The latest medical research on Sleep Medicine

The research magnet gathers the latest research from around the web, based on your specialty area. Below you will find a sample of some of the most recent articles from reputable medical journals about sleep medicine gathered by our medical AI research bot.

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The COVID-19 pandemic and sleep medicine: a look back and a look ahead.

J Clin Sleep

The COVID-19 pandemic is a reminder that global infectious disease outbreaks are not new, and they have the potential to cause catastrophic morbidi...

Targeting the human βc receptor inhibits inflammatory myeloid cells and lung injury caused by acute cigarette smoke exposure.


Chronic obstructive pulmonary disease (COPD) is a devastating disease commonly caused by cigarette smoke (CS) exposure that drives tissue injury by persistently recruiting myeloid cells into the lungs. A significant portion of COPD patients also present with overlapping asthma pathology including eosinophilic inflammation. The βc cytokine family includes granulocyte monocyte-colony-stimulating factor, IL-5 and IL-3 that signal through their common receptor subunit βc to promote the expansion and survival of multiple myeloid cells including monocytes/macrophages, neutrophils and eosinophils.

We have used our unique human βc receptor transgenic (hβc Tg) mouse strain that expresses human βc instead of mouse βc and βIL3 in an acute CS exposure model. Lung tissue injury was assessed by histology and measurement of albumin and lactate dehydrogenase levels in the bronchoalveolar lavage (BAL) fluid. Transgenic mice were treated with an antibody (CSL311) that inhibits human βc signalling.

hβc Tg mice responded to acute CS exposure by expanding blood myeloid cell numbers and recruiting monocyte-derived macrophages (cluster of differentiation 11b+ [CD11b+ ] interstitial and exudative macrophages [IM and ExM]), neutrophils and eosinophils into the lungs. This inflammatory response was associated with lung tissue injury and oedema. Importantly, CSL311 treatment in CS-exposed mice markedly reduced myeloid cell numbers in the blood and BAL compartment. Furthermore, CSL311 significantly reduced lung CD11b+ IM and ExM, neutrophils and eosinophils, and this decline was associated with a significant reduction in matrix metalloproteinase-12 (MMP-12) and IL-17A expression, tissue injury and oedema.

This study identifies CSL311 as a therapeutic antibody that potently inhibits immunopathology and lung injury caused by acute CS exposure.

Examining the impact of multilevel upper airway surgery on the obstructive sleep apnoea endotypes and their utility in predicting surgical outcomes.


Upper airway surgery for obstructive sleep apnoea (OSA) is an alternative treatment for patients who are intolerant of continuous positive airway pressure (CPAP). However, upper airway surgery has variable treatment efficacy with no reliable predictors of response. While we now know that there are several endotypes contributing to OSA (i.e., upper airway collapsibility, airway muscle response/compensation, respiratory arousal threshold and loop gain), no study to date has examined: (i) how upper airway surgery affects all four OSA endotypes, (ii) whether knowledge of baseline OSA endotypes predicts response to surgery and (iii) whether there are any differences when OSA endotypes are measured using the CPAP dial-down or clinical polysomnographic (PSG) methods.

We prospectively studied 23 OSA patients before and ≥3 months after multilevel upper airway surgery. Participants underwent clinical and research PSG to measure OSA severity (apnoea-hypopnoea index [AHI]) and endotypes (measured in supine non-rapid eye movement [NREM]). Values are presented as mean ± SD or median (interquartile range).

Surgery reduced the AHITotal (38.7 [23.4 to 79.2] vs. 22.0 [13.3 to 53.5] events/h; p = 0.009). There were no significant changes in OSA endotypes, however, large but variable improvements in collapsibility were observed (CPAP dial-down method: ∆1.9 ± 4.9 L/min, p = 0.09, n = 21; PSG method: ∆3.4 [-2.8 to 49.0]%Veupnoea , p = 0.06, n = 20). Improvement in collapsibility strongly correlated with improvement in AHI (%∆AHISupineNREM vs. ∆collapsibility: p < 0.005; R2  = 0.46-0.48). None of the baseline OSA endotypes predicted response to surgery.

