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)

beta-receptor antagonists have for many years been considered appropriate alternatives in the primary management of mild to moderate hypertension. Generally, they have been shown to be safe with a low frequency of serious side-effects. Among the predictable and usually doserelated side-effects are bradycardia, bronchospasm, hypotension, muscle fatigue and cold extremities. Examples of unexpected side-effects are gastrointestinal symptoms such as nausea and disturbed intestinal motility, skin reactions, sexual dysfunction, as well as effects related to the central nervous system (CNS) such as emotional disturbances. The CNS-related side-effects, the mechanisms of which are unclear, consist of subtle effects on general well-being, decreased initiative, a depressed frame of mind and disturbed sleep. Generally, however, beta-blockers in therapeutic dosages do not affect the qualitative functions of the brain. Thus, all beta-blockers on the market seem to have high benefit-risk ratio, but independent of their physiochemical properties and pharmacodynamic profile, they seem to cause side-effects to about the same extent. The results so far available have been obtained by primarily using objective methods. Further comparison has now been initiated using documented subjective methods to investigate whether the objectively documented differences are of any clinical relevance to the patient's quality of life. Although it cannot be claimed with certainty, nonselective beta-blockers seem to cause CNS-related side-effects to a greater extent than beta 1-selective blockers. Differences in the degree of hydrophilicity of the beta-blocker are apparently of no clinical relevance in this respect.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Quality of life/subjective symptoms during beta-blocker treatment. 198 27

A Phase I study of intravenous (IV) bolus 4'-0-tetrahydropyranyladriamycin (Pirarubicin) was done in 55 patients in good performance status with refractory tumors. Twenty-six had minimal prior therapy (good risk), 23 had extensive prior therapy (poor risk), and six had renal and/or hepatic dysfunction. A total of 167 courses at doses of 15 to 70 mg/m2 were evaluable. Maximum tolerated dose in good-risk patients was 70 mg/m2, and in poor-risk patients, 60 mg/m2. The dose-limiting toxic effect was transient noncumulative granulocytopenia. Granulocyte nadir was on day 14 (range, 4-22). Less frequent toxic effects included thrombocytopenia, anemia, nausea, mild alopecia, phlebitis, and mucositis. Myelosuppression was more in patients with hepatic dysfunction. Pharmacokinetic analyses in 21 patients revealed Pirarubicin plasma T 1/2 alpha (+/- SE) of 2.5 +/- 0.85 minutes, T beta 1/2 of 25.6 +/- 6.5 minutes, and T 1/2 gamma of 23.6 +/- 7.6 hours. The area under the curve was 537 +/- 149 ng/ml x hours, volume of distribution (Vd) 3504 +/- 644 l/m2, and total clearance (ClT) was 204 + 39.3 l/hour/m2. Adriamycinol, doxorubicin, adriamycinone, and tetrahydropyranyladriamycinol were the metabolites detected in plasma and the amount of doxorubicin was less than or equal to 10% of the total metabolites. Urinary excretion of Pirarubicin in the first 24 hours was less than or equal to 10%. Activity was noted in mesothelioma, leiomyosarcoma, and basal cell carcinoma. The recommended starting dose for Phase II trials is 60 mg/m2 IV bolus every 3 weeks.
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PMID:A phase I study of 4'-0-tetrahydropyranyladriamycin. Clinical pharmacology and pharmacokinetics. 222 62

Individuals who report illness (e.g. nausea, headache) from common chemical odors tend to report CNS symptoms suggestive of olfactory-limbic system involvement. This study compared the resting quantitative electroencephalographic (qEEG) patterns of young adult college students reporting subjectively elevated chemical odor intolerance ratings (HICI) with those of controls reporting little or no odor intolerance (LOCI). Each group was subdivided into those with higher (HIDEP) vs. lower (LODEP) ratings of concomitant depression. Nineteen channels of EEG were recorded during a single session over four separate rest periods, respectively, following baseline, cognitive, chemical exposure and olfactory identification tests. Each recording involved two 30-s, eyes-closed, filtered room air breathing conditions: (1) nose inhalation followed by mouth exhalation and (2) mouth inhalation followed by mouth exhalation. HICI showed significantly less beta 1 (beta 1) over the temporal-central region during nose than during mouth inhalation. Over some temporal and central leads, task, DEP and CI interacted to influence beta 1 as well. For theta (theta), CI differences emerged during nose inhalation after the cognitive task at Cz, after chemical exposures at C3, Cz and C4 and after the olfactory ID task at C4. CI differences emerged during mouth breathing after the olfactory ID task at Cz, C4 and T4. The T5-T6 coronal array showed significant CI differences after chemical exposures during nose breathing and during mouth breathing after the cognitive and olfactory ID tasks. The theta findings in the HICI may be related to reports of disturbed attention in CI.
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PMID:Quantitative EEG patterns during nose versus mouth inhalation of filtered room air in young adults with and without self-reported chemical odor intolerances. 950 9