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1. Biomedical articles (top 50; 2010 to 2015)
1. Jinnur P, Kumar N, Vassallo R, St Louis EK: A 54-year-old man with acute onset orthopnea and sleep-related hypoxia. J Clin Sleep Med; 2014 May 15;10(5):595-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A 54-year-old man with acute onset orthopnea and sleep-related hypoxia.

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  • (PMID = 24812547.001).
  • [ISSN] 1550-9397
  • [Journal-full-title] Journal of clinical sleep medicine : JCSM : official publication of the American Academy of Sleep Medicine
  • [ISO-abbreviation] J Clin Sleep Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC4013390
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2. Shepard P, Lam EM, St Louis EK, Dominik J: Sleep disturbances in myotonic dystrophy type 2. Eur Neurol; 2012;68(6):377-80
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Sleep disturbances in myotonic dystrophy type 2.
  • Sleep disorders in myotonic dystrophy type 1 (DM1) are common and include sleep-disordered breathing, hypersomnia, and fatigue.
  • Little is known regarding the occurrence of sleep disturbance in myotonic dystrophy type 2 (DM2).
  • We hypothesized that DM2 patients may frequently harbor sleep disorders.
  • We reviewed medical records of all genetically confirmed cases of DM2 seen at our sleep center between 1997 and 2010 for demographic, laboratory, overnight oximetry, and polysomnography (PSG) data.
  • Obstructive sleep apnea was diagnosed in 3 of 5 patients (60%) studied with PSG.
  • The clinical spectrum of DM2 may include a wide range of sleep disturbances.
  • Although respiratory muscle weakness was frequent, sustained sleep-related hypoxia suggestive of hypoventilation was not seen in our patients.
  • Further prospective studies are needed to examine the frequency and scope of sleep disturbances in DM2.
  • [MeSH-major] Disorders of Excessive Somnolence / physiopathology. Myotonic Disorders / complications. Sleep Disorders / etiology

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  • [Copyright] Copyright © 2012 S. Karger AG, Basel.
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  • (PMID = 23108384.001).
  • [ISSN] 1421-9913
  • [Journal-full-title] European neurology
  • [ISO-abbreviation] Eur. Neurol.
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / UL1 RR024150; United States / NCATS NIH HHS / TR / UL1 TR000135
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Switzerland
  • [Other-IDs] NLM/ NIHMS645958; NLM/ PMC4259012
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3. Miyamura M, Schnell O, Yamashita C, Yoshioka T, Matsumoto C, Mori T, Ukimura A, Kitaura Y, Matsumura Y, Ishizaka N, Hayashi T: Effects of acarbose on the acceleration of postprandial hyperglycemia-induced pathological changes induced by intermittent hypoxia in lean mice. J Pharmacol Sci; 2010;114(1):32-40
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  • [Title] Effects of acarbose on the acceleration of postprandial hyperglycemia-induced pathological changes induced by intermittent hypoxia in lean mice.
  • Postprandial hyperglycemia (PPH) and intermittent hypoxia related to the sleep apnea syndrome are important predictors of cardiovascular disease.
  • We investigated the effects of intermittent hypoxia on pathological changes in the left ventricular (LV) myocardium caused by PPH in lean mice and evaluated the influence of acarbose, an α-glucosidase inhibitor.
  • Male C57BL/6J mice aged 8 weeks were exposed to intermittent hypoxia (8 h/day during the daytime) or kept under normoxia.
  • Intermittent hypoxia exacerbated cardiomyocyte hypertrophy and interstitial fibrosis in the LV myocardium of RD mice.
  • Superoxide production and expression of 4-hydroxy-2-nonenal in the LV myocardium with intermittent hypoxia were increased in RD mice, but not AL mice.

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  • (PMID = 20703014.001).
  • [ISSN] 1347-8648
  • [Journal-full-title] Journal of pharmacological sciences
  • [ISO-abbreviation] J. Pharmacol. Sci.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] T58MSI464G / Acarbose
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4. Lombardi C, Meriggi P, Agostoni P, Faini A, Bilo G, Revera M, Caldara G, Di Rienzo M, Castiglioni P, Maurizio B, Gregorini F, Mancia G, Parati G, HIGHCARE Investigators: High-altitude hypoxia and periodic breathing during sleep: gender-related differences. J Sleep Res; 2013 Jun;22(3):322-30
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High-altitude hypoxia and periodic breathing during sleep: gender-related differences.
  • High-altitude exposure is characterized by the appearance of periodic breathing during sleep.
  • Only limited evidence is available, however, on the presence of gender-related differences in this breathing pattern.
  • Females started to present a significant number of central sleep apneas only at the highest reached altitude.
  • [MeSH-major] Anoxia / complications. Monitoring, Ambulatory / instrumentation. Sleep / physiology. Sleep Apnea, Central / physiopathology

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  • [Copyright] © 2013 European Sleep Research Society.
  • [ErratumIn] J Sleep Res. 2014 Oct;23(5):605
  • (PMID = 23294420.001).
  • [ISSN] 1365-2869
  • [Journal-full-title] Journal of sleep research
  • [ISO-abbreviation] J Sleep Res
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't; Validation Studies
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiotensin II Type 1 Receptor Blockers; 0 / Benzimidazoles; 0 / Benzoates; 0 / Placebos; S88TT14065 / Oxygen; U5SYW473RQ / telmisartan
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5. Cooper IF, Siadaty MS: 'Spatial Concepts' associated with 'Disturbance In Sleep Behavior': Top Publications. BioMedLib Review; SpatialConcept;DisturbanceInSleep:707395026. ISSN: 2331-5717. 2014/7/9
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  • [Title] 'Spatial Concepts' associated with 'Disturbance In Sleep Behavior': Top Publications.
  • [Transliterated title]
  • Background: There are articles published each month which present 'Spatial Concept' for 'disturbance in sleep behavior'.
  • Finding such articles is important for researchers, clinicians, and patients.
  • However these articles are spread across thousands of journals, and there are many types of 'Spatial Concept'.
  • This makes searching and locating the relevant publications a challenge.
  • We have used BioMedLib's semantic search technology to address the issue, and gathered all the pertinent publications in this review article.
  • Methods: We categorized the publications we found into two groups.
  • We used the strength of textual-association to separate the groups.
  • In group one there are publications with the strongest evidence of association. We focused finding the most relevant publications pertinent to our goal, rather than combining them into a conclusion section. Such textual synthesis will be the focus of our next project.
  • Results: Group one includes 40 publications, and group two 8499 publications.
  • Here are the top 10.
  • Jones CR: Diagnostic and management approach to common sleep disorders during pregnancy.
  • Iacono Isidoro S et al: Quality of life in patients at first time visit for sleep disorders of breathing at a sleep centre.
  • Suzuki T et al: [The efficacy of imidafenacin in patients with over active bladder, nocturia, or sleep disorders (Sayama-Iruma-Hannou study)].
  • Rener-Sitar K et al: Exploration of dimensionality and psychometric properties of the Pittsburgh Sleep Quality Index in cases with temporomandibular disorders.
  • Sharma PK et al: Primary sleep disorders seen at a Neurology service-based sleep clinic in India: Patterns over an 8-year period.
  • Babson KA et al: The comorbidity of sleep apnea and mood, anxiety, and substance use disorders among obese military veterans within the Veterans Health Administration.
  • Johannessen B: Nurses experience of aromatherapy use with dementia patients experiencing disturbed sleep patterns. An action research project.
  • Jernelöv S et al: Development of atopic disease and disturbed sleep in childhood and adolescence--a longitudinal population-based study.
  • Ritter PS et al: Disturbed sleep in bipolar disorder is related to an elevation of IL-6 in peripheral monocytes.
  • Passàli D et al: The undisclosed role of disturbed sleep and hypoxia on metabolism: the importance of upper airways pathology.

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  • [Copyright] Copyright 2014 Siadaty and Cooper; licensee BioMedLib LLC.
  • (UID = 707395026.001).
  • [ISSN] 2331-5717
  • [Journal-full-title] BioMedLib Review
  • [Language] eng
  • [Publication-type] Review
  • [Publication-country] UNITED STATES
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6. Yin T, Li NF, Ai LG, Yao XG, Hong J, Zhou L, Kong JQ: [Association of glucose transporter 4 gene polymorphism with hypoxia caused by obstructive sleep apnea syndrome and with related inflammatory factors]. Zhongguo Yi Xue Ke Xue Yuan Xue Bao; 2014 Aug;36(4):400-9
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  • [Title] [Association of glucose transporter 4 gene polymorphism with hypoxia caused by obstructive sleep apnea syndrome and with related inflammatory factors].
  • OBJECTIVE: To investigate the relationship between genetic polymorphisms of glucose transporter 4 (GLUT4) and hypoxia caused by obstructive sleep apnea syndrome (OSAS) as well as with related inflammatory factors.
  • A total of 859 subjects with possible OSAS base on their histories and physical examination findings udner went the polysomnography and inflammatory factor determination, of whom 616 (72%) were diagnosed with moderate and severe hypoxia with OSAS (case group) and 243 (28%) without hypoxia or OASA (control group).
  • TaqMan PCR was used to genotyping then analyzed the relationship between locis of GLUT4 and hypoxia.
  • A significant association of GLUT4 SNP rs5417 allele carried in control subjects, compared with moderate and severe hypoxia in OSAS patients (P<0.05); AA+AC genotype relative to CC with low oxygen levels in subjects significantly reduced.
  • AA was still an independent protective factor for hypoxia caused by OSAS (OR=0.385, 95%CI = 0.210-0.704, P=0.002).
  • Male (OR=1.635, 95% CI=1.037-2.577, P=0.034) and total cholesterol (OR=1.600, 95% CI=1.287-1.987, P<0.001) were independent risk factors associated with hypoxia.
  • Normal weight(OR=0.059, 95% CI=0.037-0.094, P<0.001) and high density lipoprotein cholesterol (OR=0.337, 95% CI=0.171-0.666, P=0.002)were independent protective factors for hypoxia.
  • CONCLUSION: Hypoxia caused by OSAS is associated with GLUT4 gene SNP rs5417.
  • [MeSH-major] Anoxia / etiology. Glucose Transporter Type 4 / genetics. Polymorphism, Single Nucleotide. Sleep Apnea, Obstructive / genetics

