Immune disruptions and night shift work in hospital healthcare professionals : the intricate effects of social jet-lag and sleep debt

Objectives: We aimed to examine the effects of circadian and sleep rhythm disruptions on immune biomarkers among hospital healthcare professionals working night shifts and rotating day shifts. Methods: Hospital nurses working either as permanent night shifters (n=95) or as day shifters rotating between morning and afternoon shifts (n=96) kept a daily diary on their sleep and work schedules over a full working week. Blood samples were collected at the beginning and end of the last shift during the week, and participants were categorized into three groups based on work shift: morning shift (39 day shifters sampled at 7:00 and 14:00), afternoon shift (57 day shifters sampled at 14:00 and 21:00), and night shift (95 night shifters sampled at 21:00 and 7:00). Circulating blood counts in immune cells, interleukin-6 and C-reactive protein concentrations as well as total sleep time per 24 hours during work days (TST24w) and free days (TST24f), sleep debt (TST24f — TST24w) and social jet-lag (a behavioral proxy of circadian misalignment) were assessed. Results: Compared with day shifters, night shifters had shorter sleep duration (TST24w=5.4 ± 1.4h), greater sleep debt (3.2 ± 1.4 h) and social jet-lag (6.7 ± 2.4 h). Variations of immune biomarkers concentrations were consistent with the expected diurnal variations among day shifters (i.e., low level in the morning, increase during the day, peak value in the evening). By contrast, in night shifters, blood concentrations of total lymphocytes, T-helper cells, cytotoxic T-cells, memory B-cells and interleukin-6 were lower at 21:00, increased during the night, and reached higher values at 7:00. Multivariate analyses ruled out significant impact of TST24w, sleep debt, and social jet-lag on immune biomarkers concentrations among day shifters. In contrast, among night shifters, multivariate analyses indicated a combined effect of total sleep time (TST24w), sleep debt and social jet-lag for total lymphocytes and T-helper cells but only a social jet-lag effect for interleukin-6 and a single total sleep time effect for neutrophil and B-Cells. Conclusions: Altogether, our results point to intricate response patterns of immune rhythms to circadian misalignment and sleep debt in night shifters. Specifically, these altered pattern expressions of immune cells may increase vulnerability to infections and reduce vaccination efficiency in night workers

National Accounts ESA. Aggregates 1970-1975. 1976

<p>Model 3 multiple logistic regression analysis for burnout diagnosis.</p

EFFETS DE LA PRIVATION AIGUE DE SOMMEIL SUR LA REGULATION DE LA PRESSION ARTERIELLE ET LE CONTROLE DE LA VASOMOTRICITE

Sleep deprivation is associated with an increase in sympathetic nervous system activity, blood pressure (BP) and pro-inflammatory status that may induce endothelial dysfunction, a key factor in the development of cardiovascular diseases. Mechanisms that link endothelial dysfunction to total sleep deprivation (TSD) are not actually known. The aim of our work was to assess the impact of TSD on vasomotricity and relationships with BP changes and immuno-inflammatory responses. In the first part, we observed, in healthy young men, that 40 hours TSD induce a decrease of acetylcholine (ACh)-induced vasodilatation and an increase in plasma levels of endothelial activation markers. This endothelial dysfunction appeared before the increase in BP and sympathetic activity and was associated with higher plasma levels of TNF-α, and TNF-α mRNA levels in white blood cells. In a second study, we showed that 29 hours TSD induce a decrease in digital skin temperature and vascular conductance during a cold water immersion test (30 min, 5°C bath) and during the subsequent passive rewarming. This decrease of local tolerance to cold, found without modification in BP and central temperature, was associated with an increase of plasma levels of endothelin-1. In the second part, we demonstrated that the decrease of endothelial- and current- induced vasodilation observed after 24 hours of awaking were independent of BP changes, in sympathectomised (reserpined) rats. We also observed a decrease of NO and prostacyclines (PGI2) pathways activity after TSD. These results were associated with an increase in plasma levels of TNF-α, and IL-6. In conclusion, our results suggest that TSD, in healthy subjects, is a sufficient stress to trigger an endothelial dysfunction and low grade inflammation, leading to a decrease in vascular reactivity. This phenomenon is initially independent on changes in BP and sympathetic activity and is the consequence of immuno-inflammatory responses.Les troubles du sommeil sont associés à une augmentation de l'activité du système nerveux sympathique, de la pression artérielle (PA) et une inflammation qui peuvent induire une dysfonction endothéliale. Les mécanismes impliqués dans cette dysfonction et les effets de la privation aiguë et totale de sommeil (PTS) ne sont pas encore élucidés. L'objectif de ce travail est d'évaluer l'effet de la PTS sur la vasomotricité et les liens avec des modifications de la PA et de la réponse immuno-inflammatoire. Dans une première partie, chez l'homme sain, nous observons au cours de 40 heures de PTS, une diminution de la vasodilatation cutanée induite par l'acétylcholine et une augmentation des concentrations plasmatiques de marqueurs de l'activation endothéliale. Cette dysfonction apparait avant les modifications de la PA et est associée à une augmentation de la concentration plasmatique de TNF-α et de la production d'ARNm du TNF-α par les cellules de la lignée blanche. Nous montrons également au cours d'un test d'immersion de la main dans l'eau froide (30 minutes, 5°C) et la récupération, une diminution de la température digitale et de la conductance vasculaire cutanée, associées à l'augmentation de la concentration plasmatique d'endothéline-1. Dans une deuxième partie, réalisée chez des rats sympathectomisés (réserpine), nous démontrons que la diminution des vasodilatations dépendante de l'endothélium, après 24 heures de PTS, est indépendante des modifications de la PA. Cette altération est liée à une diminution de l'activité des voies de production du NO et des prostacyclines (PGI2) et est associé à une augmentation des concentrations plasmatiques de TNF-α et d'IL-6. En conclusion, l'ensemble des résultats suggère que la PTS est un stress suffisant pour induire une dysfonction endothéliale, responsable d'une altération de la vasomotricité. Celle-ci semble être est initialement la conséquence de la réponse immuno-inflammatoire