Surgery unpredictably alters upper airway collapsibility but does not alter the non-anatomical endotypes. There are no baseline predictors of response to surgery.

Discrepancy between subjective and objective sleep duration among dementia caregivers and non-caregivers.

J Clin Sleep

Poor sleep, including short sleep duration, is common among caregivers of persons with dementia. However, it is unclear whether poor sleep is consistent across both self-reported and objective measures of sleep in caregivers. This study aimed to test the role of caregiving status (caregivers vs. non-caregivers) on the discrepancy between self-reported and objective sleep duration.

This was a cross-sectional study. Study participants were community-dwelling caregivers of spouses with dementia (n=122) and non-caregivers (n=53). A sleep duration discrepancy index was created by subtracting objective sleep duration measured with three consecutive 24-hour periods of actigraphy from self-reported sleep duration measured with the Pittsburgh Sleep Quality Index. Covariates included participants' demographic characteristics, depressive symptoms, positive and negative affect, personal mastery, and caregiving-role overload.

Caregivers showed a greater discrepancy in sleep duration than did non-caregivers (-0.46 hour vs. 0.22 hour, respectively; p=0.003). In a regression model, however, caregiving status was no longer associated with this sleep duration discrepancy, when accounting for covariates. Higher positive affect was significantly associated with less sleep duration discrepancy (R2=11.3%, p=0.014). Sobel's test of mediation showed that 26% of the effect of caregiving on this sleep discrepancy was attributable to caregivers with low positive affect.

The findings suggest a potential mediating role of positive affect on the relationship between caregiving status and sleep duration discrepancy. As an aid for understanding the role of lower positive affect, use of actigraphy may be useful to address sleep discrepancy in caregivers.

Contemporary Concise Review 2021: Pulmonary nodules from detection to intervention.


The US Preventive Task Force (USPSTF) has updated screening criteria by expanding age range and reducing smoking history required for eligibility; ...

Sleep-disordered breathing was associated with lower health-related quality of life and cognitive function in a cross-sectional study of older adults.


The clinical significance of sleep-disordered breathing (SDB) in older age is uncertain. This study determined the prevalence and associations of SDB with mood, daytime sleepiness, quality of life (QOL) and cognition in a relatively healthy older Australian cohort.

A cross-sectional analysis was conducted from the Study of Neurocognitive Outcomes, Radiological and retinal Effects of Aspirin in Sleep Apnoea. Participants completed an unattended limited channel sleep study to measure the oxygen desaturation index (ODI) to define mild (ODI 5-15) and moderate/severe (ODI ≥ 15) SDB, the Centre for Epidemiological Studies Scale, the Epworth Sleepiness Scale, the 12-item Short-Form for QOL and neuropsychological tests.

Of the 1399 participants (mean age 74.0 years), 36% (273 of 753) of men and 25% (164 of 646) of women had moderate/severe SDB. SDB was associated with lower physical health-related QOL (mild SDB: beta coefficient [β] -2.5, 95% CI -3.6 to -1.3, p < 0.001; moderate/severe SDB: β -1.8, 95% CI -3.0 to -0.6, p = 0.005) and with lower global composite cognition (mild SDB: β -0.1, 95% CI -0.2 to 0.0, p = 0.022; moderate/severe SDB: β -0.1, 95% CI -0.2 to 0.0, p = 0.032) compared to no SDB. SDB was not associated with daytime sleepiness nor depression.

SDB was associated with lower physical health-related quality of life and cognitive function. Given the high prevalence of SDB in older age, assessing QOL and cognition may better delineate subgroups requiring further management, and provide useful treatment target measures for this age group.

Equal effect of a non-custom versus a custom mandibular advancement device in treatment of obstructive sleep apnea.

