Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the present discussion, the author summarized the toxicological and biological features of thirty kinds of trichothecene mycotoxins which are produced by a wide range of Fusarium, Myrothecium and others. The 12, 13-epoxytrichothecenes induce nausea, emesis, vomiting, skin inflamation, leukopenia, diarrhea, hemorrhage in lung and brain, and destruction of bone marrow. Since these toxicological characteristics coincide with a major symptom of intoxicated humans and farm animals induced by consumption of moldy cereals and feeds, the red-mold toxicosis and bean-hulls poisoning in Japan, moldy corn toxicosis in U.S.A., A.T.A., stachybotryotoxicosis and dendrochiotoxicosis in Europe, are originated from a common toxicant, trichothecenes. Orally administered trichothecenes are rapidly absorbed and eliminated into the feces and urine upon deacetylation at C-4 by the microsomal esterase of liver. Biochemical approaches to the mode of action revealed that the trichothecenes are a potent inhibitor of protein and D.N.A. syntheses in eukaryotic cells. Bindings to the eukaryotic polysomes and ribosomes and the subsequent inactivation of ribosomal cycle is responsible for their inhibitory effect to initiation and termination reactions. Microbial approaches revealed that the trichothecenes are mutagenic to yeast cells, but are negative in D.N.A.-attacking ability to Bacillus subtilis and reversion assay with Salmonella typhimurium. Reactivity of the epoxide ring of trichothecenes with S.H.-group of proteins will be discussed in relation to the molecular mechanism of action.
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PMID:Mode of action of trichothecenes. 61 39

Major findings from our work on exposures and effects from organophosphate-containing pesticides in selected occupational and community patients and groups in Israel are reviewed as a basis for recommending control measures. The worker groups were pilots, ground-crews, and field workers; exposed nonworkers were adults and children living in kibbutzim with drift exposures, and household residents in houses treated by pest exterminators. In all groups, evidence of exposure-illness associations was found even though persons with acute poisoning were not seen. Complaints (headache, dizziness, fatigue, nausea, breathing problems, abdominal cramps, and tingling in extremities) were associated with within-normal depressions in cholinesterase activity. Whole blood and plasma cholinesterase activity were slightly more sensitive indicators of mixed exposure than red blood cell cholinesterase activity. High alkyl phosphate levels and symptoms were seen in individuals with within-normal limit depressions in cholinesterase activity. Complaints of weakness and tingling in hands and feet, together with low-grade changes in nerve conduction, suggest the possible influence of agents with a neurotoxic esterase-type activity independent of cholinesterase activity. Transient in-season neuropsychological changes in tests of mood status and performance were associated with exposure. Recommendations for exposure reduction include: accelerating the already declining use of pesticides in general, and organophosphates in particular; promoting the shift from more to less toxic organophosphates and other pesticides; and introducing rigid performance specifications for closed systems in loading and mixing at end-user sites. Dermal protection remains a problem. Cholinesterase activity levels and symptom interviews are useful for monitoring workers at risk, but alkyl phosphate levels are the definitive measure of exposure, surveys, investigations and surveillance.
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PMID:Health effects from exposure to organophosphate pesticides in workers and residents in Israel. 133 Sep 77

A 44-year-old woman with C1q esterase inhibitor deficiency was seen in consultation for recurrent right upper quadrant abdominal discomfort, nausea, and vomiting. Each of these episodes was accompanied by concomitant peripheral edema. Initial diagnostic efforts were fruitless. In time, intermittent elevations in amylase and lipase developed, and a diagnosis of relapsing pancreatitis was made. We contend that the patient's recurrent acute pancreatitis is associated with her hereditary angioedema. Possible pathogenesis could involve intermittent intrapancreatic edema with partial ductal obstruction or loss of inhibition on the kallikrein-kinin system.
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PMID:Hereditary angioedema associated with pancreatitis. 143 59

For two years a 19-year-old patient had been complaining of recurrent abdominal symptoms consisting of severe colicky pain, nausea, vomiting and diarrhoea. Occasionally he noticed concomitant subcutaneous swellings in the limbs. There were no swellings in the face or the region of the upper airway. The symptoms occurred once or twice a month, spontaneously receding within 3-4 days. These signs and symptoms indicated hereditary angio-oedema. Serum concentration of C1-esterase inhibitor was normal (13 mg/dl), but its serum activity was reduced to 16% (normal range 80-125%). This is thus a case of type II C1-esterase inhibitor deficiency. Since starting low-dosage treatment with Danazol (initially, for two months, 200 mg daily, then 200 mg five times per week) the patient has been symptom-free.
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PMID:[Hereditary angioedema type II with predominantly abdominal symptoms]. 204 85