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  • (PMID = 25176209.001).
  • [ISSN] 1000-503X
  • [Journal-full-title] Zhongguo yi xue ke xue yuan xue bao. Acta Academiae Medicinae Sinicae
  • [ISO-abbreviation] Zhongguo Yi Xue Ke Xue Yuan Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Glucose Transporter Type 4; 0 / SLC2A4 protein, human
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7. Cooper IF, Siadaty MS: 'Diseases or Syndromes' associated with 'Respiratory Hypoxia': Top Publications. BioMedLib Review; DiseaseOrSyndrome;RespiratoryHypoxia:705309855. ISSN: 2331-5717. 2014/8/31
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  • [Title] 'Diseases or Syndromes' associated with 'Respiratory Hypoxia': Top Publications.
  • [Transliterated title]
  • Background: There are articles published each month which present 'Disease or Syndrome' for 'respiratory hypoxia'.
  • Finding such articles is important for researchers, clinicians, and patients.
  • However these articles are spread across thousands of journals, and there are many types of 'Disease or Syndrome'.
  • This makes searching and locating the relevant publications a challenge.
  • We have used BioMedLib's semantic search technology to address the issue, and gathered all the pertinent publications in this review article.
  • Methods: We categorized the publications we found into two groups.
  • We used the strength of textual-association to separate the groups.
  • In group one there are publications with the strongest evidence of association. We focused finding the most relevant publications pertinent to our goal, rather than combining them into a conclusion section. Such textual synthesis will be the focus of our next project.
  • Results: Group one includes 21 publications, and group two 5838 publications.
  • Here are the top 10.
  • Lüneburg N et al: The endothelial ADMA/NO pathway in hypoxia-related chronic respiratory diseases.
  • Mahamed S et al: Is there a link between intermittent hypoxia-induced respiratory plasticity and obstructive sleep apnoea?.
  • Tafil-Klawe M et al: Reflex respiratory responses to progressive hyperoxic hypercapnia and normocapnic hypoxia in normocapnic and hypercapnic obstructive sleep apnea patients.
  • Thylefors J et al: Dark adaptation during systemic hypoxia induced by chronic respiratory insufficiency.
  • Ecevit A et al: Association of respiratory distress syndrome and perinatal hypoxia with histologic chorioamnionitis in preterm infants.
  • Höhne C et al: Low sodium intake does not impair renal compensation of hypoxia-induced respiratory alkalosis.
  • Han F et al: [Respiratory control during sleep and the development of nocturnal hypoxia in patients with obstructive sleep apnea hypopnea syndrome].
  • de Theije C et al: Hypoxia and muscle maintenance regulation: implications for chronic respiratory disease.
  • Mel'nikova IP et al: [Intermittent normobaric hypoxia in rehabilitation of young seamen with respiratory diseases].
  • Bernardi L et al: Respiratory and cerebrovascular responses to hypoxia and hypercapnia in familial dysautonomia.

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  • [Copyright] Copyright 2014 Siadaty and Cooper; licensee BioMedLib LLC.
  • (UID = 705309855.001).
  • [ISSN] 2331-5717
  • [Journal-full-title] BioMedLib Review
  • [Language] eng
  • [Publication-type] Review
  • [Publication-country] UNITED STATES
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8. Beuchée A, Hernández AI, Duvareille C, Daniel D, Samson N, Pladys P, Praud JP: Influence of hypoxia and hypercapnia on sleep state-dependent heart rate variability behavior in newborn lambs. Sleep; 2012 Nov;35(11):1541-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Influence of hypoxia and hypercapnia on sleep state-dependent heart rate variability behavior in newborn lambs.
  • STUDY OBJECTIVES: Although hypercapnia and/or hypoxia are frequently present during chronic lung disease of infancy and have also been implicated in sudden infant death syndrome (SIDS), their effect on cardiac autonomic regulation remains unclear.
  • The authors' goal is to test that hypercapnia and hypoxia alter sleep-wake cycle-dependent heart rate variability (HRV) in the neonatal period.
  • DESIGN: Experimental study measuring HRV during sleep states in lambs randomly exposed to hypercapnia, hypoxia, or air.
  • INTERVENTIONS: Each lamb underwent polysomnographic recordings while in a chamber flowed with either air or 21% O(2) + 5% CO(2) (hypercapnia) or 10% O(2) + 0% CO(2) (hypoxia) on day 3, 4, and 5 of postnatal age.
  • MEASUREMENTS AND RESULTS: Hypercapnia increased the time spent in wakefulness and hypoxia the time spent in quiet sleep (QS).
  • Compared with QS, active sleep (AS) was associated with an overall increase in HRV magnitude and short-term self-similarity and a decrease in entropy of cardiac cycle length in air.
  • This AS-related HRV pattern persisted in hypercapnia and was even more pronounced in hypoxia.
  • CONCLUSION: Enhancement of AS-related sympathovagal coactivation in hypoxia, together with increased heart rate regularity, may be evidence that AS + hypoxia represent a particularly vulnerable state in early life.
  • This should be kept in mind when deciding the optimal arterial oxygenation target in newborns and when investigating the potential involvement of hypoxia in SIDS pathogenesis.
  • [MeSH-major] Anoxia / physiopathology. Heart Rate. Hypercapnia / physiopathology. Sleep

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  • (PMID = 23115403.001).
  • [ISSN] 1550-9109
  • [Journal-full-title] Sleep
  • [ISO-abbreviation] Sleep
  • [Language] eng
  • [Grant] Canada / Canadian Institutes of Health Research / / MOP 15558
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC3466801
  • [Keywords] NOTNLM ; Entropy / REM sleep / frequency domain analysis / quiet sleep / scale-invariance / sympathovagal coactivation
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9. Jara SM, Benke JR, Lin SY, Ishman SL: The association between secondhand smoke and sleep-disordered breathing in children: a systematic review. Laryngoscope; 2015 Jan;125(1):241-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The association between secondhand smoke and sleep-disordered breathing in children: a systematic review.
  • OBJECTIVE: To systematically review existing literature on the association between secondhand smoke and sleep-disordered breathing in children.
  • Fifteen (83%) articles found a statistically significant association between secondhand smoke and sleep-disordered breathing.
  • Sleep-disordered breathing was quantified by polysomnography in only four (22%) of the studies and only one (6%) classified subject using polysomnography exclusively.
  • Habitual snoring was the most common form of sleep-disordered breathing studied in 14/18 (78%) studies, whereas obstructive sleep apnea was reported in one (6%) study and sleep-related hypoxia in another (6%) study.
  • CONCLUSIONS: Although the majority of studies included in this review found a significant association between secondhand smoke and sleep-disordered breathing, all of them were evidence level 3b, for an overall grade of B (Oxford Centre for Evidence-based Medicine).
  • Further higher-quality studies should be performed in the future to better evaluate the relationship between second- smoke and sleep-disordered breathing in children.
  • [MeSH-major] Sleep Apnea Syndromes / etiology. Tobacco Smoke Pollution / adverse effects
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Humans. Infant. Polysomnography. Sleep Apnea, Obstructive / diagnosis. Sleep Apnea, Obstructive / etiology. Snoring / diagnosis. Snoring / etiology. Statistics as Topic


10. Inamoto S, Yoshioka T, Yamashita C, Miyamura M, Mori T, Ukimura A, Matsumoto C, Matsumura Y, Kitaura Y, Hayashi T: Pitavastatin reduces oxidative stress and attenuates intermittent hypoxia-induced left ventricular remodeling in lean mice. Hypertens Res; 2010 Jun;33(6):579-86
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  • [Title] Pitavastatin reduces oxidative stress and attenuates intermittent hypoxia-induced left ventricular remodeling in lean mice.
  • We have reported previously that intermittent hypoxia related to sleep apnea induces cardiovascular remodeling secondary to the oxidative stress.
  • The aim of this study was to examine the effect of pitavastatin as an antioxidant to prevent intermittent hypoxia-induced left ventricular (LV) remodeling in mice without hypercholesterolemia.
  • Eight-week-old male C57BL/6J mice (n=35) were exposed to intermittent hypoxia (30 s exposure to 5% oxygen, followed by 30 s exposure to 21% oxygen) for 8 h per day during the daytime or maintained under normoxic conditions; in addition, they were either treated with pitavastatin (3 mg kg(-1) per day) or vehicle for 10 days.
  • Intermittent hypoxia significantly increased the expression levels of 4-hydroxy-2-nonenal (4-HNE) proteins, TNF-alpha and TGF-beta mRNA, and also the number of terminal deoxynucleotidyl transferase-mediated dUTP-biotin end labeling (TUNEL)-positive myocardial cells in the LV myocardium.
  • Treatment with pitavastatin significantly suppressed the expression levels of the 4-HNE proteins, cytokines, superoxide production and TUNEL-positive myocardial cells in the LV myocardium, consequently attenuating the hypoxia-induced histological changes.
  • Pitavastatin preserved, at least partially, the morphological structure of the LV myocardium in lean mice exposed to intermittent hypoxia, through its antioxidant effect.
  • [MeSH-major] Anoxia / complications. Antioxidants / therapeutic use. Hydroxymethylglutaryl-CoA Reductase Inhibitors / therapeutic use. Oxidative Stress / drug effects. Quinolines / therapeutic use. Sleep Apnea Syndromes / complications. Ventricular Remodeling / drug effects

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  • [CommentIn] Hypertens Res. 2010 Jun;33(6):535-6 [20448637.001]
  • (PMID = 20300107.001).
  • [ISSN] 1348-4214
  • [Journal-full-title] Hypertension research : official journal of the Japanese Society of Hypertension
  • [ISO-abbreviation] Hypertens. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aldehydes; 0 / Antioxidants; 0 / Hydroxymethylglutaryl-CoA Reductase Inhibitors; 0 / Quinolines; 0 / Transforming Growth Factor beta; 0 / Tumor Necrosis Factor-alpha; 29343-52-0 / 4-hydroxy-2-nonenal; 97C5T2UQ7J / Cholesterol; M5681Q5F9P / pitavastatin
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11. Ramar K, Caples SM: Vascular changes, cardiovascular disease and obstructive sleep apnea. Future Cardiol; 2011 Mar;7(2):241-9
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  • [Title] Vascular changes, cardiovascular disease and obstructive sleep apnea.
  • Vascular changes related to obstructive sleep apnea (OSA) can lead to chronic cardiovascular consequences such as hypertension.
  • The cardiovascular consequences are owing to nocturnal perturbations related to intrathoracic pressure changes, intermittent hypoxia, sympathetic neural activation, endothelial dysfunction, oxidative stress and systemic inflammation.
  • Intermittent hypoxia due to sleep-related events in OSA activates the renin-angiotensin system and increases the levels of endothelin-1.
  • Intermittent hypoxia also results in oxidative stress, as evidenced by elevated levels of xanthine oxidoreductase, lipid peroxidation and the presence of reactive oxygen species.
  • [MeSH-major] Cardiovascular Diseases / etiology. Endothelium, Vascular / physiopathology. Sleep Apnea, Obstructive / complications. Vasodilation / physiology

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  • (PMID = 21453030.001).
  • [ISSN] 1744-8298
  • [Journal-full-title] Future cardiology
  • [ISO-abbreviation] Future Cardiol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
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12. Dergacheva O, Weigand LA, Dyavanapalli J, Mares J, Wang X, Mendelowitz D: Function and modulation of premotor brainstem parasympathetic cardiac neurons that control heart rate by hypoxia-, sleep-, and sleep-related diseases including obstructive sleep apnea. Prog Brain Res; 2014;212:39-58
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Function and modulation of premotor brainstem parasympathetic cardiac neurons that control heart rate by hypoxia-, sleep-, and sleep-related diseases including obstructive sleep apnea.
  • Whereas prior reviews have focused on glutamatergic, GABAergic and glycinergic pathways, and the receptors in CVNs activated by these neurotransmitters, this review focuses on the alterations in CVN activity with hypoxia-, sleep-, and sleep-related cardiovascular diseases including obstructive sleep apnea.
  • [MeSH-major] Brain Stem / physiology. Heart / physiology. Heart Rate / physiology. Parasympathetic Nervous System / physiology. Sleep / physiology. Sleep Apnea, Obstructive / physiopathology

