Examining Employment Conditions During the COVID-19 Pandemic in Pasifika Communities.

Introduction: Pasifika (Native Hawaiian and Pacific Islander) people living in the United States experience health, economic, and social inequities, and a disproportionate burden of COVID-19 cases and deaths. This study examines employment among Pasifika living in the 10 US states with the largest Pasifika populations during the COVID-19 pandemic. Methods: We use the Current Population Survey to examine racial differences in employment status, paid work from home (PWFH), and industry telework friendliness. We use data from the Washington Office of Fiscal Management and the Washington State (WA) Employment Security Department to examine county-level unemployment claims. Results: Nationally, Pasifika did not self-report unemployment significantly more than Black, Latino, Asian, and American Indian/Alaska Native respondents, but in WA counties with high Pasifika concentrations, unemployment insurance claim rates were higher compared with all other racial groups, particularly Whites and Asians. Surprisingly, Pasifika had more PWFH opportunities, but worked in less telework-friendly industries nationally. Discussion: This study demonstrates the complexity of employment among Pasifika during the COVID-19 pandemic. The findings correspond with national reports of racialized communities impacted by unemployment, including Pasifika. Marginally significant differences in unemployment nationally may be due to Pasifika working largely in essential industries requiring workplace attendance. Health Equity Implications: Although overlooked or overshadowed by size, our findings highlight the need for continued advocacy to support data disaggregation and Pasifika data sovereignty. This can be achieved through collaborations between researchers as well as local and community organizations to address data needs of Pasifika communities.

Deletion of activating Fcgamma receptors does not confer protection in murine cryoglobulinemia-associated membranoproliferative glomerulonephritis.

Many types of glomerulonephritis are initiated by the deposition of immune complexes, which induce tissue injury via either engagement of Fc receptors on effector cells or via complement activation. Four murine Fcgamma receptors (FcgammaRs) have been identified at present. Ligand binding to FcgammaRI, III, and IV induces cell activation via the immunoreceptor tyrosine-based activation motif on the common gamma chain (FcRgamma). In this study, FcRgamma chain knockout (FcRgamma(-/-)) mice were crossed with thymic stromal lymphopoietin transgenic (TSLPtg) mice, which develop cryoglobulinemic membranoproliferative glomerulonephritis (MPGN). Female mice were studied at 30 and 50 days of age, when MPGN is in early and fully developed stages, respectively. Both TSLPtg and TSLPtg/FcRgamma(-/-) mice developed MPGN with massive glomerular immune deposits, mesangial cell proliferation, extensive mesangial matrix accumulation, and macrophage influx. TSLPtg/FcRgamma(-/-) mice had more glomerular immune complex deposits and higher levels of circulating cryoglobulins, IgG2a, IgG2b, and IgM, compared with TSLPtg mice. TSLPtg and TSLPtg/FcRgamma(-/-) mice developed similar levels of proteinuria. These results demonstrated that deletion of activating FcgammaRs does not confer protection in this model of immune complex-mediated MPGN. The findings contradict accepted paradigms on the role of activating FcgammaRs in promoting features of glomerulonephritis as seen in other model systems. We speculate engagement of FcgammaRs on cells such as monocytes/macrophages may be important for the clearance of deposited immune complexes and extracellular matrix proteins.

Renin-angiotensin system blockade is renoprotective in immune complex-mediated glomerulonephritis.

Blockade of the renin-angiotensin system is renoprotective in a variety of chronic nephropathies, but the direct effect of such treatment in active, immune complex-mediated glomerulonephritis is unknown. This study investigated the short- and long-term effects of an angiotensin-converting enzyme inhibitor (enalapril) and an angiotensin II type 1 receptor blocker (losartan) in thymic stromal lymphopoietin transgenic (TSLPtg) mice, which develop mixed cryoglobulinemia and severe cryoglobulinemia-associated membranoproliferative glomerulonephritis. Enalapril and losartan each reduced hypertension, proteinuria, glomerular extracellular matrix deposition, and mesangial cell activation in TSLPtg mice. These renoprotective effects were not observed with hydralazine treatment, despite a similar antihypertensive effect. Treatment with enalapril or losartan also decreased renal plasminogen activator inhibitor-1 in TSLPtg mice, assessed by immunohistochemistry and quantitative real-time reverse transcriptase-PCR. None of the treatments affected immune complex deposition or macrophage infiltration. Overall, enalapril- and losartan-treated TSLPtg mice survived significantly longer than untreated TSLPtg mice. These studies demonstrate that angiotensin blockade may provide renoprotective benefits, independent of its BP-lowering effect, in the treatment of active immune complex-mediated glomerulonephritis.