Biology subjects

Reis, C.

Publications and source records attributed to Reis, C..

4 recordsLinked to original sources

bioRxiv2025

Circadian disruption beneath the surface: a screening approach to identify actigraphy-based markers of split shift work in submariners

Identifying behavioral markers of disease risk associated with circadian disruption remains challenging due to reproducibility concerns, as human studies are often under-powered to detect the effects of interest. Submarines provide an extreme example of cir-cadian disruption, depriving individuals of natural light-dark cycles and limiting oppor-tunities for physical activity. To address these challenges, we developed an effect size-based method to robustly screen potential actigraphy-derived markers of the submarine environment. Actigraphy data was collected across the pre-mission, mission and post-mission periods. During the mission, crew members followed a 6-hours-on/6-hours-off split shift schedule, except for submariners with on-call duty or extended hours. Forty-one actigraphy variables were screened for their ability to differentiate between study periods and shifts. A Monte Carlo permutation test was used for this initial screening, followed by receiver operating characteristic (ROC) curve analysis for pairwise compar-isons. Light-related features, the slopes of regression lines fitted to the daily predicted dim light melatonin onset (DLMO) trajectories, and Pearson correlation coefficients be-tween each recording day and its corresponding predicted DLMO demonstrated the great-est potential to distinguish between study periods. Most high-performing features dis-criminated between split shift work schedules and on-call or extended-hours schedules. Only the relative amplitude (RA) and the average light intensity during the five least-illuminated hours of the day (L5) reliably distinguished between the shift performing the bulk of nighttime work and its counterpart. Although submarine settings offer an oppor-tunity to study a healthy population living under confined movement and dim light, de-tecting biological signals through actigraphy in this environment is inherently challeng-ing. Demonstrating robust effects under these conditions supports the use of actigraphy in dimly-lit, isolated, confined, and extreme (DICE) environments, but also its applica-bility to study other operational or clinical populations with reduced activity levels.

bioinformatics↗

bioRxiv2021

Validation of the Munich Actimetry Sleep Detection Algorithm for estimating sleep-wake patterns from activity recordings

Periods of sleep and wakefulness can be estimated from wrist-locomotor activity recordings via algorithms that identify periods of relative activity and inactivity. Here, we evaluated the performance of our Munich Actimetry Sleep Detection Algorithm (MASDA). MASDA uses a moving 24-hour-threshold and correlation procedure estimating relatively consolidated periods of sleep and wake. MASDA was validated against sleep logs and polysomnography. Sleep-log validation was performed on 2 field samples collected over 54 and 34 days (median) in 34 adolescents and 28 young adults. Polysomnographic validation was performed on a clinical sample of 23 individuals undergoing 1 night of polysomnography. Epoch-by-epoch analyses were conducted and comparisons of sleep measures via Bland-Altman plots and correlations. Compared with sleep logs, MASDA classified sleep with a median sensitivity of 80% (IQR = 75-86%) and specificity of 91% (87-92%). Mean onset and offset times were highly correlated (r = 0.86-0.91). Compared with polysomnography, MASDA reached a median sensitivity of 92% (85-100%), but low specificity of 33% (10-98%), owing to the low frequency of wake episodes in the nighttime polysomnographic recordings. MASDA overestimated sleep onset (~21 min) and underestimated wake after sleep onset (~26 min), while not performing systematically different from polysomnography in other sleep parameters. These results demonstrate the validity of MASDA to faithfully estimate sleep-wake patterns in field studies. With its good performance across day- and nighttime, it enables analyses of sleep-wake patterns in long recordings performed to assess circadian and sleep regularity and is therefore an excellent objective alternative to sleep logs in field settings.

neuroscience↗

bioRxiv2018

Thalamocortical dynamics underlying spontaneous transitions in beta power in Parkinsonism

Parkinsons disease (PD) is a neurodegenerative condition in which aberrant oscillatory synchronization of neuronal activity at beta frequencies (15-35 Hz) across the cortico-basal ganglia-thalamocortical circuit is associated with debilitating motor symptoms, such as bradykinesia and rigidity. Mounting evidence suggests that the magnitude of beta synchrony in the parkinsonian state fluctuates over time, but the mechanisms by which thalamocortical circuitry regulates the dynamic properties of cortical beta in PD are poorly understood. Using the recently developed generic dynamic causal modelling framework, we recursively optimised a set of plausible models of the thalamocortical circuit (n=144) to infer the neural mechanisms that best explain the transitions between low and high beta power states observed in recordings of field potentials made in the motor cortex of anesthetized Parkinsonian rats. Bayesian model comparison suggests that upregulation of cortical rhythmic activity in the beta-frequency band results from changes in the coupling strength both between and within the thalamus and motor cortex. Specifically, our model indicates that high levels of cortical beta synchrony are mainly achieved by a delayed (extrinsic) input from thalamic relay cells to deep pyramidal cells and a fast (intrinsic) input from middle pyramidal cells to superficial pyramidal cells. We therefore hypothesize that beta synchronisation at the cortical level could selectively be modulated via interventions that are capable of finely regulating cortical excitability in a spatial (delivered to either the superficial or deep cortical laminae) and time specific manner.

neuroscience↗

bioRxiv2018

SSU72 phosphatase is a telomere replication terminator

Telomeres, the protective ends of eukaryotic chromosomes, are replicated through concerted actions by conventional DNA polymerases and telomerase, though the regulation of this process is not fully understood. Telomere replication requires (C)-Stn1-Ten1, a telomere ssDNA-binding complex that is homologous to RPA. Here, we show that the evolutionarily conserved phosphatase Ssu72 is responsible for terminating the cycle of telomere replication in fission yeast. Ssu72 controls the recruitment of Stn1 to telomeres by regulating Stn1 phosphorylation at S74, a residue that lies within the conserved OB fold domain. Consequently, ssu72{Delta} mutants are defective in telomere replication and exhibit long 3 overhangs, which are indicative of defective lagging strand DNA synthesis. We also show that hSSU72 regulates telomerase activation in human cells by controlling the recruitment of hSTN1 to telomeres. Thus, in this study, we demonstrate a previously unknown yet conserved role for the phosphatase SSU72, whereby this enzyme controls telomere homeostasis by activating lagging strand DNA synthesis, thus terminating the cycle of telomere replication.

cell biology↗