A Cross-Sectional Factor Analysis of COVID-19 and Influenza Vaccination Decisions in a Racially Diverse Western Pennsylvania Community.

Introduction: Influenza and COVID-19 vaccination rates remain suboptimal, demanding new community-centric approaches that improve targeted counseling and increase vaccine uptake. Notably, racially diverse communities show high vaccine hesitancy, yet most existing vaccine studies focus on white, college-educated cohorts.

Objective: Here, we identify factors influencing vaccination decisions of patients at Turtle Creek Primary Care clinic in Turtle Creek, PA, a racially-diverse borough.

A Cross-Sectional Analysis of Community Perceptions of Flu and COVID-19 Vaccines at Turtle Creek Primary Care Center.

Background: Influenza (flu) and COVID-19 vaccination rates are subpar across the US, especially in racial and/or socioeconomic minority groups who are understudied in public health literature.

Objective: The objective of this mixed-methods study was to elucidate attitudes of patients at the Turtle Creek Primary Care Center, a clinic that cares for ∼70% non-white patients, towards flu and COVID-19 vaccines, with the goal of establishing vaccine education gaps and increasing vaccine uptake in minority communities.

Design/patients: This study was conducted as a cross-sectional analysis.

Reduced hepatocyte mitophagy is an early feature of NAFLD pathogenesis and hastens the onset of steatosis, inflammation and fibrosis.

Nonalcoholic fatty liver disease (NAFLD) encompasses a spectrum of pathologies that includes steatosis, steatohepatitis (NASH) and fibrosis and is strongly associated with insulin resistance and type 2 diabetes. Changes in mitochondrial function are implicated in the pathogenesis of NAFLD, particularly in the transition from steatosis to NASH. Mitophagy is a mitochondrial quality control mechanism that allows for the selective removal of damaged mitochondria from the cell via the autophagy pathway.

Hepatocyte-derived GDF15 suppresses feeding and improves insulin sensitivity in obese mice.

Growth differentiation factor 15 (GDF15) is a stress-induced secreted protein whose circulating levels are increased in the context of obesity. Recombinant GDF15 reduces body weight and improves glycemia in obese models, which is largely attributed to the central action of GDF15 to suppress feeding and reduce body weight. Despite these advances in knowledge, the tissue-specific sites of GDF15 production during obesity are unknown, and the effects of modulating circulating GDF15 levels on insulin sensitivity have not been evaluated directly.

Implementation and challenges of portable blood gas measurements in air medical transport.

Objectives: Ventilator management in prehospital settings using end-tidal CO can lead to inappropriate ventilation in the absence of point of care blood gas (POCBG) measurements. Implementation of POCBG testing in helicopter Emergency Medical Services (HEMS) is limited in part because of concern for preanalytical and analytical errors due to altitude, vibration, and other associated environmental factors and due to insufficient documentation of implementation challenges.

Methods: We performed accuracy and precision verification studies using standard materials tested pre-, in-, and post-flight (n=10) in a large HEMS agency.

Liver-specific Prkn knockout mice are more susceptible to diet-induced hepatic steatosis and insulin resistance.

Objective: PARKIN is an E3 ubiquitin ligase that regulates mitochondrial quality control through a process called mitophagy. Recent human and rodent studies suggest that loss of hepatic mitophagy may occur during the pathogenesis of obesity-associated fatty liver and contribute to changes in mitochondrial metabolism associated with this disease. Whole-body Prkn knockout mice are paradoxically protected against diet-induced hepatic steatosis; however, liver-specific effects of Prkn deficiency cannot be discerned in this model due to pleotropic effects of germline Prkn deletion on energy balance and subsequent protection against diet-induced obesity.

Prenatal hypoxia increases susceptibility to kidney injury.

Prenatal hypoxia is a gestational stressor that can result in developmental abnormalities or physiological reprogramming, and often decreases cellular capacity against secondary stress. When a developing fetus is exposed to hypoxia, blood flow is preferentially redirected to vital organs including the brain and heart over other organs including the kidney. Hypoxia-induced injury can lead to structural malformations in the kidney; however, even in the absence of structural lesions, hypoxia can physiologically reprogram the kidney leading to decreased function or increased susceptibility to injury.

Von Hippel-Lindau Acts as a Metabolic Switch Controlling Nephron Progenitor Differentiation.

Background: Nephron progenitors, the cell population that give rise to the functional unit of the kidney, are metabolically active and self-renew under glycolytic conditions. A switch from glycolysis to mitochondrial respiration drives these cells toward differentiation, but the mechanisms that control this switch are poorly defined. Studies have demonstrated that kidney formation is highly dependent on oxygen concentration, which is largely regulated by von Hippel-Lindau (VHL; a protein component of a ubiquitin ligase complex) and hypoxia-inducible factors (a family of transcription factors activated by hypoxia).