This study aimed to explore the causal association between obstructive sleep apnea (OSA) and frailty traits using a bidirectional two-sample Mendelian randomization (MR) analysis. Summary data from large-scale European genome-wide association studies were used to assess the genetic link between OSA and frailty traits, including frailty index, appendicular lean mass, grip strength, and walking pace. Effect estimates were primarily evaluated using inverse-variance weighted (IVW) analysis, complemented by MR-Egger, weighted median (WM), simple mode, and weighted mode analyses. Sensitivity analyses were performed to assess heterogeneity, outliers, and horizontal pleiotropy. Forward MR analysis showed no significant effect of OSA on frailty traits. However, reverse MR analysis suggested that a higher frailty index was associated with an increased risk of OSA (IVW: odds ratio [OR], 1.777; 95

Electrocochleography (ECochG) provides an objective assessment of cochlear and auditory nerve function and is widely used clinically, particularly during cochlear implant surgery for hearing preservation monitoring. However, ear-canal ECochG recordings remain technically challenging because unstable electrode-tissue contact can compromise signal consistency. Conventional transtympanic electrodes contact the tympanic membrane (TM) through the ear canal but often exhibit limited conformability due to their rigid metallic structure. Although transtympanic ECochG provides high-quality signals, it requires TM penetration and therefore remains invasive. Here, we report a fibrous inner-ear ECochG electrode (ECochGel) that forms a conformal and reversible adhesive interface with the TM, enabling stable recordings without conductive pastes or mechanical fixation. The ECochGel exhibits a mild thermally triggered sol-gel transition and tissue-matched mechanical compliance, resulting in strong interfacial adhesion (60.0 +/- 8.0 kPa) and reduced mechanical mismatch (tensile modulus: 13.5 +/- 1.4 kPa). Electrochemical characterization shows low interfacial impedance (10.23 +/- 0.09 Omega at 1 kHz). In recordings, ECochGel produces lower detection thresholds and larger compound action potential (CAP) amplitudes than commercial electrodes. Histological analysis confirms good biocompatibility with minimal tissue perturbation. These results demonstrate ECochGel as a soft, conformal interface for stable ECochG recording with potential applications in auditory diagnostics and intraoperative monitoring.

Type 2 inflammation (T2I) drives chronic airway diseases such as eosinophilic chronic rhinosinusitis (eCRS) and asthma, which are frequently accompanied by coagulation activation and platelet recruitment. However, whether and how these associated processes actively contribute to shaping inflammation remain largely unknown. Here, using single-cell transcriptomic profiling of human nasal polyp samples from eCRS patients with or without comorbid asthma, we identified a TGM2hi macrophage population enriched in inflamed tissues and strongly correlated with local eosinophilia and systemic disease burden. Using dust mite-induced type 2 airway inflammation models in mice, we showed that the loss of Tgm2, either globally or in macrophages, selectively impaired alternative macrophage activation and attenuated both eosinophilic inflammation and epithelial remodeling. Mechanistically, TGM2 catalyzes the recently described histone modification H3Q5 serotonylation (H3Q5Ser), promoting an epigenetically permissive chromatin state for alternative macrophage activation. We further revealed a transcellular circuit driven by the activated platelet-derived monoamine metabolite serotonin (5-HT), which acts as a critical paracrine signal to fuel this epigenetic reprogramming of macrophages. Crucially, pharmacological inhibition of platelet 5-HT release or TGM2 activity ameliorated both nasal and pulmonary pathology in a mouse model of type 2 inflammation, underscoring the therapeutic potential of this pathway. Our findings establish a serotonin-TGM2-H3Q5Ser axis that couples platelet activation to macrophage epigenetic programming. This transcellular mechanism drives type 2 inflammation and reveals novel therapeutic opportunities across airway diseases.

