Addressing Native Hawaiian and Pacific Islander Data Deficiencies Through a Community-based Collaborative Response to the COVID-19 Pandemic.

Early evidence of disproportionate COVID-19 infection and death rates in Native Hawaiian and Pacific Islander communities in the continental US raised concerns for similar disparities in Hawai'i, where these communities make up 25% of the state's population. Representatives from more than 40 different government, academic, institutional and community-based organizations partnered to form the Hawai'i Native Hawaiian and Pacific Islander COVID-19 Response, Recovery, and Resilience Team. The team consists of 5 committees including the Data & Research Committee. This committee is tasked with examining issues regarding the acquisition, quality, public reporting, and utilization of race/ethnicity-related health data used to inform priorities and guide resource allocation. Problems addressed by this committee include: inconsistency across agencies in the use of race identifiers, defaulting to the Office of Management and Budget standards which aggregated Native Hawaiian and Pacific Islanders, and methods of data collection and reporting by the Department of Health. Outcomes include: 2 forms with race categories that reflect the population of Hawai'i; the reporting of disaggregated data by the Department of Health; and conversations with testing sites, laboratories, and health institutions urging a standardized form for race/ethnicity data collection. The collection and reporting of disaggregated race/ethnicity data is critical to guiding organizations in addressing underlying inequities in chronic disease and social determinants of health that can exacerbate the adverse effects of COVID-19. The Data and Research Committee's network offers a community-based model for collaborative work that honors culture and ensures Native Hawaiian, Pacific Islander, and other minority populations are recognized and counted.

Pre-B-cell colony-enhancing factor is a secreted cytokine-like protein from the human amniotic epithelium.

OBJECTIVE: The purpose of this study was to determine whether pre-B-cell colony-enhancing factor is a secreted cytokine in the human amnion and to study its chemotaxic and antiapoptotic properties. STUDY DESIGN: Pre-B-cell colony-enhancing factor secretion was studied from amniotic epithelial-like WISH cells and primary amniotic epithelial cells that were seeded on squares of immobilon-P membrane and stimulated with lipopolysaccharide or tumor necrosis factor-alpha, respectively. The pre-B-cell colony-enhancing factor protein was detected both intracellularly and after secretion, as bound to the membrane, by immunostaining and densitometry. Medium and cell lysates that were obtained from WISH cells that were treated with lipopolysaccharide alone or together with a pre-B-cell colony-enhancing factor antisense oligonucleotide to block pre-B-cell colony-enhancing factor translation were also analyzed for secreted pre-B-cell colony-enhancing factor by Western blotting and densitometry. A chemotaxic effect of pre-B-cell colony-enhancing factor on human neutrophils was compared with the chemoattractants interleukin-8 and N-Formyl-Met-Leu-Phe methyl ester in a rapid fluorescence-based neutrophil migration assay. Apoptosis was induced in primary amniotic epithelial cells and fibroblasts by actinomycin D (1 microg/mL); the antiapoptotic effects of pre-B-cell colony-enhancing factor on early apoptosis were measured by the annexin V assay, and the late effects were determined by measurement of nuclear matrix protein in the media. RESULTS: Treatment of amnion cells that adhered to immobilon-P membrane to induce the secretion of pre-B-cell colony-enhancing factor showed significantly (P<.05) more pre-B-cell colony-enhancing factor protein surrounding the cells compared with the controls. Although the addition of lipopolysaccharide to cultured WISH cells caused the secretion of pre-B-cell colony-enhancing factor into the medium, co-treatment with an antisense oligonucleotide to pre-B-cell colony-enhancing factor obliterated it. Analysis of the cell lysates showed no significant change, which suggests that most of the pre-B-cell colony-enhancing factor protein had been secreted. No significant chemotaxic effects of pre-B-cell colony-enhancing factor were observed; however, pre-B-cell colony-enhancing factor treatment (100 ng/mL), together with actinomycin D, cancelled the early induction of apoptosis, although there was a dose-dependent and significant late antiapoptotic effect on primary amnion epithelial cells (P<.001) and fibroblasts (P<.01). CONCLUSION: Pre-B-cell colony-enhancing factor is a secreted protein from amniotic epithelial cells. Although it had no chemotaxic effects, it was antiapoptotic for both amniotic epithelial cells and fibroblasts and may protect these cells against apoptosis that is induced by chronic distension, labor, or infection.