Brain-derived neurotrophic factor (BDNF) is a neurotrophin involved in the regulation of synaptic plasticity and metabolic processes, including glucose metabolism and insulin sensitivity. In patients with obstructive sleep apnea (OSA), recurrent episodes of intermittent hypoxia may stimulate BDNF expression as a compensatory neuroprotective response. OSA is associated with metabolic disturbances, such as increased insulin resistance and a higher risk of type 2 diabetes. Continuous positive airway pressure (CPAP) therapy may influence both BDNF levels and metabolic outcomes. The aim of this study was to evaluate changes in BDNF concentration and glucose metabolism in patients with OSA, with particular emphasis on the effect of long-term CPAP therapy. Sixty-six adult patients with OSA confirmed by polysomnography were enrolled and divided into severe (s-OSA) and non-severe (ns-OSA) groups. Fasting blood samples were collected to measure glucose, insulin, and BDNF concentrations. Patients with s-OSA were re-evaluated after 12 months of CPAP therapy and further classified as compliant (sc-OSA) or non-compliant (snc-OSA) based on recorded device usage. The same biochemical parameters were assessed after the 12-month follow-up. Baseline BDNF levels were significantly higher in the s-OSA group compared to the ns-OSA group (20.1 ng/mL vs. 8.1 ng/mL, p = 0.02) and correlated with the apnea–hypopnea index (AHI, r = 0.38, p = 0.02). In the nsc-OSA group, BDNF concentrations increased significantly after 12 months (16.2 ng/mL vs. 35.5 ng/mL, p < 0.001), while no significant change was observed in the sc-OSA group (24.4 ng/mL vs. 27.4 ng/mL, p = 0.33). Among sc-OSA patients, a significant improvement in insulin resistance was noted, although no significant changes were observed in fasting glucose or insulin levels. Increased BDNF levels were observed in patients with s-OSA compared to ns-OSA. Compliant CPAP therapy was associated with reduced insulin resistance and no further BDNF increase, in contrast to non-compliance, suggesting a beneficial effect of CPAP on glucose metabolism and BDNF regulation. These findings support the hypothesis that both neurotrophic and metabolic responses in OSA may be modulated by disease severity and therapy adherence.

Obstructive sleep apnea (OSA) is associated with increased risks of systemic comorbidities, leading to significant morbidity and mortality. This study investigates predictors of all-cause mortality, emphasizing the interplay of clinical symptoms, polysomnographic findings, and comorbidities. The aim of this study was to identify and compare respiratory predictors of all-cause mortality over 5, 10, and 15 years. A single-center study was conducted at a Sleep Medicine Department between 2005 and 2019, 4025 patients with suspected OSA who underwent polysomnography were admitted, 853 died during the study. We performed Cox regression analyses with dynamic hazard ratios to evaluated predictors of mortality. Prevalence of OSA was high—75.6% in the cohort: 929 patients with mild OSA (23.1%), 770 with moderate OSA (19.1%), and 1343 with severe OSA (33.4%). Survival rates were 89.7%, 81.9%, and 78.8% at 5, 10, and 15 years, respectively. Cardiovascular causes dominated mortality (33.3%), followed by cancer (26.5%). AHI_REM was associated with higher mortality risk in 0–5, 0–10, 0–15 years of observation in contrast to AHIN_REM and AHI_TST. The hazard ratio analysis showed that mortality risk changed over time depending on sleep stage and event type: risk increased for AHI_REM and AHI_TST, while it stayed the same or decreased for AHI_NREM and most central apneas.

Sleep is tightly regulated by thermoregulatory processes that include core body temperature (CBT) modulation, the distal–proximal temperature gradient (DPG), and melatonin rhythms. In this review, we examine how these factors intersect with sleep physiology and contribute to the pathophysiology of common sleep disorders such as ADHD, insomnia, narcolepsy, Obstructive Sleep Apnea (OSA), depression, and Restless Legs Syndrome (RLS). We discuss evidence showing that delayed or disrupted CBT minima, impaired DPG, and altered melatonin secretion can prolong sleep latency, fragment rest, and lead to daytime symptoms. In addition, we explore temperature-based interventions, including foot baths, passive body heating, whole-body hyperthermia, and adjustments in room temperature, which have demonstrated potential to mitigate symptoms and enhance sleep quality. Collectively, these findings emphasize the need for personalized interventions to address thermoregulatory disruptions, presenting a noninvasive avenue for more effective sleep disorder management.

