Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01350 (gastrin)
 9,683 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a mechanical ileus model in 70 rabbits, the effects of PGF2alpha-infusions, PGE1- and PGA1-injections on jejunal pressure and serum gastrin levels were studied. PGF2alpha increases, whereas PGE1 inhibits jejunal motility. PGA1 produces no significant response. A modulation of neurotransmission is discussed. The serum gastrin levels can be decreased by PGE1-injections, whereas PGA1 effects only small decreases. The importance of the vagal mechanism for the release of gastrin is emphasized.
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PMID:[Behavior of intestinal motility and serum gastrin level after administration of prostaglandin A1, E1 and F2alpha in recent mechanical ileus of the rabbit]. 103 27

In 29 rabbits the action of PGF2 alpha and PGE2 was compared with prostigmine in a mechanical ileus model. PGE2 produces no therapeutical effect. PGF2 alpha delivered a significant increase of intraluminal intestinal pressure and of the amplitudes of peristalsis, lasting for about 5 minutes, whereas prostigmine made a long lasting significant enlargment of the amplitudes of peristalsis without any modification of intraluminal pressure. Serum gastrin levels increased after application of PGE2 and PGF2 alpha and remained constant after prostigmine. A possible way of action of PG's in the gastrointestinal tract is discussed, based on experiments concerning PG-application after different periods of time.
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PMID:[Behavior of intestinal motility and serum gastrin level during prostaglandin administration in acute mechanical ileus of the rabbit]. 120 49

The plasma gastrin levels in fasted horses (21.1 +/- 15.6 pg/ml), in horses with spasmodic colic (7.3 +/- 5.4 pg/ml) and in horses with impaction of the left ventral large colon and/or pelvic flexure (11.4 +/- 3.1 pg/ml) were not significantly different. The plasma gastrin concentrations of horses with strangulation obstruction of the small intestine, large colon displacement or adynamic ileus, and which had no gastric reflux, were 12.9 +/- 8.7 pg/ml and did not differ from fasted gastrin levels. Horses which had 5-10 litres of stomach content reflux had a higher mean gastrin level (32.2 +/- 22.6 pg/ml) (range 8.7-83.0) than the fasted horses. The mean plasma gastrin level (69.0 +/- 32.2 pg/ml) (range 27.0-122.0 pg/ml) in horses which had gastric reflux and 11-20 litres of stomach content outflow through the nasogastric tube were significantly higher (P less than 0.0004) than in fasted horses or in horses with spasmodic colic, impaction of the left ventral large colon or in horses from which no gastric reflux could be obtained.
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PMID:[Plasma gastrin levels in horses with colic]. 141 32

Motility disturbances of the large intestine, which appear in various conditions of a disease, are based on a reduction, the loss or an intensivation of the contractility as well as on a disorganization of the motor activity. Also in the region of the large intestine the normal motoricity can underlie such disturbances, such as retarded or accelerated passage, passage in wrong direction as well as increased turbulence or increased content. Retarded passage of the large intestine leads to obstipation and in advanced form to ileus. The leading symptom in accelerated passage is the diarrhoea. The passage in wrong direction disturbs the motoricity of the colon in the case of a lesion of the ileocaecal valves. Increased turbulence of the content of the large intestine is one of the causes of obstipation, particularly, when it appears in a retarded passage. The disturbances of the laminary flow are characteristic for a diverticulosis. The motor activity of the colon is influenced by many factors, mainly by the central nervous system, the gastrointestinal hormones (cholecystokinin, gastrin, serotonin, insulin and prostaglandins), the diet and the way of life. The motor disturbances are accompanied by bioelectric disturbances of the colon. In the second part of the lecture some pathogenetic and clinical aspects of the most frequently appearing motor disturbance of the large intestine, the irritable colon, are discussed.
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PMID:[Motility disturbances of the large intestine]. 722 37