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  • [Copyright] © 2014 Elsevier B.V. All rights reserved.
  • (PMID = 25194192.001).
  • [ISSN] 1875-7855
  • [Journal-full-title] Progress in brain research
  • [ISO-abbreviation] Prog. Brain Res.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / HL49965; United States / NHLBI NIH HHS / HL / HL59895; United States / NHLBI NIH HHS / HL / HL72006
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] Netherlands
  • [Keywords] NOTNLM ; REM / ambiguus / apnea / cardiac / non-REM / obstructive / parasympathetic / serotonin / sleep / vagal
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13. Feng J, Wu Q, Zhang D, Chen BY: Hippocampal impairments are associated with intermittent hypoxia of obstructive sleep apnea. Chin Med J (Engl); 2012 Feb;125(4):696-701
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  • [Title] Hippocampal impairments are associated with intermittent hypoxia of obstructive sleep apnea.
  • Obstructive sleep apnea (OSA), which is the most common sleep-related breathing disorder, is characterized as frequent upper airway collapse and obstruction.
  • In studies of OSA, it is difficult to differentiate the effects of its two main pathologic traits, intermittent hypoxia (IH) and sleep fragmentation.
  • IH, continuous hypoxia and intermittent continuous hypoxia can all result in decreases in arterial O2.
  • [MeSH-major] Anoxia / physiopathology. Hippocampus / physiopathology. Sleep Apnea, Obstructive / physiopathology

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  • (PMID = 22490498.001).
  • [ISSN] 0366-6999
  • [Journal-full-title] Chinese medical journal
  • [ISO-abbreviation] Chin. Med. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
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14. Hoshikawa M, Uchida S, Ganeko M, Sumitomo J, Totoki M, Kojima T, Nakamura Y, Kawahara T: Sleep quality under mild hypoxia in men with low hypoxic ventilatory response. Eur J Sport Sci; 2014;14 Suppl 1:S205-12
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  • [Title] Sleep quality under mild hypoxia in men with low hypoxic ventilatory response.
  • The present study evaluated whether slow-wave sleep and whole-night delta power of the non-rapid eye movement (NREM) sleep electroencephalogram (EEG) decrease during sleep at a simulated altitude of 2000 m, and whether such changes related to measures of hypoxic ventilatory response (HVR).
  • This study consisted of two parts; in the first, HVR was measured in 41 subjects and each seven subjects with the lowest or the highest HVR were selected for the subsequent sleep study.
  • Hypoxia decreased SpO2 and increased respiratory disturbances for both groups.
  • The low HVR group, but not the high HVR group, showed decreases in the whole-night delta power of NREM sleep EEG under hypoxia.
  • On the other hand, two subjects in the high HVR group, who showed relatively high apnoea indices, also showed lower SpO2 nadirs and decreases in the whole-night delta power under hypoxia.
  • These results suggest that acute hypoxia equivalent to that at a 2000 m altitude decreases slow-wave sleep in individuals that show low HVR.
  • However, low HVR may not be the only, but one of some factors that decrease the whole-night delta power under hypoxia.
  • Therefore, it was not sufficient to identify individuals likely to be susceptible to deteriorated sleep quality at a simulated altitude of 2000 m only using the HVR test.
  • [MeSH-major] Anoxia / physiopathology. Oxygen Consumption / physiology. Sleep / physiology

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  • (PMID = 24444208.001).
  • [ISSN] 1536-7290
  • [Journal-full-title] European journal of sport science
  • [ISO-abbreviation] Eur J Sport Sci
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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15. Kubin L: Sleep-wake control of the upper airway by noradrenergic neurons, with and without intermittent hypoxia. Prog Brain Res; 2014;209:255-74
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  • [Title] Sleep-wake control of the upper airway by noradrenergic neurons, with and without intermittent hypoxia.
  • Hypoglossal (XII) motoneurons innervate muscles of the tongue whose tonic and inspiratory modulated activity protects the upper airway from collapse in patients affected by the obstructive sleep apnea (OSA) syndrome.
  • Both norepinephrine and serotonin provide wakefulness-related excitatory drives that maintain activity in XII motoneurons, with the noradrenergic system playing a particularly prominent role in rats.
  • When noradrenergic and serotonergic drives are antagonized, no further decline of XII nerve activity occurs during pharmacologically induced rapid eye movement (REM) sleep-like state.
  • This is the best evidence to date that, at least in this model, the entire REM sleep-related decline of upper airway muscle tone results from withdrawal of these two excitatory inputs.
  • A major component of noradrenergic input to XII motoneurons originates from pontine noradrenergic neurons that have state-dependent patterns of activity, maximal during wakefulness, and minimal, or absent during REM sleep.
  • Our data suggest that not all ventrolateral medullary catecholaminergic neurons follow this pattern, with adrenergic C1 neurons probably increasing their activity during REM sleep.
  • When rats are subjected to chronic-intermittent hypoxia, noradrenergic drive to XII motoneurons is increased by mechanisms that include sprouting of noradrenergic terminals in the XII nucleus, and increased expression of α1-adrenoceptors; an outcome that may underlie the elevated baseline activity of upper airway muscles during wakefulness in OSA patients.
  • [MeSH-major] Adrenergic Neurons / physiology. Anoxia / physiopathology. Respiratory System / innervation. Sleep / physiology. Sleep Apnea, Obstructive / physiopathology. Wakefulness / physiology

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  • [Copyright] © 2014 Elsevier B.V. All rights reserved.
  • (PMID = 24746052.001).
  • [ISSN] 1875-7855
  • [Journal-full-title] Progress in brain research
  • [ISO-abbreviation] Prog. Brain Res.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / HL-47600; United States / NHLBI NIH HHS / HL / HL-60287; United States / NHLBI NIH HHS / HL / HL-74385
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Netherlands
  • [Keywords] NOTNLM ; REM sleep / adrenergic receptors / atonia / genioglossus / norepinephrine / obstructive sleep apnea
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16. Feng J, Chiang AA, Wu Q, Chen BY, Cui LY, Liang DC, Zhang ZL, Yao W: Sleep-related hypoxemia aggravates systematic inflammation in emphysematous rats. Chin Med J (Engl); 2010 Sep;123(17):2392-9
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  • [Title] Sleep-related hypoxemia aggravates systematic inflammation in emphysematous rats.
  • BACKGROUND: Sleep disturbance is common in patients with emphysema.
  • This study aimed to develop a novel model of sleep-related hypoxemia (SRH) in emphysema (SRHIE) with rats, and to explore the inflammatory status of SRHIE in lung, liver, pancreas, carotid artery and whole blood.
  • The protocols varied with the degree of hypoxia exposure and severity of pre-existing emphysema caused by cigarette smoke exposure:.
  • (1) SRH control (SRHCtrl) group, sham smoke exposure (smoke exposure, exposed to smoke of 15 cigarettes twice everyday, 16 weeks) and SRH exposure (12.5% O2, 3 hours, SRH exposure, divide total hypoxia time (1.5 hours or 3 hours) into 4 periods evenly (22.5 minutes or 45 minutes) and distribute these hypoxia periods evenly into physiological sleep time of rats identified by electroencephalogram, week 9 to week 16);.
  • [MeSH-major] Anoxia / complications. Emphysema / complications. Inflammation / etiology. Sleep / physiology

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  • (PMID = 21034555.001).
  • [ISSN] 0366-6999
  • [Journal-full-title] Chinese medical journal
  • [ISO-abbreviation] Chin. Med. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Hemoglobins
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17. Tkacova R, McNicholas WT, Javorsky M, Fietze I, Sliwinski P, Parati G, Grote L, Hedner J, European Sleep Apnoea Database study collaborators: Nocturnal intermittent hypoxia predicts prevalent hypertension in the European Sleep Apnoea Database cohort study. Eur Respir J; 2014 Oct;44(4):931-41
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  • [Title] Nocturnal intermittent hypoxia predicts prevalent hypertension in the European Sleep Apnoea Database cohort study.
  • Systemic hypertension is associated with obstructive sleep apnoea syndrome (OSAS) but the pathophysiological mechanisms are incompletely understood.
  • A collaborative European network of 24 sleep centres established a European Sleep Apnoea Database to evaluate cardiovascular morbidity associated with OSAS.
  • 11 911 adults referred with suspected OSAS between March 2007 and September 2013 underwent overnight sleep studies, either cardiorespiratory polygraphy or polysomnography.
  • Both AHI and ODI independently related to prevalent hypertension after adjustment for relevant covariates (p<0.0001 for linear trend across quartiles (Q) of severity for both variables).
  • This cross sectional study suggests that chronic intermittent hypoxia plays an important role in OSAS-related hypertension.

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  • [Copyright] ©ERS 2014.
  • [CommentIn] Eur Respir J. 2014 Oct;44(4):835-8 [25271222.001]
  • (PMID = 25102963.001).
  • [ISSN] 1399-3003
  • [Journal-full-title] The European respiratory journal
  • [ISO-abbreviation] Eur. Respir. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Investigator] Barbé F; Bonsignore M; Basoglu O; Escourrou P; Fietze I; Grote L; Hedner J; Kvamme JA; Lavie P; Lévy P; Lombardi C; Marrone O; Masa JF; McNicholas WT; Montserrat JM; Nolan G; Parati G; Penzel T; Pepin JL; Pretl M; Riha R; Rodenstein D; Saaresranta T; Schulz R; Sliwinski P; Tkacova R; Varoneckas G; Verbraecken J; Vitols A; Vrints H; Zielinski J
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18. Nakagawa Y, Kishida K, Kihara S, Yoshida R, Funahashi T, Shimomura I: Nocturnal falls of adiponectin levels in sleep apnea with abdominal obesity and impact of hypoxia-induced dysregulated adiponectin production in obese murine mesenteric adipose tissue. J Atheroscler Thromb; 2011;18(3):240-7
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  • [Title] Nocturnal falls of adiponectin levels in sleep apnea with abdominal obesity and impact of hypoxia-induced dysregulated adiponectin production in obese murine mesenteric adipose tissue.
  • AIM: Obstructive sleep apnea-hypopnea syndrome (OSAS) is associated with atherosclerotic cardio-vascular disease.
  • Venous blood samples were collected before sleep and after waking up.
  • We investigated the effect of hypoxia on adiponectin expression in mesenteric and subcutaneous fat tissues of obese yellow-KKAy mice.
  • In obese yellow-KKAy mice, exposure to hypoxia for 2 days suppressed plasma adiponectin levels, with no apparent change in mesenteric and subcutaneous fat tissue adiponectin mRNA expression.
  • CONCLUSIONS: These findings suggest that abdominal obesity, representing abundant mesenteric fat tissue susceptible to hypoxic stress, partly explains Δadiponectin in OSAS patients, and that reduction of visceral fat accumulation may combat OSAS-related atherosclerotic cardiovascular diseases in abdominal obesity.
  • [MeSH-major] Adiponectin / metabolism. Adipose Tissue / metabolism. Anoxia. Circadian Rhythm / physiology. Mesentery / metabolism. Sleep Apnea, Obstructive / metabolism