Noise-induced hearing loss (NIHL) is a complex disorder arising from the interplay between noise, as well as contributions from other environmental and genetic risk factors. Although occupational noise exposure is a well-established risk factor, the extent to which other variables contribute remains poorly understood. This study aimed to investigate the nonlinear relationships among these variables using several machine learning algorithms, and to evaluate the relative contributions of environmental and genetic factors to the development of occupational NIHL. Data were collected from 2077 shipyard workers between 2012 and 2021. Noise exposure was quantified as cumulative noise exposure (CNE), estimated from workplace noise measurements and individual career duration. Genetic factors were identified through whole-exome sequencing-based association analyses and SNaPshot genotyping. The impact of co-variables, including sex, age, smoking status, and alcohol consumption were addressed. The classification model achieved 86 % accuracy (area under the curve [AUC]=0.80). Ranking analysis and logistic regression indicated that long-term equivalent (Leq) noise level had the strongest association with occupational NIHL (Leq noise level 80-85 dBA: odds ratio [OR]=7.04; 95 % confidence interval [CI], 2.37-20.89, p < 0.001; Leq noise level 90-95 dBA: odds ratio [OR]=10.87; 95 % confidence interval [CI], 1.42-82.97, p = 0.021), followed by age (OR=1.02; 95 % CI, 1.00-1.03, p = 0.028) and the CNPY2 rs10783780 single nucleotide polymorphism. The G allele of CNPY2, which regulates endoplasmic reticulum stress and cell survival, was associated with increased risk of NIHL (OR=1.39; 95 % CI, 1.16-1.67, p < 0.001). NIHL severity is significantly influenced not only by CNE and age, but also by mutations in the CNPY2 gene, which regulates endoplasmic reticulum stress and cell survival. These findings suggest that effective prevention of occupational NIHL should encompass not only noise control measures to reduce CNE, but also consideration of individual factors such as age and genetic susceptibility, including CNPY2 variants.

Sleep profoundly impacts health, yet current gold-standard Polysomnography (PSG) is constrained by cost, discomfort, and limited scalability for longitudinal monitoring. Ballistocardiography (BCG) offers a non-invasive and user-friendly alternative but often lacks the precision needed for reliable real-world applications. To address this gap, we propose BCGNet, a two-stage transfer learning model that is first pre-trained on 580,865 h of PSG and then fine-tuned and validated on 15,081 h of BCG (total 595,946 h of recordings). Across multiple validation cohorts, BCGNet achieves strong performance in 4-class sleep staging (F1: 0.710-0.817), Apnea-Hypopnea Index (AHI3%) estimation (Pearson's r > 0.95), and robust quantification of sleep continuity and architecture (ICC and Pearson's r generally >0.8). Notably, BCGNet maintains strong performance even on short daytime naps and demonstrates excellent generalizability across diverse external datasets. Deployed as a portable, contactless sleep tracking mat, BCGNet represents a major step towards scalable, user-friendly solutions for longitudinal home sleep monitoring, with important implications for population screening and personalized sleep medicine.

