Health Equity in an Age-Friendly Health System: Identifying Potential Care Gaps.

BACKGROUND: The Age-Friendly Health Systems (AFHS) initiative uses a 4Ms framework-What Matters, Mentation, Medication, and Mobility-to encourage patient-centered care for older adults. Many health systems have implemented the core elements of AFHS with the goal to uniformly apply them to all patients 65 years and older. However, equity in AFHS delivery has not yet been examined. METHODS: Five health equity factors-gender, race, ethnicity, preferred language, and electronic patient portal (MyChart) activation-were cross-sectionally analyzed against the 4Ms framework for patients in an academic internal medicine clinic seen between April 2020 and April 2021 (N = 3 370). Bivariate analysis and multiple logistic regression models analyzed the relationship of health equity variables to the 4Ms metrics and were represented with odds ratios and 95% confidence intervals. RESULTS: Preferred language, gender, and MyChart activation yielded significant 4M metric pairings. Females were 1.22 times more likely than males, and English-speaking patients were 2.27 times more likely than non-English-speaking patients to receive advance care planning (p < .01). Females and patients with MyChart activation were about 2 times more likely to have a high-risk medication on their medication list compared to males and patients without MyChart activation (p < .01). Patients with MyChart activation were 2.08 times more likely than patients without MyChart activation to get cognitive screening (p < .001). CONCLUSION: This study, the first to incorporate demographic data into AFHS outcomes, suggests a need to develop best practices for equitable Age-Friendly care at the clinical team and institutional policy levels.

Autocrine hemokinin-1 functions as an endogenous adjuvant for IgE-mediated mast cell inflammatory responses.

BACKGROUND: Efficient development of atopic diseases requires interactions between allergen and adjuvant to initiate and amplify the underlying inflammatory responses. Substance P (SP) and hemokinin-1 (HK-1) are neuropeptides that signal through the neurokinin-1 receptor (NK1R) to promote inflammation. Mast cells initiate the symptoms and tissue effects of atopic disorders, secreting TNF and IL-6 after FcεRI cross-linking by antigen-IgE complexes (FcεRI-activated mast cells [FcεRI-MCs]). Additionally, MCs express the NK1R, suggesting an adjuvant role for NK1R agonists in FcεRI-MC-mediated pathologies; however, in-depth research addressing this relevant aspect of MC biology is lacking. OBJECTIVE: We sought to investigate the effect of NK1R signaling and the individual roles of SP and HK-1 as potential adjuvants for FcεRI-MC-mediated allergic disorders. METHODS: Bone marrow-derived mast cells (BMMCs) from C57BL/6 wild-type (WT) or NK1R(-/-) mice were used to investigate the effects of NK1R signaling on FcεRI-MCs. BMMCs generated from Tac1(-/-) mice or after culture with Tac4 small interfering RNA were used to address the adjuvancy of SP and HK-1. WT, NK1R(-/-), and c-Kit(W-sh/W-sh) mice reconstituted with WT or NK1R(-/-) BMMCs were used to evaluate NK1R signaling on FcεRI-MC-mediated passive local and systemic anaphylaxis and on airway inflammation. RESULTS: FcεRI-activated MCs upregulated NK1R and HK-1 transcripts and protein synthesis, without modifying SP expression. In a positive signaling loop HK-1 promoted TNF and IL-6 secretion by MC degranulation and protein synthesis, the latter through the phosphoinositide 3-kinase/Akt/nuclear factor κB pathways. In vivo NK1R signaling was necessary for the development of passive local and systemic anaphylaxis and airway inflammation. CONCLUSIONS: FcεRI stimulation of MCs promotes autocrine secretion of HK-1, which signals through NK1R to provide adjuvancy for efficient development of FcεRI-MC-mediated disorders.