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  • (PMID = 21139317.001).
  • [ISSN] 1880-3873
  • [Journal-full-title] Journal of atherosclerosis and thrombosis
  • [ISO-abbreviation] J. Atheroscler. Thromb.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Adiponectin
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19. Türkay C, Ozol D, Kasapoğlu B, Kirbas I, Yıldırım Z, Yiğitoğlu R: Influence of obstructive sleep apnea on fatty liver disease: role of chronic intermittent hypoxia. Respir Care; 2012 Feb;57(2):244-9
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  • [Title] Influence of obstructive sleep apnea on fatty liver disease: role of chronic intermittent hypoxia.
  • BACKGROUND: Currently the common pathogenetic mechanisms in nonalcoholic fatty liver disease (NAFLD) and obstructive sleep apnea (OSA) are gaining increased attention.
  • The aim of this study is to find out the influence of chronic intermittent hypoxemia and OSA related parameters to the severity of NAFLD.
  • Our multivariate analysis showed that AHI, oxygen desaturation index, lowest desaturation values, and percentage of sleep duration with S(pO(2)) < 90% were independent predictors of NAFLD after adjustment for BMI, weight, and insulin resistance.
  • Furthermore, the most correlated parameter for the severity of NAFLD was found as the duration of hypoxia during sleep.
  • [MeSH-major] Anoxia. Fatty Liver. Oxygen / analysis. Sleep Apnea, Obstructive

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  • (PMID = 21762556.001).
  • [ISSN] 0020-1324
  • [Journal-full-title] Respiratory care
  • [ISO-abbreviation] Respir Care
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] S88TT14065 / Oxygen
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20. Giusi G, Zizza M, Facciolo RM, Chew SF, Ip YK, Canonaco M: Aestivation and hypoxia-related events share common silent neuron trafficking processes. BMC Neurosci; 2012;13:39
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  • [Title] Aestivation and hypoxia-related events share common silent neuron trafficking processes.
  • BACKGROUND: The availability of oxygen is a limiting factor for neuronal survival since low levels account not only for the impairment of physiological activities such as sleep-wake cycle, but above all for ischemic-like neurodegenerative disorders.
  • This functional relationship might have therapeutic bearings for hypoxia-related dysfunctions, above all in view of recently identified silent neuron-dependent motor activity ameliorations in mammals.
  • [MeSH-major] Anoxia. Estivation / physiology. Gene Expression Regulation / physiology. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Neurons / metabolism

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  • (PMID = 22520032.001).
  • [ISSN] 1471-2202
  • [Journal-full-title] BMC neuroscience
  • [ISO-abbreviation] BMC Neurosci
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / HSP72 Heat-Shock Proteins; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / RNA, Messenger; 0 / Receptors, AMPA; 0 / glutamate receptor ionotropic, AMPA 1; 0 / glutamate receptor ionotropic, AMPA 2
  • [Other-IDs] NLM/ PMC3407487
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21. Julian GS, de Oliveira RW, Perry JC, Tufik S, Chagas JR: Validation of housekeeping genes in the brains of rats submitted to chronic intermittent hypoxia, a sleep apnea model. PLoS One; 2014;9(10):e109902
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  • [Title] Validation of housekeeping genes in the brains of rats submitted to chronic intermittent hypoxia, a sleep apnea model.
  • Obstructive sleep apnea (OSA) is a syndrome characterized by intermittent nocturnal hypoxia, sleep fragmentation, hypercapnia and respiratory effort, and it has been associated with several complications, such as diabetes, hypertension and obesity.
  • Quantitative real-time PCR has been performed in previous OSA-related studies; however, these studies were not validated using proper reference genes.
  • We have examined the effects of chronic intermittent hypoxia (CIH), which is an experimental model mainly of cardiovascular consequences of OSA, on reference genes, including beta-actin, beta-2-microglobulin, glyceraldehyde-3-phosphate dehydrogenase, hypoxanthine guanine phosphoribosyl transferase and eukaryotic 18S rRNA, in different areas of the brain.

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  • (PMID = 25289636.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC4188622
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22. Park SY, Kim SM, Sung JJ, Lee KM, Park KS, Kim SY, Nam HW, Lee KW: Nocturnal hypoxia in ALS is related to cognitive dysfunction and can occur as clusters of desaturations. PLoS One; 2013;8(9):e75324
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  • [Title] Nocturnal hypoxia in ALS is related to cognitive dysfunction and can occur as clusters of desaturations.
  • Consequently, most patients with ALS exhibit progressive hypoventilation, which worsens during sleep.
  • The aim of this study was to evaluate the relationship between nocturnal hypoxia and cognitive dysfunction and to assess the pattern of nocturnal hypoxia in patients with ALS.
  • Patients were grouped according to the presence of nocturnal hypoxia (SpO2<95% for ≥10% of the night) and their clinical characteristics and cognitive function were compared.
  • RESULTS: Compared to patients without nocturnal hypoxia, those with nocturnal hypoxia (n = 10, 40%) had poor memory retention (p = 0.039) and retrieval efficiency (p = 0.045).
  • A cluster-of-desaturation pattern was identified in 7 patients (70%) in the Hypoxia Group.
  • CONCLUSIONS: These results suggest that nocturnal hypoxia can be related to cognitive dysfunction in ALS.
  • In addition, a considerable number of patients with ALS may be exposed to repeated episodes of deoxygenation-reoxygenation (a cluster-of-desaturation pattern) during sleep, which could be associated with the generation of reactive oxygen species.

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  • (PMID = 24058674.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC3776791
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23. Perry JC, Guindalini C, Bittencourt L, Garbuio S, Mazzotti DR, Tufik S: Whole blood hypoxia-related gene expression reveals novel pathways to obstructive sleep apnea in humans. Respir Physiol Neurobiol; 2013 Dec 1;189(3):649-54
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Whole blood hypoxia-related gene expression reveals novel pathways to obstructive sleep apnea in humans.
  • In this study, our goal was to identify the key genes that are associated with obstructive sleep apnea (OSA).
  • Thirty-five volunteers underwent full in-lab polysomnography and, according to the sleep apnea hypopnea index (AHI), were classified into control, mild-to-moderate OSA and severe OSA groups.
  • [MeSH-major] Gene Expression Regulation / physiology. Sleep Apnea, Obstructive / metabolism

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  • [Copyright] Copyright © 2013 Elsevier B.V. All rights reserved.
  • (PMID = 23994550.001).
  • [ISSN] 1878-1519
  • [Journal-full-title] Respiratory physiology & neurobiology
  • [ISO-abbreviation] Respir Physiol Neurobiol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / PRPF40A protein, human; 0 / RNA, Messenger; EC 1.14.11.4 / Procollagen-Lysine, 2-Oxoglutarate 5-Dioxygenase
  • [Keywords] NOTNLM ; CPAP / Gene expression / Hypoxia / Obstructive sleep apnea / Sleep
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24. Minville C, Hilleret MN, Tamisier R, Aron-Wisnewsky J, Clement K, Trocme C, Borel JC, Lévy P, Zarski JP, Pépin JL: Nonalcoholic fatty liver disease, nocturnal hypoxia, and endothelial function in patients with sleep apnea. Chest; 2014 Mar 1;145(3):525-33
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  • [Title] Nonalcoholic fatty liver disease, nocturnal hypoxia, and endothelial function in patients with sleep apnea.
  • BACKGROUND: Nocturnal hypoxia, the hallmark of OSA, is a potential contributing factor for nonalcoholic fatty liver disease (NAFLD).
  • NAFLD severity and its implication in OSA-related endothelial dysfunction have not been investigated in a large, unselected OSA population, including nonobese subjects.
  • The dose-response relationship between the severity of nocturnal hypoxia and liver injury was established only in morbid obesity and not in lean.
  • CONCLUSIONS: In a large, unselected OSA population, the severity of nocturnal hypoxia was independently associated with steatosis.
  • [MeSH-major] Anoxia / complications. Endothelium, Vascular / physiopathology. Fatty Liver / etiology. Sleep Apnea, Obstructive / complications. Vasodilation / physiology

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  • [CommentIn] Chest. 2014 Aug;146(2):e67-8 [25091773.001]
  • [CommentIn] Chest. 2014 Aug;146(2):e67 [25091772.001]
  • (PMID = 24264333.001).
  • [ISSN] 1931-3543
  • [Journal-full-title] Chest
  • [ISO-abbreviation] Chest
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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25. Palma JA, Urrestarazu E, Lopez-Azcarate J, Alegre M, Fernandez S, Artieda J, Iriarte J: Increased sympathetic and decreased parasympathetic cardiac tone in patients with sleep related alveolar hypoventilation. Sleep; 2013 Jun;36(6):933-40
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  • [Title] Increased sympathetic and decreased parasympathetic cardiac tone in patients with sleep related alveolar hypoventilation.
  • OBJECTIVE: To assess autonomic function by heart rate variability (HRV) during sleep in patients with sleep related alveolar hypoventilation (SRAH) and to compare it with that of patients with obstructive sleep apnea (OSA) and control patients.
  • SETTING: Sleep Unit, University Hospital of University of Navarra.
  • PATIENTS: Fifteen idiopathic and obesity related-SRAH patients were studied.
  • MEASUREMENTS AND RESULTS: Time- and frequency-domain HRV measures (R-R, standard deviation of normal-to-normal RR interval [SDNN], very low frequency [VLF], low frequency [LF], high frequency [HF], LF/HF ratio) were calculated across all sleep stages as well as during wakefulness just before and after sleep during a 1-night polysomnography.
  • In patients with SRAH and OSA, LF was increased during rapid eye movement (REM) when compared with control patients, whereas HF was decreased during REM and N1-N2 sleep stages.
  • Correlation analysis showed that LF and HF values during REM sleep were correlated with minimal SatO2 and mean SatO2.
  • CONCLUSIONS: Patients with SRAH exhibited an abnormal cardiac tone during sleep.
  • This fact appears to be related to the severity of nocturnal oxygen desaturation.
  • Moreover, there were no differences between OSA and SRAH, supporting the hypothesis that autonomic changes in OSA are primarily related to a reduced nocturnal oxygen saturation, rather than a consequence of other factors such as nocturnal respiratory events.
  • [MeSH-major] Heart Rate / physiology. Sleep Apnea, Central / physiopathology
  • [MeSH-minor] Case-Control Studies. Cross-Sectional Studies. Female. Heart / innervation. Heart / physiology. Heart / physiopathology. Humans. Male. Middle Aged. Parasympathetic Nervous System / physiology. Parasympathetic Nervous System / physiopathology. Polysomnography. Sleep / physiology. Sleep Apnea, Obstructive / physiopathology. Sympathetic Nervous System / physiology. Sympathetic Nervous System / physiopathology

