Sleep Medicine

ABSTRACT Background Medical students face demanding academic schedules and elevated stress levels, predisposing them to poor sleep quality. Sleep hygiene, a set of behavioural and environmental practices aimed at optimising sleep, has been identified as a modifiable determinant of sleep quality, yet its role among medical students in Sudan remains unstudied. Objectives To assess current sleep hygiene practices among medical students at UMST and determine their association with sleep quality outcomes. Methods A facility based cross-sectional study was conducted at UMST among 240 medical students from three academic batches (3rd, 4th, and 5th year), selected via stratified random sampling. Data were collected using two validated self administered instruments: the Pittsburgh Sleep Quality Index (PSQI) and the Sleep Hygiene Index (SHI). Descriptive statistics, independent sample t tests, one way ANOVA, chi-square tests, Pearson correlation, and binary logistic regression were performed using SPSS version 23. Results Poor sleep quality (PSQI >5) was prevalent in 72.1% of participants (mean PSQI 7.25 +/- 2.66), and poor sleep hygiene (SHI >16) in 92.5% (mean SHI 27.1 +/- 7.9). SHI score (continuous) was the only significant independent predictor of sleep quality on logistic regression (OR = 1.13 per unit increase; 95% CI: 1.08-1.19; p < 0.001), equivalent to a 3.4-fold increase in odds per 10-unit rise in SHI score. Female sex was additionally identified as a significant predictor (OR = 1.88; 95% CI: 1.00-3.53; p = 0.049). A significant positive correlation was observed between PSQI and SHI scores (r = 0.359, p < 0.001). Conclusion Poor sleep hygiene is highly prevalent among UMST medical students and is the most significant modifiable predictor of poor sleep quality, with each unit increase in SHI score increasing the odds of poor sleep quality by 13%. These findings highlight a gap in sleep health education within Sudanese medical institutions and support the integration of targeted sleep hygiene interventions into the medical curriculum. Keywords: sleep hygiene; sleep quality; medical students; Sudan; PSQI; SHI; cross-sectional study

We completed a video-based, four-night, in-home, level 3 sleep apnea study of healthy, low-risk pregnant participants and their bed partners in order to characterize sleep physiology in the third trimester of pregnancy. Demographic, anthropometric, and baseline sleep health characteristics were recorded, and the NightOwl home sleep apnea test device was used to measure sleep breathing, posture, and architecture parameters. Symptoms of restless legs syndrome were elicited in the exit interview. Forty-one pregnant participants and 36 bed partners completed the study. Bed partners had a significantly higher prevalence of sleep apnea than their pregnant co-sleepers (31% vs. 5.9%). Bed partners also had more severe sleep apnea than their pregnant co-sleepers, and this persisted on an adjusted analysis for baseline differences in factors known to increase risk of sleep apnea. In pregnant participants, increasing gestational age was found to be protective against mild respiratory events but not more severe events. While the correlation between STOP-Bang score and measures of sleep apnea severity was weak, an affirmative response to the witnessed apneas item on the STOP-Bang questionnaire was a strong predictor of more severe sleep apnea for all participants. Smoking history also increased sleep apnea risk. Pregnant participants had lower sleep efficiency and longer self-reported sleep onset latency. Restless legs syndrome was experienced by 39.5% of the pregnant participants but no bed partners. From a sleep breathing perspective, people with healthy, low-risk pregnancies have better sleep than their bed partners despite lower sleep efficiency and higher rates of restless legs syndrome.

A systematic review and meta-analysis of sleep studies in schizoaffective disorder were conducted using published articles researched in major databases within the period from inception to December 1, 2025. The sleep parameters: total sleep time, sleep efficiency, sleep latency, wakefulness, REM time and percentage, REM latency, REM density, stage 1, 2, 3 and 4 sleep time and percentage, delta sleep time and percentage, of drug-free schizoaffective patients were analyzed and, where available, compared with case-control data of healthy controls, depressed unipolar patients and schizophrenic patients. Forty studies were identified in the systematic review. Nine case-control studies with 67 schizoaffective patients, 88 schizophrenic patients, 79 healthy controls and 131 depressed patients were included in the meta-analyses. The primary outcome was the standard mean difference. Data were fitted with a random-effects model. Publication bias assessment was checked by Egger's Regression and funnel plot asymmetry. Patients with schizoaffective disorder showed reduced total sleep time, increased sleep latency and wakefulness, along with reduced REM time and shortened REM latency, reduced stage 4 sleep time and percentage compared to healthy controls. Patients with schizoaffective disorder differed from depressed patients only for increased sleep latency, while they did not show any difference compared to patients with schizophrenia. SZA showed a non-significant trend (p=0.08) towards increased REM density compared to SCZ, suggesting the need to better clarify the role of REM density in mood and psychotic disorders.

