The evolving COVID-19 pandemic has unevenly affected academic medical centers (AMCs), which are experiencing resource-constraints and liquidity challenges while at the same time facing high pressures to improve patient access and clinical outcomes. Technological advancements in the field of data analytics can enable AMCs to achieve operational efficiencies and improve bottom-line expectations. While there are vetted analytical tools available to track physician productivity, there is a significant paucity of analytical instruments described in the literature to adequately track clinical and financial productivity of physician assistants (PAs) and nurse practitioners (NPs) employed at AMCs. Moreover, there is no general guidance on the development of a dashboard to track PA/NP clinical and financial productivity at the individual, department, or enterprise level. At our institution, there was insufficient tracking of PA/NP productivity across many clinical areas within the enterprise. Thus, the aim of the project is to leverage our institution's existing visualization tools coupled with the right analytics to track PA/NP productivity trends using a dashboard report.MethodsWe created an intuitive and customizable highly visual clinical/financial analytical dashboard to track productivity of PAs/NPs employed at our AMC.ResultsThe APP financial and clinical dashboard is organized into two main components. The volume-based key performance indicators (KPIs) included work relative value units (wRVUs), gross charges, collections (payments), and payer-mix. The session utilization (KPIs) included (e.g., new versus return patient ratios, encounter type, visit volume, and visits per session by provider). After successful piloting, the dashboard was deployed across multiple specialty areas and results showed improved data transparency and reliable tracking of PAs/NPs productivity across the enterprise. The dashboard analytics were also helpful in assessing PA/NP recruitment requests, independent practice sessions, and performance expectations.ConclusionTo our knowledge, this is the first paper to highlight steps AMCs can take in developing, validating, and deploying a financial/clinical dashboard specific to PAs/NPs. However, empirical research is needed to assess the impact of qualitative and quantitative dashboards on provider engagement, revenue, and quality of care.

The neurotoxin beta-N-methylamino-l-alanine (BMAA) was first identified as a toxin of interest in regard to the amyotrophic lateral sclerosis-Parkinsonism Dementia Complex of Guam (ALS/PDC); studies in recent years highlighting widespread environmental sources of BMAA exposure and providing new clues to toxic mechanisms have suggested possible relevance to sporadic ALS as well. However, despite clear evidence of uptake into tissues and a range of toxic effects in cells and animals, an animal model in which BMAA induces a neurodegenerative picture resembling ALS is lacking, possibly in part reflecting limited understanding of critical factors pertaining to its absorption, biodistribution and metabolism. To bypass some of these issues and ensure delivery to a key site of disease pathology, we examined effects of prolonged (30day) intrathecal infusion in wild type (WT) rats, and rats harboring the familial ALS associated G93A SOD1 mutation, over an age range (80±2 to 110±2days) during which the G93A rats are developing disease pathology yet remain asymptomatic. The BMAA exposures induced changes that in many ways resemble those seen in the G93A rats, with degenerative changes in ventral horn motor neurons (MNs) with relatively little dorsal horn pathology, marked ventral horn astrogliosis and increased 3-nitrotyrosine labeling in and surrounding MNs, a loss of labeling for the astrocytic glutamate transporter, GLT-1, surrounding MNs, and mild accumulation and aggregation of TDP-43 in the cytosol of some injured and degenerating MNs. Thus, prolonged intrathecal infusion of BMAA can reproduce a picture in spinal cord incorporating many of the pathological hallmarks of diverse forms of human ALS, including substantial restriction of overt pathological changes to the ventral horn, consistent with the possibility that environmental BMAA exposure could be a risk factor and/or contributor to some human disease.

The neurotoxin beta-N-methylamino-l-alanine (BMAA) was first identified as a "toxin of interest" in regard to the amyotrophic lateral sclerosis-Parkinsonism Dementia Complex of Guam (ALS/PDC); studies in recent years highlighting widespread environmental sources of BMAA exposure and providing new clues to toxic mechanisms have suggested possible relevance to sporadic ALS as well. However, despite clear evidence of uptake into tissues and a range of toxic effects in cells and animals, an animal model in which BMAA induces a neurodegenerative picture resembling ALS is lacking, possibly in part reflecting limited understanding of critical factors pertaining to its absorption, biodistribution and metabolism. To bypass some of these issues and ensure delivery to a key site of disease pathology, we examined effects of prolonged (30day) intrathecal infusion in wild type (WT) rats, and rats harboring the familial ALS associated G93A SOD1 mutation, over an age range (80±2 to 110±2days) during which the G93A rats are developing disease pathology yet remain asymptomatic. The BMAA exposures induced changes that in many ways resemble those seen in the G93A rats, with degenerative changes in ventral horn motor neurons (MNs) with relatively little dorsal horn pathology, marked ventral horn astrogliosis and increased 3-nitrotyrosine labeling in and surrounding MNs, a loss of labeling for the astrocytic glutamate transporter, GLT-1, surrounding MNs, and mild accumulation and aggregation of TDP-43 in the cytosol of some injured and degenerating MNs. Thus, prolonged intrathecal infusion of BMAA can reproduce a picture in spinal cord incorporating many of the pathological hallmarks of diverse forms of human ALS, including substantial restriction of overt pathological changes to the ventral horn, consistent with the possibility that environmental BMAA exposure could be a risk factor and/or contributor to some human disease.