Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Evidence is presented for the existence of three distinct enterotoxins detected in concentrated cell-free culture filtrates of selected Bacillus cereus strains. The first was a product capable of stimulating the adenylate cyclase-cyclic-AMP system in intestinal epithelial cells and, possibly through this, causing fluid accumulation in ligated ileal sections ("loops") of young rabbits. This was elaborated by a strain isolated from an incident of diarrhoea and which caused diarrhoea in 6 of 10 monkey feedings. The second was tentatively identified as a factor which caused fluid accumulation in rabbit loops but not, apparently, through stimulation of the adenylate cyclase-cyclic-AMP system; this was elaborated by a strain isolated from raw rice which failed to produce symptoms in eight monkey feedings. Together, the behaviour of these two factors indicates that diarrhoea caused by B. cereus enterotoxin may be a cyclic-AMP-mediated event. The third, here referred to as "pyogenic toxin", caused severe tissue damage in the ileal mucosa and was elaborated by a strain isolated from a brain abscess. A factor produced by a strain isolated from an outbreak of vomiting which caused vomiting in 10 of 24 monkey feedings could bot be detected in tests reported here but appears to be a fourth enterotoxin type. Cytopathic effects in tissue cultures, suckling mouse tests, and assays of glycerol production by fat cells were not found to be of value in the detection of any of the enterotoxins.
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PMID:Studies on the production of enterotoxins by Bacillus cereus. 82 25

Prostacyclin (PGI2) is known to cause vasorelaxation and inhibit platelet aggregation by receptor-mediated mechanisms. While cyclic (c) AMP is known to act as a second messenger for inhibition of platelet aggregation, vasorelaxation by hyperpolarization has been described only recently and may provide an explanation, in addition to stimulation of cAMP for the PGI2 mechanism of action on blood vessels. When PGI2 is infused into healthy volunteers it reduces blood pressure only at infusion rates that also cause significant side-effects, primarily, nausea, emesis, flushing, diaphoresis, and restlessness. In hypertensive patients blood-pressure responses are complex and are influenced to some extent by renin secretion. PGI2 stimulates renin secretion by a direct effect on the juxtaglomerular apparatus, and it also has an indirect effect by activating the sympathetic nervous system. Thus, it is useless as an antihypertensive agent even apart from its debilitating side-effects. Vascular PGI2 is synthesized endogenously by both the endothelial cells and the muscularis of arteries. While the endothelial cells undoubtedly synthesize large amounts of PGI2, the muscularis comprises a much larger tissue mass so that the overall synthesis is about equally distributed between the endothelial and muscle cells. In patients with pregnancy-induced hypertension and some patients with essential hypertension endogenous synthesis of PGI2 has been evaluated by measuring 2,3-dinor-6-keto-PGF1 alpha and has proved to be greatly reduced. Some drugs (thiazides, propranolol) have been shown to stimulate PGI2 synthesis, and inhibition of cyclooxygenase has been shown to reduce their antihypertensive effects. The effects of low- and high-dose aspirin on prostacyclin and thromboxane synthesis are discussed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Prostacyclin in hypertension]. 149 51

Prostacyclin (PGI2) is known to cause vasorelaxation and inhibit platelet aggregation by receptor-mediated mechanisms. While cyclic (c)AMP is known to act as a second messenger for platelet aggregation, vasorelaxation by hyperpolarization has been described only recently and may provide an explanation, in addition to stimulation of cAMP, for the PGI2 mechanism of action on blood vessels. When PGI2 is infused into healthy volunteers it reduces blood pressure only at infusion rates that also cause significant side effects, primarily nausea, emesis, flushing, diphoresis and restlessness. In hypertensive patients blood pressure responses are complex and are influenced to some extent by secretion. PGI2 stimulates renin secretion by a direct effect on the juxtaglomerular apparatus, and also has an indirect effect by activating the sympathetic nervous system. Thus it is useless as an antihypertensive agent even apart from its debilitating side effects. Vascular PGI2 is synthesized endogenously by both the endothelial cells and the muscularis of arteries. While the endothelial cells undoubtedly synthesize larger amounts of PGI2, the muscularis comprises a much larger tissue mass so that the overall synthesis is about equally distributed between the endothelial and muscle cells. In patients with pregnancy-induced hypertension and some patients with essential hypertension, endogenous synthesis of PGI2 has been evaluated by measuring 2,3-dinor-6-keto-PGF1 alpha and has proved to be defective. Some drugs (cicletanine, thiazides, propranolol) have been shown to stimulate PGI2 synthesis, and inhibition of cyclooxygenase has been shown to abolish their antihypertensive effects. Whether stimulation of PGI2 synthesis affects the antihypertensive efficacy of these drugs is not yet known.
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PMID:Prostacyclin in hypertension. 225 88

