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)

The presence of beta-endorphin (beta-end) was immunohistologically identified in synovial tissue samples biopsied from patients with rheumatoid arthritis (RA) and osteoarthritis (OA). The amount of beta-end in culture supernatants of synovial tissue explants was also determined by RIA. beta-end was strongly detected in mainly superficial synovial cells, vascular endothelial cells and a few synovial interstitial cells in RA patients, but not in OA patients. In RA patients the beta-end concentration was significantly higher in the supernatants of tissue explants (26.4 +/- 8.3 pg/ml) than in the plasma of the same patients (15.3 +/- 2.5 pg/ml) (p < 0.01). Using isolated synovial cells, the beta-end concentration in the culture supernatants of non-adherent cells (19.4 pg/ml) was higher than that of adherent cells (4.0 pg/ml). It is suggested that beta-end is produced by non-adherent cells such as lymphocytes and neutrophils in addition to synovial lining cells and endothelial cells and may play some role in the pathology of RA synovial inflammation.
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PMID:[Role of opioid peptide in rheumatoid arthritis--detection of beta-endorphin in synovial tissue]. 144 37

Several new problems in obesitology were pointed out in this book and commented with respect to experiments and experiences of our working group. The problem of the low triiodothyronine (T3) syndrome was treated in chapter 2. The decrease of serum T3 and increase of serum reverse T3 in obese subjects was induced by several factors, namely by fasting. A resistance to administered thyroxine and triiodothyronine was observed in these patients. This energy saving mechanism is at variance with slimming regimens. The prevention and treatment of this awkward complication was discussed. The next chapter (3) is concerned with the hormonal and metabolic effects of diet and motor activity in the course of slimming regimens. The different effects of diet and motor activity on epinephrine and norepinephrine in obese subjects were similar to those obtained by other investigators in nonobese humans. A great importance was attributed to an increased plasma level of cortisol in obese and nonobese subjects in the course of different forms of motor activity and related to a different intensity of exercise. Parallel to several of these experiments, beta-endorphin, thyroid hormones and glucagon were also estimated. It was suggested that motor activity for exercising subjects should not lead to an enhanced secretion of cortisol in view of the health deteriorating effects of increased cortisolemia and in view of an already stimulated secretion of this hormone in obese subjects on basal conditions. Vice versa, a decreased cortisolemia should be obtained in obese subjects treated with an appropriate motor activity and diet. It has been shown that diet without motor activity reduced the level of plasma androgens but in cooperation with motor activity, the level of androgens remained unaltered in the course of the reducing regimen. The conservation of a normal or even higher level of androgens is probably prerequisite for a positive nitrogen balance observed in the course of a combined slimming regimen, while diet without motor activity led in the studied conditions to a negative nitrogen balance. Chapter 4 was devoted to the role of motor activity in slimming regimens. In view of the metabolic effects of motor activity and the clinical late effects of obesity (osteoarthritis of the knees, hips and spine, arterial hypertension, overload of the cardiovascular system, diabetes mellitus etc.), a selection of motor activities was proposed. According to our long experience, we do not recommend jogging, running, jumping and all sports leading to collisions of players.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:New trends in obesitology. 307 25

Serum concentrations of luteinizing hormone, follicle-stimulating hormone, prolactin, 17 beta-estradiol, testosterone, androstenedione, dehydrotestosterone, dehydroepiandrosterone sulfate, and cortisol were examined in 14 men with rheumatoid arthritis (RA) and in age-matched osteoarthritis controls. Hypophyseal, adrenal, and testicular responses to stimulation with luteinizing hormone-releasing hormone, adrenocorticotropin, and human chorionic gonadotropin, respectively, were evaluated in 8 RA patients and in 8 age-matched healthy volunteers. Basal serum testosterone concentrations were significantly lower in male RA patients than in the osteoarthritis control subjects (P less than 0.01). After human chorionic gonadotropin stimulation, serum concentrations of testosterone were also lower in the RA patients than in normal healthy controls (P less than 0.05). These findings suggest that diminished testicular steroid biosynthesis might contribute to the serum testosterone deficiency observed in male RA patients.
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PMID:Sex hormone status of male patients with rheumatoid arthritis: evidence of low serum concentrations of testosterone at baseline and after human chorionic gonadotropin stimulation. 314 Aug 23

