Background: Circadian Syndrome (CircS) encompasses cardiometabolic risk factors and comorbidities, indicating an elevated susceptibility to cardiovascular disease and type 2 diabetes. Methods: This cross-sectional study aimed to investigate the association between vitamin D levels and each of the following: CircS, metabolic syndrome (MetS), and the individual components of CircS. Data from 14,907 adults who participated in the National Health and Nutrition Examination Survey (NHANES) between 2007 and 2018 were utilized. CircS was defined based on MetS components, alongside depression, short sleep, and non-alcoholic fatty liver disease (NAFLD). Results: Our results indicated that low vitamin D levels exhibited meaningful associations with CircS, with vitamin D deficiency and inadequacy demonstrating 2.21-fold (95% CI 1.78–2.74, p < 0.001) and 1.33-fold (95% CI 1.14–1.54, p < 0.001) increases in CircS odds, respectively. The association between vitamin D deficiency and CircS was stronger than that with MetS. Additionally, a dose-response gradient in odds of CircS components, particularly with short sleep duration, was noted as serum vitamin D levels decreased. Conclusions: our findings highlight a significant association between low serum vitamin D levels and CircS and its components, particularly with short sleep. This suggests a potentially pivotal role of vitamin D in the pathogenesis of Circadian syndrome.

Transient Receptor Potential Vanilloid (TRPV) channels represent one of the seven subfamilies of TRP receptors and are widely expressed throughout the human body where they play pivotal roles in various physiological processes. In the gastrointestinal (GI) system, TRPV channels regulate critical functions such as nutrient absorption, motility, and secretions. Beyond maintaining cellular homeostasis, these channels are involved in pain and inflammation, contributing to diverse pathologies. Their central role in the pathophysiology of different digestive system disorders has made TRPV channels a significant focus of research. Moreover, the involvement of TRPV channels in numerous GI cancers has further heightened research interest in the role of these channels. Accordingly, this review elucidates the structural components and intricate signaling pathways of TRPV channels, focusing on the unique characteristics of each family member (TRPV1–6) in GI physiology. Furthermore, we explore the therapeutic potential of targeting these channels to modulate their physiological and pathological roles, highlighting their promise in treating GI disorders. Additionally, we address the challenges associated with their therapeutic application, considering their interactions in different systems, inherent biochemical characteristics, and the alterations required for effective design.

Transient Receptor Potential Vanilloid (TRPV) channels represent one of the seven subfamilies of TRP receptors and are widely expressed throughout the human body where they play pivotal roles in various physiological processes. In the gastrointestinal (GI) system, TRPV channels regulate critical functions such as nutrient absorption, motility, and secretions. Beyond maintaining physiological equilibrium, these channels are involved in pain and inflammation, contributing to diverse pathologies. Their central role in the pathophysiology of different digestive system disorders has made TRPV channels a significant focus of research. Moreover, the involvement of TRPV channels in numerous GI cancers has further heightened research interest in the role of these channels. Accordingly, this review elucidates the structural components and intricate signaling pathways of TRPV channels, focusing on the unique characteristics of each family member (TRPV1-6) in GI physiology. Furthermore, we explore the therapeutic potential of targeting these channels to modulate their physiological and pathological roles, highlighting their promise in treating GI disorders. Additionally, we address the challenges associated with their therapeutic application, considering their interactions in different systems, inherent biochemical characteristics, and the alterations required for effective design.

Multiple myeloma (MM) is a malignant hematologic neoplasm that primarily affects the bone marrow and can invade other organs, leading to diverse clinical manifestations. Presentation with gastrointestinal bleeding as the initial symptom is exceptionally rare. We report a case of MM in a 46‐year‐old man who presented with gastrointestinal bleeding and severe anemia. Routine endoscopic evaluation was inconclusive, but further hematologic and imaging investigations confirmed multiple myeloma. The patient was successfully treated with bortezomib‐based chemotherapy and supportive care. This case emphasizes the importance of considering plasma cell dyscrasias in patients with unexplained GI bleeding and anemia, particularly when conventional gastrointestinal causes are excluded.

Background: Head and neck cancers (HNCs) represent a global health burden, with high morbidity and mortality largely driven by late-stage diagnosis and heterogeneous clinical outcomes. Reliable biomarkers are needed to improve early detection, prognostic stratification, and therapeutic decision-making. This study evaluates the diagnostic and prognostic value of chemokines in HNCs and identifies candidates with clinical relevance. Methods: A comprehensive literature search was conducted on 28 March 2026 across PubMed, Embase, Scopus, Web of Science, and EBSCO. Observational studies involving patients or biological samples with confirmed HNCs were included if they evaluated chemokines as diagnostic or prognostic biomarkers. Risk of bias was assessed using the Newcastle–Ottawa Scale (NOS) for prognostic studies and the Quality Assessment of Diagnostic Accuracy Studies-2 (QUADAS-2) tool for diagnostic studies. Meta-analyses were performed for chemokines evaluated in ≥3 studies using the inverse-variance heterogeneity model. Results: Forty-four studies encompassing 7294 participants were included. Prognostic findings were heterogeneous across biomarkers. MIP-3α demonstrated consistently significant associations with poorer survival outcomes. In contrast, IL-8, CXCL10, and CXCR4 showed inconsistent or predominantly non-significant associations with overall survival (OS), disease-free survival (DFS), and locoregional control (LRC). For diagnostic performance, IL-8, in saliva, demonstrated relatively high sensitivity and specificity for oral squamous cell carcinoma. Chemerin showed high diagnostic accuracy, although evidence remains limited. Conclusions: Certain chemokines show potential as diagnostic and prognostic biomarkers in HNCs. However, heterogeneity across tumor types, samples, and methodologies limits evidence. Larger, well-designed studies are needed to validate their clinical utility in risk stratification and personalized management of HNCs.

Diabetes mellitus (DM) is a rapidly growing global health burden and a major driver of infection-related morbidity and mortality. Chronic hyperglycemia disrupts both innate and adaptive immunity through impaired complement activity, dysfunctional dendritic cells and natural killer cells, altered macrophage polarization and efferocytosis, and neutrophil defects including reduced chemotaxis, impaired phagocytosis, and dysregulated NETosis. These immune abnormalities, compounded by endothelial dysfunction and microvascular disease, increase susceptibility to severe and recurrent infections such as urinary tract infections, tuberculosis, pneumonia, skin and soft tissue infections, and invasive fungal diseases. Emerging evidence also supports a bidirectional relationship in which infections may precipitate or aggravate DM via mechanisms including molecular mimicry, β-cell injury, chronic inflammation, and gut microbiota dysbiosis, contributing to insulin resistance and β-cell dysfunction. Recurrent infections and frequent exposure to broad-spectrum antibiotics, together with altered pharmacokinetics, chronic wounds with biofilm formation, and prolonged healthcare exposure, create strong selective pressure for antimicrobial resistance (AMR) in diabetic populations. Using clinical and scientific based evidence, this review explores mechanisms linking DM, infection risk, and AMR, highlighting implications for the diagnosis, therapy, stewardship, and vaccination, as well as outlines key research gaps including improved AMR surveillances stratified by diabetes status and integrated predictive models incorporating glycemic control, host factors, and microbial genomics.