The role of payment and financing in achieving health equity

Objective

The aim was to identify healthcare payment and financing reforms to promote health equity and ways that the Agency for Healthcare Research and Quality (AHRQ) may promote those reforms.

Data Sources and Study Setting

AHRQ convened a payment and financing workgroup–the authors of this paper–as part of its Health Equity Summit held in July 2022. This workgroup drew from its collective experience with healthcare payment and financing reform, as well as feedback from participants in a session at the Health Equity Summit, to identify the evidence base and promising paths for reforms to promote health equity.

Study Design

The payment and financing workgroup developed an outline of reforms to promote health equity, presented the outline to participants in the payment and financing session of the July 2022 AHRQ Health Equity Summit, and integrated feedback from the participants.

Data Collection/Extraction Methods

This paper did not require novel data collection; the authors collected the data from the existing evidence base.

Principal Findings

The paper outlines root causes of health inequity and corresponding potential reforms in five domains: (1) the differential distribution of resources between healthcare providers serving different communities, (2) scarcity of financing for populations most in need, (3) lack of integration/accountability, (4) patient cost barriers to care, and (5) bias in provider behavior and diagnostic tools.

Conclusions

Additional research is necessary to determine whether the proposed reforms are effective in promoting health equity.     

Evaluation of the bioequivalence and food effect on the bioavailability of CC-486 (oral azacitidine) tablets in adult patients with cancer

Cancer Chemotherapy and Pharmacology - CC-486 is an oral formulation of azacitidine that allows for extended dosing schedules to prolong azacitidine exposure to malignant cells and maximize...     

Dexamethasone potentiates in vitro blood-brain barrier recovery after primary blast injury by glucocorticoid receptor-mediated upregulation of ZO-1 tight junction protein

Owing to the frequent incidence of blast-induced traumatic brain injury (bTBI) in recent military conflicts, there is an urgent need to develop effective therapies for bTBI-related pathologies. Blood-brain barrier (BBB) breakdown has been reported to occur after primary blast exposure, making restoration of BBB function and integrity a promising therapeutic target. We tested the hypothesis that treatment with dexamethasone (DEX) after primary blast injury potentiates recovery of an in vitro BBB model consisting of mouse brain endothelial cells (bEnd.3). DEX treatment resulted in complete recovery of transendothelial electrical resistance and hydraulic conductivity 1 day after injury, compared with 3 days for vehicle-treated injured cultures. Administration of RU486 (mifepristone) inhibited effects of DEX, confirming that barrier restoration was mediated by glucocorticoid receptor signaling. Potentiated recovery with DEX treatment was accompanied by stronger zonula occludens (ZO)-1 tight junction immunostaining and expression, suggesting that increased ZO-1 expression was a structural correlate to BBB recovery after blast. Interestingly, augmented ZO-1 protein expression was associated with specific upregulation of the α⁺ isoform but not the α⁻ isoform. This is the first study to provide a mechanistic basis for potentiated functional recovery of an in vitro BBB model because of glucocorticoid treatment after primary blast injury.