Plasma concentrations of [met]enkephalin (ME) and beta-endorphin (beta E) were measured in samples obtained immediately before and after physiotherapeutic exercises for patients with ankylosing spondylitis (AS), osteoarthritis (OA), or knee injuries. Correlations were sought between opioid peptide concentrations or changes therein, and nature, severity and duration of disease, age, severity of pain reported and pain threshold. No correlation was found with any of the pain parameters. However, there was a possible relationship between age or duration of disease and changes in ME concentrations.
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PMID:Changes in plasma opioid concentrations after physiotherapeutic exercises for arthritic patients. 315 38

Serum beta-endorphin levels have been determined in patients with a wide variety of rheumatic disorders as well as a group of healthy men and women controls. Normal levels of endorphin have been found in patients with juvenile rheumatoid arthritis. Patients with rheumatoid arthritis, osteoarthritis, systemic lupus erythematosus, gout, ankylosing spondylitis, pseudogout and psoriatic arthritis have diminished levels of endorphins. Speculation is offered to explain these changes. Perturbations in endorphins are postulated to be part of the organism's protective mechanism in inflammatory arthritis.
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PMID:Serum beta-endorphin in rheumatic disorders. 716 73

Inflammation normally results in enhanced synthesis and secretion of hypothalamic corticotropin-releasing hormone (CRH) which, in turn, exerts antiinflammatory effects by virtue of increased adrenal glucocorticoid production. CRH and CRH binding sites are also expressed in the peripheral nervous and immune systems. Our groups have recently shown that CRH is secreted locally in acute carrageenin-induced inflammation in rats and has predominantly proinflammatory effects. We have also shown that CRH is expressed in the joints of Lewis rats with experimental arthritis. To determine if CRH is present in human inflammatory arthritis, we examined synovial fluids and tissues from patients with rheumatoid arthritis (RA) or osteoarthritis (OA) and normal individuals. We found markedly enhanced expression of immunoreactive CRH in situ in synovium from patients, which was significantly greater in RA than in OA (p < 0.01). CRH concentrations were also significantly higher in RA (140 +/- 33 pg/ml, mean +/- SEM; n = 10) than OA (25 +/- 4 pg/ml; n = 6) synovial fluids (p < 0.005). HPLC showed immunoreactive CRH extracted from RA and OA synovial tissues and fluids coeluted with CRH 1-41. CRH mRNA was present in low levels in synovial tissue from patients with RA and, to a lesser extent, OA. In summary, immunoreactive CRH is locally secreted in the synovium of patients with RA and, at lower levels, OA. These data support the view that CRH functions as an autocrine and/or paracrine mediator of inflammation in humans.
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PMID:Corticotropin-releasing hormone in synovial fluids and tissues of patients with rheumatoid arthritis and osteoarthritis. 833 47

The aim of this study was to determine if the anticytokine neuropeptide alpha-melanocyte-stimulating hormone (alpha-MSH) occurs, along with interleukin 1 receptor antagonist (IL-1ra) and soluble tumor necrosis factor receptor (sTNFr), in synovial fluid of patients with rheumatoid arthritis (RA), juvenile chronic arthritis (JCA), or osteoarthritis. The data show that alpha-MSH does occur in the synovial fluid and its concentrations are greater in patients with RA than in those with osteoarthritis. Synovial fluid concentrations of IL-1ra and sTNFr were likewise greater in RA. Further, concentrations of alpha-MSH, IL-1-ra, and sTNFr were greater in patients with polyarticular/systemic-onset JCA than in those with pauciarticular disease, that is in patients with greater joint inflammation. Concentrations of alpha-MSH were greater in synovial fluid than in plasma in a substantial proportion of patients, suggesting local production of the peptide; this is the first indication that the anticytokine molecule alpha-MSH is produced within a site of inflammation. Further, it appears that local production of alpha-MSH is induced particularly in those arthritic joints that have more intense inflammatory reactions. This finding, combined with previous evidence of the marked anti-inflammatory activity of alpha-MSH, suggests that the peptide acts locally to modulate proinflammatory influences in rheumatic diseases.
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PMID:The anticytokine neuropeptide alpha-melanocyte-stimulating hormone in synovial fluid of patients with rheumatic diseases: comparisons with other anticytokine molecules. 852 99