We present a 15-year-old woman with acute myelomonocytic leukemia without marrow eosinophilia, M4 in the FAB classification. She was admitted to our hospital with nausea and headaches. Upon admission, the leukocyte count was 284,000/microliters with 95% leukemic cells. The bone marrow aspirate was hypercellular with 74.8% blasts and 0.2% eosinophils. Leukemic cells were positive for myeloperoxidase and esterase staining. Initially, the karyotype of the bone marrow cells on admission was considered to be normal. However, the PEBP2 beta/MYH11 fusion transcript was detected in the bone marrow mononuclear cells by using the reverse transcriptase-polymerase chain reaction (RT-PCR). Reevaluation of karyotypes showed a t(16;16) (p13;q22) in the bone marrow cells. After achieving complete remission, she was treated with low-dose etoposide. Chromosome analysis showed a normal karyotype and no amplified chimeric transcripts were observed. This case indicates that the molecular analysis of PEBP2 beta and MYH11 genes is a useful tool to detect inv (16) and t(16;16) which were often difficult to find, and that leukemic cells from some cases of M4 without marrow eosinophilia have these chromosome abnormalities.
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PMID:[Detection of PEBP2 beta/MYH11 fusion mRNA in acute myelomonocytic leukemia without marrow eosinophilia]. 877 82

Although angiotensin-converting enzyme inhibitors (ACEIs) are well-known causes of orofacial angioedema, angioedema from these agents involving the bowel is not often considered. We report a case of simultaneous onset of small bowel and orofacial angioedema due to captopril. A 61-year-old black man with hypertension, coronary artery disease, and congestive heart failure had been treated with captopril for 5 years. He had sudden swelling of the lips, face, and tongue, followed by nausea, emesis, abdominal pain, and diarrhea. Other medications included aspirin, indomethacin, allopurinol, colchicine, and nifedipine. Examination showed swelling of the tongue, buccal mucosa, and neck; he also had midabdominal tenderness but no respiratory distress. Laboratory data were normal. A C1-esterase inhibitor level was normal. An ileus pattern was present on abdominal x-ray film. Angioedema was diagnosed, and all signs and symptoms resolved in 24 hours after captopril was discontinued. Clinicians need to be vigilant for bowel involvement from ACEI angioedema.
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PMID:Simultaneous mucosal and small bowel angioedema due to captopril. 982 92

Exatecan mesylate (DX-8951f) is a new hexacyclic camptothecin analogue with favorable attributes compared to topotecan and CPT-11, including watersolubility, greater potency against topoisomerase I, lack of esterase-dependent activation, broad antitumor activity, and low cross-resistance against MDR-1 overexpressing tumors. In preclinical studies, the compound demonstrated a favorable toxicology profile with hematologic dose-limiting toxicity and moderate gastrointestinal toxicity, linear pharmacokinetics, P450 hepatic metabolism (CYP3A4 and CYP1A2), and predominately fecal excretion. The results of six U.S. and European phase I clinical trials as well as two Japanese studies are presented including total DX-8951 and lactone DX-8951 pharmacokinetics. The toxicity profile was similar for all schedules of administration. Hematologic toxicity was dose-dependent and reversible. Neutropenia was dose-limiting in minimally pretreated patients, whereas neutropenia and thrombocytopenia were dose-limiting in heavily pretreated patients. Non-hematologic toxicity included moderate gastrointestinal toxicity (nausea, vomiting > diarrhea), transient elevation of hepatic transaminases, asthenia, and alopecia. Two cases of acute pancreatitis not predicted by preclinical toxicology were also observed. Antineoplastic activity was detected in several solid tumor types: non-small cell lung cancer, extrapulmonary small cell cancer, colorectal cancer, hepatocellular cancer, and sarcoma. Antitumor activity was seen in CPT-11 and topotecan-resistant tumors. Pharmacokinetics were linear within the dose range tested. A pharmacokinetic/pharmacodynamic model predictive of DX-8951f-induced neutropenia in individual patients was developed. The daily x5, every 3-week schedule with the drug administered as a 30-minute intravenous infusion was selected for future phase II clinical trials based on its superior antitumor activity.
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PMID:DX-8951f: summary of phase I clinical trials. 1119 1

We compared Remifentanil, an esterase-metabolized opioid, with Alfentanil as part of the total intravenous anesthesia with propofol and atracurium for out-patient laparoscopic gynaecological procedures in a multicenter randomized, double-blind study. We chose Remifentanil 1 mg./kg.for bolus injection and a continuous infusion of 0.25-0.5 microg./kg./min, compared to Alfentanil 20 microg./kg. For bolus injection and a continuous infusion of 0.5-1 microg./kg./min. Fifty-nine patients received Remifentanil, and sixty-three received Alfentanil. Patients who received Remifetanil experienced significantly fewer stress responses to surgical stimuli (p < 0.05) and required fewer additional boluses of study drugs and propofol (p < 0.05) than Alfentanil during the intraoperative period. Response time to verbal commands, spontaneous respiration, adequate respiration and tracheal extubation, were not significantly different between these two opioids. Remifentanil patients, required more fentanyl for post operative pain control, 40 from 59 cases in the Remifentanil group and 22 from 63 cases in the Alfentanil group (p < 0.05) but still showed significantly better recovery of psychomotor function by Aldrete score of ten at 50 and 60 min (p < 0.05) than Alfentanil patients. The incidence of intraoperative bradycardia was significantly higher with Remifentanil. Other incidences of nausea, emesis, urinary retention and postural hypotension were similar. All patients were ready to be discharged from the hospital within two hours after extubation except for one patient in the Alfentanil group who needed five hours of hospital stay because of urinary retention, nausea and severe emesis.
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PMID:A multicenter randomized double-blind comparison of remifentanil and alfentanil during total intravenous anaesthesia for out-patient laparoscopic gynaecological procedures. 1121 62

