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)

Gastric function was studied in 69 peptic ulcer patients in the long-term period after gastric resection according to Billroth-I and Billroth-II. Enzyme-producing function of the stomach was appraised according to the blood pepsinogen content, acid-forming function was assessed with the aid of intragastric pH-metry, and mucus-forming one in accordance with the content of hexosamines and sialic acids in gastric juice. The patients showed different alterations in gastric function. A correlation analysis was used to establish the role played by the neurohormonal systems (leu-enkephalin, beta-endorphin, gastrin, somatotropin, triiodothyronine, thyroxine, cortisol) in the derangement of secretory function of the resected stomach. The data obtained enable one to come closer to understanding the ineffectiveness in some cases of drug and surgical therapy of peptic ulcer. On the other hand, specification of the regularities of the impairment of secretory function of the stomach will be helpful in elaborating methods of gastric function correction at the neurohormonal level.
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PMID:[Changes in gastric secretory function in peptic ulcer patients after gastric resection]. 204 10

RIA method was used in this study to determine immunoreactive beta-endorphin (ir-beta-EP) in gastric mucosa of patients with benign and malignant gastric diseases. The results showed that the content of ir-beta-EP in gastric mucosa in the peptic ulcer group was the highest (68 +/- 9.5 pg/mg wet weight tissue, P less than 0.01), while its content in gastric carcinoma was closely related to the degree of differentiation of the tumor, that is, in poorly differentiated carcinoma it was lower than that in well differentiated carcinoma (P less than 0.02), and was also lower than that in gastritis (P less than 0.05). At the same time, we found that beta-endorphin can markedly augment the 3H-TdR incorporation of lymphocytes (P less than 0.01). This effect was not blocked by naloxone.
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PMID:Changes and significance of immunoreactive beta-endorphin in gastric mucosa of patients with benign and malignant gastric diseases. 214 73

Although the generally accepted belief in the psychological benefits of exercise for children has very little documentation by well controlled studies, the risk:benefit ratio nonetheless tends to favor exercise when competition is sensibly controlled. The field is a fertile one for longitudinal and developmental investigations employing more sophisticated psychological measures and appropriate physiological assessment. Studies using self-concept measures in very young children may find less change after exercise than those using a more age-specific developmental scale, such as the Vineland Social Maturity Scale or human figure drawings. Exercise programs for childhood research may be more informative when natural exercise patterns are observed than when artificial regimens are imposed. The mechanism through which exercise effects psychological change remains unidentified; the beta-endorphin theory suggested by Carr was not documented when Markoff, Ryan, and Young discovered that naloxone, an endorphin antagonist, failed to reverse the mood elevation associated with running. The important effects of exercise on the immune system recently reported in adults have not been investigated in children. The possible implications of my recent finding of a significantly reduced level of absolute lymphocytes among a large group of hospitalized depressed adults remain to be assessed but suggest directions for research. Having treated a 10-year-old Little League player with a generalized anxiety disorder; a 7-year-old Pony League outfielder terrified over the possibility of being hit in the head with a baseball; and a 9-year-old with peptic ulcer associated with a Little League all-star selection, I plead for the encouragement of sports for pleasure rather than glory, while at the same time recommending regular and age-appropriate exercise for children. Using our research findings, we have developed a profile of psychosomatic fitness, an optimal state of health in which there is an accurate balancing process involving mind, body, and spirit through attention to how we live and regard others. No one may possess all the characteristics of this profile, but it is an ideal. The extent to which one may achieve psychosomatic fitness may vary from time to time, depending on one's unique circumstances, but its attainment seems to be related to will power, motivation, and respect for the dire consequences of failure.
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PMID:Exercise and mental health in the pediatric population. 676 95

The purpose of this study was to identify the CNS neurons that express Fos protein after i.p. injection of ulcergenic drug cinchophen (300 mg/kg). This was done in unanesthetized Wistar rats with careful physiological controls. The population of Fos-immunoreactive (Fos-ir) neurons was the largest in the medial parvicellular part of the paraventricular nucleus of the hypothalamus (PVH). Distribution of Fos-ir neurons in the PVH corresponds with that of the parvicellular neurons in the PVH which secrete corticotropin-releasing hormone (CRH). This study strongly suggests that the cinchophen-induced peptic ulcer may originate in excitation of the CRH-secreting neurons in the parvicellular part of the PVH.
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PMID:Neuronal expression of Fos protein in the paraventricular nucleus of the hypothalamus after i.p. injection of ulcergenic cinchophen. 791 44