BackgroundSleep fragmentation impairs health and quality of life, yet its relationship with glucose–lipid metabolic dysregulation remains unclear. This study investigated this association in obstructive sleep apnea (OSA), with a focus on nocturnal hypoxia and hypoxia-related brainstem cellular responses.MethodsThis large-scale cross-sectional study included 5,885 adults with suspected OSA from the Shanghai Sleep Health Study. Glucose–lipid metabolic status was assessed using the triglyceride–glucose (TyG) index, TyG-body mass index (TyG-BMI), metabolic score for insulin resistance (METS-IR), and metabolic syndrome. Sleep fragmentation was quantified by the micro-arousal index (MAI). Multivariable regression, restricted cubic spline, threshold effect, multiplicative and additive interaction, stratified analyses, Benjamini–Hochberg false discovery rate (FDR) correction were performed. GEO single-nucleus analyses were conducted to explore intermittent hypoxia-related cellular and metabolic pathway responses in the brainstem (metabolic activity scoring, GSVA, scTenifoldKnk).ResultsTyG, TyG-BMI, and METS-IR were independently positively associated with MAI. Each 1-unit increase in TyG was associated with a 4.0-unit increase in MAI (β = 4.0, p < 0.001). TyG-BMI and METS-IR showed significant nonlinear dose–response relationships with thresholds at 310.31 and 57.25, respectively. OSA severity and nocturnal hypoxia significantly strengthened these associations through both multiplicative and additive interactions. When AHI > 5, the associations of TyG (β = 4.04), TyG-BMI (β = 0.08), and METS-IR (β = 0.41) on MAI were more pronounced. Combined exposure was associated with 4.07–5.91-fold higher odds of elevated MAI. All primary associations remained significant after FDR correction. Single-nucleus analyses suggested widespread glucose–lipid metabolic reprogramming in brainstem cells, particularly neurons and oligodendrocytes.ConclusionGlucose–lipid metabolic abnormalities were significantly associated with OSA-related sleep fragmentation, and these associations were stronger among participants with greater OSA severity and nocturnal hypoxia.

OBJECTIVE:Obstructive sleep apnea (OSA) is associated with autonomic imbalance and glucose metabolism disorders. However, whether autonomic imbalance mediates the association between sleep apnea-specific hypoxic burden (SASHB) and glucose metabolism disorders was also unknown. METHODS:We enrolled 2470 suspected OSA patients between January 2021 and May 2025, who underwent polysomnography, biochemical testing, and heart rate variability (HRV) assessment. Logistic regression was performed to estimate odds ratios for glucose metabolism disorders across quartiles of both SASHB and HRV indices. Mediation analysis examined five classic HRV indices (Mean R-R intervals; SDNN index; Centroid of R-R distribution; Approximate Entropy; LF/HF) as autonomic imbalance markers. RESULTS:Compared with the lowest quartile, higher SASHB levels were significantly associated with increased risks of hyperglycemia (ORs: 1.161, 1.021, and 1.653; P < 0.001), hyperinsulinemia (ORs: 1.455, 1.725, and 2.459; P < 0.001), and insulin resistance (ORs: 1.431, 1.733, and 2.381; P < 0.001). Conversely, higher AppEn levels were associated with decreased risks of hyperglycemia (ORs: 0.799, 0.680, and 0.825; P = 0.043), hyperinsulinemia (ORs: 0.865, 0.771, and 0.538; P < 0.001), and insulin resistance (ORs: 0.794, 0.694, and 0.598; P < 0.001). Mediation analysis revealed that HRV indices exerted partial mediating effects, with indirect effect (OR) values of 1.044, 1.042, and 1.043 for the three outcomes, respectively. CONCLUSIONS:The study results indicate that SASHB is associated with glucose metabolism disorders, and autonomic imbalance may play a mediating role in such an association. These findings suggest that targeting autonomic imbalance might be a promising therapeutic strategy for OSA-related glucose metabolism disorders.

Background:Implantable hypoglossal nerve stimulation (HNS) is an established neuromodulatory therapy for obstructive sleep apnea (OSA) in patients intolerant to continuous positive airway pressure (CPAP). However, no domestically developed HNS system has been clinically implemented in China to date. Methods:We report the first clinical implantation of a novel, Chinese-developed HNS system in a patient with severe OSA. The patient was a 39-year-old man with a 20-year history of nocturnal snoring and apnea. Preoperative polysomnography (PSG) demonstrated an apnea-hypopnea index (AHI) of 46.3 events per hour and a lowest oxygen saturation of 83%. The device selectively activates the medial branch of the hypoglossal nerve, which induces genioglossus contraction and anterior tongue displacement, thereby stabilizing the upper airway during sleep. Results:The procedure was successfully performed. At short-term follow-up, the patient showed marked improvements: AHI decreased from 46.3 to 11.8 events/hour, LSaO2 increased from 83% to 86%, and the Epworth Sleepiness Scale Score improved from 1 to 0. No adverse events occurred. Conclusions:This first‑in‑human experience confirms that the domestic HNS system is feasible, safe, and clinically effective in patient with severe OSA who is intolerant to CPAP. These preliminary results support further clinical development and validation of this domestically manufactured HNS technology for broader application in China.

