Cervical cancer remains a significant public health challenge, disproportionately affecting women in low- and middle-income countries (LMICs). Persistent infection with high-risk types of human papillomavirus (HPV), particularly HPV16 and HPV18, is the central cause of cervical carcinogenesis, driven by the viral oncoproteins E6 and E7, which disrupt the host tumor suppressors p53 and retinoblastoma protein (pRb). Advances in molecular understanding have catalyzed effective primary and secondary prevention strategies. Prophylactic HPV vaccination, especially the nonavalent formulation, has demonstrated high efficacy in reducing HPV infections and cervical precancer. Concurrently, HPV deoxyribonucleic acid (DNA) testing, self-sampling, and screen-and-treat protocols are transforming screening paradigms, particularly in resource-limited settings. However, global disparities in vaccine access, screening coverage, and health infrastructure persist, impeding progress toward the World Health Organization’s (WHO) 90–70–90 elimination targets. By synthesizing recent advances in virology, prevention strategies, and implementation innovations, such as therapeutic vaccines, artificial-intelligence (AI)-driven diagnostics, and mobile health solutions, this review sheds light on their potential to narrow these equity gaps.

Gestational diabetes mellitus (GDM) is one of the most common metabolic complications during pregnancy, affecting up to 14% of pregnancies globally. GDM is characterized by glucose intolerance that arises or is first identified during pregnancy and is linked to significant short- and long-term adverse outcomes for both mothers and their offspring. The pathophysiology of GDM involves more than maternal insulin resistance and β-cell dysfunction. It is influenced by complex interactions among placental hormones, adipokines, inflammatory mediators, and oxidative stress pathways. Additionally, placental-derived exosomes and metabolomic signatures have emerged as promising biomarkers for early prediction and monitoring of the disease. Despite advancements in clinical diagnosis and management, including lifestyle interventions and pharmacological treatments, current strategies are still inadequate to prevent complications for both mothers and newborns entirely. Recent molecular insights into GDM development have been explored, along with emerging biomarkers and potential therapies. This synthesis also considers prospects for precision medicine strategies that could significantly improve GDM management. The urgent need for improved prevention and treatment of GDM is evident. A deeper understanding of the molecular foundations of GDM is essential and urgent, as it may enhance clinical outcomes and provide opportunities for early prevention of intergenerational metabolic disease risk.

In patients diagnosed with multiple myeloma (MM), the primary complaints at the time of diagnosis are often related to bone involvement, significantly impacting quality of life and increasing both morbidity and mortality. Obesity is associated with a chronic inflammatory state that results in the production of various cytokines and adipokines, which may promote bone destruction. Adiponectin, an adipokine predominantly secreted by adipocytes, is notably diminished in circulation among individuals with obesity, a phenomenon that has also been observed in MM. This reduction may contribute to the disruption of an already compromised bone architecture. The increase in adipose tissue is associated with heightened leptin production, a key adipokine, which can play a significant role in the pathophysiology of MM and its related bone complications. Obesity is associated with hyperinsulinemia and increased levels of free IGF-1. In MM, IGF-1 plays a critical role as a growth factor, produced by both myeloma cells and osteoclasts within the bone marrow microenvironment. Our gathered data indicates a significant relationship between the adipokines produced by adipose tissue and the bone matrix, particularly in the context of obesity and MM. However, it is important to note that the existing body of research on this topic is relatively sparse, with the majority of studies conducted on murine models rather than human subjects. This limitation highlights a critical need for further investigation to elucidate the precise mechanisms that contribute to bone destruction under these conditions.

Adiponectin and omentin are adipose tissue-derived adipokines implicated in insulin sensitivity and cardiometabolic regulation. Their behavior across different stages of dysglycemia, as well as in relation to visceral adiposity and cardiometabolic phenotypes, remains incompletely understood. In this cross-sectional study, circulating adiponectin and omentin levels were evaluated in individuals with prediabetes (PreDM, n = 100) and newly diagnosed type 2 diabetes mellitus (T2DM, n = 128). Associations with insulin resistance-related indices, including the triglyceride–glucose (TyG) index and TyG-derived composites, the visceral adiposity index (VAI), cardiometabolic phenotypes, and cardiovascular risk categories, were assessed using correlation and multivariable regression analyses. Discriminatory performance for metabolically unhealthy obesity was evaluated using receiver operating characteristic (ROC) curve analysis. Both adiponectin and omentin levels were lower in T2DM compared with PreDM (22.05 vs. 30.30 and 25.72 vs. 38.84, p < 0.0001 for both). In PreDMs, omentin showed a significant inverse correlation with the TyG index (weak correlation, ρ = −0.197, p = 0.050), whereas adiponectin demonstrated only weak trends. In multivariable models, VAI and male sex were independent predictors of circulating omentin levels, whereas fasting insulin was not. In contrast, adiponectin did not retain independent associations with metabolic or visceral adiposity indices. In T2DM, adipokine–metabolic associations were largely absent. Neither adipokine differed substantially across cardiometabolic phenotypes or cardiovascular risk categories. ROC analyses revealed modest overall discriminatory performance for metabolically obese phenotypes, with poor discrimination after stratification by glycemic status (area under the ROC curve (AUC) of 0.704 for adiponectin and 0.710 for omentin, and AUC of 0.431 for adiponectin and 0.461 for omentin, respectively). Circulating adipokines appear to exhibit stage-dependent relationships with metabolic dysfunction, being more informative in PreDM than in established T2DM. Omentin may reflect visceral adiposity-related metabolic alterations in early dysglycemia, whereas adiponectin shows limited independent associations. Overall, these findings suggest that adipokines have limited diagnostic or cardiovascular risk-stratification utility when considered in isolation and may be better interpreted within multimarker cardiometabolic assessment frameworks.