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  • (PMID = 23729937.001).
  • [ISSN] 1550-9109
  • [Journal-full-title] Sleep
  • [ISO-abbreviation] Sleep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC3648676
  • [Keywords] NOTNLM ; Autonomic nervous system / heart rate variability / hypoxia / obesity hypoventilation syndrome / sleep apnea / sleep disordered breathing
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26. Han Q, Yeung SC, Ip MS, Mak JC: Cellular mechanisms in intermittent hypoxia-induced cardiac damage in vivo. J Physiol Biochem; 2014 Mar;70(1):201-13
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  • [Title] Cellular mechanisms in intermittent hypoxia-induced cardiac damage in vivo.
  • Obstructive sleep apnea (OSA), characterized by intermittent hypoxia (IH) during sleep, is increasingly recognized as an independent risk factor of cardiovascular diseases.
  • [MeSH-minor] Adiponectin / blood. Animals. Apoptosis. Cell Hypoxia. Chemokine CXCL1 / blood. Heme Oxygenase-1 / metabolism. Interleukin-6 / metabolism. Male. Malondialdehyde / blood. NF-E2-Related Factor 2 / metabolism. Rats. Rats, Sprague-Dawley. Sleep Apnea, Obstructive / blood. Sleep Apnea, Obstructive / pathology. Troponin I / metabolism. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 24122132.001).
  • [ISSN] 1877-8755
  • [Journal-full-title] Journal of physiology and biochemistry
  • [ISO-abbreviation] J. Physiol. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Adiponectin; 0 / Chemokine CXCL1; 0 / Cxcl1 protein, rat; 0 / Interleukin-6; 0 / NF-E2-Related Factor 2; 0 / Nfe2l2 protein, rat; 0 / Troponin I; 0 / Tumor Necrosis Factor-alpha; 4Y8F71G49Q / Malondialdehyde; EC 1.14.99.3 / Heme Oxygenase-1
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27. Chai LP, Xie X, Zeng YH, Wang ZF, Tu XP: [Rapid eye movement-related and none rapid eye movement-related classification in obstructive sleep apnea hypopnea syndrome]. Zhonghua Er Bi Yan Hou Tou Jing Wai Ke Za Zhi; 2010 Feb;45(2):105-10
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  • [Title] [Rapid eye movement-related and none rapid eye movement-related classification in obstructive sleep apnea hypopnea syndrome].
  • OBJECTIVE: To study the value of a new measurement that divided obstructive sleep apnea-hypopnea syndrome (OSAHS) into rapid-eye-movement (REM) related and non-rapid-eye-movement (NREM) related subgroups.
  • METHODS: According to Siddiqui classification, 137 adult patients with OSHAS were diagnosed as REM-related OSAHS [REM apnea hypopnea index (AHI)/NREM AHI > 1] or NREM-related OSAHS (REM AHI/NREM AHI < 1).
  • (1) There were 72 cases defined as REM-related OSAHS (52.6%) and 65 cases defined as NREM-related OSAHS (47.4%). (2) In all cases, total AHI and NREM AHI in REM-related OSAHS were significantly lower than those in NREM-related OSAHS, while lowest arterial oxygen saturation (LSaO₂), REM LSaO₂ and NREM LSaO₂ were significantly higher than those in NREM-related OSAHS (t were -6.466, -7.638, 3.426, 2.472, 4.873 respectively, P < 0.05).
  • No significance was found in sleep structure, REM AHI and REM LSaO₂ between REM-related and NREM-related OSAHS (P > 0.05). (3) Given the severity of OSHAS, the constituent ratio of REM-related OSAHS decreased (77.8%, 61.5%, 37.3%) from mild to severe OSAHS, while that of NREM-related OSAHS rose (22.7%, 38.5%, 62.7%; chi² = 16.996, P < 0.01).
  • In mild and moderate groups, REM LSaO₂ of REM-related OSAHS was significantly lower than those in NREM-related OSAHS (t were -4.273 and -2.136, P < 0.05), while the differences of total AHI and LSaO₂, NREM LSaO₂ between these two types were not significant.
  • In severe group, AHI in NREM-related OSAHS was significantly higher than that in REM-related OSAHS, while LSaO₂, REM LSaO₂ and NREM LSaO₂ was significantly lower than those in REM-related OASHS (t were -4.943, 2.574, 1.996, 3.571, P ≤ 0.05). (4) There was no significance in sleeping latency and efficiency between REM-related and NREM-related OSHAS.
  • CONCLUSIONS: REM-related OSHAS mainly exists in mild and moderate OSHAS, while NREM-related one mainly exists in severe OSHAS.
  • NREM-related OSAHS may be more severe in AHI and hypoxia than REM-related one.
  • Whenever obstructive apnea happened in REM or NREM period, its impacts on sleep structure, efficiency and latency have no difference.
  • [MeSH-major] Sleep Apnea, Obstructive / classification. Sleep, REM
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Humans. Male. Middle Aged. Polysomnography. Sleep Stages. Young Adult

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  • (PMID = 20398503.001).
  • [ISSN] 1673-0860
  • [Journal-full-title] Zhonghua er bi yan hou tou jing wai ke za zhi = Chinese journal of otorhinolaryngology head and neck surgery
  • [ISO-abbreviation] Zhonghua Er Bi Yan Hou Tou Jing Wai Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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28. Hui-guo L, Kui L, Yan-ning Z, Yong-jian X: Apocynin attenuate spatial learning deficits and oxidative responses to intermittent hypoxia. Sleep Med; 2010 Feb;11(2):205-12
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  • [Title] Apocynin attenuate spatial learning deficits and oxidative responses to intermittent hypoxia.
  • RATIONALE: The long-term intermittent hypoxia (LTIH) that characterizes sleep-disordered breathing impairs spatial learning and increases oxidative stress in rodents.
  • In untreated animals, LTIH exposure was related to increase of MDA levels in comparison to sham LTIH animals, and apocynin-treated animal exposure to LTIH showed reduction in MDA levels.
  • NADPH oxidase up-expression is closely associated with oxidative processes in LTIH rats, and inhibition of NADPH oxidase activity may hopefully serve as a useful strategy for cognitive function impairment from chronic intermittent hypoxia.

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  • [Copyright] 2009 Elsevier B.V. All rights reserved.
  • (PMID = 20083433.001).
  • [ISSN] 1878-5506
  • [Journal-full-title] Sleep medicine
  • [ISO-abbreviation] Sleep Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Acetophenones; 4Y8F71G49Q / Malondialdehyde; B6J7B9UDTR / acetovanillone; EC 1.15.1.1 / Superoxide Dismutase; EC 1.6.3.1 / NADPH Oxidase; EC 1.6.3.1 / neutrophil cytosolic factor 1; EC 1.6.3.1 / p22-phox protein, rat
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29. Johansson P, Svensson E, Alehagen U, Dahlström U, Jaarsma T, Broström A: Sleep disordered breathing, hypoxia and inflammation: associations with sickness behaviour in community dwelling elderly with and without cardiovascular disease. Sleep Breath; 2015 Mar;19(1):263-71
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  • [Title] Sleep disordered breathing, hypoxia and inflammation: associations with sickness behaviour in community dwelling elderly with and without cardiovascular disease.
  • BACKGROUND: Inflammation can induce a cluster of symptoms, referred to as sickness behaviour (e.g., depressive symptoms, sleep disturbances, pain and fatigue).
  • Cardiovascular disease (CVD) and sleep disordered breathing (SDB) are common in older adults.
  • CVD is associated with an increased inflammatory activity and in SDB, hypoxia can also increase inflammation.
  • The purpose of this study is to explore if SDB-related hypoxia is associated differently with inflammation and the presence of sickness behaviour in older adults with and without CVD.
  • METHODS: Three hundred and thirty-one older adults, whose mean age is 78 years, underwent one-night polygraphic recording to measure SDB and hypoxia.
  • RESULTS: Structural Equation Modelling showed that SDB-related hypoxia was associated with inflammation (β > 0.40) which mediated indirect associations with sickness behaviour (β = 0.19) and depressive symptoms (β = 0.11), but only in those with CVD (n = 119).
  • Hypoxia had the strongest effect (i.e., β = 0.41; significant) on inflammation, whereas the AHI or ODI had weak and non-significant effects (β = 0.03 and β = 0.15).
  • The effect of SDB was mainly caused by hypoxia, suggesting that hypoxia is an important marker of SDB severity in older adults with CVD.

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  • (PMID = 24859483.001).
  • [ISSN] 1522-1709
  • [Journal-full-title] Sleep & breathing = Schlaf & Atmung
  • [ISO-abbreviation] Sleep Breath
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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30. Vernet C, Redolfi S, Attali V, Konofal E, Brion A, Frija-Orvoen E, Pottier M, Similowski T, Arnulf I: Residual sleepiness in obstructive sleep apnoea: phenotype and related symptoms. Eur Respir J; 2011 Jul;38(1):98-105
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  • [Title] Residual sleepiness in obstructive sleep apnoea: phenotype and related symptoms.
  • 40 apnoeic patients, with (n = 20) and without (n = 20) RES, and 20 healthy controls underwent clinical interviews, cognitive and biological tests, polysomnography, a multiple sleep latency test, and 24-h sleep monitoring.
  • The marked subjective sleepiness in the RES group (mean ± sd score 16.4 ± 3) contrasted with moderately abnormal objective measures of sleepiness (90% of patients with RES had daytime sleep latencies >8 min).
  • Compared with patients without RES, the patients with RES had more fatigue, lower stage N3 percentages, more periodic leg movements (without arousals), lower mean sleep latencies and longer daytime sleep periods.
  • The association between RES, periodic leg movements, apathy and depressive mood parallels the post-hypoxic lesions in noradrenaline, dopamine and serotonin systems in animals exposed to intermittent hypoxia.
  • [MeSH-major] Disorders of Excessive Somnolence / diagnosis. Sleep Apnea, Obstructive / diagnosis
  • [MeSH-minor] Adult. Aged. Anoxia. Case-Control Studies. Fatigue. Female. France. Humans. Male. Middle Aged. Phenotype. Polysomnography. Sleep. Sleep Stages. Time Factors

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  • [CommentIn] Eur Respir J. 2011 Jul;38(1):7-8 [21719496.001]
  • [CommentIn] Eur Respir J. 2012 Jan;39(1):226-7; author reply 227-8 [22210820.001]
  • (PMID = 21406511.001).
  • [ISSN] 1399-3003
  • [Journal-full-title] The European respiratory journal
  • [ISO-abbreviation] Eur. Respir. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
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31. Almendros I, Wang Y, Becker L, Lennon FE, Zheng J, Coats BR, Schoenfelt KS, Carreras A, Hakim F, Zhang SX, Farré R, Gozal D: Intermittent hypoxia-induced changes in tumor-associated macrophages and tumor malignancy in a mouse model of sleep apnea. Am J Respir Crit Care Med; 2014 Mar 1;189(5):593-601
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  • [Title] Intermittent hypoxia-induced changes in tumor-associated macrophages and tumor malignancy in a mouse model of sleep apnea.
  • RATIONALE: An increased cancer aggressiveness and mortality have been recently reported among patients with obstructive sleep apnea (OSA).
  • Intermittent hypoxia (IH), a hallmark of OSA, enhances melanoma growth and metastasis in mice.
  • OBJECTIVES: To assess whether OSA-related adverse cancer outcomes occur via IH-induced changes in host immune responses, namely tumor-associated macrophages (TAMs).
  • [MeSH-major] Anoxia / immunology. Lung Neoplasms / pathology. Macrophages / pathology. Melanoma, Experimental / pathology. Sleep Apnea, Obstructive / physiopathology