Motor memory retention is impaired in Parkinson's disease (PD), affecting long-term rehabilitation outcomes. It appears that NREM sleep could be beneficial for consolidation processes in PD, and could be leveraged with non-invasive sleep interventions. This study examined the effect of auditory targeted memory reactivation (TMR) during NREM sleep on the retention of a motor sequence learning finger tapping task in 20 PD and 20 healthy older adults (HOA). TMR was applied during a 2-hour nap and its effect on motor retention was post-nap, after 24-hours and with a dual-task. The impact of TMR on sleep electrophysiology was also evaluated. Results showed no effect of TMR on motor retention or dual-tasking, with no difference between the groups. However, the TMR intervention did increase slow-wave density and decreased spindle density in both groups, and slow-wave amplitude during the presentation of the auditory cues was positively associated with performance in HOA. In conclusion, TMR applied during a 2 hour nap did not enhance motor retention, but the changes in sleep physiological features could be linked to a possible underlying effect on memory processing that warrants further investigation.

Scientists have for decades attempted to automate the manual sleep staging problem not only for human polysomnography data but also for rodent data. No model has, however, succeeded in fully replacing the manual procedure across clinics and laboratories. We hypothesize that this is due to the models limited ability to generalize to data from unseen laboratories. Our findings show that despite the high performance of four state-of-the-art models reported in initial publications, the published models struggle to generalize to other laboratories. We further show a significant improvement in model performance across labs by re-training them on a diverse dataset from five different sites. To assess the contribution of variability in manual scoring, ten experts from five laboratories all labelled the same nine mouse sleep recordings. The result revealed substantial scoring variability, particularly for rapid eye movement (REM) sleep, both within and between labs. In conclusion our study demonstrates that key challenges in the generalizability of state-of-the-art sleep scoring models are signal variability and label noise. Our study highlights the need for a standardized set of mouse sleep scoring guidelines to enable consistency and collaboration across the field. Until such a consensus is reached, we present four sufficiently robust models trained on diverse datasets that can serve as standardized tools across labs.

BackgroundThe mechanisms underpinning associations between sleep and psychiatric conditions are poorly understood, partly due to challenges with longitudinal sleep studies outside the laboratory. Children and young people with rare genetic conditions caused by micro-deletions or -duplications (Copy Number Variants or CNVs) have increased risk of disrupted sleep and poorer neurodevelopmental (ND) outcomes. The Sleep Detectives study aims to investigate this by tracking behavioural and neurophysiological signatures of sleep health in young people with ND risk or ND-CNVs. To optimally achieve this, we have worked with families with ND-CNVs and charity partners to co-design our tools, methods, study protocol, and materials. MethodWe established a Lived Experience Advisory Group (LEAP) with nine parents and 13 children and young people with ND-CNVs, alongside representatives of UK charities Max Appeal and Unique. Together, the research team and LEAP co-designed two in-person family workshops in which we collected feedback on the acceptability of sleep monitoring devices, the design of bespoke cognitive tasks, and overall study protocol. Informal interviews and surveys were conducted with LEAP members and researchers, to enable the team to reflect and learn from their Patient/Public Involvement (PPI) experiences. ResultsKey outputs included pre-workshop invitation and briefing materials and insights that iteratively refined the main study design, including the need for flexibility to increase accessibility, selection of sleep devices, customisation of cognitive tasks, and choice of language in documents. The PPI process was highly valued by LEAP members, workshop attendees, and the research team. One investigator described the PPI work as "reinvigorating my love of research by helping me focus on science that matters". Participating families also established peer support networks. ConclusionsInvolving families affected by ND-CNVs in co-designing the Sleep Detectives study maximised opportunities for acceptability, accessibility and scalability. The research team gained inspiration and deeper understanding of the impact of ND-CNVs on families. Families gained awareness about research, established connections with each other and peer support, and were enthusiastic about future research involvement. This experience empowered families to engage more deeply with the research process and helped the PPI work to be more impactful and inclusive. Plain English summaryChildren and young people with rare genetic conditions caused by small deletion or duplication of genetic material are more likely to experience sleep difficulties such as insomnia, restless sleep, and tiredness. They also show an increased likelihood of neurodevelopmental conditions such as learning disability and autism, and mental health issues such as anxiety. The Sleep Detectives team wanted to explore how these genetic conditions affect childrens sleep, cognition and psychiatric health. To make sure that the project design was well suited to the children and young people that would be invited to participate, the team worked closely with families to design the study. Parents and caregivers of affected children and young people were invited to join a Lived Experience Advisory Panel (LEAP), together with charity representatives and Sleep Detective researchers, to co-design two hands-on workshops, and advise on study design. Children and young people and parents/caregivers attending the workshops tried out and provided feedback on tools and devices that the research team were developing. They also advised on the arrangements and support families might need whilst taking part, and on the study protocol. This collaborative approach helped ensure the study design was optimally suited for the recruitment and participation of children and young people and their families. This report documents our public involvement work for the Sleep Detectives study, illustrating the difference the partnership between researchers and families has made to the project, and the wider benefits for all concerned.

