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)

Tiazofurin (2-B-D-Ribofuranosylthiazole-4-Carboxamide: NSC 286193) is a nucleoside antimetabolite that acts as a potent inhibitor of IMP dehydrogenase resulting in a guanine nucleotide deprivation. Recent in vivo biochemical observations in rats bearing hepatoma suggested a correlation between depletion of guanine nucleotides and antitumor effect. The present phase I trial utilized a weekly x 3 bolus infusion schedule, repeated every 5 weeks. Biochemical measurements of GTP and dGTP were performed in patients at each dose level. Twelve patients received 16 courses of the drug in doses ranging from 1100 to 2050 mg/m2 weekly x 3. The dose limiting toxicities were pericarditis and clinical symptoms suggestive of a more generalized serositis (chest and abdominal pain). Other toxicities included reversible elevations in CPK (MM band only) and SGOT, nausea, vomiting, and arthralgias. Neurotoxic effects were generally mild, including headaches, anxiety, and malaise. Only 1 of 6 patients evaluated for tiazofurin's biochemical activity showed a sustained depletion of guanine nucleotide pools. No antitumor activity was observed. The maximally tolerated dose of tiazofurin on this intermittent weekly x 3 schedule was 1650 mg/m2. Toxicity and the overall lack of biochemical and biologic effect at clinically achievable doses may preclude further clinical evaluation of this drug on a weekly schedule. The toxicities observed in our study were similar to those reported for phase I investigations using a considerably higher dose intensity with daily x 5 schedules.
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PMID:Phase I trial and biochemical evaluation of tiazofurin administered on a weekly schedule. 234 2

Twelve taste repellents and 3 oral emetics were tested. The taste repellents were capsaicin, capsicum, oleoresin, sucrose octaacetate, quinine tonic, quassia wood extract, vanillamide, horseradish extract, caffeine, pepperoni enhancer, acorn extract, and commercially available bitter and hot flavors. The emetics tested were: antimony potassium tartrate, apomorphine, and copper sulfate. Intake of a 20% sucrose solution by Beagles was significantly depressed by addition of vanillamide at concentrations greater than 0.001%, by capsicum and capsaicin at concentrations greater than 0.01%, and by horseradish extract, pepperoni enhancer, and a commercially available hot flavor at concentrations greater than 0.1%. Antimony potassium tartrate, when added to the 20% sucrose solution at a concentration of 0.1%, produced emesis as did apomorphine at a concentration of 0.005% and copper sulfate at 1%. When the emetic antimony potassium tartrate was combined with vanillamide in a 20% sucrose solution, intake was reduced to less than 20 ml, and vomiting occurred within 15 minutes. Capsaicin (0.02%) inhibited intake of ethylene glycol to less than the lethal dose in 5 dogs tested. Incorporation of such taste repellents and/or emetics into potentially poisonous substances would reduce accidental poisoning of animals and children.
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PMID:Use of taste repellants and emetics to prevent accidental poisoning of dogs. 647 61

Of 1,500 different types of Norwegian mushrooms, 60-100 are considered poisonous. Fatal intoxications occur very infrequently. Lack of knowledge of picking and preparing mushrooms and accidental or deliberate consumption are recognised causes of mushroom poisoning. Delayed onset of symptoms (> 5-6 hrs) indicates serious poisoning, and these patients must be admitted to hospital. Cytotoxic toxins (e.g. amatoxin, orellanin) cause serious damage to the visceral organs (liver, kidney) and require intensive treatment, including hemoperfusion. Neurotoxic toxins may cause dramatic, but less harmful peripheral or central symptoms affecting the peripheral and central nervous systems, including hallucinations. Some mushrooms cause gastroenteritis of low clinical significance within a few hours after consumption. Interaction between mushrooms and alcohol may lead to a disulfiram-like effect. Induced vomiting and activated charcoal are important initial therapeutic measures. The precise history of the patient and the collecting of mushroom remnants, including vomitus, may help to identify the particular mushroom. In Norway, the National Poison Information Centre may be contacted for further advice.
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PMID:[Poisonous mushrooms, mushroom poisons and mushroom poisoning. A review]. 941 93