Corticotropin releasing hormone (CRH) and ACTH concentrations in plasma and CRH and IL-6 concentrations in synovial fluid in patients with rheumatoid arthritis (RA) were examined to clarify the relationship between cytokines and the hypothalamic-pituitary-adrenal axis (HPA axis). Concentrations of serum amyloid A protein (SAA), one of the acute phase proteins, were also measured as an indicator of inflammation. CRH and IL-6 concentrations in synovial fluid were higher in RA patients than in control patients (osteoarthritis, OA). Plasma ACTH and CRH levels were significantly lower in RA patients than in OA patients. This suggests that CRH secretion in synovial fluid is regulated differently from plasma CRH secretion, as CRH levels in synovial fluid and plasma showed opposite changes in RA patients. SAA levels were positively correlated with the levels of CRH or IL-6 in synovial fluid, whereas there was no correlation between CRH and IL-6 levels. The results suggest that CRH and IL-6 play important independent roles in producing SAA in synovial fluid.
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PMID:Differential changes of corticotropin releasing hormone (CRH) concentrations in plasma and synovial fluids of patients with rheumatoid arthritis (RA). 902 71

The radioactive and thermal effects of radon hot spring were biochemically compared under a sauna room or hot spring conditions with a similar chemical component, using the parameters that are closely involved in the clinic for radon therapy. The results showed that the radon and thermal therapy enhanced the antioxidation functions, such as the activities of superoxide dismutase (SOD) and catalase, which inhibit lipid peroxidation and total cholesterol produced in the body. Moreover the therapy enhanced concanavalin A (ConA)-induced mitogen response and increased the percentage of CD4 positive cells, which is the marker of helper T cells, and decreased the percentage of CD8 positive cells, which is the common marker of killer T cells and suppressor T cells, in the white blood cell differentiation antigen (CD8/CD4) assay. Furthermore, the therapy increased the levels of alpha atrial natriuretic polypeptide (alpha ANP), beta endorphin, adrenocorticotropic hormone (ACTH), insulin and glucose-6-phosphate dehydrogenase (G-6-PDH), and it decreased the vasopression level. The results were on the whole larger in the radon group than in the thermal group. The findings suggest that radon therapy contributes more to the prevention of life-style-related diseases related to peroxidation reactions and immune suppression than to thermal therapy. Moreover, these indicate what may be a part of the mechanism for the alleviation of hypertension, osteoarthritis (pain), and diabetes mellitus brought about more by radon therapy than by thermal therapy.
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PMID:Biochemical comparison between radon effects and thermal effects on humans in radon hot spring therapy. 1513 94

In the present study, we have investigated the presence of pro-opiomelanocortin C-terminal fragment derived-peptides in human articular cartilage and cultured chondrocytes. beta-Lipotropin and beta-endorphin were monitored in different cell cultures and biopsies using different techniques. Biopsies were taken from patients undergoing total knee arthroplasty due to osteoarthritis. Both fresh tissue sections and chondrocytes cultured in monolayer were used in the study. Immunohistochemistry, immunocytochemistry, reverse transcriptase-polymerase chain reaction and qualitative Western blots were carried out. The results of the reverse transcriptase-polymerase chain reaction showed transcription of a truncated-form of mRNA for pro-opiomelanocortin in native cartilage and cultured chondrocytes. There was no detection of endogenous production of beta-lipotropin or beta-endorphin in human articular chondrocytes, either in situ or in vitro. Whether pro-opiomelanocortin-derived peptides of non-cartilaginous origin are present in articular cartilage itself still remains unclear.
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PMID:Detection of mRNA transcripts of truncated opiate precursor (POMC) in human cartilage. 1589 26


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