Physiological regulatory mechanisms of gastric acid secretion are the basis for all those studies which attempt to analyze the pathophysiological role of acid secretion. The major stimulus of parietal cell function is food intake which acts via activation of cephalic-vagal and gastric mechanisms. Cephalic phase of acid secretion is augmented predominantly by acetylcholine and gastrin while histamine is of major importance during the gastric phase. A contribution of neuropeptides located in the ex- and intrinsic nervous system such as enkephalin, beta-endorphin, gastrin-releasing peptide and neuromedin C ist most likely, however, their exact physiological role remains to be determined especially in man. Following maximal acid secretion parietal cell function is turned down which is paralleled by the decrease of intragastric pH. The mechanisms responsible for this effect originate in the stomach and small intestine. In contrast to the stimulatory factors the physiologically relevant inhibitors of acid secretion are less well known. Hormones such as somatostatin, glucagon-like peptide-1 (7-36)-NH2 and peptide YY are presumably of importance. The role of secretin, GIP, CCK and neurotensin is somewhat more controversial and remains to be examined in greater detail in humans. Especially the synergistic action of gastrointestinal hormones is virtually unknown. The increasing knowledge of the complex regulatory mechanisms in the stomach should result in new perspectives for the pathogenesis of peptic ulcer disease.
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PMID:[Physiologic regulation of gastric acid secretion]. 847 47

When exposed to prolonged stress, rats develop gastric ulceration, enhanced colon motility with depletion of its mucin content and signs of physiological and behavioral arousal. In this model, we tested whether antidepressants (fluoxetine and bupropion), anxiolytics (diazepam and buspirone) or the novel nonpeptide corticotropin-releasing hormone (CRH) type-1 receptor (CRH-R1) antagonist, antalarmin, modify these responses. Fluoxetine, bupropion, diazepam and antalarmin all suppressed stress-induced gastric ulceration in male Sprague-Dawley rats exposed to four hours of plain immobilization. Antalarmin produced the most pronounced anti-ulcer effect and additionally suppressed the stress-induced colonic hypermotility, mucin depletion, autonomic hyperarousal and struggling behavior. Intraperitoneal CRH administration reproduced the intestinal but not the gastric responses to stress while vagotomy antagonized the stress-induced gastric ulceration but not the intestinal responses. We conclude that brain CRH-R1 and vagal pathways are essential for gastric ulceration to occur in response to stress and that peripheral CRH-R1 mediates colonic hypermotility and mucin depletion in this model. Nonpeptide CRH-R1 antagonists may therefore be prophylactic against stress ulcer in the critically ill and therapeutic for other pathogenetically related gastrointestinal disorders such as peptic ulcer disease and irritable bowel syndrome.
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PMID:Marked suppression of gastric ulcerogenesis and intestinal responses to stress by a novel class of drugs. 1208 65

Overproduction of corticotropin-releasing hormone (CRH) and stress system abnormalities are seen in psychiatric diseases such as depression, anxiety, eating disorders, and addiction. Investigations of CRH type 1 receptor (CRHR1) nonpeptide antagonists suggest therapeutic potential for treatment of these and other neuropsychiatric diseases. However, overproduction of CRH in the brain and on its periphery and disruption of the hypothalamic-pituitary-adrenal axis are also found in 'somatic' disorders. Some rare forms of Cushing's disease and related pituitary/adrenal disorders are obvious applications for CRHR1 antagonists. In addition, however, these antagonists may also be effective in treating more common somatic diseases. Patients with obesity and metabolic syndrome who often have subtle, but chronic hypothalamic-pituitary-adrenal hyperactivity, which may reflect central dysregulation of CRH and consequently glucocorticoid hypersecretion, could possibly be treated by administration of CRHR1 antagonists. Hormonal, autonomic, and immune aberrations are also present in chronic inflammatory, autoimmune, and allergic diseases, with considerable evidence linking CRH with the observed abnormalities. Furthermore, autonomic dysregulation is a prominent feature of common gastrointestinal disorders, such as irritable bowel syndrome and peptic ulcer disease. Patients with irritable bowel syndrome and other gastrointestinal disorders frequently develop altered pain perception and affective symptoms. CRH acts peripherally to modulate bowel activity both directly through the autonomic system and centrally by processing viscerosensory and visceromotor neural signals. This review presents clinical and preclinical evidence for the role of CRH in the pathophysiology of these disorders and for potential diagnostic and therapeutic applications of CRHR1 antagonists. Recognition of a dysfunctional stress system in these and other diseases will alter the understanding and treatment of 'psychosomatic' disorders.
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PMID:Nonpeptide corticotropin-releasing hormone receptor type 1 antagonists and their applications in psychosomatic disorders. 1552 86