BackgroundGrowing evidence suggests that sleep plays an important role in PTSD outcomes, potentially due to its influence on emotional memory consolidation, though these mechanisms remain unknown. This study sought to test the hypotheses that sleep neurophysiology, PTSD status, and sex moderates the degree to which the late positive potential (LPP) mediates memory accuracy for affective visual stimuli. MethodsN = 39 participants (18 female) viewed 75 negative and 75 neutral IAPS images while EEG was recorded. After viewing the images, participants took a two-hour long nap which was followed by a memory assessment. Memory accuracy was measured using d = Z(hit rate) - Z(false alarm rate), where hit rate refers to the proportion of images seen during the memory assessment that are correctly identified as being previously seen, false alarm rate refers to the proportion of images seen during the memory assessment that are incorrectly identified as being previously seen, and Z() is the inverse cumulative distribution function of the standard normal distribution function. ResultsThe early (300 - 1000 ms) and late (1000 - 1500 ms) LPP mediated enhanced discrimination accuracy for emotional compared to neural stimuli (d) (ps < 0.001). The association between the late LPP and d was moderated by sleep such that the association was stronger when participants spent proportionately more time in N3 and REM (p = 0.02). The differences in reactivity between emotional and neutral images for both the early and late LPP were attenuated in PTSD+ individuals vs. controls (ps < 0.001). Despite mediation results showing greater d for emotional compared to neutral stimuli, women showed overall worse memory accuracy for negative compared to neutral stimuli (p < 0.001) whereas men showed no difference (p = 0.64). ConclusionsN3 and REM sleep play a critical role for memory of stimuli that produce large and sustained neural responses. PTSD is marked by a diminished ability to distinguish between negative and neutral information. More research is critical to understand sex effects on emotional memory.

Study ObjectivesIdiopathic hypersomnia (IH) is a central nervous system hypersomnia frequently accompanied by autonomic symptoms, yet objective physiological data are limited. We sought to characterize autonomic nervous system (ANS) dysfunction in IH using nocturnal heart rate variability (HRV) and diurnal autonomic reflex testing (ART), compared to individuals with type 1 narcolepsy (NT1) and healthy controls (HCs). MethodsTwenty-four adults with IH, 10 with NT1, and 14 HCs underwent overnight video polysomnography with HRV analyses in time and frequency domains during stable slow-wave sleep and REM sleep. Comprehensive ART included sympathetic adrenergic (head-up tilt (HUT), Valsalva BP responses), parasympathetic cardiovagal (HRV to deep breathing, Valsalva ratio), and sudomotor (Q-Sweat) measures. ResultsIH participants were predominantly female, with over half reporting long sleep duration. Compared to NT1 and HC, participants with IH demonstrated a greater magnitude of orthostatic tachycardia on tilt ({Delta}HR 41.0 {+/-} 16.3 vs. 26.3 {+/-} 9.3 vs. 30.8 {+/-} 9.3 bpm, p = 0.0086), as well as frequent sudomotor dysfunction (64.3%). IH participants demonstrated greater nocturnal and REM HR with reduced parasympathetic indices during REM, indicating diminished vagal modulation compared with HCs ConclusionsIH is characterized by a distinct pattern of autonomic dysfunction, including pronounced orthostatic tachycardia, frequent sudomotor abnormalities, and reduced parasympathetic activity during sleep. These findings provide objective physiological evidence of ANS involvement in IH and delineate features that distinguish IH from NT1 and HCs.

