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OBJECTIVES/GOALS: Scholarly achievement metrics are essential for academic researchers since they are used for promotion and funding opportunities. Our objective was to create awareness among pilot project PIs about how these scholarly activities are evaluated and about the need for continuous auto-evaluation. METHODS/STUDY POPULATION: NIH-sponsored Clinical & Translational Research (CTR) infrastructure grants are a critical mechanism to increase scholarly activity. The Pilot Project Program Core (PPP) of The Alliance IDeA-CTR created a weighted metrics system to evaluate activities including presentations, publications, promotion, honors, & community service. We used the revised evidence-based medicine pyramid to develop the metric instrument. Pilot project PIs received the metric table and met quarterly with a PPP member to discuss progress. The top PIs were acknowledged during the Alliance Research Day with a platform presentation and a monetary award for research expenses or travel to scientific meetings. RESULTS/ANTICIPATED RESULTS: During our first 2 pilot project calls (2020-2022) the PPP funded 7 one-year pilot projects for ($50,000 each). We had a total of 10 PIs, 2 of the projects were MPI. Seven PIs were early or new stage investigators (ESI/NSI). Using the productivity award metric we had a total of 33 presentations, 10 publications, 12 events of community service, and 2 external grant funding. These are significant outcomes considering the pandemics impact on clinical & translational research. A total of 3 awards were given, one award per year for funding and an overall award. The activity was well received by the PIs who actively participated in the tracking of their scholarly activities using the metric. DISCUSSION/SIGNIFICANCE: Productivity metrics are crucial for the career development of ESI and NSI by raising awareness regarding the importance of scholarly activities in their career. This activity will help them track their productivity in an ongoing manner while becoming independent researchers.

OBJECTIVES/GOALS: Non-alcoholic fatty liver disease increases with aging and may be associated with MCI. Thus, adults >65 years with NAFLD have a greater risk of MCI. Our objective is to associate NAFLD with MCI and, therefore, optimize the management of MCI through prevention strategies and early interventions. METHODS/STUDY POPULATION: We will recruit 100 patients >65 of all sexes from the GI and Geriatrics clinics of the University of Puerto Rico (UPR). NAFLD prevalence in aging adults will be estimated via ICD-10 codes and definition will be liver fat accumulation or steatosis (AASLD) without secondary causes. We will exclude patients RESULTS/ANTICIPATED RESULTS: We expect to find a higher NAFLD prevalence in aging adults >65 years old compared to younger ones. Furthermore, we aim to elucidate an association of NAFLD with MCI in aging adults. Besides, as the literature has shown, we anticipate that the main cognitive domains affected by NAFLD will be the visuospatial and executive functions. As the population ages, this study will help identify future targets for early interventions in people diagnosed with NAFLD that could have a greater risk for cognitive impairment. DISCUSSION/SIGNIFICANCE: To our knowledge, no study has determined the association of NAFLD with MCI in Hispanics >65 in PR. Raising awareness of NAFLD as a possible treatable or preventable risk factor for MCI by screening NAFLD patients for MCI may improve not only their global health but their quality of life as well.

Human immunodeficiency virus (HIV‐1) remains a public health threat. The introduction of combined antiretroviral treatments has markedly increase life expectancy but inflammation has remained unsolved. Recent studies, in control subjects, link macrophage's alpha7 nicotinic acetylcholine receptor (α7‐nAChR) activation with anti‐inflammatory response. This response normally prevents exaggerated immune responses through the cholinergic anti‐inflammatory pathway (CAP) which inhibits the release of pro‐inflammatory cytokines through the activation of the α7‐nAChR. Nonetheless, little is known if this neuroimmune regulation is affected in HIV‐1 infected patients. Here we examined the secretion of 9 cytokines and chemokines from control subjects exposed to HIV gp120 envelope protein to determine if the CAP is disrupted. We found that HIV gp120 induce α7‐nAChR upregulation and a pro‐inflammatory phenotype in macrophages as demonstrated by the inability to control the release of 8 of 9 pro‐inflammatory cytokines. These results suggest that HIV mitigates the natural strategy to control inflammation by promoting the upregulation of α7‐nAChR, a key player in the CAP, contributing to one crucial, unresolved problem of HIV infection despite therapy: inflammation. Sponsored by NIH‐NINDS Specialized Neuroscience Program U54NS0430311