Cardinal signs of red mold toxicosis in man and farm animals are vomiting, nausea, diarrhea, and food refusal. The red mold toxicosis has been suggested to be induced by trichothecenes, which are produced by Fusarium fungi. Fusarenon-X (F-X) is one of the trichothecene mycotoxins. The ip injection of F-X to rats causes an expansion of the small intestine and watery diarrhea. In this study, we measured the concentrations of protein, sodium, potassium, and calcium in the serum of rat treated with F-X for the sake of demonstrating the loss of serum protein and the decreases of serum sodium and calcium by F-X. Since it is well known that some diarrheal diseases are due to the increase of cyclic nucleotide level in the intestinal mucosa, we also measured cyclic AMP and cyclic GMP levels in the intestinal mucosa. It was demonstrated that F-X did not increase the cyclic AMP and cyclic GMP levels in the jejunal and the ileal mucosa at 8 and 24 hr after F-X treatment. The results obtained in this work suggest that F-X-induced diarrhea is not mediated by the cyclic nucleotide system.
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PMID:Studies on mechanisms of diarrhea induced by fusarenon-X, a trichothecene mycotoxin from Fusarium species: fusarenon-X-induced diarrhea is not mediated by cyclic nucleotides. 282 46

Sixteen children with refractory hematological malignancies were treated with a combination of BH.AC, aclacinomycin-A, 6-MP and predonisolone (BH-AC.AMP protocol). They were ALL(6), ANLL(8), CML(1) and NHL(1). The CR ratio was 17% in ALL, 50% in ANLL, and blast crisis of CML was treated successfully but NHL failed in the induction remission. Major complications were vomiting, nausea, gastrointestinal bleeding, hematuria and hemorrhagic cystitis. More than 10 days or 120 mg/m2 administration of aclacinomycin-A was thought to induce more severe side effects.
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PMID:[BH-AC.AMP protocol in the treatment of refractory childhood acute leukemia]. 317 40

A 45-year-old female manifested lower abdominal fullness and symptoms of hypercalcemia with nausea, vomiting, and thirst. Physical examination showed a right ovarian mass and laboratory data demonstrated hypercalcemia (14.6 mg/dl). The radiographic findings confirmed a right ovarian tumor without any evidence of bone metastasis. Tests revealed that her PTH, nephrogenic urinary cyclic AMP, and 1-25 (OH)2 Vitamin D were not high but that her prostaglandin E2 (PGE2) was elevated. After correction of her calcium elevation with infusion and prednisolone, right oophorectomy with tumor excision was performed. A histological examination of the tumor revealed a mucinous cysto-adenocarcinoma. The postoperative course has been uneventful, with normal calcium and PGE2 values. This case illustrates that hypercalcemia associated with an ovarian carcinoma (Malignancy-associated hypercalcemia) can be mediated by the patient's PGE2 in part.
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PMID:[A case of hypercalcemia with ovarian carcinoma]. 323 Jun 42

A 57-year-old-male patient with acute myelogenous leukemia in second relapse who was refractory to BHAC . AMP [behenoyl arabinosyl cytosine (BHAC), aclacinomycin, 6-mercaptopurine and prednisolone (PSL)] and BHAC . DVP [BHAC, daunomycin, vincristine and PSL] was treated with an intermediate-dose cytosine arabinoside (ID Ara-C) regimen. This schedule consisted of a 1-h infusion of Ara-C at a dose of 500 mg/m2 every 12 h for 6 d (days 3-8), in combination with doxorubicin 50 mg/m2 on day 1 and vincristine 1 mg/m2 on day 2. The patient achieved a complete remission 23 days after completion of Ara-C and was treated with ID Ara-C (Ara-C days 3-6) as a consolidation. Remission duration was only 2.5 months. Plasma Ara-C concentrations were assayed by HPLC and the peak level was 6.7 micrograms/ml. Side effects were mild nausea, vomiting, alopecia and moderate skin rash.
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PMID:[A case of complete remission from acute myelogenous leukemia in second relapse achieved using an intermediate-dose cytosine arabinoside (ID Ara-C) regimen]. 345 5