INTRODUCTIONLocus coeruleus and glymphatic dysfunction are linked both to Alzheimers disease (AD) and, recently, to infraslow oscillation in sleep spindle (sigma) activity (ISO). Here we hypothesise ISO integrity is a critical link between sleep and AD. METHODSWe analyzed non-rapid eye movement sleep EEG from AD and controls, extracting ISO peak amplitude, intrinsic frequency, and bandwidth from the sigma-power time course. We assessed group differences and correlations with plasma biomarkers (A{beta}42/40, pTau181 and 217, NfL, GFAP). RESULTSISO peak amplitude was significantly reduced in AD, while intrinsic frequency and bandwidth were preserved. ISO peak amplitude positively correlated with A{beta}42/40 ratio, and ISO bandwidth correlated with GFAP and NfL levels, and with lower verbal memory retention. DISCUSSIONSuch selective weakening of ISO in AD is consistent with LC dysfunction and impaired glymphatic cycling. ISO may be a novel mechanism and electrophysiological marker linking sleep microarchitecture to AD pathology.

Study objectives Consumer sleep technologies (CSTs) enable low-burden longitudinal sleep monitoring, and their output measures are often interpreted as equivalent to polysomnography (PSG) measures. We applied a measurement reliability-aware approach to determine whether CST-derived 'sleep' measures (1) are interchangeable or device-specific, (2) can reliably assess trait-like sleep characteristics of an individual, (3) can be reduced to latent principal components of sleep, and (4) can be used for classification and biomarker discovery. Methods Data from 74 older adults (20 people living with dementia [PLWD]) were collected at-home (upto 14 nights; Total=752nights) using four tools simultaneously: research-grade actigraphy (Axivity), a wearable (Withings Watch), a nearable (Withings Sleep Analyzer) and Sleep Diary, followed by one in-lab PSG assessment. We used repeated-measures correlation analyses, intraclass correlation coefficients (ICC), principal component analysis (PCA) and binary classification models to address our objectives. Results Single-night between-device correlations and correlations with PSG were moderate (0.3[&le;]r<0.7) for some duration- and timing-related measures, but other associations were weak (r<0.3). Seventy-one percent of sleep measures reached acceptable reliability (ICC[&ge;]0.7) within seven nights of aggregation, but the required aggregation window varied across measures, tools and between PLWD and Controls. Reliability-filtered PCA yielded stable and interpretable principal components, but Duration was the only component showing moderate between-device association. Principal components were successfully used to classify PLWD vs Controls but feature importance varied across devices. Conclusions Aggregation of CST derived measures across 7-14 nights, yielded reliable measures, most of which were device-specific, with duration being the only essential aspect transferable between devices.

Background: Narcolepsy is a debilitating sleep disorder caused by hypocretin deficiency. Aside from its role to induce wakefulness, hypocretin is linked to modulated appetite and metabolism, often resulting in weight gain. Study objectives: We aimed to unravel the comprehensive epidemiological connection between narcolepsy and major cardiometabolic outcomes. Methods: We analyzed cardiovascular and metabolic disease distribution in the FinnGen study. Using longitudinal electronic health records, we assessed associations between narcolepsy, cardiac/metabolic markers, and prescriptions for relevant drugs. Results: Our findings demonstrate significant associations between narcolepsy and metabolic traits (OR [95% CI] = 2.65 [1.81, 3.89]) as well as stroke (OR = 2.36 [1.38, 4.04]). Narcolepsy patients exhibit a less favourable metabolic profile, including higher glucose levels (OR = 1.1143 [1.0599, 1.1715]) and dyslipidaemia. This is supported by increased prescriptions of insulin (OR = 2.269 [1.46, 3.53]), simvastatin (OR = 2.292 [1.59, 3.31]), and metformin (OR = 2.327 [1.66, 3.25]), reflecting high metabolic disturbances. Furthermore, positive associations with antihypertensive and antiplatelet medications were observed, consistent with elevated cardiovascular risk. Conclusion: Taken together, our findings highlight the cardiometabolic burden in narcolepsy. This study enhances understanding of the metabolic and cardiovascular consequences of narcolepsy and offers timely guidance for effective disease control.