Background: Digestive system cancers remain a major public-health challenge in Asia, where rapid population ageing and heterogeneous socioeconomic transitions could reshape future cancer burden. We quantified long-term trends, drivers, inequalities, and future trajectories of digestive system cancers across Asia. Methods: Using Global Burden of Disease Study 2023 estimates, we analysed incidence, deaths, and disability-adjusted life-years for six digestive system cancers in 51 Asian countries and territories from 1990 to 2023. We assessed age-standardised rates, estimated annual percentage changes, socioeconomic inequalities, decomposition of burden change, and projections to 2050 using Bayesian age–period–cohort models. Findings: In 2023, Asia had 3·33 million incident cases and 2·37 million deaths from digestive system cancers. The age-standardised incidence rate was 61·55 per 100 000 population and the age-standardised mortality rate was 44·36 per 100 000 population. From 1990 to 2023, both rates declined, with estimated annual percentage changes of –1·15% for incidence and –1·82% for mortality. East Asia had the highest age-standardised burden, whereas South Asia showed increasing trends. Population ageing was the dominant contributor to increases in absolute burden. Colon and rectum cancer had the highest age-standardised incidence rate in 2023, whereas stomach cancer remained the leading cause of deaths. By 2050, incident cases and deaths are projected to increase to 13·50 million and 9·37 million, respectively. Interpretation: Despite declining age-standardised rates, digestive system cancers will impose an increasing absolute burden in Asia, mainly because of population ageing. Prevention, screening, early diagnosis, and guideline-concordant cancer care should be strengthened, particularly in settings with rising trends and limited health-system capacity.

Tympanic membrane (TM) perforation is a common otologic problem that can lead to conductive hearing loss and increase the risk of middle ear infection. However, current clinical repair techniques rely on complex procedures and autologous graft harvesting, which cause extra tissue injury and make rapid intervention difficult. Herein, we presented a convenient liquid-based TM repair strategy in which a “liquid TM bandage” can be dropwise applied onto the perforation and transformed to a thin and adherent membrane within 30 s at room temperature. This liquid-to-film transition enabled rapid functional restoration, improving auditory thresholds by approximately 20–30 dB sound pressure level (dB SPL) across multiple frequency bands and approaching normal hearing levels. Meanwhile, the liquid TM bandage possessed broad-spectrum antibacterial activity, reducing in vivo bacterial load by approximately 88% and thereby minimizing infection risk following perforation. Long-term evaluation demonstrated that liquid TM bandage induced no excessive inflammation or abnormal tissue reactions. This rapid, minimally invasive, and infection-resistant strategy represents a promising approach for TM repair and warrants further investigation toward future clinical translation.

Spontaneous calcium (Ca2+) waves play a critical role as internal stimuli in the early developing auditory system before the onset of sensory experiences. However, neither the spatiotemporal control of spontaneous Ca2+ waves nor their impacts on auditory development are well understood. Here we report that a lateral array of inner supporting cells (ISCs) beneath the inner hair cells displays a spontaneous ultra-long, ultra-fast, transient Ca2+ flash, termed "Ca2+ lightning", which triggers a series of simultaneous bursts of Ca2+ waves in the whole cochlea, before the ear canal opening. The Ca2+ lightning margins the cochlear ISCs at different developmental stages that correspondingly exhibit different Ca2+ activities. Triggered by an ATP-induced high-level Ca2+ wave, the Ca2+ lightning rapidly propagates laterally into neighboring ISCs through the intricate interplay of the T-type Ca2+ channel, Anoctamin 1 (Ano1) Ca2+-activated Cl- channel and Connexin 26 (Cx26). The genetic deletion of Cav3.2, Ano1, or Cx26 abrogates Ca2+ lightning flashes and dysregulates cell development and functions in peripheral cochleae. We propose that cochlear Ca2+ lightning flashes orderly with Ca2+ waves together orchestrate the spatiotemporal maturation processes of the peripheral auditory system before the onset of hearing.