Spontaneous bacterial peritonitis (SBP) is one of the main infectious complications of cirrhosis and occurs in 8-30% of hospitalized patients with ascites. SBP is characterized by infection of the ascitic fluid (AF) in the absence of any primary focus of intra-abdominal infection. The main route by which the AF becomes infected is the hematogenous route. The pathogenic mechanism by which infection develops is bacterial translocation from the intestinal flora to the mesenteric lymph nodes and from there to the bloodstream. Contributing factors are an increased growth of Gram-negative aerobic bacilli in the jejunum, changes in the intestinal barrier and in addition factors which could reduce the local flow of blood. For clinical diagnosis, patients with SBP may present signs of peritoneal irritation and pain, together with changes in gastrointestinal motility, sometimes with nausea, vomiting, diarrhea or ileus. Many patients, however, may not present any symptoms or signs as a result of the presence of SBP. Diagnostic paracentesis of the AF must be performed for every patient with cirrhosis, hospitalized with ascites. Laboratory diagnosis of SBP is carried out by polymorphonuclear count in the AF, together with a positive culture from the AF, which is characteristically monomicrobial. Escherichia coli has been the main bacterium isolated from AF as well as other Gram-negative bacteria from the Enterobacteriaceae family and Streptococcus genus. A more rapid diagnosis of SBP can be obtained via the use of leukocyte esterase, which is present in biological fluids and reacts with a component of the dipstick, changing its color. During the acute phase of SBP, antibiotics should be initiated promptly once the clinical and laboratory diagnosis of SBP has been made, before the result of AF culture. Cefotaxime or other third-generation cephalosporins have been considered the first-choice empirical antibiotics in the treatment of cirrhotic patients with SBP, and is efficacious in approximately 90% of cases. Broad-spectrum quinolones, which are almost completely absorbed after oral administration and diffuse rapidly through the AF, are currently used for oral treatment of uncomplicated SBP. Patients who have already had a previous episode of SBP, with a 69% probability of recurrence within a year, will benefit from prophylactic treatment. Cirrhotic patients with a high risk of SBP and other infections, such as those with gastrointestinal bleeding, also benefit from primary prophylaxis and norfloxacin has been used with success.
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PMID:Spontaneous bacterial peritonitis: a therapeutic update. 1659 6

Cancer is a hyper-proliferative disorder that involves transformation, dysregulation of apoptosis, Proliferation, invasion, angiogenesis and metastasis. The conventional methods to treat cancer are surgery, radiotherapy and chemotherapy. Chemotherapy, being a major treatment modality used for the control of advanced stages of malignancies and as a prophylactic against possible metastasis, exhibits severe toxic side effects like diarrhea, fatigue, nausea, vomiting etc. Plants have been used for treating various diseases of human beings since time immemorial. In this study, methanolic extract of Decalepis hamiltonii was studied for its chemoprotective and antioxidant activity. Intraperitoneal administration of the extract significantly increased the total WBC count (3166 +/- 202 cells/cm2), bone marrow cellularity (680 +/- 70.1cells/femur), alpha-esterase positive cells (641 +/- 26.2 cells/4000 cells), Weights of organs such as a spleen and lungs, in Cyclophosphamide (CTX) treated animals when compared to control. D. hamiltonii administration significantly decreased the levels of Serum glutamate pyruvate transaminase (SGPT), Serum glutamate oxaloacetate transaminase (SGOT), creatinine and urea in serum and increased their levels in liver and kidney. Histopathological analysis of small intestine also suggests that extract could reduce the CTX induced intestinal damage. Analysis of the antioxidant status revealed that treatment with D. hamiltonii could significantly inhibit the free radical generation in vitro. Similarly in vivo studies using D. hamiltonii showed that the extract could significantly decrease the level of SOD in serum of the treated animals compared to control animals. In conclusion the finding of this study suggested that the extract from D. hamiltonii has strong chemo protective effect against CTX induced toxicity.
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PMID:Chemoprotective effect of Decalepis hamiltonii against cyclophosphamide induced toxicity. 2254 22


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