Background: Peri-lead edema (PLE) occurs in up to 15% of Deep Brain Stimulation (DBS) cases, can cause morbidity, and its etiology remains unknown. We hypothesized that PLE represents a secondary brain injury modulated by hypoxemia, and that patients with obstructive sleep apnea (OSA) are at elevated risk. Methods: We conducted a retrospective case-control study of 121 Parkinson's disease (PD) patients undergoing DBS at a single center (2019-2024). PLE severity was quantified by CT volumetric segmentation and Hounsfield unit (HU) measures. Perioperative SpO2 and PaO2 were recorded. Polysomnography (PSG) was available in 26 patients; and the REM Sleep Behavior Disorder Screening Questionnaire (RBDSQ) was administered retrospectively. Results: Symptomatic PLE occurred in 12 patients (9.9%), with onset at 3.5 (2-9) days postoperatively. PLE patients had higher body mass index (p = 0.022) and higher OSA prevalence (75% vs. 30%; p = 0.002). Perioperative SpO2 was lower in the PLE group in both the operating room and post-anesthesia care unit (PACU; p < 0.05); PaO2 was lower in the PACU (p = 0.037). In the PSG subgroup, REM Sleep Behavior Disorder (RBD) incidence was lower in PLE patients (20% vs. 60%; unadjusted p = 0.048), and PLE severity correlated significantly with sleep-related hypoxemia and respiratory indices. RBDSQ scores were positively associated with edema density (normalized HU: rho = 0.86, p = 0.024). Conclusions: OSA and perioperative hypoxemia are associated with symptomatic PLE following DBS, while RBD appears protective. Preoperative sleep evaluation and optimized perioperative airway management warrant prospective investigation as PLE prevention strategies.

Chronic short sleep (CSS) is an emerging public health issue that frequently begins in adolescence and is common among healthcare professionals and others engaged in shift work. Epidemiological studies associate CSS and sleep disruption with metabolic disorders, cardiovascular disease, cognitive decline, and heightened Alzheimers disease risk. Building on our prior findings that sleep deprivation perturbs proteostasis and activates endoplasmic reticulum (ER) stress pathways, we investigated the long-term consequences of CSS in young adult wild-type mice over the course of one year. Mice exposed to CSS displayed impaired cognition in hippocampal dependent tasks by 28 weeks of age, indicating emerging memory deficits. At the molecular level, CSS disrupted hippocampal proteostasis--particularly protein folding processes--and triggered ER stress and activation of the unfolded protein response (UPR). Importantly, disrupted proteostasis preceded the behavioral decline, with diminution of the key chaperone and UPR regulator BiP occurring at 20-22 weeks of age. CSS also increased markers of cellular stress and neuroinflammation while reducing the expression of proteins associated with memory function. Age also seemed to be a cellular stressor, causing a longitudinal increase in UPR, ISR, and neuroinflammation markers. Together, these results indicate that both chronic short sleep and age compromise proteostasis and promote neuroinflammation, contributing to progressive cognitive dysfunction.

