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)

Megavoltage CNS irradiation was given to 20 patients with clinically definite multiple sclerosis (MS) to determine if de novo CNS IgG synthesis could be eradicated. In all five patients given 1,200 rads, a transient reduction in the de novo CNS IgG synthesis rate was noted. In ten patients given 1,800 rads, the following occurred: a reduction in synthesis rate in three patients, a reduction followed by enhancement in two, only enhancement in four, and no change in one. In all five additional patients, a therapy of adrenocorticotropic hormone (ACTH) followed by prednisone in combination with 1,800 rads produced greater and more persistent decreases in CNS IgG synthesis, but did not block the enhancement effect. Only two of 19 patients who had abnormal CNS IgG synthesis rates had reductions to normal; no patients showed changes in the number or pattern CSF IgG oligoclones. Hence, no treatment eradicated de novo CNS IgG synthesis. A persistent decrease in CSF leukocytes occurred in all 20 patients due to the reduction of small lymphocytes (not dose related). The blood-brain-barrier to albumin concentration was transiently damaged in 11 of 15 patients given irradiation, but when patients were premedicated with ACTH/prednisone therapy, no damage was found. None of the patients demonstrated neurological improvement, change in the activity of their disease, or persistent adverse effects.
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PMID:Multiple sclerosis de novo CNS IgG synthesis. Effect of CNS irradiation. 625 76

Mice were injected with adrenocorticotropic hormone (ACTH) and the glomerular lesion that was induced was studied by light and immunofluorescence microscopy. By light microscopy, kidneys from ACTH-treated mice showed typical ACTH-induced glomerular lesions. Immunofluorescence of kidneys from ACTH-treated mice revealed intense staining for IgG and IgM in the extraglomerular mesangium (EGM), in Bowman's space, and in the ascending thick limb of Henle near the macula densa. Staining for immunoglobulins was unchanged after treatment with acid buffer. Immunoreactivity for complement (C3) was confined largely to the EGM and Bowman's space. Staining for albumin was almost exclusively in Bowman's space or the peripheral glomerular tuft in discrete aggregates. The above patterns of IgG, IgM, C3 and albumin were seen in control mice, although much less frequently. The results show that in mice, treatment with ACTH results in the increased accumulation of plasma proteins in the juxtaglomerular apparatus (JGA). This effect may reflect a role for the JGA in the normal clearing of plasma proteins from the glomerulus and/or directly from the blood.
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PMID:An ACTH-induced renal glomerular lesion in the mouse: immunofluorescence microscopy. 630 Mar 62

The hypothesis that lipolytic hormones reduce the mitochondrial electrical potential in rat white adipocytes via free fatty acids (FFA) was examined. Hormonal effects on plasma and mitochondrial membrane potentials were evaluated with [3H]triphenylmethylphosphonium (TPMP+) and 86Rb+. FFA generation was controlled by varying medium albumin concentrations. In 4.0% albumin buffer, adrenocorticotropin or l-epinephrine increased intracellular FFAs, produced cellular TPMP+ efflux, ATP depletion, release of FFAs and glycerol, and no change in 86Rb+ distribution. In 0.5% albumin buffer, greater intracellular FFA accumulation accompanied greater TPMP+ and ATP depletion, significant loss of cell-associated 86Rb+, and a concomitant inhibition of FFA and glycerol release. Exogenous addition of FFAs mimicked the effect of hormones on adipocyte TPMP+ distribution. TPMP+ and 86Rb+ uptake into adipocyte "ghosts" were unaffected by hormones. We suggest that mitochondrial membrane depolarization is a metabolic response to hormones via FFA accumulation by white adipocytes. The additional hormonal effects that were observed in 0.5% albumin buffer may be related to inhibition of lipolysis secondary to intracellular ATP depletion.
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PMID:Hormones modulate adipocyte membrane potential ATP and lipolysis via free fatty acids. 631 Oct 25