BACKGROUND:Noise exposure at work can damage hearing at speech-frequency essential for speech perception, leading to communication difficulties, life quality decline, and adverse mental and cognitive outcomes. Early identification of individuals at high risk is crucial for occupational health management. This study aims to develop prediction models to estimate the risk of speech-frequency hearing loss among noise-exposed workers. METHODS:We developed and validated multimodal prediction models using epidemiological, hearing assessment, and genetic information from shipyard workers. The training cohort included 5053 workers and the testing cohort included 2086 workers recruited between 2012 and 2024. Noise exposure was estimated using detailed work durations and workplace measurements. Participants completed questionnaires, underwent standardized hearing examinations, and provided blood samples for genetic analysis. Sex-specific models were constructed based on two commonly used definitions of speech-frequency hearing loss. Longitudinal risk was evaluated using repeated-measures statistical approaches. RESULTS:Here we show that binaural hearing thresholds at 3 and 6 kHz are the strongest predictors of subsequent speech-frequency hearing loss, together with age and noise exposure (P < 0.001). Longitudinal prediction models demonstrate good discrimination and calibration, with AUCs exceeding 0.80 and C-indices above 0.78 in both training and testing cohorts. Incorporation of genetic variants further improves predictive performance, increasing discrimination by approximately 2% in males and 3% in females. CONCLUSIONS:These findings provide evidence-based prediction tools that enable individualized risk assessment. Practically, identifying workers at high risk would benefit the hearing preservation in the frequencies more relevant to speech sounds and maintain good communication.

Low-burden screening of sleep apnea-hypopnea syndrome (SAHS) is of great significance for expanding screening coverage, enabling early intervention, and reducing the burden on healthcare systems. Polysomnography (PSG), although the current gold standard, remains difficult to find widespread use due to its cost, complexity, and limited patient compliance. Through non-contact monitoring of vital signs such as respiration and body movements, radar enables comprehensive sleep assessment, including sleep apnea-hypopnea events (SAHE) detection and sleep structure prediction. Reductions in pulse oxygen saturation (SpO2) may also reflect diminished ventilation and provide supportive evidence for SAHE detection. In this paper, we propose a novel low-burden method using millimeter-wave radar and pulse oximeter for SAHS screening (ROSA). ROSA employs a radar-based SAHE detection network, a radar-based sleep structure prediction network, and a learnable fusion strategy integrating SpO2 signals to refine the radar-detected SAHE events. The respiratory event index (REI) is then estimated from SAHE detection and sleep structure prediction results. Experimental results on a real-world dataset (overnight recordings of over 1000 hours, 141 subjects) demonstrated high statistical agreement (ICC = 0.9894) between estimated REI and PSG-derived apnea-hypopnea index (AHI), which outperforms previous studies. The high accuracy and low burden of ROSA show its potential to improve the accessibility of SAHS screening in the population and to integrate with medical Internet of Things (IoT) platforms in future healthcare systems.