Abstract Background: Poor sleep quality is associated with increased cardiovascular risk, although its relationship with left ventricle (LV) structure is poorly understood and ethnic differences in the relationship between sleep and LV structure have not been studied. We investigated the association between poor sleep quality and LV structure in a tri-ethnic cohort. Methods: A total of 1284 participants were analysed from the Southall and Brent Revisited (SABRE) study (age=49.9{+/-} 6.2y; male 75.9%, Europeans (EU)=615, South Asians (SA)=457, African/African-Caribbean (AC)=212). A composite sleep quality score was calculated, and LV structure was measured using echocardiography. Associations between sleep quality and LV mass indexed to height1.7 (LVMi), relative wall thickness (RWT) and LV end-diastolic volume indexed to height1.7 (LVEDVi) were estimated using multivariable linear regression with adjustment for demographic and lifestyle factors across three models. Analyses were performed in the whole cohort and stratified by ethnicity. Results: Compared with those who reported very good sleep quality, participants with poorer sleep quality had higher LVMi (4.8 (95% CI 1.4; 8.2)g/(m1.7*unit sleep score); p=0.006). When stratifying by ethnicity, the association between sleep quality and LVMi was unconvincing in EU (1.9(-3.5, 7.3)g/(m1.7*unit sleep score); p=0.493), whereas poor sleep was associated with higher LVMi in AC and SA participants (9.1(1.3;16.8)g/(m1.7*unit sleep score); p=0.023 and 5.8(0.5;11.0)g/(m1.7*unit sleep score); p=0.031 respectively). Conclusions: Poor sleep quality is associated with higher LVMi in older African/African-Caribbeans and South Asians, but not in Europeans. This may contribute to cardiovascular risk. Keywords: sleep, left ventricle, hypertrophy, remodelling

Cannabis use is an increasingly common therapeutic for a variety of chronic diseases. In addition, people with sleep problems may self-medicate using cannabis products. However, genetic architecture of cannabis use and its shared genetic predispositions with sleep traits has not been systematically examined. We performed a meta-analysis of cannabis use within the All of Us and UK Biobank cohorts, consisting of 152,807 cases and 220,272 controls. Our meta-analysis identified 39 independent loci, including the previously reported CADM2 locus associated with cannabis use and replicating previous work. Additionally our associations include neuronal and sleep-regulating genes such as HTR1A, RAI1, SLC39A8, and NCAM1. Moreover, tissue-specific analyses revealed that the genetic architecture of cannabis use is heavily enriched within the central nervous system and specific brain cell types. In addition, we observed significant positive genetic correlations with clinical insomnia, insomnia-related medication usage, and objectively measured nighttime physical activity, alongside negative correlations with morningness chronotype and daytime activity. Fine-mapping and colocalization analyses identified shared genetic signals between cannabis use and clinical insomnia including a near-perfect colocalization at SLC39A8 and CADM2. Together, these results highlight the shared genetic risk between cannabis use and sleep disorders. Additionally, our findings indicate the importance of investigating the genetic effects of cannabis use as its use becomes more widespread, both recreationally and medicinally.

Study ObjectivesTo evaluate wearable sleep staging across sleep apnea severity, including very severe sleep apnea defined as an apnea-hypopnea index (AHI)[&ge;] 50 events/h, and to assess how training-set composition affects performance in this subgroup. MethodsWe analyzed 552 overnight recordings, 318 from the Sleep Lab Dataset and 234 from the Hospital Dataset. In the Hospital Dataset, 26.5% had very severe sleep apnea. We developed a deep learning model for sleep staging using RR intervals from wrist-worn photoplethysmography and three-axis accelerometry. Baseline performance was assessed by cross-validation under 5-stage and 4-stage staging. We examined night-level associations with AHI severity. We also compared the baseline model with an ablation model trained on the same number of recordings but with more Sleep Lab Dataset and lower-AHI Hospital Dataset recordings, evaluating both models in the very severe subgroup. ResultsIn 5-stage classification, Cohens kappa was 0.586 in the Sleep Lab Dataset and 0.446 in the Hospital Dataset. Under 4-stage staging, the gap narrowed, with kappa values of 0.632 and 0.525, respectively. In the Hospital Dataset, performance declined with increasing AHI severity. Among 62 recordings with very severe sleep apnea, reducing high-AHI representation in training lowered kappa from 0.365 to 0.303. ConclusionsWearable sleep staging performance declined across greater sleep apnea severity in this clinical cohort. Clinical utility may benefit from training data that better represent the target severity spectrum and from selecting staging granularity to match the intended use case. Statement of SignificanceRepeated laboratory polysomnography is impractical for long-term sleep apnea management. Wearable sleep staging could support scalable monitoring, yet its reliability in clinically severe sleep apnea has remained unclear. This study developed and evaluated a wearable sleep staging approach in both sleep-laboratory and hospital cohorts. The hospital cohort included many severe and very severe cases. Performance was lower in the hospital cohort and declined with greater sleep apnea severity. A coarser staging scheme reduced the gap between cohorts, and models trained without representative very severe cases performed worse in this target population. These findings highlight the value of severity-aware model development and motivate future multi-night home validation with reliability cues.