CSF proteins in 107 children ranging from 3 to 24 months of age were analyzed by means of quantitative zone electrophoresis on agarose gel. Subjects included 50 children with infantile spasms, 41 children without CNS disease serving as controls, and 16 infants with acute aseptic meningitis who demonstrated the protein pattern of blood-CSF barrier disturbance. Children with infantile spasms were subdivided into several groups according to etiological categories: symptomatic (pre-, peri-, and postnatal), doubtful, and cryptogenetic. Before any treatment was started, these children showed the protein profile of increased permeability of the blood-CSF barrier, especially for albumin. There was an association between the severity of the changes and the etiological category. Changes were most marked in the symptomatic group, intermediate in the doubtful group, and slight in the cryptogenetic group. No child with infantile spasms of doubtful or unknown etiology revealed changes of the immunoglobulin-containing gamma fractions. Ten children who had received adrenocorticotropic hormone (ACTH) or dexamethasone for 2-11 weeks no longer showed any protein leakage into the CSF. The period of ACTH or dexamethasone treatment was characterized by the following findings: the disappearance or reduction of hypsarrhythmia; the reappearance of normal cerebrovascular permeability for protein; and the occurrence of reversible dilatation of the subarachnoid and intraventricular spaces.
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PMID:CSF protein profile in infantile spasms. Influence of etiology and ACTH or dexamethasone treatment. 632 52

To study the effects of beta-endorphin in chronic schizophrenia, nine male patients participated in a double-blind crossover comparison of a single intravenous 20-mg injection of beta-endorphin and saline. Bolus injection of beta-endorphin from an albumin-coated syringe produced markedly higher plasma concentrations than did slow intravenous infusion from a non-albumin-coated syringe. Beta-endorphin intravenously injected in nine patients produced a statistically significant increase in serum prolactin levels. In one patient, both 10 mg of morphine sulfate and 20 mg of beta-endorphin produced similar increases in the alpha power of the EEG. In eight patients, beta-endorphin administration was associated with a statistically significant but not clinically obvious improvement in schizophrenic symptoms.
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PMID:beta-Endorphin and schizophrenia. 738 35

We hypothesized that increased levels of blood cytokines occur in brain-dead patients, and that these cytokines are responsible for some of the endocrine and/or acute-phase reactant abnormalities found in these patients. We measured blood levels of cytokines, hormones, and acute-phase reactants in 18 brain-dead potential organ donors at the moment of establishing the legal diagnosis of brain death and compared them with levels found in a control group. Although interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha) levels were within the normal range, interleukin-6 (IL-6) levels were clearly above the normal range in all patients (median, 1,444 pg/mL; range, 75 to 11,780). In the brain-dead group, total thyroxine (tT4), free T4 (fT4), triiodothyronine (T3), thyrotropin (TSH), dehydroepiandrosterone sulfate (DHEA-S), testosterone, albumin, Zn, and osteocalcin levels were decreased, T3 resin uptake index (T3 RUI), corticotropin (ACTH), cortisol, 11-deoxycortisol (11-DOC), 17-hydroxyprogesterone (17-OHPr), aldosterone, luteinizing hormone, and follicle-stimulating hormone levels were normal, and reverse T3 (rT3), renin, and C-reactive protein (CRP) levels were increased. Multiple regression analysis demonstrated significant interrelations between IL-6 and T4, T3, testosterone, and CRP. We also studied the evolution of some of these parameters in four patients with severe head injury who finally developed brain death. IL-6 levels on admission to the intensive care unit (ICU) were above the normal limits, as in other patients with cranial trauma, but when the patients developed brain death, there was a pronounced increase in IL-6 levels.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Blood levels of cytokines in brain-dead patients: relationship with circulating hormones and acute-phase reactants. 754 Feb 49

We have compared the properties of AtT20 cells cultivated in a Dulbecco's modified Eagles medium containing 10% fetal calf serum (FCS) and of AtT20 cells adapted to a chemically better defined medium with transferrin, albumin, insulin, sodium selenit and 0.2% FCS. Our interest was focused on the hypothalamo-pituitary-adrenal axis (HPA) involved adrenocorticotropic hormone (ACTH) and the potent opioid peptide beta-endorphin (beta-END). There were no differences in basal secretion of ACTH and beta-END by cells cultivated in medium containing 10% or 0.2% serum, respectively. In combination to the decreased proliferation activity of AtT20 cells, grown in the serum-reduced medium we found a strongly enhanced ACTH secretion activity stimulated by the corticotropin releasing hormone (CRH) in contrast to normally cultivated AtT20 cells (10% serum). In addition, the proopiomelanocortin (POMC) gene expression was significantly down regulated in serum-reduced medium and was normalized again after further cultivation in a 10% serum containing medium. This leads to the conclusion that under standard conditions (10% serum) the gene transcription is increased by hitherto uncharacterized modulators present in the serum. The unexpected unchanged amounts of ACTH and beta-End could be the result of increased protein convertases activities. These enzymes are responsible for the POMC precursor processing into beta-End and ACTH.
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PMID:The proopiomelanocortin (POMC) gene expression of AtT20 mouse pituitary cells is dependent on cell culture conditions. 800 51

