerogenesis. Semax (MEHFPGP) is a nootropic analogue of adrenocorticotropin 4-7 stabilized by PGP in the C-terminal region. In this study we examined the impact of these peptides on the development and healing of acetic ulcers in rats. The histomorphological and dynamical characteristics of acetic ulcers are most similar to human chronic ulcers. All the peptides were shown to accelerate the process of ulcer cicatrisation in a varying degree (GP semax PG PGP). The dynamics of structural changes in the place of ulcer formation investigated with the use of cytohistological control demonstrated that their anti-ulcer effects can be related to their ability to accelerate ulcer clarification from necrotic tissues and to activate the process of cicatrisation and epithelization. PGP and GP were also shown to reduce the inflammation in the ulcer zone on the fifth day after acetic acid application.
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PMID:[Semax and some glyproline peptides accelerate the healing of acetic ulcers in rats]. 1465 48

Like primary reinforcers, the anticipation of reward ought to affect neurochemical release in brain regions, such as the medial prefrontal cortex (mPFC), which are associated with appraisal processes. To assess the neurochemical changes associated with anticipation, rats were exposed to the pairing of auditory (60-dB white noise), visual, and olfactory cues with the daily presentation of a palatable snack (Cue Relevant group). Rats of a second group were similarly trained, but for a 2-week period, the snack was no longer provided following cue presentation (Extinction group). In the third condition, the presentation of the snack and cues was uncorrelated (Cue Irrelevant group). Analyses of dialysates collected in vivo from the mPFC revealed that release of corticotropin-releasing hormone (CRH), gastrin-releasing peptide (GRP), and the 5-HT catabolite, 5-hydroxyindole acetic acid (5-HIAA), had increased bilaterally in response to the anticipatory cues, whereas DA release increased only within the right mPFC. In the case of CRH and GRP, these increases were also apparent in the extinction condition, despite the fact that behavioral arousal to the anticipatory cues (increased exploration, rearing, grooming, and vigilance) was only evident in the Cue Relevant condition. In contrast, the elevated DA and 5-HIAA were apparent exclusively in the Cue Relevant condition. Thus, CRH and GRP systems may serve to allocate salience and/or incentive reward value to biologically significant stimuli or reflect the emotional response to the anticipatory stimulus. The activity of DA and 5-HT neurons, in contrast, is more closely aligned with the cognitive appraisal of predictor stimuli.
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PMID:Anticipatory cues differentially provoke in vivo peptidergic and monoaminergic release at the medial prefrontal cortex. 1503 70


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