BACKGROUND:Substantial variability in susceptibility to noise-induced hearing loss (NIHL) with comparable noise exposures suggests a genetic contribution, but population-based evidence remains limited. This study evaluated whether a polygenic risk score (PRS), summarizing the effect of genetic variants, was associated with NIHL susceptibility. METHODS:Participants were recruited from an ongoing Occupational Noise Exposure and Health Study (ONEHS), including 3836 NIHL cases and 2028 normal hearing (NH) controls. A weighted PRS, calculated from seven genetic variants, stratified participants into low (0-20%), moderate (20-80%), and high (80-100%) PRS groups. Cross-sectional associations with prevalence of NIHL were assessed using logistic regression, while longitudinal associations with incident NIHL and hearing deterioration were evaluated using Cox proportional hazards models and generalized estimating equations. RESULTS:For cross-sectional analyses, participants with high PRS had an increased NIHL risk relative to low PRS participants (odds ratio [OR] = 1.35, 95% confidence interval [CI]: 1.13-1.63, P = 0.001). PRS exhibited an interaction with cumulative noise exposure (CNE). For the longitudinal study (907 with NH and 897 with mild hearing loss at baseline), approximately one-third of participants experienced hearing deterioration. High PRS participants showed increased risk of developing NIHL (hazard ratio [HR] = 1.57, 95% CI: 1.13-2.18, P = 0.008) and further hearing deterioration (HR = 1.49, 95% CI: 1.08-2.07, P = 0.017). Joint associations were observed for high PRS with CNE and age. CONCLUSIONS:Common genetic variation, captured by PRS, contributes to NIHL susceptibility and modifies the relationship between noise exposure and hearing outcomes.

Chronic intermittent hypoxia (CIH), a hallmark pathological feature of obstructive sleep apnea (OSA), is extensively linked to hepatic steatosis in high-fat-diet-induced mice. However, the association between CIH and hepatic steatosis in lean mice, as well as the potential involvement of gut microbiota-related mechanisms, remains poorly understood. Four hundred participants in the Shanghai Sleep Health Study were included to assess the association between apnea-hypopnea index (AHI) and hepatic steatosis index (HSI). To characterize CIH-associated phenotypes and explore microbiota-related alterations in lean mice, liver histology, inflammatory cytokine profiling, metagenomic sequencing with antibiotic intervention, plasma untargeted metabolomics, and liver transcriptomics were performed. As a result, AHI was positively associated with HSI in non-obese participants. In lean mice, 16-week CIH alone induced hepatic steatosis and inflammation, accompanied by significant alterations in gut microbiota composition. Antibiotic treatment attenuated hepatic steatosis and inflammation in 16-week CIH-exposed mice. Metagenomic analysis revealed CIH-associated depletion of Bacteroides uniformis, which was reversed by antibiotic treatment. Plasma metabolomic profiling identified deoxycholic acid as a metabolite exhibiting opposite, phenotype-aligned alterations between CIH and CIH plus antibiotic groups and showing the strongest correlation with Bacteroides uniformis abundance. In parallel, liver transcriptomics revealed coordinated alterations in bile acid-related metabolic pathways and PPAR signaling consistent with CIH-induced and antibiotic-sensitive metabolic remodeling. Together, these findings indicate that prolonged CIH exposure induces hepatic lipid accumulation in lean mice and is associated with coordinated, antibiotic-sensitive alterations in gut microbiota composition, bile acid metabolism, and hepatic transcriptional programs, suggesting a potential involvement of gut microbiota-bile acid-liver interactions in CIH-associated hepatic steatosis.IMPORTANCEObstructive sleep apnea (OSA) is increasingly recognized as a contributor to metabolic dysfunction, yet its role in hepatic steatosis independent of obesity remains incompletely understood. This study shows that chronic intermittent hypoxia (CIH), a defining pathological feature of OSA, is sufficient to induce hepatic steatosis and inflammation in lean mice, independent of dietary manipulation. These findings broaden current understanding of OSA-associated liver disease beyond the context of obesity and metabolic syndrome. By integrating metagenomic sequencing, plasma metabolomics, and liver transcriptomics, this work highlights coordinated alterations in gut microbial composition, bile acid profiles, and hepatic lipid-related transcriptional programs associated with CIH exposure. Depletion of Bacteroides uniformis and elevation of deoxycholic acid were linked to CIH-induced hepatic phenotypes and were sensitive to antibiotic intervention, supporting a contributory role of gut microbiota-bile acid interactions in this process. Together, these findings underscore the potential importance of gut microbiota-host metabolic crosstalk in OSA-associated hepatic steatosis and suggest that microbiota- or bile acid-targeted strategies may warrant further investigation as adjunctive approaches for risk stratification and therapeutic intervention in OSA-related liver disease.