We describe the clinical and pathological findings in two Japanese men with small cell carcinoma of the prostate; case 1 was 58 years old and case 2 was 24 years old. Case 1 was initially diagnosed as a poorly differentiated adenocarcinoma of the prostate, stage D2, with marked elevation of serum neuron-specific enolase (NSE), carcinoembryonic antigen (CEA), and CA 19-9 levels. The patient had undergone castration and systemic chemotherapy. After three courses of chemotherapy, tumour markers were normalized. However, 6 months later serum levels of tumour markers again rose, and biopsy of the prostate revealed a small cell carcinoma component in the adenocarcinoma of the prostate and benign prostate hypertrophy. The patient was again treated with systemic chemotherapy but died within 1 year after relapse. In case 2, the patient presented with initial symptoms of lumbago and dysuria, and an enlarged prostate was radiologically diagnosed. Shortly after admission he developed ileus, and an exploratory laparotomy revealed a large tumour arising from the prostate and invading the peritoneal cavity. This tumour was pathologically diagnosed as a small cell carcinoma. The patient died shortly thereafter without responding to chemotherapy. Immunohistological evaluation was done using a panel of antibodies against NSE, chromogranin A, CEA, CA 19-9, prostatic acid phosphatase (PAP), prostate-specific antigen (PSA), leukocyte common antigen (LCA), epithelial membrane antigen (EMA), adrenocorticotropic hormone (ACTH), calcitonin, serotonin, gastrin, vasoactive intestinal peptide (VIP), and glucagon. CEA was intensely positive in the tumour lesions from case 1, and NSE and ACTH were focally positive, and calcitonin, serotonin, CA 19-9, and PSA were weakly positive only in several cells in the tumour lesions from case 1. In the tumour lesion from case 2, NSE was intensely positive, and chromogranin A was weakly positive. These findings support the neuroendocrine nature of this neoplasm.
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PMID:Two cases of small cell carcinoma of the prostate. 900 36

Short-bowel syndrome is functionally defined as a state of malabsorption following loss of small bowel. Most cases occur in the neonatal period after extensive resection for necrotizing enterocolitis, or due to congenital anomalies of the gastrointestinal tract. A smaller percentage originate later in life from surgical treatment of Crohn's disease, neoplastic disorders, or vascular events. The physiological, morphological and functional intestinal gradient determines the clinical picture leading to better tolerance of jejunal than ileal resections. The subsequent adaptation process requires enteral feeding with a different impact of specific nutrients, and is also influenced by a number of humoral mediators such as enteroglucagon, gastrin, growth factors, prostaglandins and polyamines. Nutritional management starts parenterally via a central venous line covering basic demands, substituting current losses and restoring pre-existing deficiencies. Continuous enteral tube feeding is added as soon as postoperative ileus resolves, beginning with an elemental diet, which is gradually increased first in concentration, then in quantity, and supplemented by small oral meals. Cycling of parenteral nutrition is the next step. As soon as sufficient stability is reached, the child should be discharged home under continued outpatient care. Main long-term problems comprise bacterial overgrowth, fluid and electrolyte disequilibration, nutritional deficiencies, parenteral nutrition-related liver disease, and central venous line complications such as sepsis and thrombosis.
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PMID:Enteral and parenteral nutrition in patients with short-bowel syndrome. 1053 60

Thyroid disease is common, and its effects on the gastrointestinal system are protean, affecting most hollow organs. Hashimoto disease, the most common cause of hypothyroidism, may be associated with an esophageal motility disorder presenting as dysphagia or heartburn. Dyspepsia, nausea, or vomiting may be due to delayed gastric emptying. Abdominal discomfort, flatulence, and bloating occur in those with bacterial overgrowth and improve with antibiotics. Reduced acid production may be due to autoimmune gastritis or low gastrin levels. Constipation may result from diminished motility, leading to an ileus, megacolon, or rarely pseudoobstruction. Ascites in myxedema is characterized by a high protein concentration. Graves' disease accounts for 60% to 80% of thyrotoxicosis. Hyperthyroidism is accompanied by normal gastric emptying with low acid production, partly due to an autoimmune gastritis with hypergastrinemia. Transit time from mouth to cecum is accelerated, resulting in diarrhea. Steatorrhea is due to hyperphagia and stimulation of the adrenergic system. Diarrhea in medullary carcinoma of the thyroid (MCT) may be due to elevated calcitonin, prostaglandins, or 5-hydroxyindoleacetic acid. Ileal or colonic function may be abnormal. The esophagus may be compressed by benign processes, but more often by malignancies. MRI and CT scans are the best diagnostic modalities. The gastrointestinal manifestations of thyroid disease are generally due to reduced motility in hypothyroidism, increased motility in hyperthyroidism, autoimmune gastritis, or esophageal compression by a thyroid process. Symptoms usually resolve with treatment of the thyroid disease.
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PMID:The thyroid and the gut. 2035 69