Systemic tachykinin NK1 receptor antagonists and resiniferatoxin are known to abolish vomiting mediated by vagal afferents. Emetic vagal afferents have been shown to make synaptic contact with neurons in the medial solitary nucleus. These results suggest that substance P participates in the synapse as a mediator. To examine this possibility, the effects of 4th-ventricular application of capsaicin (0.033-33 mM, 20-30 microl) and resiniferatoxin (1.6-160 microM, 20-30 microl) on the activity of neurons in the medial solitary nucleus and fictive retching induced by vagal stimulation were observed in paralyzed decerebrate dogs. Capsaicin (33 mM) and resiniferatoxin (160 microM) initially increased the neuronal firing and occasionally produced retching, then abolished both neuronal and retching responses. However, stimulation of the medial solitary nucleus continued to provoke retching. Field potential changes in the medial solitary nucleus evoked by pulse-train vagal stimulation decreased in amplitude, but did not disappear. Latencies of neuronal firing and evoked potentials were about 300 ms. These results suggest that emetic vagal afferents are capsaicin-sensitive C fibers which may have substance P as an excitatory transmitter or modulator.
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PMID:Capsaicin in the 4th ventricle abolishes retching and transmission of emetic vagal afferents to solitary nucleus neurons. 947 34

The potential of resiniferatoxin and capsaicin to modulate emesis and genital grooming was investigated in Suncus murinus. Resinifertoxin (3-30 nmol, i.c.v.), E-capsaicin (10-100 nmol, i.c.v.) and Z-capsaicin (100 nmol, i.c.v.) induced emesis (P<0.05) and subsequently antagonised the emetic response induced by intragastric copper sulphate (480.6 micromol/kg; P<0.05). However, resiniferatoxin failed to affect nicotine-induced (30.7 mol/kg, s.c.) emesis (P>0.05). Only resiniferatoxin induced genital grooming that was antagonised (P<0.05) by capsazepine (300-600 nmol, i.c.v.) and ruthenium red (3 nmol, i.c.v.). E-capsaicin-induced emesis was antagonised by capsazepine (300-600 nmol, i.c.v.; P<0.05) and ruthenium red (3 nmol, i.c.v.; P<0.05) but resiniferatoxin-induced emesis was resistant to capsazepine (30-600 nmol, i.c.v.; P>0.05). The emetic action of resiniferatoxin but not E-capsaicin was subject to tachyphylaxis. In cross-tachyphylaxis experiments, E-capsaicin reduced the genital grooming induced by resiniferatoxin (P<0.05). The data are discussed in relation to the classification of vanilloid receptors and mechanisms involved in emesis and genital grooming.
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PMID:Genital grooming and emesis induced by vanilloids in Suncus murinus, the house musk shrew. 1143 Sep 30

The major syndromes of mushroom poisoning can be divided by presentation timing: Early syndromes (symptom onset <6 hrs after ingestion) have little probability to cause organ damage. Epigastric pain, nausea, vomiting and diarrhea occur in most cases and treatment includes initial gastrointestinal decontamination with oral activated charcoal and fluid rehydration. In addition, an acute gastrointestinal syndrome can be combined with cholinergic toxicity, epileptiformic response or immuno-hemolytic anemia. Neurotoxic Syndromes may present as dysphoria, delirium, hallucinations or disulfiram-like reactions. Treatment is entirely supportive and if performed in hospital, the prognosis is good. Late syndromes (symptom onset >6 hrs after ingestion) are life-threatening due to liver- and renal failure. Patients who are jaundiced after an acute gastrointestinal episode, are suspected to be poisoned with Amatoxins. Patients with flank pain, hematuria, polyuria or oliguria in the absence of jaundice are suspected to have an intoxication with Cortinarius mushrooms. In both cases an intensive care management is indicated.
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PMID:[Mushroom poisonings: syndromic diagnosis and treatment]. 1803 May 54

Brown widow spider (Latrodectus geometricus) venom (BrWSV) produces few local lesions and intense systemic reactions such as cramps, harsh muscle pains, nausea, vomiting and hypertension. Approximately 16 protein bands under reducing conditions and approximately 14 bands under non-reducing conditions on a 12.5% sodium dodecyl sulfate-polyacrylamide gel electrophoresis were observed. Neurotoxic clinical manifestations were confirmed in vivo, while proteolytic activity was demonstrated on gelatine film. Severe ultrastructural damages in mice skeletal muscles were observed at 3, 6, 12 and 24 h postinjection with at total of 45 microg of venom protein. Infiltration of eosinophils and ruptures of the cellular membranes were observed in the muscles along with swelling of the nuclear cover and interruption of the collagen periodicity. Altered mitochondrias and autophage vacuoles, nuclear indentation and mitochondria without cristae, slight increment of intermyofibrillar and subsarcolemic spaces and myelinic figures formation were also observed. In the capillary, endothelial membrane unfolding into the lumen was noticed; along with myelinic figures compatible with a toxic myopathy. Swollen sarcotubular systems with lysis of membrane, intense mitochondria autophagia and areas without pinocytic vesicles were observed. Swollen mitochondria surrounded by necrotic areas, myofibrillar disorganization and big vacuolas of the sarcotubular system, degenerated mitochondrium with formation of myelinic figure was seen. Glycogenosomes with small particulate, muscle type glycogen was noticed. Autophagic vacuole (autophagolysosomes) and necrotic areas were also noticed. These damages may be due to interactive effects of the multifactorial action of venom components. However, Latrodectus geometricus venom molecules may also be utilized as neuro therapeutic tools, as they affect neuronal activities with high affinity and selectivity. To our knowledge, the present study is the first ultrastructural report in the literature of muscle injuries and neurological and proteolytic activities caused by BrWSV.
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PMID:Neurotoxic activity and ultrastructural changes in muscles caused by the brown widow spider Latrodectus geometricus venom. 1939 Jul 38