The unidirectional brain-to-blood transport system for corticotropin-releasing hormone (CRH) across the blood-brain barrier could be instrumental in the homeostasis of central CRH. To characterize this system, the intracerebroventricular injection of 125I-CRH was used in mice. CRH was rapidly transported out of the brain with a half-time disappearance (t1/2) of 15 min, much faster than albumin (t1/2 = 50 min). Kinetic analysis revealed a saturable component with a low maximum velocity (apaproximately 0.020 nmol x min(-1) x brain(-1)) and low capacity (Michaelis constant approximately 1.4 nmol/brain). Transport was inhibited by verapamil, ouabain, and colchicine but not by cyclosporin. Transport was increased by corticosterone and inhibited by tumor necrosis factor-alpha and beta-endorphin. These results suggest that the specific unidirectional brain-to-blood transport system for CRH is dependent on energy and calcium channels, involves microtubules, is independent of the P-glycoprotein transporter, and is acutely modulated by adrenal steroids, cytokines, and endogenous opiates. This suggests its participation in the control of the stress response.
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PMID:Acute modulation of active carrier-mediated brain-to-blood transport of corticotropin-releasing hormone. 912 40

Spinal cord injury (SCI) in mammals has a poor outcome because of a lack of regeneration. Alteration of the local environment after injury may induce regeneration. However, the passage of blood-borne or exogenous neurotrophic substances through the blood-brain barrier (BBB) is not well characterized in either normal or injured states. We investigated the permeability of the BBB in normal and injured states to two markers of permeability (albumin and sucrose), to a peptide (ebiratide), and to a cytokine [tumor necrosis factor-alpha(TNF)]. We found that in normal mice the cervical and lumbar areas of the spinal cord were more permeable than the thoracic area and the brain to all four substances. The penetration of the alpha-MSH/ACTH analogue ebiratide and of TNF, substances that have saturable transport systems across the BBB and may be involved in regenerative processes in the CNS, followed a regional pattern of differential permeability comparable to that of albumin and sucrose. Complete transection at the lumbar level induced a temporal change in the permeability of the BBB. The increased permeability, as measured by the radioactively labeled tracers albumin and sucrose, was most apparent in the lumbar region proximal to the transection. After SCI, the permeability to ebiratide remained unchanged, suggesting that disruption of the BBB did not affect the transport system for ebiratide. By contrast, the increase of permeability to TNF exceeded that detected by the markers albumin and sucrose. This enhanced permeability was inhibited by excess unlabeled TNF in the blood, showing saturability. This suggests that the transport system for TNF may be activated in SCI.
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PMID:Blood-brain barrier permeability to ebiratide and TNF in acute spinal cord injury. 927 46

To determine the effectiveness of gamma-oryzanol supplementation, weight-trained males were randomly divided into supplemented (G-O) and control placebo (Con) groups. The G-O group ingested 500 mg.day-1 of gamma-oryzanol according to manufacturer's instructions. Test batteries were administered before (T1), after 4 weeks (T2), and after 9 weeks (T3) of a periodized resistance exercise program. Both groups demonstrated significant increases in 1 repetition maximum muscular strength (bench press and squat) and vertical jump power, with no differences between the groups. No differences between groups were observed for measures of circulating concentrations of hormones (testosterone, cortisol, estradiol, growth hormone, insulin, beta-endorphin), minerals (calcium, magnesium), binding protein (albumin), or blood lipids (total cholesterol, triglycerides, HDL-cholesterol). Resting cardiovascular variables decreased similarly for both groups. These data suggest that 9 weeks of 500 mg.day-1 of gamma-oryzanol supplementation does not influence performance or related physiological parameters in moderately weight-trained males.
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PMID:The effects of gamma-oryzanol supplementation during resistance exercise training. 940 58


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