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)

1. Despite advances in the art and science of fluid balance, exertional heat illness -- even life-threatening heat stroke -- remains a threat for some athletes today. 2. Risk factors for heat illness include: being unacclimatized, unfit, or hypohydrated; certain illnesses or drugs; not drinking in long events; and a fast finishing pace. 3. Heat cramps typically occur in conditioned athletes who compete for hours in the sun. They can be prevented by increasing dietary salt and staying hydrated. 4. Early diagnosis of heat exhaustion can be vital. Early warning signs include: flushed face, hyperventilation, headache, dizziness, nausea, tingling arms, piloerection, chilliness, incoordination, and confusion. 5. Pitfalls in the diagnosis of heat illness include: confusion preventing self-diagnosis; the lack of trained spotters; rectal temperature not taken promptly; the problem of "seek not, find not;" and the mimicry of heat illness. 6. Heat stroke is a medical emergency. Mainstays of therapy include: emergency on-site cooling; intravenous fluids; treating hypoglycemia as needed; intravenous diazepam for seizures or severe cramping or shivering; and hospitalizing if response is slow or atypical. 7. The best treatment is prevention. Tips to avoiding heat illness include: rely not on thirst; drink on schedule; favor sports drinks; monitor weight; watch urine; shun caffeine and alcohol; key on meals for fluids and salt; stay cool when you can; and know the early warning signs of heat illness.
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PMID:Treatment of suspected heat illness. 969 24

The authors prospectively assessed symptoms induced by the interruption of antidepressants in 16 patients (11 women and 5 men), aged from 33 to 85 years (mean = 52.4 +/- 16.4), treated with antidepressants since at least two weeks. All patients were free of alcohol abuse or dependence disorder and of other dependence to psychoactive substances. None of them presented medical illness. Diagnosis were made by separate evaluations by two authors and confirmed with a semistructered assessment instrument: the Schedule for Affective Disorders and Schizophrenia (Lifetime Version). All patients were submitted to a brutal discontinuation of their antidepressant agent. Patients were assessed twice, before the interruption of the antidepressant, and 72 hours later. Effects of antidepressant interruption were assessed by several means. Modification of anxiety and depression were evaluated using the Montgomery Asberg Depression Rating Scale (MADRS) and the Hamilton Anxiety Scale. Symptoms of withdrawal were assessed with Cassano and al.'s scale SESSH including an evaluation of anxiety, agitation, irritability, anergy, difficulty on concentrating, depersonalization, sleep and appetite disorders, muscle pains, nausea, tremor, sweating, altered taste, hyperosmia, paresthesias, photophobia, motor incoordination, dizziness, hyperacousia pain, delirium. Fourteen of the 16 patients (87.5%) presented modifications of their somatic or psychic state 3 days after the interruption of the antidepressant treatment. Most frequent symptoms were: increase in anxiety (31%), increase in irritability (25%), sleep disorders (19%), decrease of anergia and fatigue (19%). Mean scores of anxiety and depression were not significantly modified by the withdrawal. Following TCAs interruption (7 patients) most frequent symptoms were sleep disorders; increase in anxiety, nausea. Among patients withdrawn from SSRIs (6 patients), most frequent symptoms were increase in anxiety, increase in irritability, headache. Patients also presented a decrease of nausea, and of anorexia.
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PMID:[Prospective evaluation of antidepressant discontinuation]. 969 14

Methyl parathion - MP (C[8]H[10rsqbNO[5rsqbPS) is a restricted-use pesticide that has been widely used as an agricultural insecticide. It belongs to the class of organophosphate chemicals characterized by their ability to inhibit acetylcholinesterase activity. The main route of human exposure is inhalation, but dermal contact and inadvertent ingestion can also be substantial. Populations that are susceptible to MP exposure primarily are applicators, manufacturers and individuals living near application and/or disposal sites. Exposure has also been reported as a result of illegal indoor application. MP related health effects include headaches, nausea, night-waking, diarrhea, difficulty breathing, excessive sweating and salivation, incoordination, and mental confusion. Other symptoms including behavior problems, motor skill problems and impairment of memory recall have also been reported. The primary targets of toxicity are the hematopoietic system (serum cholinesterase inhibition), the cardiovascular system (cardiovascular lesions, abnormalities in heart rate and increase in heart-to-body ratio), the reproductive system (placental morphology, fibrosis and hemorrhage, and inhibition of DNA synthesis in seminiferous tubules), and the nervous system (headache, muscle weakness, insomnia, dizziness, and impaired memory). MP is believed to not have any carcinogenic effects. In an attempt to update its toxicologic profile, we hereby provide a critical review of MP-related environmental and toxicologic effects, with a special emphasis on their potential implications for public health.
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PMID:Environmental toxicology and health effects associated with methyl parathion exposure--a scientific review. 1681 98