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  • (PMID = 24471484.001).
  • [ISSN] 1535-4970
  • [Journal-full-title] American journal of respiratory and critical care medicine
  • [ISO-abbreviation] Am. J. Respir. Crit. Care Med.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / HL-086662; United States / NHLBI NIH HHS / HL / HL-107160; United States / NHLBI NIH HHS / HL / HL-65270; United States / NIDDK NIH HHS / DK / T32 DK087703
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC3977714
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32. Donovan L, Welford SM, Haaga J, LaManna J, Strohl KP: Hypoxia--implications for pharmaceutical developments. Sleep Breath; 2010 Dec;14(4):291-8
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  • [Title] Hypoxia--implications for pharmaceutical developments.
  • Lowered oxygen availability (hypoxia) is theoretically important in the consideration of pharmacology because (1) hypoxia can alter cellular function and thereby the therapeutic effectiveness of the agent, (2) therapeutic agents may potentiate or protect against hypoxia-induced pathology, (3) hypoxic conditions may potentiate or mitigate drug-induced toxicity, (4) hypoxia may alter drug metabolism and thereby therapeutic effectiveness, and (5) therapeutic agents might alter the relative coupling of blood flow and energy metabolism in an organ.
  • The prototypic biochemical effect of hypoxia is related to its known role as a cofactor in a number of enzymatic reactions, e.g., oxidases and oxygenases, which are affected independently from the bioenergetic effect of low oxygen on energetic functions.
  • With chronic hypoxia, many of these processes are reversed, suggesting that hypoxia induces the drug-metabolizing systems.
  • Support for this comes from observations that hypoxia can induce the hypoxic inducible factors which in turn alters transcription and function of some but not all cytochrome P-450 isoforms.
  • Hypoxia is identified as a cofactor in cancer expression and metastatic potential.
  • Thus, the effects of hypoxia play an important role in pharmacology, and the signaling pathways that are affected by hypoxia could become new targets for novel therapy or avenues for prevention.
  • [MeSH-minor] Biotransformation / physiology. Cell Hypoxia / physiology. Cytochrome P-450 Enzyme System / physiology. Cytochromes c / physiology. Humans. Inactivation, Metabolic / physiology

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  • (PMID = 20625934.001).
  • [ISSN] 1522-1709
  • [Journal-full-title] Sleep & breathing = Schlaf & Atmung
  • [ISO-abbreviation] Sleep Breath
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / R33 HL087340; United States / NHLBI NIH HHS / HL / R33 HL087340-01A1
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 9007-43-6 / Cytochromes c; 9035-51-2 / Cytochrome P-450 Enzyme System
  • [Other-IDs] NLM/ NIHMS223042; NLM/ PMC3236526
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33. Nespoulet H, Wuyam B, Tamisier R, Saunier C, Monneret D, Remy J, Chabre O, Pépin JL, Lévy P: Altitude illness is related to low hypoxic chemoresponse and low oxygenation during sleep. Eur Respir J; 2012 Sep;40(3):673-80
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Altitude illness is related to low hypoxic chemoresponse and low oxygenation during sleep.
  • We compared 12 AMS-susceptible individuals with recurrent and severe symptoms (AMS+) with 12 "AMS-nonsusceptible" subjects (AMS-), assessing sleep-breathing disorders in simulated altitude as well as chemoresponsive and pulmonary vasoconstrictive responses to hypoxia.
  • During exposure to simulated altitude, mean blood oxygen saturation during sleep was lower in AMS+ subjects (81.6 ± 2.6 versus 86.0 ± 2.4%, p<0.01), associated with a lower central apnoea/hypopnoea index (18.2 ± 18.1 versus 33.4 ± 24.8 events · h(-1) in AMS+ and AMS- subjects, respectively; p=0.038).
  • This represented the only significant and independent predictive factor for altitude intolerance, despite a higher increase in pulmonary artery systolic pressure in response to hypoxia, a lower lung diffusing capacity and a higher endothelin-1 level at baseline in AMS+ subjects (p<0.05).
  • AMS+ subjects were more hypoxaemic whilst exhibiting fewer respiratory events during sleep owing to lower hypoxic (isocapnic) chemoresponsiveness.
  • [MeSH-major] Altitude Sickness / physiopathology. Anoxia / physiopathology. Oxygen / blood. Sleep / physiology

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  • (PMID = 22523356.001).
  • [ISSN] 1399-3003
  • [Journal-full-title] The European respiratory journal
  • [ISO-abbreviation] Eur. Respir. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Endothelin-1; S88TT14065 / Oxygen
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34. Dale-Nagle EA, Hoffman MS, MacFarlane PM, Satriotomo I, Lovett-Barr MR, Vinit S, Mitchell GS: Spinal plasticity following intermittent hypoxia: implications for spinal injury. Ann N Y Acad Sci; 2010 Jun;1198:252-9
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  • [Title] Spinal plasticity following intermittent hypoxia: implications for spinal injury.
  • One frequently studied model of respiratory plasticity is long-term facilitation of phrenic motor output (pLTF) following acute intermittent hypoxia (AIH).
  • pLTF arises from spinal plasticity, increasing respiratory motor output through a mechanism that requires new synthesis of brain-derived neurotrophic factor, activation of its high-affinity receptor, tropomyosin-related kinase B, and extracellular-related kinase mitogen-activated protein kinase signaling in or near phrenic motor neurons.
  • Because intermittent hypoxia induces spinal plasticity, we are exploring the potential to harness repetitive AIH as a means of inducing functional recovery in conditions causing respiratory insufficiency, such as cervical spinal injury.
  • [MeSH-minor] Animals. Brain-Derived Neurotrophic Factor / physiology. Cervical Vertebrae / injuries. Enzyme Activation. Humans. Hypertension / etiology. Learning Disorders / etiology. Learning Disorders / physiopathology. Phrenic Nerve / physiology. Phrenic Nerve / physiopathology. Protein Kinase C / metabolism. Rats. Receptors, Serotonin, 5-HT2 / physiology. Respiratory Physiological Phenomena. Sleep Disorders / etiology. Sleep Disorders / physiopathology

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  • (PMID = 20536940.001).
  • [ISSN] 1749-6632
  • [Journal-full-title] Annals of the New York Academy of Sciences
  • [ISO-abbreviation] Ann. N. Y. Acad. Sci.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / F31 HL092785; United States / NHLBI NIH HHS / HL / F31 HL092785-02; United States / NHLBI NIH HHS / HL / HL69064; United States / NHLBI NIH HHS / HL / HL80209; United States / NINDS NIH HHS / NS / NS05777; United States / NINDS NIH HHS / NS / P01 NS057778; United States / NINDS NIH HHS / NS / P01 NS057778-05; United States / NHLBI NIH HHS / HL / R01 HL080209; United States / NHLBI NIH HHS / HL / R01 HL080209-06; United States / NHLBI NIH HHS / HL / R37 HL069064; United States / NHLBI NIH HHS / HL / R37 HL069064-10; United States / NHLBI NIH HHS / HL / T32 HL007654; United States / NHLBI NIH HHS / HL / T32 HL007654-25; United States / NHLBI NIH HHS / HL / T32HL07654
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Brain-Derived Neurotrophic Factor; 0 / Receptors, Serotonin, 5-HT2; EC 2.7.11.13 / Protein Kinase C
  • [Number-of-references] 60
  • [Other-IDs] NLM/ NIHMS261289; NLM/ PMC3030965
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35. Stettner GM, Fenik VB, Kubin L: Effect of chronic intermittent hypoxia on noradrenergic activation of hypoglossal motoneurons. J Appl Physiol (1985); 2012 Jan;112(2):305-12
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  • [Title] Effect of chronic intermittent hypoxia on noradrenergic activation of hypoglossal motoneurons.
  • In obstructive sleep apnea patients, elevated activity of the lingual muscles during wakefulness protects the upper airway against occlusions.
  • A possibly related form of respiratory neuroplasticity is present in rats exposed to acute and chronic intermittent hypoxia (CIH).
  • [MeSH-major] Adrenergic Neurons / metabolism. Anoxia / physiopathology. Hypoglossal Nerve / physiology. Motor Neurons / physiology. Receptors, Adrenergic / metabolism. Sleep Apnea, Obstructive

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  • (PMID = 22016369.001).
  • [ISSN] 1522-1601
  • [Journal-full-title] Journal of applied physiology (Bethesda, Md. : 1985)
  • [ISO-abbreviation] J. Appl. Physiol.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / HL-047600
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenergic alpha-1 Receptor Antagonists; 0 / Receptors, Adrenergic; X4W3ENH1CV / Norepinephrine; XM03YJ541D / Prazosin
  • [Other-IDs] NLM/ PMC3349609
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36. da Rosa DP, Forgiarini LF, e Silva MB, Fiori CZ, Andrade CF, Martinez D, Marroni NP: Antioxidants inhibit the inflammatory and apoptotic processes in an intermittent hypoxia model of sleep apnea. Inflamm Res; 2015 Jan;64(1):21-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Antioxidants inhibit the inflammatory and apoptotic processes in an intermittent hypoxia model of sleep apnea.
  • BACKGROUND: Sleep apnea causes intermittent hypoxia (IH).
  • We aimed to investigate the proteins related to oxidative stress, inflammation and apoptosis in liver tissue subjected to IH as a simulation of sleep apnea in conjunction with the administration of either melatonin (MEL, 200 μL/kg) or N-acetylcysteine (NAC, 10 mg/kg).
  • The animals were subjected to simulations of sleep apnea for 8 h a day for 35 days.

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  • (PMID = 25380745.001).
  • [ISSN] 1420-908X
  • [Journal-full-title] Inflammation research : official journal of the European Histamine Research Society ... [et al.]
  • [ISO-abbreviation] Inflamm. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
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37. Faiz SA, Balachandran D, Hessel AC, Lei X, Beadle BM, William WN Jr, Bashoura L: Sleep-related breathing disorders in patients with tumors in the head and neck region. Oncologist; 2014 Nov;19(11):1200-6
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  • [Title] Sleep-related breathing disorders in patients with tumors in the head and neck region.
  • BACKGROUND: Sleep disturbance is a prominent complaint of cancer patients.
  • Most studies have focused on insomnia and cancer-related fatigue.
  • Obstructive sleep apnea (OSA) has been reported in small studies and case reports.
  • METHODS: In a retrospective review of patients who underwent formal sleep evaluation and polysomnography (PSG) from 2006 to 2011, 56 patients with tumors in the head and neck region were identified.
  • Clinical characteristics, sleep-related history, and PSG data were reviewed.
  • Significant sleep-related breathing disorder was noted in 93% of patients, and 84% met clinical criteria for OSA.
  • The majority of patients (79%) underwent radiation prior to sleep study, of which 88% had OSA, and in the group without prior radiation, 67% had OSA.
  • A subset of patients with persistent hypoxia despite advanced forms of PAP required tracheostomy.
  • CONCLUSION: Sleep-related breathing disorder was common in patients with tumors in the head and neck region referred for evaluation of sleep disruption, and most met clinical criteria for OSA.
  • A heightened clinical suspicion for sleep-related breathing disorder and referral to a sleep specialist would be beneficial for patients with these complaints.