J Clin Sleep

Numerous types of mandibular advancement devices (MADs) are available to treat patients with obstructive sleep apnea (OSA), varying from non-custom to custom devices. Only a limited number of studies have been performed to determine whether a non-custom MAD could be used to predict treatment success of a custom MAD. In this study, we investigated the potential of a new generation non-custom MAD, by comparing its effectiveness with a custom MAD. We hypothesize that the effectiveness of the devices is similar with regard to both objective (polysomnography; PSG) and self-reported (questionnaires, adherence, and patient satisfaction) outcomes.

Single-center prospective randomized cross-over study including a consecutive series of patients with OSA. Patients were randomized to start either with the non-custom or custom MAD. Both MADs were applied for 12 weeks, followed by a PSG with MAD in situ and questionnaires. After the first 12 weeks of follow-up, a wash out period of one week was applied. Equal effectiveness was defined as no significant differences in both objective and self-reported outcomes between both devices.

Fifty-eight patients were included; forty completed the full follow-up. The median apnea-hypopnea index significantly reduced from 16.3 [7.7; 24.8] events/h to 10.7 [5.6; 16.6] events/h with the custom MAD (p=0.010) and to 7.8 [2.9; 16.1] events/h with the non-custom MAD (p<0.001). Self-reported outcomes significantly improved in both groups. No significant differences were found between both devices.

The effectiveness of a non-custom and custom MAD is comparable, which suggest that a non-custom MAD can be used as a selection tool for MAD treatment eligibility to improve MAD treatment outcome.

Registry: Netherlands Trial Register; Title: The use of a boil and bite Mandibular Advancement Device versus a custom Mandibular Advancement Device in Obstructive Sleep Apnea management; Identifier: NL64738.100.18; URL:

Association of accelerometry-derived social jetlag and sleep with temperament in children less than 6 years of age.

J Clin Sleep

Social jetlag (SJL) measures the discrepancy between circadian and social clocks. Using accelerometry-derived data, our objective was to assess the prevalence of SJL in young healthy children and determine the association of SJL and sleep with temperament.

Of 117 children participating in TARGet Kids!, a Canadian cohort of healthy preschool-aged children, 78 children (39 girls (50%)); mean age [SD]: 35.1[20.5] months) were included. Sleep was measured objectively using accelerometry. Temperament dimensions (surgency, negative affectivity, and effortful control) were assessed with the very short forms of Rothbart's child and infant behavior questionnaires. We examined associations of SJL and sleep with temperament using multivariable linear regression models adjusted for sex, age, ethnicity, and preschool/daycare attendance.

20 out of 78 (25.6%) experienced SJL of greater than 30 minutes. SJL was greater in children who attended preschool/daycare compared with children who did not (26.3[18.8]min vs. 17.6[14.8]min; p<0.05). There was no evidence of an association between SJL and any temperament dimension. We found evidence of an association between increased sleep duration and increased negative affectivity scores (longer 24h sleep (ß:0.347, 95% CI:0.182,0.512, p<0.0001); longer nighttime sleep duration (ß:0.413, 95% CI:0.163,0.663, p=0.002)).

In our cohort, 1 in 4 preschool-aged children experienced SJL. Increased sleep duration was associated with increased negative affect, which could have implications for children developing internalizing behavior such as depression or low-self-esteem. We found that sleep duration, but not SJL, was associated with temperament and may impact daytime behavior of young children.

Optical coherence tomography angiography and Humphrey visual field in patients with obstructive sleep apnea.

J Clin Sleep

To determine if obstructive sleep apnea (OSAS) predisposes patients to glaucoma and macular disease due to vascular compromise by evaluating retinal and optic nerve vasculature and function using optical coherence tomography angiography (OCT-A) and Humphrey visual field testing, respectively.

In this prospective, observational, cross-sectional study forty-five patients undergoing polysomnography ordered per standard of care were selected and stratified based on apnea-hypopnea index (AHI). Medical history, visual acuity testing, 24-2 Humphrey visual field (HVF), intra-ocular pressure measurement, optical coherence tomography angiography (OCT-A) studies of the macular and peripapillary retina were obtained. Correlations between polysomnography parameters and imaging data were analyzed.

