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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
MeSH Review

Polysomnography

 
 
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Disease relevance of Polysomnography

 

Psychiatry related information on Polysomnography

 

High impact information on Polysomnography

  • The timing of the production of endogenous melatonin was measured as a marker of the circadian time (phase), and sleep was monitored by polysomnography [11].
  • Data included questionnaire information on medical and family history, SDB symptoms; measurement of height, weight, blood pressure, waist and hip circumference, and serum cholesterol concentration; and overnight sleep monitoring [12].
  • The effect of cyproheptadine on plasma growth hormone and cortisol levels was studied in seven male volunteers with polygraphic sleep monitoring [13].
  • Eighteen clinically stable male schizophrenic patients taking haloperidol were studied with 3 nights of polysomnography for baseline measures and again after neuroleptic withdrawal [14].
  • Social engagement was assessed by questionnaire, sleep was assessed by using the NightCap in-home sleep monitoring system and the Pittsburgh Sleep Quality Index, and blood samples were obtained for analysis of plasma levels of IL-6 [15].
 

Chemical compound and disease context of Polysomnography

 

Biological context of Polysomnography

 

Anatomical context of Polysomnography

 

Associations of Polysomnography with chemical compounds

  • All-night polysomnography was performed in a sleep laboratory during the last 2 days of placebo treatment and on days 13, 14, 89, and 90 of tenoxicam treatment [27].
  • Plasma levodopa concentrations were measured serially and all-night polysomnography was performed [28].
  • Each subject completed a questionnaire including questions on sleep-related symptoms and underwent overnight polysomnography in which we evaluated the apnea-hypopnea index (AHI) and the percentage of time during which arterial O2 saturation was less than 90% (T90) [29].
  • DESIGN: Patients with OSA were studied by polysomnography during APAP therapy (Somnosmart) [30].
  • The agreement between both strategies, visual and computer analysis, was tested using data from a pharmacological sleep study with 16 elderly insomniacs, which was aimed at comparing the effects of lormetazepam and zopiclone on polysomnography [31].
 

Gene context of Polysomnography

  • Polysomnography demonstrated that the percentage of SWS was not different when saline and GHRH antagonist nights were compared (P=0.607); other quantifiable sleep parameters were also unchanged [32].
  • A clinical follow-up was performed approximately 1 decade after depressed and psychiatrically "normal" control adolescents, who were now young adults, had undergone baseline serial GH measurements over a 24-hour period on the third night of sleep polysomnography studies [33].
  • After polysomnography, venous blood was collected at 5:00 A.M. from 44 patients with OSAS and 18 control subjects who were obese, and serum levels of MMP-9, TIMP-1, and enzymatic activity of MMP-9 were measured [34].
  • METHODS: Serum and plasma BDNF concentrations, BDNF secretion by peripheral blood mononuclear cells, and overnight polysomnography were evaluated in 17 men with newly diagnosed OSAS (as defined by a respiratory disturbance index of >10/hour with >70% obstructive events and corresponding daytime symptoms) and 12 healthy control men [35].
  • Forty-seven ADHD children referred to the sleep clinic (ADHDcl), 53 ADHD children from a community survey (ADHDcom), and 49 control children underwent overnight polysomnography [36].
 

Analytical, diagnostic and therapeutic context of Polysomnography

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