Prévalence des troubles du sommeil chez les militaires dans l exercice de la médecine générale d unité

Introduction Les troubles du sommeil touchent plus d'un tiers de la population et peuvent retentir sur l'activité professionnelle, la vigilance au volant et l'état de santé. Leur prise en charge est faible et souvent tardive. Les militaires sont particulièrement exposés aux troubles du sommeil. L'objectif était de déterminer la prévalence des troubles du sommeil dans une population militaire puis d évaluer la proportion de troubles non prise en charge, leur répercussion diurne et d identifier des facteurs de risque. Méthode Cette étude, prospective par questionnaire, menée sur les militaires de la Région Parisienne se présentant en visite systématique annuelle, évaluait les troubles et la qualité du sommeil et la somnolence. Résultats Sur les 510 répondeurs, la prévalence des troubles du sommeil était de 11,8%, de l hypersomnie de 9%, de l insomnie 2,4% et de signes cliniques d'apnée du sommeil de 11,4%. Une hypersomnolence diurne était observée dans 30,2% des cas. 23,3% reconnaissaient une chance, moyenne ou forte, de s'assoupir au volant d une voiture. Les principaux facteurs de risque de troubles du sommeil étaient : une durée habituelle de sommeil inférieure à 6h, des antécédents de troubles du sommei, un âge supérieur à 40 ans, le sexe féminin, le statut de militaire du rang et l'appartenance au service de santé, à la marine, ou à la gendarmerie. Conclusion L hypersomnie et de l hypersomnolence diurne avaient une prévalence importante dans les armées, avec un fort retentissement diurne. L exploration des troubles du sommeil est donc nécessaire dans cette population, accompagnée d une sensibilisation des praticiens et des militaires et de contre-mesures préventivesPARIS12-CRETEIL BU Médecine (940282101) / SudocSudocFranceF

Limitations of stroke volume estimation by non-invasive blood pressure monitoring in hypergravity.

Altitude and gravity changes during aeromedical evacuations induce exacerbated cardiovascular responses in unstable patients. Non-invasive cardiac output monitoring is difficult to perform in this environment with limited access to the patient. We evaluated the feasibility and accuracy of stroke volume estimation by finger photoplethysmography (SVp) in hypergravity.Finger arterial blood pressure (ABP) waveforms were recorded continuously in ten healthy subjects before, during and after exposure to +Gz accelerations in a human centrifuge. The protocol consisted of a 2-min and 8-min exposure up to +4 Gz. SVp was computed from ABP using Liljestrand, systolic area, and Windkessel algorithms, and compared with reference values measured by echocardiography (SVe) before and after the centrifuge runs.The ABP signal could be used in 83.3% of cases. After calibration with echocardiography, SVp changes did not differ from SVe and values were linearly correlated (p<0.001). The three algorithms gave comparable SVp. Reproducibility between SVp and SVe was the best with the systolic area algorithm (limits of agreement -20.5 and +38.3 ml).Non-invasive ABP photoplethysmographic monitoring is an interesting technique to estimate relative stroke volume changes in moderate and sustained hypergravity. This method may aid physicians for aeronautic patient monitoring

Sleep and COVID-19. A Case Report of a Mild COVID-19 Patient Monitored by Consumer-Targeted Sleep Wearables

