Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033377 (prolapse)
 11,717 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Ouabain given by intracerebroventricular injection to mice in small doses (0.1-0.4 mug) produced a dose related depression of central nervous activity, characterized by a reduction in spontaneous locomotor activity, hypothermia, catalepsy and ptosis, lowered body posture and lack of response to external stimuli. Doses above 0.4 mug were excitatory, convulsant and lethal.2. The depressant effects could be antagonized by (+)-amphetamine, desmethylimipramine, dibutyryl cyclic 3'5'-adenosine monophosphate and caffeine.3. The MAO inhibitor nialamide produced only a small antagonism of ouabain, resulting in a greater rate of recovery from the depressant effects of ouabain.4. The depressant effects were associated with a marked elevation of whole-brain dopamine levels with little change in noradrenaline or 5-hydroxytryptamine.5. The dopamine-beta-hydroxylase inhibitor sodium diethyldithiocarbamate, administered by intracerebroventricular injection, produced effects qualitatively similar to those seen after ouabain.6. An interference with central transmitter function is postulated as a possible mode of action of intracerebroventricularly injected ouabain.
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PMID:Pharmacological properties of centrally administered ouabain and their modification by other drugs. 432 23

The adenosine A2a receptor (A2aAR) is thought to be implicated in the pathogenesis of panic disorder because caffeine, a potent antagonist for A2aAR, can precipitate panic attacks, and because disruption of the A2aAR gene increased anxiety-behaviors in mice. Recent studies demonstrated that the A2aAR 1976T > C genetic variant confers susceptibility to panic disorder though not by all studies. The present study tested the hypothesis that the A2aAR 1976T > C genetic variant confers susceptibility to panic disorder using a Chinese population of 104 panic disorder patients and 192 normal controls. We also tested whether the A2aAR 1976T > C polymorphism relates to the age of onset or subtype of panic disorders. Neither the distribution of the A2aAR 1976T > C genotypes (P = 0.296) or alleles (P = 0.864), nor the age of onset (P = 0.719) were significantly different among genotype groups. Furthermore, no association was demonstrated between this A2aAR polymorphism and either mitral-valve prolapse or agoraphobia in panic-disorder patients. These findings suggested that it is unlikely that the A2aAR 1976T > C polymorphism plays a major role in panic disorder pathogenesis in the Chinese population. The positive association between this polymorphism and panic disorder found in western population but not in Asian population suggests that this association could be ethnicity-dependent. The 1976C > T polymorphism may be in linkage disequilibrium with a functional variant that affects panic disorder, and the extent of this linkage disequilibrium is not similar for all ethnic populations.
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PMID:Association study of A2a adenosine receptor genetic polymorphism in panic disorder. 1577 65

Hypnic headache (HH) is a rare sleep-associated primary headache disorder, usually affecting aged people, first described by Raskin in 1988. The headache attacks, single or multiple in one night, occur exclusively during sleep and tend to present at a consistent time each night, sometimes during a dream. Compared to the original description, newly reported cases have expanded the clinical spectrum of the disorder to include unilateral forms (about 40%, half of which are side-locked), forms with a longer duration (up to 3 h) and cases with onset in juvenile/adult age. The male predominance found in Raskin's series has not been confirmed by subsequent observations. To date the reported F/M ratio is 1.7/1. Pain is of severe intensity in less then one-third of cases and mild-moderate in about two-thirds. The location of pain is fronto-temporal in over 40% of cases; headache is throbbing in 38% of cases, dull in 57% and stabbing in less than 5%. Nausea is reported in 19% of cases; photophobia, phonophobia or both are present in 6.8%. Mild autonomic signs (lacrimation, nasal congestion, ptosis) may rarely be present. In 2004, HH was included in Group 4 of the International Classification of Headache Disorders-II (Other primary headaches). Sufficient evidence, mainly from polysomnographic studies, indicates that HH is a primary rapid eye movement (REM) sleep-related headache disorder of chronobiological origin. Lithium, melatonin, indomethacin and caffeine at bedtime are among the most effective therapeutic options. The pathophysiology of HH is still unclear. Available data allow speculation that, in predisposed subjects, an age-related impairment of suprachiasmatic nucleus could cyclically activate a disnociceptive mechanism leading to both a sudden awakening and headache. The mechanism may be precipitated by neurophysiologic events such as the strong reduction of firing occurring in the dorsal raphe nucleus during a REM sleep phase.
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PMID:Hypnic headache: an update. 1668 19

p-Synephrine is an adrenergic amine found in Citrus aurantium L. fruits and has been used for weight loss in dietary supplements. There are commercial products containing this substance associated to caffeine, salicin, and ephedrine. The aim of this study was to evaluate the acute toxicity of this mixture in mice of both sexes. The significative results observed after acute oral administration to male and female mice of 300, 350, and 400 mg/kg total of p-synephrine, ephedrine, salicin, plus caffeine in a 10:4:6:80 w/w ratio included a reduction in locomotor activity and ptosis in all treated groups for both sexes. Seizures were also observed in male (400 mg/kg) and female groups (350 and 400 mg/kg). Gasping and tearing were observed in males. Salivation (400 mg/kg), agitation (350 and 400 mg/kg), and piloerection (all treated groups) were significantly observed only in females. Deaths occurred in males at 350 and 400 mg/kg treated groups and the necropsy showed cardiopulmonary hemorrhage. A reduction in locomotor activity was confirmed through the spontaneous locomotor activity test, in which the number of crossings considerably decreased (P < .01) in all treated groups. The rotarod test showed a decrease in motor coordination at 400 mg/kg. Body temperature decreased significantly (P < .01) in all treated groups compared to controls. The results suggested clear signs of toxicity of p-synephrine, ephedrine, salicin, and caffeine association; this toxicity augments the attentiveness on commercial products containing this mixture, given the expressive number of adverse events related to its utilization.
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PMID:Toxicological effects of a mixture used in weight loss products: p-synephrine associated with ephedrine, salicin, and caffeine. 2240 69