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MeSH Review

Sleep Stages

 
 
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Disease relevance of Sleep Stages

  • Of the 153 children who took at least one dose of diazepam, 39 percent had ataxia, lethargy, or irritability or at least one other moderate side effect that was reversed after a reduction in the dose [1].
  • The central nervous dysfunctions of lethargy, fever and anorexia are manifestations of sepsis that seem to be mediated by increased cytokine production [2].
  • Treatment was discontinued in 28 patients because of dose-limiting toxicity consisting of a syndrome of malaise, fatigue, and lethargy; recurrent reduction in creatinine clearance of 50% or more; or axonal neuropathy [3].
  • The treated animals show normalization of metabolic abnormalities including hyperglycemia, insulin resistance, impaired glucose tolerance, and lethargy [4].
  • RAPA-treated mice had no clinical (e.g., weight loss, diarrhea, lethargy) or histologic evidence of classical acute or chronic GVHD but did develop a clinical-pathological syndrome consisting of ulcerative dermatitis, bile duct proliferation, and a nondestructive peribronchiolar pulmonary infiltration [5].
 

Psychiatry related information on Sleep Stages

 

High impact information on Sleep Stages

  • The median interval between the onset of major symptoms (vomiting and lethargy, seizures, and coma) and diagnosis was 16 months (range, 1 to 142) [11].
  • OBJECTIVE: To determine the chronology of age-related changes in sleep duration and quality (sleep stages) in healthy men and whether concomitant alterations occur in GH and cortisol levels [12].
  • Mutants were isolated by their ability to suppress lethargy of an unc-64 syntaxin mutant that restricts neurotransmitter release [13].
  • Sleep stage was graded by continuous electroencephalogram, and systemic glucose turnover was estimated by isotope dilution [14].
  • When cisapride was given, there was frequent irregular contractile activity, faster gastric emptying, and no symptoms of lethargy [15].
 

Chemical compound and disease context of Sleep Stages

  • Tryptophan loading produced lethargy and drowsiness within 30 minutes of ingestion under all loading conditions [16].
  • The intrinsic and network properties of thalamic reticular (RE) neurons, which release the potent inhibitory neurotransmitter gamma-aminobutyric acid (GABA), endow them with oscillatory properties within the frequency range of sleep spindles (7-15 Hz), a hallmark brain rhythm that characterizes early sleep stages [17].
  • Side effects for aminoglutethimide (including lethargy, rash, and depression) were more common than for tamoxifen, and 7% of aminoglutethimide-treated patients had to discontinue treatment because of these compared with 0% on tamoxifen [18].
  • Three patients, who received all 18 doses of suramin per protocol, developed severe, but not dose-limiting, malaise, fatigue, and lethargy [19].
  • Thirty to 48 hr after the initial acetaminophen dose, the animals begin to exhibit symptoms of encephalopathy and progress from lethargy to the inability to maintain posture and then coma, seizures and death [20].
 

Biological context of Sleep Stages

 

Anatomical context of Sleep Stages

 

Gene context of Sleep Stages

 

Analytical, diagnostic and therapeutic context of Sleep Stages

References

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  2. Upregulation of RGS7 may contribute to tumor necrosis factor-induced changes in central nervous function. Benzing, T., Brandes, R., Sellin, L., Schermer, B., Lecker, S., Walz, G., Kim, E. Nat. Med. (1999) [Pubmed]
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