BACKGROUND:Hereditary hearing loss is one of the most common disabling disorders in children and lacks effective pharmacological treatments. Recent breakthroughs in OTOF gene therapy clinical trials necessitate standardized frameworks to guide emerging therapies. This study aims to establish the first international consensus on the clinical application of gene therapy for hereditary hearing loss. METHODS:A modified Delphi process was conducted from March 2024 to March 2025, involving 46 multidisciplinary experts from several countries across otology, genetics, audiology, gene therapy, and hearing rehabilitation. After a systematic literature review, as well as integration of research and clinical expertise and experience, three iterative voting rounds (two anonymous surveys and one online consensus meeting) were performed. Statements required ≥75% agreement for inclusion. FINDINGS:From 9,093 publications, 69 were used to draft and support the consensus statements. A total of 30 statements relevant to six domains achieved consensus on gene therapy for hereditary hearing loss, including ethical review (1 statement), patient selection criteria (12 statements), diagnosis and preoperative evaluation (9 statements), gene therapy drug delivery (4 statements), follow-up (3 statements), and post-treatment auditory and speech rehabilitation (1 statement). CONCLUSIONS:This consensus provides the first globally endorsed framework for gene therapy in hereditary hearing loss. It standardizes clinical trial design and patient management, accelerating translation from research to practice while ensuring safety. The guidelines are immediately applicable to OTOF-related hearing loss and adaptable to other genetic forms. FUNDING:This work was supported by the National Natural Science Foundation of China, the German Research Foundation (DFG) via the Cluster of Excellence, and others.

Background Obstructive sleep apnea (OSA) is associated with cardiac autonomic dysfunction and impaired lipid homeostasis. We investigated whether cardiac autonomic imbalance mediates the association between hypoxic burden (HB) and dyslipidemia.Methods Between January 2022 and March 2026, we consecutively enrolled 2,580 patients with suspected OSA for cross-sectional evaluation. All underwent overnight polysomnography and fasting lipid profiling. HB served as the exposure, heart rate variability (HRV) indices (pNN50 and LF/HF ratio) as mediators, and lipid parameters (LDL-C, total cholesterol, triglycerides) as outcomes. Multivariable logistic regression estimated odds ratios (ORs) for dyslipidemia across HB quartiles, and mediation analysis quantified indirect effects transmitted through HRV.Results Higher HB quartiles were progressively associated with increased risk of elevated LDL-C (OR, 2.372; p < 0.001), hypercholesterolemia (OR, 2.518; p < 0.001), and hypertriglyceridemia (OR, 1.933; p = 0.021). These associations were robust among younger (<45 years), female, and normal-weight (BMI < 24 kg/m2) individuals but were attenuated in older (>60 years) and obese individuals. Mediation analysis indicated that the HRV indices statistically accounted for part of these associations, consistent with a potential mediating role. The indirect effects (bootstrap 95% CI) of pNN50 on LDL-C, total cholesterol, and triglycerides were 0.004, 0.010, and 0.007, accounting for approximately 4.3%, 8.4%, and 3.8% of the total effect; the corresponding indirect effects of the LF/HF ratio were 0.004, 0.006, and 0.007, accounting for approximately 4.3%, 5.1%, and 3.8% of the total effect.Conclusions HB is independently associated with dyslipidemia, an association that is partially mediated by cardiac autonomic imbalance, particularly in younger, female, and non-obese populations.

