Heart failure (HF) remains a significant health challenge globally, placing a heavy burden on individuals, families, and healthcare systems. The prevalence of HF continues to rise, posing substantial public health concerns. This burden is particularly pronounced among the Black Population, who face higher prevalence, earlier onset, and greater severity of HF compared to other racial and ethnic groups. This review explores the multifaceted landscape of HF in Black individuals by examining epidemiological patterns, pathophysiological mechanisms, clinical presentations, treatment disparities, and clinical outcomes. Black individuals exhibit distinct pathophysiological characteristics, such as genetic variations contributing to heightened susceptibility and severity of HF. Social determinants of health, including socioeconomic status, education, and healthcare access, further exacerbate these disparities. Despite advancements in medical science, Black individuals receive less optimal HF care, reflected in lower rates of guideline-directed medical therapy and cardiac rehabilitation. Addressing these disparities requires targeted interventions and a holistic approach that emphasizes social determinants of health, improved healthcare access, and health equity. This review synthesizes existing literature to illuminate the unique challenges faced by Black HF patients and advocates for evidence-based strategies to enhance management and outcomes, aiming to reduce disparities and improve the well-being of this vulnerable population.

Objective: Clinical trials are the cornerstone of medical innovation and set the standard for medical care. Cancer clinical trials drive critical innovation and availability of new treatments. However, obstacles to successful recruitment and participation of patients in clinical trials still significantly limit their success. Our objective is to evaluate trial enrollment trends according to both patient and trial demographics/features for those who have sought care at our multi-center, mixed-setting Gynecologic Oncology practice, allowing for us to describe specific trial criteria designs that are negatively associated with diverse enrollment or lack of enrollment completion on cancer clinical trials. Methods: An IRB-approved, retrospective cohort study was completed to evaluate patients who screened positive for a clinical trial through the Gynecologic Oncology practice’s manual screening process. We looked at how trial characteristics affect enrollment success. Results: After adjustment, there were no significant differences between patient factors and enrollment status. Higher rates of enrollment were seen among Asian patients and patients whose race was reported as “unknown” (>50%, p = 0.125). There was a drastic, unadjusted estimated increase in enrollment for Medicaid patients compared to patients with other insurance types (55.2% vs. 32%, p = 0.031), but multivariable logistic regression showed that insurance status (Medicaid vs. others) lost significance, p = 0.148. Patients with Stage I cancer accounted for 42.1% of patients enrolled, and enrollment rates were higher than for other cancer stages (p = 0.087). There was a significant increase in enrollment likelihood if the trial did not exclude subjects with prior cancer (50.0% vs. 33.3%, p = 0.046). Conclusions: We demonstrated equitable trial enrollment across different races and insurance statuses and were able to identify criteria that lend itself towards higher rates of enrollment. These findings can be used to tailor cancer trial portfolios to a diverse patient catchment.

Acne vulgaris is an inflammatory cutaneous condition that disproportionately affects the pediatric population. While there are several risk factors, emerging evidence suggests that ultra-processed foods (UPFs), as part of Western dietary patterns, may contribute to acne pathophysiology through activation of inflammatory pathways, such as mTORC1. This comprehensive review synthesizes current evidence regarding acne pathogenesis in conjunction with diet-associated inflammatory cascades to better illustrate the potential role of diet as an adjunct to clinical management in pediatric patients. The current literature suggests that increased insulin/IGF-1 levels may contribute to alterations in the skin and gut microbiota. Additionally, components commonly found in UPFs have been proposed to activate the mechanistic target of rapamycin complex (mTORC1) through insulin/IGF-1-dependent and -independent mechanisms, perpetuating inflammatory pathways that give rise to acne pathogenesis. However, the majority of available evidence is derived from adult cohorts; pediatric-specific evidence remains limited. While studies have demonstrated clinical significance in acne severity with dietary interventions, future high-quality studies are required. Through understanding the relationship between diet and acne pathogenesis, future therapeutic and preventative strategies may be developed to improve pediatric acne clinical outcomes.