Despite the importance of sleep to overall health and well-being, there is a high prevalence of undiagnosed sleep disorders and adverse sleep health, particularly among vulnerable populations. Such vulnerable populations include people experiencing homelessness (PEH), refugees, and incarcerated individuals. In this narrative review, we provide an overview of the literature on sleep health and disorders among key and vulnerable populations (e.g., PEH, refugees, and incarcerated individuals). The limited research among these populations indicated a high prevalence of sleep disorders, mainly insomnia, short sleep duration, and fatigue. Substance abuse and PTSD were commonly found among PEH and refugee populations, respectively, which were was related to poor sleep. Similar across the included vulnerable populations, the individuals reside in environments/facilities with inopportune light exposure, noise disruption, inadequate bedding, and forced sleep schedules. Studies also found a high prevalence of psychosocial stress and reports of threats to safety, which were associated with poor sleep health outcomes. Additionally, several studies reported environmental barriers to adherence to sleep disorder treatment. This paper highlighted the conditions in which these vulnerable populations reside, which may inform interventions within these various facilities (homeless shelters, refugee camps, prisons/jails). The improvement of these facilities with a sleep equity focus may in turn improve quality of life and daily functioning.

Hepatocellular carcinoma (HCC), the most common primary liver cancer, remains a leading cause of cancer-related mortality worldwide. Its often-silent progression results in late-stage diagnosis, limiting curative options and necessitating systemic therapy for many patients. The presence of underlying cirrhosis in most cases further complicates treatment decisions. While the approval of sorafenib in 2007 marked a major milestone in systemic therapy for HCC, the treatment landscape has since evolved significantly, particularly with the advent of immune checkpoint inhibitors and anti-angiogenic agents. Combination regimens, such as atezolizumab plus bevacizumab, have demonstrated superior outcomes and are now considered standard first-line options. Despite these advances, efforts to translate insights from HCC’s molecular pathogenesis into personalized treatments have been limited. This narrative review explores the current systemic therapy options for HCC, from first-line to subsequent-line treatments, and highlights emerging strategies, including novel immunotherapies and targeted agents. We emphasize the need for individualized treatment approaches that consider tumor biology, liver function, and performance status, and we outline future directions for research aimed at improving outcomes in this complex and evolving field.

Purpose: To synthesize current evidence on how sleep deprivation, impaired sleep architecture, and circadian misalignment affect cardiovascular and metabolic regulation across autonomic, hormonal, inflammatory, and behavioral pathways, and to highlight remaining research gaps in cardiometabolic sleep medicine. Methods: A structured literature search was conducted using PubMed, Scopus, and Google Scholar to identify peer‑reviewed primary and review articles published within the past decade, using chronobiological and cardiometabolic search terms. Reference lists of retrieved articles were screened to identify additional relevant studies. Results: Experimental and epidemiologic data consistently link short or disturbed sleep with increased incidence of hypertension, coronary artery disease, stroke, obesity, type 2 diabetes, and metabolic syndrome. Sleep loss activates the sympathetic nervous system and elevates cortisol, while suppressing growth hormone, thereby promoting vasoconstriction, endothelial dysfunction, and cardiac remodeling. Parallel disruption of leptin, ghrelin, and endocannabinoid signaling increases hunger, caloric intake, and preference for energy‑dense foods, driving weight gain, visceral adiposity, and insulin resistance. Circadian misalignment from shift work and social jet lag further amplifies inflammatory signaling and metabolic risk across the lifespan. Limited interventional data suggest that sleep extension can improve appetite regulation, blood pressure, and some glycemic indices, but mechanistic and long‑term outcomes remain underexplored. Conclusion: Sleep deprivation and circadian disruption mediate cardiometabolic disease through converging neuroendocrine, autonomic, inflammatory, and behavioral pathways. Future research should employ longitudinal designs and integrated multi- “omics” approaches combined with sleep phenotyping to clarify causal mechanisms and identify novel biomarkers and therapeutic targets in clinical sleep medicine.

Introduction: The COVID‐19 pandemic, caused by the SARS‐CoV‐2 virus, was first identified in Wuhan, China, in December 2019 and has had a significant impact on global health. The virus uncovered multifaceted complications across various organ systems, including the cardiovascular system. Pulmonary hypertension, often exacerbated in settings of severe or prolonged viral infections, presents unique challenges in the context of COVID‐19 due to its complex pathophysiology involving vascular inflammation and thrombotic events. Methods: This narrative review aims to delineate the emerging relationship between COVID‐19 and pulmonary hypertension, focusing on pathophysiological insights, clinical implications, and evolving therapeutic strategies, enriching clinical practice and guiding future research of this complex interaction. We conducted a comprehensive literature review using databases such as MEDLINE, PubMed, and Google Scholar with keywords related to pulmonary hypertension and COVID‐19, covering studies published between December 2019 and February 2025. Results: COVID‐19 has been linked to an increased incidence of pulmonary hypertension due to direct viral effects on pulmonary vasculature and secondary inflammatory responses. Clinical manifestations of pulmonary hypertension in COVID‐19 include typical symptoms such as dyspnea and chest pain. Effective management strategies include the use of vasodilators, anticoagulants, and tailored experimental treatments. The review also emphasizes the importance of long‐term follow‐up and monitoring to evaluate disease progression and treatment response. Conclusion: The intersection of COVID‐19 and pulmonary hypertension presents a significant challenge in cardiovascular medicine, necessitating advanced diagnostic and therapeutic approaches. The insights gained from the current pandemic will likely influence broader public health strategies and clinical protocols, improving outcomes for patients with pulmonary hypertension and those at risk of severe viral infections. Future research should focus on personalized medicine approaches and the development of innovative treatments to manage the unique aspects of pulmonary hypertension in the context of COVID‐19.