INTRODUCTION:Metropolitan cities in the United States suffer from higher rates of gun violence. However, the specific structural factors associated with increased gun violence are poorly defined. We hypothesized that firearm homicide in metropolitan cities would be impacted by Black-White segregation index. METHODS:This cross-sectional analysis evaluated 51 US metropolitan statistical areas (MSAs) using data from 2013 to 2017. Several measures of structural racism were examined, including the Brooking Institute's Black-White segregation index. Demographic data were derived from the US Census Bureau, US Department of Education, and US Department of Labor. Crime data and firearm homicide mortality rates were obtained from the Federal Bureau of Investigation and the Centers for Disease Control. Spearman ρ and linear regression were performed. RESULTS:Firearm mortality was associated with multiple measures of structural racism and racial disparity, including White-Black segregation index, unemployment rate, poverty rate, single parent household, percent Black population, and crime rates. In regression analysis, percentage Black population exhibited the strongest association with firearm homicide mortality (β = 0.42, p < 0.001). Black-White segregation index (β = 0.41, p = 0.001) and percent children living in single-parent households (β = 0.41, p = 0.002) were also associated with higher firearm homicide mortality. Firearm legislation scores were associated with lower firearm homicide mortality (β = −0.20 p = 0.02). High school and college graduation rates were not associated with firearm homicide mortality and were not included in the final model. CONCLUSION:Firearm homicide disproportionately impacts communities of color and is associated with measures of structural racism, such as White-Black segregation index. Public health interventions targeting gun violence must address these systemic inequities. Furthermore, given the association between firearm mortality and single-parent households, intervention programs for at-risk youth may be particularly effective.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) or coronavirus disease 2019 , first identified in December 2019 in Wuhan, China, has rapidly spread worldwide, is now a public health emergency, and has been declared a pandemic. While SARS-CoV-2 is known to cause significant pulmonary disease, ranging from pneumonia to acute respiratory distress syndrome (ARDS), various extrapulmonary manifestations of COVID-19 have also been reported. Growing evidence suggests that COVID-19 leads to a hypercoagulable state leading to micro and macro-vascular angiopathies. We present a case of an 80-yearold male without a previous history of prothrombotic disorders who developed descending aortic thrombosis, approximately 40% stenosis, at the level of the diaphragmatic hiatus and acute limb ischemia secondary to COVID-19 requiring emergent surgical intervention. After 12 days of persistent ischemic left lower extremity imaging despite thrombectomy, bypass, and therapeutic heparin, the patient's limb was deemed non-salvageable and underwent left above-knee amputation. Transthoracic echocardiogram revealed normal left ventricular function, moderate pulmonary hypertension, and no evidence of atrial septal defect, aortic root abnormalities, or intraventricular thrombi. Evaluation of autoimmune and inflammatory vasculitis was negative. While further study into the prothrombotic nature of this condition still needs to be pursued, the thromboembolic risk of COVID-19 represents an urgent need for appropriate anticoagulation for venous thrombosis. Arterial thrombosis requires other kinds of management to avoid the severe adverse effects of emboli and related ischemia. This current case highlights the need for randomized control trials testing different prophylactic strategies. Further evidence is also required for the role of amputation surgery when initial interventions for revascularization fail to restore blood flow.

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Background: The blood-brain barrier inhibits the central nervous system penetration of 98% of small molecule drugs and virtually all biologic agents, which has limited progress in the treatment of neurologic disease. Vasoactive peptides have been shown in animal studies to transiently disrupt the blood-brain barrier and regadenoson is currently being studied in humans to determine if it can improve drug delivery to the brain. However, there are many other vasoactive peptides that could potentially be used for this purpose. Methods: We performed a review of the literature evaluating the physiologic effects of vasoactive peptides on the vasculature of the brain and systemic organs. To assess the likelihood that a vasoactive peptide might transiently disrupt the blood-brain barrier, we devised a four-tier classification system to organize the evidence available. Results: We identified 33 vasoactive peptides with potential blood-brain barrier permeability-altering properties. To date, none of these are shown to open the blood-brain barrier in humans. 12 vasoactive peptides increased blood-brain barrier permeability in rodents. The remaining 23 had favorable physiologic effects on blood vessels but lacked specific information on permeability changes to the blood-brain barrier. Conclusion: Vasoactive peptides remain an understudied class of drugs with the potential to increase drug delivery and improve treatment in patients with brain tumors and other neurologic diseases. Dozens of vasoactive peptides have yet to be formally evaluated for this important clinical effect. This narrative review summarizes the available data on vasoactive peptides, highlighting agents that deserve further in vitro and in vivo investigations.