Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017168 (gastroesophageal reflux disease)
 11,783 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The possible participation of a stimulated ACTH secretion in the promotion of the pineal gland reactive response under conditions of injection stress was studied. Morphine was used as a pharmacological mimicry of the stress-induced ACTH outflow in the post-injection period of 10-45 min. In animals subjected to injection stress (administration of the physiological solution), in the 10-th min. light pinealocytes exhibited a significant rise in the relative volume of the GER field and the Gogli apparatus, as well as bouquets of presecretory or secretory forms of the cell processes and frequent extrusion of lipid droplets. From 20-th min. on, the relative volume of their membranous elaborative compartment gradually decreased, the cell processes were missing and the lipid droplet extrusion was rare. The rich arbourisation of the GER tubules, the active appearance of the Golgi apparatus and a more abundant occurrence of lipid droplets--a picture which persisted even in 30 min.--showed that the intensified elaborative activity of dark pinealocytes, a minor cell population, was of longer duration in comparison with light pinealocytes. The subsequent fall in their stress-reactive response points out that the function of light and dark pinealocytes is driven by different regulative systems. Based on the principle that the function is the reflection of morphometabolic changes, in can be concluded that 10 min. after the injection act, the pineal gland has a short-term crescendo of its stress-reactive response. The morphine injection did not cause any significant changes in both pinealocyte populations in 10 min. A considerable increase of the relative volume of the constituents of the membrane elaborative compartment was found in light pinealocytes in the next observational periods, i.e., in the 20-th and the 30-th min. The lack of any conspicuous signs of an enhanced secretory activity, in contrast with frequent findings of lipid droplets and prosecretory granules, shows that the facilitation of the elaborative activity leads more to a restitution and increase of the pinealocyte potential than to a stimulation of their current secretion. Characteristic of this period was a frequent finding of newly generated lipid droplets. Their presence within the fields of GER tubules, as well as the communication of the lumens of these tubules with the matrix of the arising lipid droplet suggest a close connection of lipid droplets with the pinealocyte peptidergic activity Unexpected was the finding of a conglomerate of fasciculated lamellae--structures of a so far unknown function.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Morphodynamic response of the pineal gland to an initial stress attack--the effect of morphine]. 213 14

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

Allgrove syndrome (triple A) is a rare autosomal recessive disease. The classic triad includes, congenital adrenal insufficiency due to ACTH resistance, achalasia of the cardia and alacrimia. Neurological abnormalities are associated with autonomic neuropathy, sensory and motor defects, deafness, mental retardation, Parkinsonism and dementia. The gene responsible is the ADRACALIN or AAAS encoding a protein called ALADIN. We report a case of a 19 year-old male, assessed when he was 10 years old in our department due to suspected storage disease. Mild mental and language retardation, hypernasal voice, sensory-motor neuropathy with autonomic involvement and signs of spastic paraparesis, alacrimia. gastroesophageal reflux, and achalasia. Molecular studies showed to mutations, the undescribed p.Tyr 19 Cys, and IVS14 +1 G.
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PMID:[Allgrove syndrome (triple A). Finding of a mutation not described in the AAAS gene]. 2282 7