The classical enterotoxins are known primarily for their ability to cause emesis and diarrhoea in cases of staphylococcal food poisoning but they also exhibit other biological activities. The seven antigenic types of toxin have molecular weights in the range 25 000-35 000. All types induce emesis in man and monkey and are of comparable potency. The enterotoxins seem to induce emesis by stimulating neural receptors in the intestine rather than acting on the medulla directly. The mechanism whereby diarrhoea is produced is unclear. Another product of Staphylococcus aureus which meets the more recent definition of an enterotoxin is the delta toxin. This toxin is an amphipathic peptide having an Mr of 2977 and possessing the ability to interact with a variety of hydrophobic substances. It is cytotoxic, can increase vascular permeability in guinea-pig skin, and can increase cellular cyclic AMP levels in guinea-pig ileum. In the ileum delta toxin also inhibits water absorption, apparently by increasing the bidirectional movement of Na+ and Cl- across the mucosa. This response does not appear to be mediated by cyclic AMP since the changes in ion fluxes precede the increases in cellular cyclic AMP levels. In high doses delta toxin also elicits a positive response in the neonatal mouse after intragastric inoculation.
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PMID:Staphylococcus aureus delta toxin as an enterotoxin. 384 37

Aclacinomycin A (ACM) is different from other anthracycline antibiotics in its antitumor activity and clinical effect. We report a case of acute promyelocytic leukemia complicated with severe esophageal ulcer by BH-AC . AMP therapy. The patient was 24 years old. In 1983, he achieved complete remission with BH-AC . DMP therapy but we confirmed relapse in April, 1984. ACM caused nausea, vomiting, diarrhea, alimentary tract bleeding and sore throat, together with a complication of esophageal stenosis. In about half of 10 cases receiving BH-AC . AMP therapy in our hospital, we noticed severe bleeding in the urinary treat, genital organs and alimentary tract. Care should therefore be taken with regard to mucosal injury when ACM therapy is used.
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PMID:[A case of acute promyelocytic leukemia complicated with severe esophageal stenosis caused by aclacinomycin A]. 386 Nov 36

1. The effect of prostaglandin E(1) (PGE(1)) on gastric secretion was studied in dogs equipped with gastric fundic pouches, either innervated (Pavlov) or denervated (Heidenhain).2. PGE(1) inhibited gastric secretion (volume, acid concentration, acid output, pepsin output) when given either by constant intravenous infusion or by single intravenous injection. The degree of inhibition was dose dependent.3. The antisecretory effect of PGE(1) was demonstrated against gastric stimulants which operate through different mechanisms. Thus, PGE(1) counteracted the secretogogue effect of:(a) histamine dihydrochloride; the ED(50) was 0.5-1.0 mug/kg. min for a submaximal dose, and 1.0-1.5 mug/kg. min for a maximal dose;(b) pentagastrin; the ED(50) was around 0.25 mug/kg. min;(c) food; the ED(50) was 0.5 to 0.75 mug/kg. min;(d) 2-deoxyglucose; the ED(50) was less than 0.1 mug/kg. min.4. Although in some experiments, nausea and vomiting were observed during administration of PGE(1), the antisecretory property of the substance is not related to a vomiting reflex, since(a) an antiemetic, such as atropine, prevented vomiting without interfering with the effect of PGE(1), and(b) profuse vomiting elicited by apomorphine did not reduce gastric secretion stimulated by either histamine or pentagastrin.5. The mechanism by which PGE(1) inhibits gastric secretion is unknown. Studies by others have shown that the compound reduces gastric mucosal blood flow, inhibits acid formation from gastric mucosa when applied in vitro and may change the rate of formation of gastric cyclic AMP. It is likely that PGE(1) interferes with biochemical processes, within parietal and chief cells, which lead to elaboration of gastric juice.6. Unlike most gastric inhibitors, PGE(1) appears to act as a protective shield against most, if not all, gastric stimulants. Since prostaglandins of the E series are naturally occurring substances and are normally present in the stomach, they may play a role in the regulation of gastric secretion.
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PMID:Inhibition by prostaglandin E 1 of gastric secretion in the dog. 439 9


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