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  • [Copyright] ©AlphaMed Press.
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  • [ISO-abbreviation] Oncologist
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA016672; United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC4221368 [Available on 05/01/15]
  • [Keywords] NOTNLM ; Cancer / Head and neck squamous cell carcinoma / Head and neck tumors / Obstructive sleep apnea / Polysomnography / Radiation therapy / Sleep disruption / Sleep-related breathing disorder
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38. Angelo MF, Aguirre A, Avilés Reyes RX, Villarreal A, Lukin J, Melendez M, Vanasco V, Barker P, Alvarez S, Epstein A, Jerusalinsky D, Ramos AJ: The proinflammatory RAGE/NF-κB pathway is involved in neuronal damage and reactive gliosis in a model of sleep apnea by intermittent hypoxia. PLoS One; 2014;9(9):e107901
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  • [Title] The proinflammatory RAGE/NF-κB pathway is involved in neuronal damage and reactive gliosis in a model of sleep apnea by intermittent hypoxia.
  • Sleep apnea (SA) causes long-lasting changes in neuronal circuitry, which persist even in patients successfully treated for the acute effects of the disease.
  • Evidence obtained from the intermittent hypoxia (IH) experimental model of SA has shown neuronal death, impairment in learning and memory and reactive gliosis that may account for cognitive and structural alterations observed in human patients.
  • The Receptor for Advanced Glycation End products (RAGE) and its downstream effector Nuclear Factor Kappa B (NF-κB) have been related to neuronal death and astroglial conversion to the pro-inflammatory neurodegenerative phenotype.

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  • (PMID = 25265561.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC4180086
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39. Diogo LN, Monteiro EC: The efficacy of antihypertensive drugs in chronic intermittent hypoxia conditions. Front Physiol; 2014;5:361
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  • [Title] The efficacy of antihypertensive drugs in chronic intermittent hypoxia conditions.
  • Sleep apnea/hypopnea disorders include centrally originated diseases and obstructive sleep apnea (OSA).
  • The mechanisms involved in the pathogenesis of HT can be summarized in relation to two main pathways: sympathetic nervous system stimulation mediated mainly by activation of carotid body (CB) chemoreflexes and/or asphyxia, and, by no means the least important, the systemic effects of chronic intermittent hypoxia (CIH).
  • First, we explore the experimental animal models, developed to mimic HT related to CIH, which have been used to investigate the effect of antihypertensive drugs (AHDs).

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  • (PMID = 25295010.001).
  • [ISSN] 1664-042X
  • [Journal-full-title] Frontiers in physiology
  • [ISO-abbreviation] Front Physiol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Other-IDs] NLM/ PMC4170135
  • [Keywords] NOTNLM ; antihypertensive drugs / blood pressure / chronic intermittent hypoxia / hypertension / obstructive sleep apnea
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40. Davis EM, O'Donnell CP: Rodent models of sleep apnea. Respir Physiol Neurobiol; 2013 Sep 15;188(3):355-61
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  • [Title] Rodent models of sleep apnea.
  • Rodent models of sleep apnea have long been used to provide novel insight into the generation and predisposition to apneas as well as to characterize the impact of sleep apnea on cardiovascular, metabolic, and psychological health in humans.
  • Given the significant body of work utilizing rodent models in the field of sleep apnea, the aims of this review are three-fold: first, to review the use of rodents as natural models of sleep apnea; second, to provide an overview of the experimental interventions employed in rodents to simulate sleep apnea; third, to discuss the refinement of rodent models to further our understanding of breathing abnormalities that occur during sleep.
  • Given mounting evidence that sleep apnea impairs cognitive function, reduces quality of life, and exacerbates the course of multiple chronic diseases, rodent models will remain a high priority as a tool to interrogate both the pathophysiology and sequelae of breathing related abnormalities during sleep and to improve approaches to diagnosis and therapy.
  • [MeSH-major] Disease Models, Animal. Sleep Apnea Syndromes / physiopathology
  • [MeSH-minor] Animals. Anoxia / physiopathology. Cognition / physiology. Mice. Rats. Respiratory System / physiopathology. Rodentia. Sleep / physiology. Sleep Apnea, Obstructive / physiopathology

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  • [Copyright] Copyright © 2013 Elsevier B.V. All rights reserved.
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  • (PMID = 23722067.001).
  • [ISSN] 1878-1519
  • [Journal-full-title] Respiratory physiology & neurobiology
  • [ISO-abbreviation] Respir Physiol Neurobiol
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / T32 HL082610
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Other-IDs] NLM/ NIHMS569974; NLM/ PMC4010146
  • [Keywords] NOTNLM ; Breathing / Central sleep apnea / Intermittent hypoxia / Mice / Obstructive sleep apnea / Rats / Upper airway
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41. Rambaud C, Guilleminault C: Death, nasomaxillary complex, and sleep in young children. Eur J Pediatr; 2012 Sep;171(9):1349-58
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  • [Title] Death, nasomaxillary complex, and sleep in young children.
  • This is an investigation of anatomical and sleep history risk factors that were associated with abrupt sleep-associated death in seven children with good pre-mortem history.
  • Seven young children with abrupt deaths and information on health status, sleep history, death scene report, and autopsy performed in a specialized unit dedicated to investigation of abrupt death in young children were investigated Seven age and gender matched living children with obstructive-sleep-apnea (OSA) were compared to the findings obtained from the dead children.
  • History revealed presence of chronic indicators of abnormal sleep in all cases prior death and history of an acute, often mild, rhinitis just preceding death in several.
  • All children were concluded to have died of hypoxia during sleep.
  • Their presence should lead to greater attention to sleep-related complaints that may be present very early in life and indicate impairment of well been and presence of sleep disruption.
  • [MeSH-major] Anoxia / mortality. Death, Sudden / etiology. Maxilla / pathology. Nose / pathology. Sleep Apnea, Obstructive / complications

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  • (PMID = 22492014.001).
  • [ISSN] 1432-1076
  • [Journal-full-title] European journal of pediatrics
  • [ISO-abbreviation] Eur. J. Pediatr.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Germany
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42. Poulain L, Thomas A, Rieusset J, Casteilla L, Levy P, Arnaud C, Dematteis M: Visceral white fat remodelling contributes to intermittent hypoxia-induced atherogenesis. Eur Respir J; 2014 Feb;43(2):513-22
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Visceral white fat remodelling contributes to intermittent hypoxia-induced atherogenesis.
  • Obstructive sleep apnoea is a highly prevalent disease characterised by repetitive upper airway collapse during sleep leading to intermittent hypoxia.
  • Cardiometabolic complications of sleep apnoea have been mostly attributed to intermittent hypoxia.
  • These consequences could be mediated through intermittent hypoxia-related alterations of the visceral white fat, as it is recognised for playing an important role in inflammation, atherogenesis and insulin resistance.
  • Epididymal adipose tissue alterations were investigated in 20-week-old nonobese male apolipoprotein E-deficient mice exposed to intermittent hypoxia (inspiratory oxygen fraction 5-21%, 60-s cycle, 8 h · day(-1)) or air for 6 weeks.
  • These adipose tissue alterations, as well as metabolic alterations and aortic atherosclerosis, were then assessed in lipectomised or sham-operated mice exposed to intermittent hypoxia or air for 6 weeks.
  • Intermittent hypoxia induced morphological (shrunken adipocytes), functional (increased uncoupling protein-1 expression) and inflammatory (increased macrophage recruitment and secretion of interleukin-6 and tumour necrosis factor-α) remodelling of epididymal adipose tissue.
  • Epididymal lipectomy attenuated both intermittent hypoxia-induced dyslipidaemia and atherogenesis, but did not improve insulin sensitivity.
  • Our results confirmed that the dyslipidaemic and proatherogenic effects of intermittent hypoxia are partly mediated through morphological, functional and inflammatory remodelling of visceral white fat, regardless of obesity.

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  • (PMID = 24072212.001).
  • [ISSN] 1399-3003
  • [Journal-full-title] The European respiratory journal
  • [ISO-abbreviation] Eur. Respir. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Ccl2 protein, mouse; 0 / Chemokine CCL2; 0 / Ion Channels; 0 / Mitochondrial Proteins; 0 / mitochondrial uncoupling protein
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43. Xiang YH, Su XL, Hu CP, Luo YQ, He RX: [A study of the related pathways of oxidative stress in chronic intermittent hypoxia rats and the effect of N-acetylcysteine]. Zhonghua Jie He He Hu Xi Za Zhi; 2010 Dec;33(12):912-6
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  • [Title] [A study of the related pathways of oxidative stress in chronic intermittent hypoxia rats and the effect of N-acetylcysteine].
  • OBJECTIVE: To study the relation of oxidative stress with systolic blood pressure (SBP) and renin-agiotensin system (RAS) in a rat model of chronic intermittent hypoxia (CIH), and to investigate the preventive effect and mechanism of N-acetylcysteine (NAC) in CIH-induced hypertension.
  • CIH rats were subjected to alternating cycles of hypoxia (6%-8% O2 in N2 for 20-25 s) and normoxia (21% O2 in N2 for 2 min) every 180 s for 7 h per day.
  • The imbalance of RAS in CIH rats was related with oxidative stress.
  • [MeSH-minor] Animals. Blood Pressure. Male. Rats. Rats, Sprague-Dawley. Renin-Angiotensin System. Sleep Apnea, Obstructive / metabolism


44. Mukai T, Nagao Y, Nishioka S, Hayashi T, Shimizu S, Ono A, Sakagami Y, Watanabe S, Ueda Y, Hara M, Tokudome K, Kato R, Matsumura Y, Ohno Y: Preferential suppression of limbic Fos expression by intermittent hypoxia in obese diabetic mice. Neurosci Res; 2013 Dec;77(4):202-7
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  • [Title] Preferential suppression of limbic Fos expression by intermittent hypoxia in obese diabetic mice.
  • Sleep apnea (SA) causes not only sleep disturbances, but also neurocognitive impairments and/or psychoemotional disorders.
  • Here, we studied the effects of intermittent hypoxia (IH) on forebrain Fos expression using obese diabetic db/db mice to explore the pathophysiological alterations in neural activities and the brain regions related to SA syndrome.
  • The present results illustrate that SA in the obese diabetic model causes neural suppression preferentially in the limbic and paralimbic regions, which may be related to the neuropsychological disturbances associated with SA.
  • [MeSH-major] Anoxia / metabolism. Limbic System / metabolism. Proto-Oncogene Proteins c-fos / metabolism. Sleep Apnea Syndromes / metabolism

