Life

Aim: Obstructive sleep apnea (OSA) causes intermittent hypoxemia and sleep fragmentation, both of which may affect bone metabolism, yet studies of OSA and bone mineral density (BMD) have produced inconsistent results. We examined whether OSA status and conventional polysomnographic indices of OSA severity and nocturnal oxygenation were associated with lumbar spine and total hip T-scores in postmenopausal women. Methods: We conducted a retrospective cross-sectional study of 101 postmenopausal women with polysomnography (PSG) and dual-energy X-ray absorptiometry (DXA) records; 40 had PSG-confirmed OSA and 61 were controls. Lumbar spine and total hip T-scores were the primary outcomes. The OSA and control groups were compared with linear regression adjusted for age and body mass index (BMI). Four conventional indices (apnea–hypopnea index [AHI], oxygen desaturation index [ODI], mean SpO₂, and minimum SpO₂) were each examined in a separate model adjusted for age and BMI. Extended models, which added calcium, phosphate, alkaline phosphatase [ALP], vitamin D, and parathyroid hormone [PTH] and entered all four indices together, were treated as sensitivity analyses and were calculated. Results: Women with OSA were older than controls (63.9 ± 7.8 vs. 60.1 ± 7.2 years) and had a higher BMI (36.0 ± 7.0 vs. 30.6 ± 4.9 kg/m²). The unadjusted T-score differences were 0.28 (95% CI −0.30 to 0.86) at the lumbar spine and 0.11 (95% CI −0.34 to 0.56) at the total hip; neither was statistically significant. None of the indices were statistically significant in the extended models. The lumbar extended model was significant overall (p = 0.023), whereas the total hip model was not (p = 0.117). Conclusions: We found no statistically significant associations between the conventional indices and lumbar spine or total hip T-scores. The findings should be interpreted cautiously because of the modest sample size, possible overfitting and collinearity in the extended models, and the lack of data on cumulative hypoxic burden. They do not show that OSA has no effect on bone health. Because fractures were not assessed, these data cannot inform screening or fracture-risk decisions.

Rhabdomyolysis is classically understood as skeletal muscle injury complicated by myoglobin-mediated acute kidney injury, but this framework does not fully explain the diagnostic and clinical complexity created by liver disease, aminotransferase abnormalities, and multiorgan dysfunction. This narrative review summarizes clinical and experimental evidence on liver, muscle, and kidney interactions in rhabdomyolysis. Relevant studies addressing aminotransferase elevation, liver-related susceptibility to muscle injury, rhabdomyolysis-associated kidney injury, interorgan communication, and shared systemic insults were reviewed. The evidence indicates that aminotransferase elevation in rhabdomyolysis often reflects muscle injury rather than primary hepatic damage, requiring interpretation with serial enzyme trends, liver-specific markers, and clinical context. Liver disease may increase vulnerability to muscle injury and kidney injury through sarcopenia, metabolic disturbance, altered drug handling, and impaired perfusion. Severe rhabdomyolysis may also contribute to hepatic stress through inflammation, heme-related pathways, and AKI-mediated effects, although direct causal evidence remains limited. A liver–muscle–kidney framework may improve integrated assessment, but prospective studies are needed to clarify temporal relationships and validate clinically useful biomarkers.

Despite advances in treating breast cancer with modern therapeutic approaches, it still causes significant morbidity and mortality in patients. Like many other diseases, oxidative stress is a significant risk factor for initiation and progression of breast cancer. Redox-sensitive transcription factors, nuclear factor-kappa B (NF-κB), activator protein-1 (AP-1), and hypoxia-induced regulators promote chronic inflammation, proliferation, angiogenesis, and metabolic adaptation of cancer cells. Therefore, regulating oxidative stress is necessary to repair cellular damage and slow or inhibit cancer progression. However, current therapeutic approaches for treating breast cancer have limitations that necessitate the development of new treatment strategies. Cannabidiol (CBD), a non-psychoactive lipophilic phytocannabinoid, acts as a context-dependent redox modulator and selectively exploits oxidative vulnerabilities in breast malignancies and provides anticancer effects via modulation of Nrf2 pathway components. It demonstrates strong antioxidant capabilities, modulating redox balance and also disrupts multiple oncogenic pathways. There is also increasing interest in developing synthetic CBD derivatives with improved therapeutic potential for cancer treatment. Inhibiting the molecular targets of cancer cell development and progression by these derivatives may provide an effective therapeutic strategy. This review provides an understanding of CBD’s potential in reducing cancer cell proliferation, metastasis, inducing apoptosis and inhibiting angiogenesis. It also highlights novel approaches of CBD analogues on molecular targets in breast cancer cell lines.