Objective: A questionnaire survey was conducted on the willingness and demand for acupuncture treatment in patients with malignant tumors, and the possible factors affecting patients' willingness and demand for acupuncture treatment were explored. Methods: A voluntary, anonymous survey was conducted between February and May 2025 among patients with malignant tumors aged 18 years and older who visited Beijing Cancer Hospital. The questionnaire included 16 questions addressing three dimensions:current medical purposes,Traditional Chinese Medicine(TCM) literacy, and acupuncture treatment needs.The questionnaire was posted online and completed by respondents using a smartphone interface. Results: A total of 511 valid questionnaires were retrieved in the survey, and 481 patients(94.1%) are willing to receive acupuncture treatment. Among the 481 patients willing to receive acupuncture treatment, the top five symptoms they hoped to improve with acupuncture were: disturbed sleep (245 participants, 50.9%); pain (229 participants, 47.6%); fatigue (177 participants, 36.8%); numbness (165 participants, 34.3%); and poor appetite (144 participants, 29.9%). Among patients who chose to "explicitly accept" acupuncture treatment and those who "accepted acupuncture treatment upon doctor's recommendation", 55% and 56% respectively had good knowledge of traditional Chinese medicine (TCM) culture. In contrast, this proportion was only 36.7% among patients who refused acupuncture treatment, and the difference was statistically significant (P<0.05). The survey results also show that Female patients reported significantly higher demands for pain relief and improved sleep than male patients, with statistically significant differences (P<0.05). Furthermore, those aged 18-45 and with better TCM literacy were more likely to desire acupuncture to improve sleep, with statistically significant differences (P<0.05). Conclusion: Differences in TCM literacy can influence patients' willingness to choose acupuncture treatment. Strengthening patient health education and improving TCM literacy will help increase cancer patients' willingness to choose TCM acupuncture treatment, thereby enabling them to benefit from acupuncture. For patients aged 18-45, those with good TCM literacy female with high acupuncture needs, acupuncture treatment may be recommended as a priority.

BACKGROUND: Observational studies have suggested an association between obstructive sleep apnea (OSA) and myocardial infarction (MI), but whether this relationship is causal or largely reflects shared risk factors remains unclear. METHODS AND RESULTS: We performed a 2-sample Mendelian randomization (MR) analysis to evaluate the causal effect of OSA on MI. Summary statistics for OSA were obtained from FinnGen, and MI data were obtained from the UK Biobank, with external validation using CARDIoGRAMplusC4D. Mediation MR was used to assess 13 potential mediators, and a 6-step multivariable MR framework was applied to estimate the direct effect of OSA after sequential adjustment for potential confounders. Reverse MR was conducted to test possible reverse causality. Genetically predicted OSA liability was associated with increased MI risk (odds ratio [OR] per log-OR increase, 1.0024 [95% CI, 1.0010-1.0039]; P=0.001). Body mass index (BMI) was the strongest mediator, explaining 35.94% of the association (P=0.030), whereas systolic blood pressure (SBP) showed minimal mediation (0.28%; P=0.678). In stepwise multivariable MR, the OSA-MI association was attenuated after adjustment for BMI and SBP (P=0.156), suggesting partial confounding by shared cardiometabolic risk. In a model including SBP and atrial fibrillation (AF), AF remained independently associated with MI (P=0.004), whereas OSA showed only a marginal direct effect (P=0.050). Reverse MR found no evidence that MI influenced OSA risk. CONCLUSIONS: These findings support a causal association between OSA and MI and suggest that this relationship may be mediated in part through obesity-related and arrhythmia-related pathways. AF may represent an important intermediate component of OSA-related cardiovascular risk beyond traditional hemodynamic factors. Keywords: obstructive sleep apnea; myocardial infarction; Mendelian randomization; mediation analysis; obesity.

