Improving the Assessment of Resident Competency: Physical Medicine and Rehabilitation Milestones 2.0.

ABSTRACT: In 2015, the Accreditation Council for Graduate Medical Education published the Physical Medicine and Rehabilitation Milestones 1.0 as part of the Next Accreditation System. This was the culmination of more than 20 yrs of work on the part of the Accreditation Council for Graduate Medical Education to improve graduate medical education competency assessments. The six core competencies were patient care, medical knowledge, systems-based practice, practice-based learning and improvement, professionalism, and interpersonal and communication skills. While providing a good foundation for resident assessment, the Physical Medicine and Rehabilitation Milestones 1.0 was not without faults. With input from program directors, national organizations, and the public, the Physical Medicine and Rehabilitation Milestones 2.0 strives to further advance resident assessment, providing improvements through the integration of the harmonized Milestones and the addition of a supplemental guide.

Resident Perspectives on the Current State of Diversity in Graduate Medical Education.

BACKGROUND: Diversity continues to be an important topic to physicians in training. OBJECTIVE: We set out to define current issues related to diversity in graduate medical education; explore these topics with a multispecialty group of current residents and fellows; and identify programmatic, institutional, and Accreditation Council for Graduate Medical Education actions to support diversity in the medical profession. METHODS: A 35-member, multispecialty council of residents and fellows used a World Café diversity and inclusion exercise to highlight current issues related to diversity. RESULTS: Several common issues in diversity were identified, including microaggressions, team member relationships, underrepresentation of workplace discrimination, and tolerance of unacceptable behavior to conform to workplace norms. Suggestions and methods to improve these diversity issues were also proposed. CONCLUSIONS: As trainees, we must continue to implement strategies and policies that allow us to embrace diversity in our workplace and community for our patients and ourselves. Only with the continued support of residency and institutional leadership can we improve the state of diversity in our training programs.

Surprising behavioral and neurochemical enhancements in mice with combined mutations linked to Parkinson's disease.

Parkinson's disease (PD) is the second most common neurodegenerative disorder behind Alzheimer's disease. There are currently no therapies proven to halt or slow the progressive neuronal cell loss in PD. A better understanding of the molecular and cellular causes of PD is needed to develop disease-modifying therapies. PD is an age-dependent disease that causes the progressive death of dopamine-producing neurons in the brain. Loss of substantia nigra dopaminergic neurons results in locomotor symptoms such as slowness of movement, tremor, rigidity and postural instability. Abnormalities in other neurotransmitters, such as serotonin, may also be involved in both the motor and non-motor symptoms of PD. Most cases of PD are sporadic but many families show a Mendelian pattern of inherited Parkinsonism and causative mutations have been identified in genes such as Parkin, DJ-1, PINK1, alpha-synuclein and leucine rich repeat kinase 2 (LRRK2). Although the definitive causes of idiopathic PD remain uncertain, the activity of the antioxidant enzyme glutathione peroxidase 1 (Gpx1) is reduced in PD brains and has been shown to be a key determinant of vulnerability to dopaminergic neuron loss in PD animal models. Furthermore, Gpx1 activity decreases with age in human substantia nigra but not rodent substantia nigra. Therefore, we crossed mice deficient for both Parkin and DJ-1 with mice deficient for Gpx1 to test the hypothesis that loss-of-function mutations in Parkin and DJ-1 cause PD by increasing vulnerability to Gpx1 deficiency. Surprisingly, mice lacking Parkin, DJ-1 and Gpx1 have increased striatal dopamine levels in the absence of nigral cell loss compared to wild type, Gpx1(-/-), and Parkin(-/-)DJ-1(-/-) mutant mice. Additionally, Parkin(-/-)DJ-1(-/-) mice exhibit improved rotarod performance and have increased serotonin in the striatum and hippocampus. Stereological analysis indicated that the increased serotonin levels were not due to increased serotonergic projections. The results of our behavioral, neurochemical and immunohistochemical analyses reveal that PD-linked mutations in Parkin and DJ-1 cause dysregulation of neurotransmitter systems beyond the nigrostriatal dopaminergic circuit and that loss-of-function mutations in Parkin and DJ-1 lead to adaptive changes in dopamine and serotonin especially in the context of Gpx1 deficiency.

An evaluation of multiple trauma severity indices created by different index development strategies

Evaluation of the effectiveness of emergency trauma care systems is complicated by the need to adjust for the widely variable case mix found in trauma patient populations. Several strategies have been advanced to construct the severety indices that can control for these population differences. This article describes a validity and reliability comparison of trauma. Severity indices developed inder three different approaches: 1) Use of a multi-attribute utility (MAU) Model;2) An actuarial approach relying on empirical data bases; and 3) An "AD HOC" approach, seven criteria were identified to serve as standards of comparison for four different indices the study's findings indicate that the index developed using the MAU theory approach associates most closely with physical judgments of trauma severity when correlated with a morbidity out-come measure. The MAU-Based index shows higher levels of agreement than the other indices. The index development approach based on the principles of mau theory has several advantages and it appears to be a powerful tool in the creation of effective severety indices (AU)