Sleep profoundly impacts health, yet current gold‐standard Polysomnogram (PSG) is constrained by cost, discomfort, and limited scalability for longitudinal monitoring. Ballistocardiogram (BCG) offers a non-invasive and user-friendly alternative but often lacks the precision needed for reliable real-world applications. To address this gap, we propose BCGNet, a two-stage transfer learning model that is first pre-trained on 580,866 hours of PSG and then fine-tuned and validated on 15,081 hours of BCG (total 595,947 hours of recordings). Across multiple validation cohorts, BCGNet achieves strong performance in 4-class sleep staging (F1: 0.710-0.817), Apnea-Hypopnea Index (AHI) estimation (Pearson's r>0.95), and robust quantification of sleep continuity and architecture (ICC and Pearson's r generally >0.8). Notably, BCGNet maintains strong performance even on short daytime naps and demonstrates excellent generalizability across diverse external datasets. Deployed as a portable, contactless sleep tracking mat, BCGNet represents a major step towards scalable, user-friendly solutions for longitudinal home sleep monitoring, with important implications for population screening and personalized sleep medicine. ### Competing Interest Statement The authors have declared no competing interest. ### Funding Statement This study was funded by by the Ministry of Science and Technology of China STI2030-Major Projects (No. 2021ZD0201900,2021ZD0201902), and the National Natural Science Foundation of China (62102008). ### Author Declarations I confirm all relevant ethical guidelines have been followed, and any necessary IRB and/or ethics committee approvals have been obtained. Yes The details of the IRB/oversight body that provided approval or exemption for the research described are given below: Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine; West China Hospital, Sichuan University; Beijing Tongren Hospital; Inner Mongolia Mental Health Center (The Third Hospital of Inner Mongolia Autonomous Region, Brain Hospital of Inner Mongolia Autonomous Region); Second Affiliated Hospital of Soochow University. The above hospitals in China gave ethical approval for this work. I confirm that all necessary patient/participant consent has been obtained and the appropriate institutional forms have been archived, and that any patient/participant/sample identifiers included were not known to anyone (e.g., hospital staff, patients or participants themselves) outside the research group so cannot be used to identify individuals. Yes I understand that all clinical trials and any other prospective interventional studies must be registered with an ICMJE-approved registry, such as ClinicalTrials.gov. I confirm that any such study reported in the manuscript has been registered and the trial registration ID is provided (note: if posting a prospective study registered retrospectively, please provide a statement in the trial ID field explaining why the study was not registered in advance). Yes I have followed all appropriate research reporting guidelines, such as any relevant EQUATOR Network research reporting checklist(s) and other pertinent material, if applicable. Yes All data produced in the present study are available upon reasonable request to the authors

Obstructive sleep apnea (OSA), is associated with dysfunction in the cardiovascular, metabolic and neurological systems. However, the relationship between OSA and memory impairment, intervention effects, and underlying pathways are not well understood. This review summarizes recent advances in the clinical characterization, treatment strategies, and mechanisms of OSA-induced memory impairments. OSA patients may exhibit significant memory declines, including impairments in working memory from visual and verbal sources. The underlying mechanisms behind OSA-related memory impairment are complex and multifactorial with poorly understood aspects that require further investigation. Neuroinflammation, oxidative stress, neuronal damage, synaptic plasticity, and blood-brain barrier dysfunction, as observed under exposures to intermittent hypoxia and sleep fragmentation are likely contributors to learning and memory dysfunction. Continuous positive airway pressure treatment can provide remarkable relief from memory impairment in OSA patients. Other treatments are emerging but need to be rigorously evaluated for cognitive improvement. Clinically, reliable and objective diagnostic tools are necessary for accurate diagnosis and clinical characterization of cognitive impairments in OSA patients. The complex links between gut-brain axis, epigenetic landscape, genetic susceptibility, and OSA-induced memory impairments suggest new directions for research. Characterization of clinical phenotypic clusters can facilitate advances in precision medicine to predict and treat OSA-related memory deficits.