Importance: Sleep-wake disturbances in midlife are common and potentially modifiable contributors to long-term brain health, yet primary care lacks a brief, validated tool that reliably identifies adults with early cognitive vulnerability. Objective: To evaluate associations between commonly used sleep questionnaires and cognitive impairment among midlife primary care patients. Design, Setting, and Participants: Cross-sectional analysis of baseline data from the MidCog cohort, an observational study of English-speaking adults aged 35 to 64 years receiving primary care at academic practices or federally qualified health centers in the Chicagoland area. Exposures: Five validated sleep questionnaires were used to assess distinct sleep-wake disturbance phenotypes: (A) unsatisfactory sleep (PROMIS Sleep Disturbance T-score >55), (B) short sleep duration (<6 hours; Munich Chronotype Questionnaire), (C) obstructive sleep apnea (OSA) risk (STOP-Bang [&ge;]3), (D) insomnia symptoms (Insomnia Severity Index [&ge;]15), and (E) poor multidimensional sleep health (RU-SATED [&le;]6). Main Outcomes and Measures: The primary outcome was cognitive impairment defined as an age- and education-adjusted NIH Toolbox Cognition Battery (NIHTB-CB) Fluid Composite T-score <40 ( >1 SD below the population mean). Cognitive impairment defined by the Montreal Cognitive Assessment (MoCA) score <23 served as the secondary outcome. Logistic regression estimated adjusted odds ratios (aOR), controlling for age, sex, education, body mass index, hypertension, hypercholesterolemia, diabetes, smoking, depressive symptoms, and recruitment site. Results: Among 646 participants (mean [SD] age, 52.3 [8.1] years; 62.4% female; 38.0% non-Hispanic Black, 38.4% non-Hispanic White, 16.0% Hispanic), cognitive impairment was present in 18.7% by NIHTB-CB and 22.3% by MoCA. Among five sleep-wake disturbance phenotypes evaluated, only poor multidimensional sleep health was consistently associated with cognitive impairment after multivariable adjustment (NIHTB-CB: adjusted OR [95% CI] = 2.03 [1.25-3.26]; MoCA: 1.98 [1.20-3.26]). Conclusions and Relevance: Poor multidimensional sleep health was associated with cognitive impairment in midlife primary care patients. Brief multidimensional sleep health screening may identify individuals with early cognitive vulnerability and represent a potential strategy for targeting sleep-focused interventions to promote long-term brain health.

Hypermobile Ehlers-Danlos Syndrome (hEDS) is a genetic connective tissue disorder characterized by hypermobile joints, chronic pain, fatigue, brain fog, orthostatic intolerance, and GI symptoms and dysmotility. Its heterogeneous presentation contributes to poor quality of life, inappropriate interventions, and prolonged diagnostic delays, often up to 10 years. This study primarily aimed to determine if physiological signals captured by a medical-grade wrist wearable could characterize autonomic patterns in hEDS and relate them to symptoms. Individuals with hEDS (n=30) and healthy controls (n=28) wore a medical grade smartwatch for 30 days, collecting continuous heart rate variability, activity, oxygen saturation, and blood pressure, alongside initial baseline symptom and quality-of-life surveys. Individuals with hEDS showed greater instability and variability in both systolic and diastolic blood pressure as well as the HRV metric LF/HF ratio, in comparison to healthy controls (p-values: 0.04, 0.02, 0.02). During sleep, metrics of parasympathetic activity (HRV measures: HF power, pNN50, RMSSD) trended lower in hEDS than healthy in comparison. As expected, survey domains assessing physiologic symptoms and quality-of-life were significantly worse in the hEDS cohort (p-values < 0.05). Notably, autonomic metrics correlated with GI symptoms in the hEDS cohort (Spearman's {rho} range: 0.38-0.60), and psychological symptoms in the healthy cohort (Spearman's {rho} range: -0.47-0.41). Principal component analysis (PCA) of physiologic and symptom features clearly separated groups, supporting distinct physiologic profiles. Combination of GI symptom index and wearable monitoring show promise as a hybrid screening approach that could substantially shorten the time to diagnosis in this population.