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Rationale: Sepsis is a syndrome of life-threatening organ dysfunction caused by a dysregulated host immune response to infection. Social risk factors including location and poverty are associated with sepsis-related disparities. Understanding the social and biological phenotypes linked with the incidence of sepsis is warranted to identify the most at-risk populations. We aim to examine how factors in disadvantage influence health disparities related to sepsis., Methods: A scoping review was performed for English-language articles published in the United States from 1990 to 2022 on PubMed, Web of Science, and Scopus. Of the 2064 articles found, 139 met eligibility criteria and were included for review., Results: There is consistency across the literature of disproportionately higher rates of sepsis incidence, mortality, readmissions, and associated complications, in neighborhoods with socioeconomic disadvantage and significant poverty. Chronic arterial hypertension and diabetes mellitus also occur more frequently in the same geographic distribution as sepsis, suggesting a potential shared pathophysiology., Conclusions: The distribution of chronic arterial hypertension, diabetes mellitus, social risk factors associated with socioeconomic disadvantage, and sepsis incidence, are clustered in specific geographical areas and linked by endothelial dysfunction. Such population factors can be utilized to create equitable interventions aimed at mitigating sepsis incidence and sepsis-related disparities., Competing Interests: Declaration of Competing Interest The authors have no conflicts of interest to report., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Restless legs syndrome (RLS) is a common, chronic neurologic condition, which causes a persistent urge to move the legs in the evening that interferes with sleep. Human and animal studies have been used to study the pathophysiologic state of RLS and much has been learned about the iron and dopamine systems in relation to RLS. Human neuropathologic and imaging studies have consistently shown decreased iron in different brain regions including substantia nigra and thalamus. These same areas also demonstrate a state of relative dopamine excess. While it is not known how these changes in dopamine or iron produce the symptoms of RLS, genetic and hormone studies of RLS have identified other biologic systems or genes, such as the endogenous opioid and melanocortin systems and BTBD9 and MEIS1, that may explain some of the iron or dopamine changes in relation to RLS. This manuscript will review what is known about the pathophysiology of RLS, especially as it relates to changes in iron, dopamine, genetics, and hormonal systems.