Stress, defined as an acute threat to homeostasis, evokes an adaptive or allostatic response and can have both a short- and long-term influence on the function of the gastrointestinal tract. The enteric nervous system is connected bidirectionally to the brain by parasympathetic and sympathetic pathways forming the brain-gut axis. The neural network of the brain, which generates the stress response, is called the central stress circuitry and includes the paraventricular nucleus of the hypothalamus, amygdala and periaqueductal gray. It receives input from the somatic and visceral afferent pathways and also from the visceral motor cortex including the medial prefrontal, anterior cingulate and insular cortex. The output of this central stress circuit is called the emotional motor system and includes automatic efferents, the hypothalamus-pituitary-adrenal axis and pain modulatory systems. Severe or long-term stress can induce long-term alteration in the stress response (plasticity). Corticotropin releasing factor (CRF) is a key mediator of the central stress response. Two CRF receptor subtypes, R1 and R2, have been described. They mediate increased colonic motor activity and slowed gastric emptying, respectively, in response to stress. Specific CRF receptor antagonists injected into the 0 block these visceral manifestations of stress. Circulating glucocorticoids exert an inhibitory effect on the stress response by receptors located in the medial prefrontal cortex and hippocampus. Many other neurotransmitters and neuroimmunomodulators are being evaluated. Stress increases the intestinal permeability to large antigenic molecules. It can lead to mast cell activation, degranulation and colonic mucin depletion. A reversal of small bowel water and electrolyte absorption occurs in response to stress and is mediated cholinergically. Stress also leads to increased susceptibility to colonic inflammation, which can be adaptively transferred among rats by sensitized CD4(+) lymphocytes. The association between stress and various gastrointestinal diseases, including functional bowel disorders, inflammatory bowel disease, peptic ulcer disease and gastroesophageal reflux disease, is being actively investigated. Attention to the close relation between the brain and gut has opened many therapeutic avenues for the future.
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PMID:Stress and the gastrointestinal tract. 1574 Apr 74

The hypothalamo-pituitary-adrenal (HPA) axis is known to relate with energy homeostasis. Appetite and food intake are assumed to be regulated by the HPA axis. Among lots of medicines that act gastrointestinal system, we focused proton pump inhibitors, which are widely used to treat peptic ulcer, gastro esophageal reflux disease and eradication of Helicobacter pylori. In this study, we investigated that the effect of three proton pump inhibitors (omeprazole, lansoprazole and rabeprazole) on plasma adrenocorticotropic hormone (ACTH) and cortisol levels in healthy human subjects. Five healthy male volunteers were treated to omeprazole, lansoprazole, rabeprazole or placebo. Venous blood samples were taken repetitively from a forearm vein before and after administration. Plasma ACTH-like immunoreactive substance (IS) levels were measured using a sensitive enzyme immunoassay, and plasma cortisol levels were measured using a fluorescence polarization immunoassay. Single administration of lansoprazole caused significant (P<0.05) increase of ACTH-IS at 60 and 120-180 min, and cortisol at 180-240 min after administration, compared with placebo group. Rabeprazole also caused significant increase of ACTH-IS at 120 min and cortisol at 240-360 min, compared with placebo group. Omeprazole had no effect on plasma ACTH-IS and cortisol levels. Lansoprazole and rabeprazole increased plasma ACTH-IS and cortisol levels. Therefore, we hypothesized that the medicines might activate the HPA axis, and have effect to promote feeding. We considered that these results might be relevant to the development of new therapeutics in the treatment of psychiatric disorders involving dysregulation of appetite.
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PMID:Comparison of the effects of proton pump inhibitors on human plasma adrenocorticotropic hormone and cortisol levels under the starved condition. 1652 91

Gout, a common inflammatory arthritis, can be diagnosed with absolute certainty. Gout results from the body's reaction to urate crystals deposited in tissues, and this pathophysiology is well understood. If used appropriately, available therapies can be entirely effective in not only treating the symptoms of gout, but also in eliminating the excess urate from the body, thereby eradicating the disease. Because of these facts, management of patients with gout should be successful. However, management of gout is particularly challenging in the elderly, even though the principles of management are the same for all age groups. The purpose of this article is to review these principles and discuss them as they pertain to the elderly. The classic gout attack is acute in onset, extremely painful and associated with marked swelling, warmth, erythema and tenderness of a single joint. However, the diagnosis of gout may be challenging in the elderly because atypical presentations are more common in this group. Treatment of acute gout involves the use of NSAIDs, colchicine, corticosteroids or corticotropin (adrenocorticotropic hormone). Unfortunately, co-morbid conditions such as chronic kidney disease, peptic ulcer disease and congestive heart failure may make the use of these agents dangerous or contraindicated. Thus, it is important to try to treat an acute flare of gout at the earliest sign, because the sooner treatment is initiated, the faster the inflammation will resolve. Urate-lowering agents include allopurinol and uricosuric agents. These also must be used judiciously in the elderly. However, if used at the lowest dose that maintains the serum urate level below 5.0-6.0 mg/dL, the excess urate in the body will be eliminated, acute flares will no longer occur and tophi will resolve. Gout is often seen in association with hypertension, excessive alcohol consumption, obesity and hypertriglyceridaemia. These conditions and the medications used to treat them may contribute to the hyperuricaemia. Treating these conditions and using medications that do not promote hyperuricaemia will aid in the management of gout. Despite the challenges that often complicate the management of gout in the elderly, an understanding of the pathophysiology of the disease and both the indications and limitations of the medications used should allow successful treatment.
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PMID:Management of gout in older adults: barriers to optimal control. 1723 45


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