Snakebite is an environmental hazard associated with significant morbidity and mortality. We report a case series of venomous snakebites in a military operational area of north India. Of 33 cases of snake bites presenting to the military hospital, 21 patients were envenomated. The median age of patients was 24 years; all were men. All of the envenomations were neurotoxic in nature. Abdominal pain (91%), headache (86%), dysphagia (86%), ptosis (77%), diplopia (72%), blurred vision (72%), dyspnea (67%), and vomiting (62%) were the predominant clinical presentation. Polyvalent AntiSnakeVenom (ASV) [mean 180 ml; range 90-320 ml] was given to all patients with systemic manifestations, and repeated as needed. Eleven (52%) patients received neostigmine with glycopyrrolate to counter cholinergic effects. Two patients were given ventilatory support. The average time of recovery from envenomation was 16 hours after administration of ASV. All patients recovered without sequelae. Soldiers during military exercise are vulnerable to snakebites. Neurotoxic snakebites predominate in our study and usually present with autonomic features along with headache, abdominal pain, ptosis, diplopia and dysphasia. Preventive measures to minimize snake bites and planned treatment regimens should be emphasized among medical and military personnel deployed in the field operations.
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PMID:Clinical profile of venomous snake bites in north Indian Military Hospital. 1956 85

Harmful algal blooms are natural phenomena caused by the massive growth of phytoplankton that may contain highly toxic chemicals, the so-called marine biotoxins causing illness and even death to both aquatic organisms and humans. Their occurrence has been increased in frequency and severity, suggesting a worldwide public health risk. Marine biotoxins can accumulate in bivalve molluscs and regulatory limits have been set for some classes according to European Union legislation. These compounds can be distinguished in water- and fat-soluble molecules. The first group involves those of Paralytic Shellfish Poisoning and Amnesic Shellfish Poisoning, whereas the toxins soluble in fat can cause Diarrheic Shellfish Poisoning and Neurotoxic Shellfish Poisoning. Due to the lack of long-term toxicity studies, establishing tolerable daily intakes for any of these marine biotoxins was not possible, but an acute reference dose can be considered more appropriate, because these molecules show an acute toxicity. Dietary exposure assessment is linked both to the levels of marine biotoxins present in bivalve molluscs and the portion that could be eaten by consumers. Symptoms may vary from a severe gastrointestinal intoxication with diarrhea, nausea, vomiting, and abdominal cramps to neurological disorders such as ataxia, dizziness, partial paralysis, and respiratory distress. The official method for the detection of marine biotoxins is the mouse bioassay (MBA) showing some limits due to ethical restrictions and insufficient specificity. For this reason, the liquid chromatography-mass spectrometry method has replaced MBA as the reference technique. However, the monitoring of algal blooms producing marine biotoxins should be regularly assessed in order to obtain more reliable, accurate estimates of bloom toxicity and their potential impacts.
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PMID:Marine Biotoxins: Occurrence, Toxicity, Regulatory Limits and Reference Methods. 2745 45

Snakebite is an environmental hazard associated with a significant morbidity and mortality. Two main types of toxicity occur due to snakebite, namely vasculotoxicity and neurotoxicity. Neurotoxic snakebites present mainly with bilateral ptosis with dilated pupils and/or difficulty in breathing. Jatropha curcas belongs to the family Euphorbiaceae and is commonly referred to as "Ratanjyot" in Gujarati. It has got many medicinal uses such as anticancerous properties and bio-oil. There are very few cases of its toxicity in adults. Toxicity from it causes meiosis, vomiting, diarrhea, etc., We will hereby discuss one such patient who consumed J. curcas seeds intentionally, became drowsy and accidentally got bit by a snake, and then, the patient started having bilateral ptosis, but with normal-sized pupils. There is no case reported yet in the literature mentioning the combined toxicity of snakebite and J. curcas, so we thought to publish this first case report of its kind in the world, thus discussing its diagnosis, symptoms, and treatment modalities.
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PMID:A mixed toxidrome presenting with bilateral ptosis with normal pupils: The first case in the literature. 2821 6


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