Since its first description in Wuhan, China, the novel Coronavirus (SARS-CoV-2) has spread rapidly around the world. The management of this major pandemic requires a close coordination between clinicians, scientists, and public health services in order to detect and promptly treat patients needing intensive care. The development of consumer wearable monitoring devices offers physicians new opportunities for the continuous monitoring of patients at home. This clinical case presents an original description of 55 days of SARS-CoV-2-induced physiological changes in a patient who routinely uses sleep-monitoring devices. We observed that sleep was specifically affected during COVID-19 (Total Sleep time, TST, and Wake after sleep onset, WASO), within a seemingly bidirectional manner. Sleep status prior to infection (e.g., chronic sleep deprivation or sleep disorders) may affect disease progression, and sleep could be considered as a biomarker of interest for monitoring COVID-19 progression. The use of habitual data represents an opportunity to evaluate pathologic states and improve clinical care

Napping and weekend catchup sleep do not fully compensate for high rates of sleep debt and short sleep at a population level (in a representative nationwide sample of 12,637 adults)

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The risks of sleeping "too much". Survey of a National Representative Sample of 24671 adults (INPES health barometer).

BACKGROUND: A significant U-shaped association between sleep duration and several morbidity (obesity, diabetes or cardiovascular disease) and mortality risks has been regularly reported. However, although the physiological pathways and risks associated with "too short sleep" (<5 hours/day) have been well demonstrated, little is known about "too much sleeping". PURPOSE: To explore socio-demographic characteristics and comorbidities of "long sleepers" (over 10 hours/day) from a nationally representative sample of adults. METHODS: A cross-sectional nationally representative sample of 24,671 subjects from 15 to 85-year-old. An estimated total sleep time (TST) on non-leisure days was calculated based on a specifically designed sleep log which allows to distinguish "long sleepers" from "short sleepers" (<5 hours/day). Insomnia was assessed according to the International classification of sleep disorders (ICSD-2). RESULTS: The average TST was 7 hours and 13 minutes (+/- 17 minutes). Six hundred and twelve subjects were "long sleepers" (2.7%) and 1969 "short sleepers" (7.5%). Compared to the whole group, "long sleepers" were more often female, younger (15-25 year-old) or older (above 65 year-old), with no academic degree, mostly clerks and blue collar workers. "Long sleepers" were significantly more likely to have psychiatric diseases and a greater body mass index (BMI). However, long sleep was not significantly associated with the presence of any other chronic medical disease assessed. Conversely, short sleep duration was significantly associated with almost all the other chronic diseases assessed. CONCLUSIONS: In the general population, sleeping too much was associated with psychiatric diseases and higher BMI, but not with other chronic medical diseases

Leukocyte Expression of Type 1 and Type 2 Purinergic Receptors and Pro-Inflammatory Cytokines during Total Sleep Deprivation and/or Sleep Extension in Healthy Subjects

The purinergic type P1 (adenosine A1 and A2A) receptors and the type P2 (X7) receptor have been suggested to mediate physiological effects of adenosine and adenosine triphosphate on sleep. We aimed to determine gene expression of A1R (receptor), A2AR, and P2RX7 in leukocytes of healthy subjects during total sleep deprivation followed by sleep recovery. Expression of the pro-inflammatory cytokines IL-1β and TNF-α were also determined as they have been characterized as sleep regulatory substances, via P2RX7 activation. Blood sampling was performed on 14 young men (aged 31.9 ± 3.9) at baseline (B), after 24 h of sleep deprivation (24 h-SD), and after one night of sleep recovery (R). We compared gene expression levels after six nights of habitual (22.30–07.00) or extended (21.00–07.00) bedtimes. Using quantitative real-time PCR, the amount of mRNA for A1R, A2AR, P2RX7, TNF-α, and IL-1β was analyzed. After 24 h-SD compared to B, whatever prior sleep condition, a significant increase of A2AR expression was observed that returned to basal level after sleep recovery [day main effect, F(2, 26) = 10.8, p &lt; 0.001]. In both sleep condition, a day main effect on P2RX7 mRNA was observed [F(2, 26) = 6.7, p = 0.005] with significant increases after R compared with 24 h-SD. TNF-α and IL-1β expressions were not significantly altered. Before 24 h-SD (baseline), the A2AR expression was negatively correlated with the latency of stage 3 sleep during the previous night, while that of the A1R positively. This was not observed after sleep recovery following 24 h-SD. This is the first study showing increased A2AR and not A1 gene expression after 24 h-SD in leukocytes of healthy subjects, and this even if bedtime was initially increased by 1.5 h per night for six nights. In conclusion, prolonged wakefulness induced an up-regulation of the A2A receptor gene expression in leukocytes from healthy subjects. Significant correlations between baseline expression of A1 and A2A receptors in peripheral cells and stage 3 sleep suggested their involvement in mediating the effects of adenosine on sleep