A variety of newer antiepileptic drugs (AEDs) are now available for treating patients with epilepsy in addition to the 'conventional' drugs that have been available throughout a large part of the last century. Since these drugs act to suppress the pathological neuronal hyperexcitability that constitutes the final substrate in many seizure disorders, it is not surprising that they are prone to causing adverse reactions that affect the CNS.Information on adverse effects of the older AEDs has been mainly observational. Equally, whilst the newer drugs have been more systematically studied, their long-term adverse effects are not clearly known. This is illustrated by the relatively late emergence of the knowledge of visual field constriction in the case of vigabatrin, which only became known after several hundred thousand patient-years of use. However, older drugs continue to be studied and there has been more recent comment on the possible effect of valproate (valproic acid) on cognition following exposure to this drug in utero.With most AEDs, there are mainly dose-related adverse effects that could be considered generic, such as sedation, drowsiness, incoordination, nausea and fatigue. Careful dose titration with small initial doses can reduce the likelihood of these adverse effects occurring. Adverse effects such as paraesthesiae are more commonly reported with drugs such as topiramate and zonisamide that have carbonic anhydrase activity. Weight loss and anorexia can also be peculiar to these drugs. Neuropsychiatric adverse effects are reported with a variety of AEDs and may not be dose related. Some drugs, such as carbamazepine when used to treat primary generalized epilepsy, can exacerbate certain seizure types. Rare adverse effects such as hyperammonaemia with valproate are drug specific. There are relatively very few head-to-head comparisons of AEDs and limited information is available in this regard.In this review, we discuss the available literature and provide a comprehensive summary of adverse drug reactions of AEDs affecting the CNS.
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PMID:CNS adverse events associated with antiepileptic drugs. 1869 74

Cannabinoid agonists have shown some promise clinically as analgesics, in particular for cancer pain, in which they have the additional benefit of decreasing nausea. However, as for most other drugs, the long-term use of cannabinoids is limited by the development of tolerance. Several molecular mechanisms have been proposed to explain drug tolerance, including receptor downregulation. The cannabinoid 1 (CB1) receptors can be downregulated in vitro through an interaction with the G-protein-coupled receptor-associated sorting protein1, GASP1, that targets CB1 receptors for degradation after their agonist-mediated endocytosis. To investigate whether GASP1-mediated postendocytic sorting of the CB1 receptor contributes to tolerance to cannabinoid drugs in vivo, we generated a mouse with a disruption of GASP1. In wild-type mice, repeated administration of the cannabinoid agonist WIN55,212-2 promoted downregulation of CB1 receptor levels and concomitant tolerance to the effects of drug on antinociception, motor incoordination, and locomotor hypoactivity. In contrast, GASP1 knockout mice did not develop tolerance to any of these effects and showed no significant receptor downregulation. Taken together, this study provides evidence that GASP1 regulates CB1 receptor downregulation in vivo, and that postendocytic receptor trafficking has a key role in the development of tolerance to WIN55,212-2.
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PMID:Differential regulation of behavioral tolerance to WIN55,212-2 by GASP1. 2016 30

The article represents a case of a young patient with atypical clinical and paraclinical presentation of vertebral artery dissection by multiple cerebral infarcts, localized at the supratentorial and infratentorial levels in the posterior circulation. A case of a 21-year-old man, without a history of trauma in the cervical area or at the cranial level, without recent chiropractic maneuvers or practicing a sport, which required rapid, extreme, rotational movements of the neck, was examined. He presented to the emergency room with nausea, numbness of the left limbs, dysarthria, and incoordination of walking, with multiple objective signs at the neurological examination, which revealed right vertebral artery subacute dissection after the paraclinical investigations. The case was particular due to the atypical debut symptomatology, through the installation of the clinical picture in stages, during 4 hours and by multiple infarcts through the artery-to-artery embolic mechanism in the posterior cerebral territory. Abbreviations: PICA = posterior inferior cerebellar artery, CT = computed tomography, MRI = magnetic resonance imaging, angio MRI = mangnetic resonance angiography, FLAIR = fluid attenuated inversion recovery, FS = fat suppression, ADC = apparent diffusion coefficient, DWI = diffusion weighted imaging, T1/ T2 = T1/ T2 weighted image-basic pulse sequences in MRI, VA = vertebral artery, 3D-TOF = 3D Time of Flight.
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PMID:Spontaneous vertebral artery dissection with multiple supratentorial and infratentorial acute infarcts in the posterior circulation Case report. 2797 38


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