Shift work is an essential component of modern occupational systems but represents a major source of circadian misalignment associated with gastrointestinal symptoms and selected gastrointestinal disorders. The biological pathways underlying these associations remain incompletely integrated across circadian, neuroendocrine, immune, epithelial, and microbial domains. This narrative review aimed to synthesize current evidence linking shift work with gastrointestinal dysfunction and disease while distinguishing epidemiological associations from experimental mechanistic evidence and biologically plausible but insufficiently validated relationships. We conducted a structured literature search in PubMed/MEDLINE, Scopus, and Web of Science, focusing primarily on studies published between January 2020 and July 2026. We prioritized recent original studies, systematic reviews, meta-analyses, and mechanistic and translational investigations, while retaining relevant landmark studies. Evidence was organized within an integrative framework encompassing occupational exposure, circadian disruption, neuroendocrine alterations, immune dysregulation, intestinal barrier dysfunction, gut microbial and metabolic alterations, and gastrointestinal outcomes, with explicit consideration of differences in evidentiary strength across these proposed relationships. Human studies consistently support an association between night or rotating shift work and circadian disruption, whereas evidence for downstream neuroendocrine, immune, epithelial, and microbial pathways varies substantially in directness and strength. Experimental studies indicate that circadian disruption can alter inflammatory signaling, epithelial barrier function, and host–microbiota interactions, while microbial metabolites, including short-chain fatty acids, secondary bile acids, and tryptophan derivatives, may participate in reciprocal interactions with mucosal immunity and barrier integrity. Epidemiological evidence is strongest for disorders of gut–brain interaction, particularly irritable bowel syndrome, whereas evidence for functional dyspepsia, inflammatory bowel disease, and colorectal neoplasia is more limited, inconsistent, or unresolved. Candidate circadian, inflammatory, intestinal barrier, microbial, and metabolomic biomarkers remain investigational and are not currently validated for gastrointestinal risk prediction or routine occupational surveillance. Shift work is associated with selected gastrointestinal outcomes, while experimental evidence provides biological plausibility for interconnected circadian, neuroendocrine, immune, epithelial, and microbial mechanisms. However, the proposed framework should be regarded as integrative and hypothesis-generating rather than as an established linear causal cascade in human shift workers. Prospective longitudinal and interventional studies are required to establish temporal and causal relationships, validate candidate biomarkers, and determine whether occupational, behavioral, or mechanism-based interventions can produce clinically meaningful gastrointestinal benefits.

Background/Objectives: Inflammatory and hematologic indices derived from routine blood tests have been increasingly investigated as prognostic biomarkers in multiple myeloma (MM). However, their clinical utility remains inconsistent, and data on novel composite indices, such as the mean corpuscular volume-to-lymphocyte ratio (MCVL) and the cumulative inflammatory index (IIC), are lacking in MM. Methods: We conducted a retrospective study including 122 patients with newly diagnosed MM. Hematologic and inflammatory indices were evaluated at baseline and after four cycles of induction therapy. Associations with progression-free survival (PFS) and overall survival (OS) were assessed using Kaplan–Meier analysis, Cox regression models, and receiver operating characteristic (ROC) curve analysis. Results: Baseline inflammatory biomarkers, including NLR, PLR, MLR, SII, as well as MCVL and IIC, were not significantly associated with PFS or OS. ROC analysis demonstrated poor discriminative ability for all evaluated markers at both baseline and post-induction timepoints (AUC values close to or below 0.50). In contrast, post-induction inflammatory indices, particularly PLR, MLR, AISI, and SIRI, were significantly associated with PFS in both univariable and multivariable Cox regression analyses. Neither baseline nor post-induction MCVL and IIC showed independent prognostic value. Conclusions: Baseline inflammatory and erythrocyte-derived indices, including the novel composite markers MCVL and IIC, have limited prognostic utility in MM. In contrast, dynamic changes in inflammatory biomarkers during treatment may provide more clinically relevant information regarding disease progression. These findings support the integration of longitudinal biomarker assessment into future risk stratification models in MM.