COVID‐19 and the Uncovering of Health Care Disparities in the United States, United Kingdom and Canada: Call to Action

Aftab Ala, Julius Wilder, Naudia L. Jonassaint, Carla S. Coffin, Carla Brady, Andrew Reynolds, Michael L. Schilsky – 19 July 2021 – The coronavirus disease 2019 (COVID‐19) pandemic created a crisis that disproportionately affected populations already disadvantaged with respect to access to health care systems and adequate medical care and treatments. Understanding how and where health care disparities are most widespread is an important starting point for exploring opportunities to mitigate such disparities, especially within our patient population with liver disease.

The E3 Ubiquitin Ligase Ring Finger Protein 5 Ameliorates NASH Through Ubiquitin‐Mediated Degradation of 3‐Hydroxy‐3‐Methylglutaryl CoA Reductase Degradation Protein 1

Qin Yang, Xi Chen, Yanfang Zhang, Sha Hu, Fengjiao Hu, Yongping Huang, Tengfei Ma, Heng Hu, Han Tian, Song Tian, Yan‐Xiao Ji, Zhi‐Gang She, Peng Zhang, Xiao‐Jing Zhang, Yufeng Hu, Hailong Yang, Yufeng Yuan, Hongliang Li – 16 July 2021

Reassessment of the Hispanic Disparity: Hepatic Steatosis Is More Prevalent in Mexican Americans Than Other Hispanics

Magda Shaheen, Deyu Pan, Katrina M. Schrode, Dulcie Kermah, Vishwajeet Puri, Ali Zarrinpar, David Elisha, Sonia M. Najjar, Theodore C. Friedman – 15 July 2021 – Hepatic steatosis (HS) is a growing problem in adults worldwide, with racial/ethnic disparity in the prevalence of the disease. The purpose of this study was to characterize the racial/ethnic prevalence of the stages (normal/mild [S0/S1], moderate [S2], and severe [S3]) of HS in Mexican Americans and other Hispanics compared to other racial/ethnic groups.

Tissue‐Specific Regulation of Ferroportin in Wild‐Type and Hjv‐/‐ Mice Following Dietary Iron Manipulations

Angeliki Katsarou, Konstantinos Gkouvatsos, Carine Fillebeen, Kostas Pantopoulos – 15 July 2021 – Hepcidin is a liver‐derived peptide hormone that limits iron egress from tissues to the bloodstream. It operates by binding to the iron exporter ferroportin, which blocks iron transport and tags ferroportin for degradation. Genetic hepcidin inactivation leads to hereditary hemochromatosis, a disease of iron overload. We used wild‐type and Hjv‐/‐ mice, a model of hemochromatosis, to examine the expression of ferroportin and other proteins of iron metabolism in hepcidin target tissues.

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