The radial peripapillary capillary (RPC) vascular density (VD) demonstrated no relationship to AHI (95% CI (-0.026,0.038)) or severity of OSAS (95% CI: (-0.772, 3.648) for moderate OSAS compared to mild/normal and (-1.295, 3.1421) for severe comparing to mild/normal. OCT-A superficial parafoveal VD (95% CI: (-0.068,0.011), deep parafoveal VD (95% CI: (-0.080,0.009)), and FAZ (95% CI: (-0.001, 0.001)) showed no statistically significant relationship to AHI or OSAS severity after controlling for confounders. OCT retinal nerve fiber layer (RNFL) thickness increased with AHI (p=0.014), but there was no statistically significant correlation with OSAS severity with RNFL thickness (95% CI: (-12.543, 6.792) for moderate comparing to normal and (-2.883, 16.551) for severe comparing to normal). Visual field parameters were unaffected by OSAS (95% CI: Mean deviation (-0.21,0.29), Pattern standard deviation: (-0.351,0.121), Visual field index: (-0.166, 0.329)). OCT choroidal thickness showed a statistically significant decrease when OSAS was grouped by severity (p=0.0092), but did not correlate with AHI (p=0.129, 95% CI: (-1.210, 0.095)).

The severity of OSAS did not show a statistically significant effect on parameters associated with glaucoma or macular vascular disease. Larger cohorts may be required to determine the physiologic consequences of OSAS on the macular and optic nerve vasculature, structure, and function.

Effects of sulfur dioxide, ozone, and ambient air pollution on lung histopathology, oxidative-stress biomarkers, and apoptosis-related gene expressions in rats.

Exp Lung Res

Ambient air pollution (AAP) has become an important health problem globally. Besides, several pieces of evidence indicate that air pollutants such as sulfur dioxide (SO2) and ozone (O3) are major contributors to a wide range of non-communicable diseases. The present study investigated the effects of AAP, sulfur dioxide, and ozone on oxidative stress, histopathology, and some apoptosis-related genes expressions of lung tissue in a rat model.

Thirty-two Wistar rats were randomly divided into the control, AAP, sulfur dioxide (10 ppm), and ozone (0.6 ppm) groups. After five consecutive weeks' exposure to the selected pollutants (3 h/day), lung tissues were harvested and immediately fixed with formalin. The samples were routinely processed, sectioned, stained with hematoxylin and eosin (H&E), and finally assessed for presence of pathological changes. Expression changes of BAX, p-53, EGFR, caspase-3, caspase-8 and caspase-9 were assayed using the RT-qPCR method. One hundred milligrams of lung tissues were extracted and the supernatants were used for assaying malondialdehyde (MDA), total antioxidant capacity (TAC), superoxide dismutase (SOD), glutathione peroxidase (GPX), and catalase activities.

GPx activity was increased in the ozone (P = 0.05) and AAP (P < 0.001) groups and also MDA level in sulfur dioxide group (P = 0.008). Pathological lesions were mild, moderate, and severe in the sulfur dioxide, ozone, and AAP groups, respectively, as compared to control group (P ˂ 0.05). Exposure to AAP and sulfur dioxide enhanced BAX (P = 0.002) and caspase-8 (P < 0.001) mRNA expression, respectively. Caspases-3 and -8 mRNA expressions were elevated in ozone group (P < 0.001).

The results indicated induction of oxidative stress. Our results suggest the apoptosis stimuli effect of AAP and also the extrinsic apoptotic pathway trigger effect of sulfur dioxide and ozone in the lung tissue in the concentrations used in the present study. The histopathological and the genes expression changes may be a result of the induced oxidative stress in the lung tissues.

Contemporary Concise Review 2021: Interstitial lung disease.


The last 2 years have presented previously unforeseen challenges in pulmonary medicine. Despite the significant impact of the SARS-CoV-2 pandemic o...

Occupational COPD-The most under-recognized occupational lung disease?


Chronic obstructive pulmonary disease (COPD) is caused by exposure to noxious particles and gases. Smoking is the main risk factor, but other facto...