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  • [Copyright] Copyright © 2013. Published by Elsevier Ireland Ltd.
  • (PMID = 24144732.001).
  • [ISSN] 1872-8111
  • [Journal-full-title] Neuroscience research
  • [ISO-abbreviation] Neurosci. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins c-fos
  • [Keywords] NOTNLM ; Fos expression / IH / Intermittent hypoxia / Limbic system / SA / Sleep apnea / db/db mice / intermittent hypoxia / sleep apnea
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45. Fava C, Montagnana M, Favaloro EJ, Guidi GC, Lippi G: Obstructive sleep apnea syndrome and cardiovascular diseases. Semin Thromb Hemost; 2011 Apr;37(3):280-97
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  • [Title] Obstructive sleep apnea syndrome and cardiovascular diseases.
  • Obstructive sleep apnea syndrome (OSAS) is a chronic disease characterized by recurrent episodes of partial or complete upper airway collapse and obstruction during sleep, associated with intermittent oxygen desaturation, sleep fragmentation, and symptoms of disruptive snoring and daytime sleepiness.
  • Increasing focus is being placed on the relationship between OSAS and all-cause and cardiovascular disease-related mortality, but it still largely unclear whether this association is causative or simply speculative and epidemiological.
  • Although it is still unclear whether OSAS might represent an independent risk factor for several acute or chronic conditions, or rather might trigger cardiovascular disease in the presence of traditional cardiovascular risk factors (e.g., obesity, diabetes, and dyslipidemia), there is a plausible biological background underlying this association, in that most of the mechanisms implicated in the pathogenesis of OSAS (i.e., hypoxia, hypercapnia, negative intrathoracic pressure, micro-arousal, sympathetic hyperactivity, metabolic and hormonal changes, oxidative stress, phlogosis, endothelial dysfunction, hypercoagulability, and genetic predisposition) might also be involved in the pathogenesis of cardiovascular disorders.
  • [MeSH-major] Cardiovascular Diseases / etiology. Sleep Apnea, Obstructive / complications

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  • [Copyright] © Thieme Medical Publishers.
  • (PMID = 21455862.001).
  • [ISSN] 1098-9064
  • [Journal-full-title] Seminars in thrombosis and hemostasis
  • [ISO-abbreviation] Semin. Thromb. Hemost.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] IY9XDZ35W2 / Glucose
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46. Pérez-Rico C, Gutiérrez-Díaz E, Mencía-Gutiérrez E, Díaz-de-Atauri MJ, Blanco R: Obstructive sleep apnea-hypopnea syndrome (OSAHS) and glaucomatous optic neuropathy. Graefes Arch Clin Exp Ophthalmol; 2014 Sep;252(9):1345-57
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Obstructive sleep apnea-hypopnea syndrome (OSAHS) and glaucomatous optic neuropathy.
  • Obstructive sleep apnea-hypopnea syndrome (OSAHS) is becoming widely accepted as a risk factor for glaucoma.
  • We discuss the proposed mechanism involved in the pathogenesis of glaucoma in OSAHS, and review the published data on the association between these two conditions, as well as papers regarding functional and structural tests related with glaucomatous damage.
  • There is increasing evidence that the prevalence of glaucoma is higher in OSAHS patients, especially in those with severe disease with apnea-hypopnea index (AHI) >30, and also that sleep disorders may be more frequent in patients with glaucoma, especially in those with normal tension glaucoma (NTG).
  • Raised intraocular pressure (IOP), possibly related to increased body mass index, thinning of retinal nerve fiber layer (RNFL), and alteration of visual field (VF) indices has been demonstrated in many studies, in patients with no history of glaucoma or evidence of glaucomatous changes in the ophthalmic examination.
  • The pathogenesis of optic nerve involvement has been related to vascular and mechanical factors.
  • Vascular factors include recurrent hypoxia with increased vascular resistance, autonomic deregulation, oxidative stress and inflammation linked to hypoxia and subsequent reperfusion, decreased cerebral perfusion pressure and direct hypoxic damage to the optic nerve.
  • Proposed mechanical factors include increased IOP at night related to supine position and obesity, raised intracranial pressure and elastic fiber depletion in the lamina cribosa and/or trabeculum.
  • In conclusion, ophthalmic evaluation should be recommended in patients with severe OSAHS, and the presence of sleep disorders should be investigated in patients with glaucoma, especially in NTG patients and in those with progressive damage despite controlled IOP, as treatment with continuous positive airway pressure may contribute to stabilizing the progression of glaucomatous damage.
  • [MeSH-major] Glaucoma / complications. Optic Nerve Diseases / complications. Sleep Apnea, Obstructive / complications

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  • (PMID = 24859387.001).
  • [ISSN] 1435-702X
  • [Journal-full-title] Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv für klinische und experimentelle Ophthalmologie
  • [ISO-abbreviation] Graefes Arch. Clin. Exp. Ophthalmol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Germany
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47. Onen F, Onen H: [Obstructive sleep apnea and cognitive impairment in the elderly]. Psychol Neuropsychiatr Vieil; 2010 Sep;8(3):163-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Obstructive sleep apnea and cognitive impairment in the elderly].
  • Obstructive Sleep Apnea Syndrome (OSAS) is characterized by repeated episodes of upper airway obstruction during sleep that result in intermittent hypoxemia and arousal.
  • OSAS causes hypoxia, fragmented sleep, daytime sleepiness, cognitive dysfunction, functional decline, and brain damage resulting from reduced cerebral blood flow, ischemic brain lesions, microvascular reactivity, white matter lesions, and grey matter loss.
  • OSAS-related cognitive dysfunction has been shown in a variety of domains including attention, executive functioning, motor efficiency, working memory, and long-term episodic memory.
  • Proposed mechanisms include hypoxemia, sleep fragmentation and inflammatory process, but it remains unclear which mechanisms underlie the relationship between OSAS and disturbances in the different cognitive domains.
  • [MeSH-major] Cognition Disorders / etiology. Sleep Apnea, Obstructive / diagnosis
  • [MeSH-minor] Aged. Alzheimer Disease / diagnosis. Alzheimer Disease / epidemiology. Alzheimer Disease / etiology. Brain Damage, Chronic / complications. Brain Damage, Chronic / diagnosis. Brain Damage, Chronic / epidemiology. Continuous Positive Airway Pressure. Cross-Sectional Studies. Humans. Hypoxia, Brain / complications. Hypoxia, Brain / diagnosis. Hypoxia, Brain / epidemiology. Neuropsychological Tests

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  • (PMID = 20739254.001).
  • [ISSN] 1760-1703
  • [Journal-full-title] Psychologie & neuropsychiatrie du vieillissement
  • [ISO-abbreviation] Psychol Neuropsychiatr Vieil
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
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48. Lurie A: Endothelial dysfunction in adults with obstructive sleep apnea. Adv Cardiol; 2011;46:139-70
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Endothelial dysfunction in adults with obstructive sleep apnea.
  • There is convincing evidence for endothelial dysfunction in obstructive sleep apnea (OSA): OSA is associated with alterations in vascular structures and their elastic properties, increased circulating cell-derived microparticles, reduced endothelial repair capacity, and vascular reactivity.
  • These alterations may be related to the reduced availability of nitric oxide, which has major vasoprotective effects including vasodilation, inhibition of platelet adhesion and aggregation, inhibition of leukocyte-endothelial adhesion and inhibition of smooth muscle cell proliferation.
  • It is unknown whether endothelial dysfunction in OSA is due to alterations in vasoconstriction mechanisms related to angiotensin II or endothelin 1.
  • In OSA, endothelial dysfunction may be related to chronic intermittent hypoxia and to sleep loss and fragmentation.
  • [MeSH-major] Continuous Positive Airway Pressure. Endothelium, Vascular / physiopathology. Sleep Apnea, Obstructive / physiopathology. Sleep Apnea, Obstructive / therapy

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  • [Copyright] Copyright © 2011 S. Karger AG, Basel.
  • (PMID = 22005191.001).
  • [ISSN] 0065-2326
  • [Journal-full-title] Advances in cardiology
  • [ISO-abbreviation] Adv Cardiol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Biological Markers; 0 / Endothelin-1; 11128-99-7 / Angiotensin II; 31C4KY9ESH / Nitric Oxide
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49. Hanly PJ, Ahmed SB: Sleep apnea and the kidney: is sleep apnea a risk factor for chronic kidney disease? Chest; 2014 Oct;146(4):1114-22
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Sleep apnea and the kidney: is sleep apnea a risk factor for chronic kidney disease?
  • Although this phenomenon has been attributed to the growth in diabetes, hypertension, and obesity, sleep apnea and nocturnal hypoxemia may also contribute to the pathogenesis of CKD and its progression to kidney failure.
  • Two pathophysiologic mechanisms responsible for CKD are glomerular hyperfiltration and chronic intrarenal hypoxia, resulting in tubulointerstitial injury, the final common pathway to end-stage kidney disease (ESKD).
  • Multiple descriptive studies have demonstrated an association between CKD and sleep apnea.
  • Although sleep apnea is common in patients with CKD and associated with significant nocturnal hypoxemia, it is often relatively free of sleep-related symptoms, making it difficult to detect without objective nocturnal monitoring.
  • Nevertheless, sleep apnea and nocturnal hypoxemia have been associated with loss of kidney function and kidney injury, suggesting that they contribute to the pathogenesis of continued deterioration in kidney function.
  • There are several pathways through which sleep apnea may achieve this, including a direct effect of intrarenal hypoxia and activation of the systemic and renal renin-angiotensin system.
  • Further research is required to better understand these relationships and determine whether specific interventions in patients with sleep apnea have an impact on clinical outcomes, such as reducing the prevalence of CKD and delaying its progression to ESKD.
  • [MeSH-major] Kidney / physiopathology. Renal Insufficiency, Chronic / etiology. Sleep Apnea Syndromes / complications


50. Gonzalez-Martín MC, Vega-Agapito MV, Conde SV, Castañeda J, Bustamante R, Olea E, Perez-Vizcaino F, Gonzalez C, Obeso A: Carotid body function and ventilatory responses in intermittent hypoxia. Evidence for anomalous brainstem integration of arterial chemoreceptor input. J Cell Physiol; 2011 Aug;226(8):1961-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Carotid body function and ventilatory responses in intermittent hypoxia. Evidence for anomalous brainstem integration of arterial chemoreceptor input.
  • Obstructive sleep apnea is a frequent medical condition consisting in repetitive sleep-related episodes of upper airways obstruction and concurrent events of arterial blood hypoxia.
  • There is a frequent association of cardiovascular diseases and other pathologies to this condition conforming the obstructive sleep apnea syndrome (OSAS).
  • Laboratory models of OSAS consist in animals exposed to repetitive episodes of intermittent hypoxia (IH) which also develop cardiovascular pathologies, mostly hypertension.
  • The overall OSAS pathophysiology appears to be linked to the repetitive hypoxia, which would cause a sensitization of carotid body (CB) chemoreflex and chemoreflex-driven hyperreactivity of the sympathetic nervous system.
  • The efferent activity was measured as ventilation in normoxia, hypoxia, and hypercapnia.
  • Findings indicate a sensitization of the CB function to hypoxia evidenced by exaggerated chemoreceptor cell and CB afferent activity.
  • [MeSH-minor] Animals. Hypercapnia / physiopathology. Hypertension / physiopathology. Male. Norepinephrine / metabolism. Norepinephrine / physiology. Rats. Rats, Wistar. Renal Artery / physiopathology. Sleep Apnea, Obstructive / physiopathology. Sympathetic Nervous System / physiopathology

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  • [Copyright] Copyright © 2010 Wiley-Liss, Inc.
  • (PMID = 21520047.001).
  • [ISSN] 1097-4652
  • [Journal-full-title] Journal of cellular physiology
  • [ISO-abbreviation] J. Cell. Physiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] X4W3ENH1CV / Norepinephrine
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