BACKGROUND Obstructive sleep apnea (OSA) is associated with increased risk of systemic comorbidities, leading to significant morbidity and mortality. This study investigates predictors of all-cause and OSA-related mortality, emphasizing the interplay of clinical symptoms, polysomnographic findings, and comorbidities. The aim of this study was to identify and compare predictors of all-cause and OSA-related mortality over 5, 10, and 15 years of follow-up. MATERIAL AND METHODS In this single-center study conducted at our Sleep Medicine Department between 2005 and 2019, 4025 patients with suspected OSA underwent polysomnography and were enrolled in this longitudinal study. Patients were categorized based on their mortality status, with a follow-up time of up to 15 years, and the cause of death if applicable. Based on the underlying cause of death, we identified 2 study groups: all-cause mortality (n=853) and OSA-related mortality (n=460). We performed Cox regression analyses to evaluate predictors of mortality. RESULTS Prevalence of OSA was high - 75.6% in the cohort: 929 patients with mild OSA (23.1%), 770 with moderate OSA (19.1%), and 1343 with severe OSA (33.4%). Survival rates were 89.7%, 81.9%, and 78.8% at 5, 10, and 15 years, respectively. Cardiovascular causes dominated mortality (33.3%), followed by cancer (26.5%). We compared the apnea-hypopnea index (AHI) a well-known, widely used metric for indicating the severity of OSA, in 0-5, 0-10, and 0-15 years of observation of all-cause mortality and OSA-related mortality. Comparing the AHI during rapid eye movement (REM) sleep, non-rapid eye movement (NREM) sleep, and total sleep time (TST), AHIREM was associated with a higher mortality risk than AHINREM and AHITST. Sleepiness (HR 1.17 95% CI: 1.09-1.26), episodes of stroke (HR 1.77 95% CI: 1.38-2.28), and use of new oral anticoagulants (HR 1.71 95% CI: 1.21-2.43) were associated with mortality at 15 years. CONCLUSIONS OSA management requires a holistic approach that extends beyond AHI, integrating clinical symptoms, comorbidities, and polysomnographic indices.

Background: Rectal neuroendocrine tumors (r-NETs) measuring 20 mm or less are increasingly diagnosed during colorectal cancer screening, but the optimal depth of endoscopic resection remains uncertain. Endoscopic submucosal dissection (ESD) is well established, whereas endoscopic intermuscular dissection (EID) may provide deeper resection for fibrotic or recurrent lesions. We hypothesized that EID would provide reliable deep-margin clearance without compromising safety. Methods: We retrospectively reviewed 42 consecutive patients treated at a tertiary center between 2018 and 2025. Thirty-two primary lesions underwent ESD and 10 lesions or scars suspicious for deep invasion underwent EID. Primary outcomes were en bloc and R0 resection; secondary outcomes were procedure time, adverse events, and length of stay. Groups were compared with the t, Mann–Whitney U, and chi-square tests. Results: En bloc resection was achieved in all cases. Histology confirmed R0 resection in all 26 primary lesions. Among 16 excision scars, 14 showed fibrosis only and 2 harbored grade 1 NET recurrence; both recurrent lesions were resected R0 with EID. Lesion size and procedure time were similar between groups. No major adverse events occurred. Self-limited intraprocedural bleeding occurred in five patients, and all patients were discharged within 2 postoperative days. Conclusions: Both techniques are safe and effective for r-NETs measuring 20 mm or less, and EID may be preferred for fibrotic or recurrent lesions. Large prospective multicentre studies are needed to validate the depth-tailored use of EID in r-NETs.

Obstructive sleep apnea (OSA) is associated with increased cardiovascular, respiratory, and all-cause mortality, yet the long-term survival impact of continuous positive airway pressure (CPAP) remains contested, and treatment is usually analysed as a binary exposure rather than by the quality of the response achieved. In a single-centre cohort of 4368 adults referred for polysomnography and followed for 8–20 years (prespecified subgroup with apnea–hypopnea index [AHI] ≥ 15, n = 2304), we applied cause-specific Cox and Fine–Gray competing-risks models, together with machine-learning classifiers, to characterise all-cause, cardiovascular, and pulmonary mortality. CPAP was associated with reduced all-cause (hazard ratio [HR] 0.75), cardiovascular (HR 0.75), and pulmonary mortality (HR 0.54), with the benefit confined to severe OSA (HR 0.66) and absent in moderate disease (HR 0.95). Good responders showed a significant 34% reduction in all-cause mortality (HR 0.66), whereas poor responders showed no significant reduction. Nocturnal desaturation (time with oxygen saturation < 90%) was the dominant independent predictor of pulmonary mortality, and baseline features predicted response category only moderately (macro-averaged AUC 0.76). Long-term CPAP confers a severity- and response-dependent survival benefit; nocturnal hypoxaemia is a key, modifiable driver of respiratory death.