When the Family Medicine for America’s Health (FMAHealth) Workforce Education and Development Tactic Team (WEDTT) began its work in December 2014, one of its charges from the FMAHealth Board was to increase family physician production to achieve the diverse primary care workforce the United States needs. The WEDTT created a multilevel interfunctional team to work on this priority initiative that included a focus on student, resident, and early-career physician involvement and leadership development. One major outcome was the adoption of a shared aim, known as 25 x 2030. Through a collaboration of the WEDTT and the eight leading family medicine sponsoring organizations, the 25 x 2030 aim is to increase the percentage of US allopathic and osteopathic medical students choosing family medicine from 12% to 25% by the year 2030. The WEDTT developed a package of change ideas based on its theory of what will drive the achievement of 25 x 2030, which led to specific projects completed by the WEDTT and key collaborators. The WEDTT offered recommendations for the future based on its 3-year effort, including policy efforts to improve the social accountability of US medical schools, strategy centered around younger generations’ desires rather than past experiences, active involvement by students and residents, engagement of early-career physicians as role models, focus on simultaneously building and diversifying the family medicine workforce, and security of the scope future family physicians want to practice. The 25 x 2030 initiative, carried forward by the family medicine organizations, will use collective impact to adopt a truly collaborative approach toward achieving this much needed goal for family medicine.
Mutations in MCOLN1, which encodes the cation channel protein TRPML1, result in the neurodegenerative lysosomal storage disorder Mucolipidosis type IV. Mucolipidosis type IV patients show lysosomal dysfunction in many tissues and neuronal cell death. The ortholog of TRPML1 in Caenorhabditis elegans is CUP-5; loss of CUP-5 results in lysosomal dysfunction in many tissues and death of developing intestinal cells that results in embryonic lethality. We previously showed that a null mutation in the ATP-Binding Cassette transporter MRP-4 rescues the lysosomal defect and embryonic lethality of cup-5(null) worms. Here we show that reducing levels of the Endosomal Sorting Complex Required for Transport (ESCRT)-associated proteins DID-2, USP-50, and ALX-1/EGO-2, which mediate the final de-ubiquitination step of integral membrane proteins being sequestered into late endosomes, also almost fully suppresses cup-5(null) mutant lysosomal defects and embryonic lethality. Indeed, we show that MRP-4 protein is hypo-ubiquitinated in the absence of CUP-5 and that reducing levels of ESCRT-associated proteins suppresses this hypo-ubiquitination. Thus, increased ESCRT-associated de-ubiquitinating activity mediates the lysosomal defects and corresponding cell death phenotypes in the absence of CUP-5.KEYWORDS CUP-5; ESCRT; lysosome; mucolipidosis type IV; TRPML1 M UCOLIPIDOSIS type IV (MLIV) is a neurodegenerative lysosomal storage disorder characterized by corneal clouding, achlorhydria, and psychomotor defects (Bach 2001;Altarescu et al. 2002). In MLIV patients, large lipid-rich vacuoles are found in many tissues, while psychomotor defects are thought to be due to neuronal cell death. MLIV is caused by mutations in MCOLN1, which encodes the human protein mucolipin-1/TRPML1; this protein belongs to the transient receptor potential cation channel family and is a nonselective cation channel (Bargal et al. 2000;Bassi et al. 2000;Sun et al. 2000;Laplante et al. 2002;Raychowdhury et al. 2004;Dong et al. 2008).Caenorhabditis elegans protein CUP-5 is the ortholog of human TRPML1 (Fares and Greenwald 2001b;Hersh et al. 2002). The phenotypes resulting from mutations in cup-5(null) mimic those found in MLIV patients: defective lysosomal degradation and the appearance of large vacuoles in most tissues (Fares and Greenwald 2001b;Schaheen et al. 2006a). In addition, this lysosomal dysfunction in the absence of CUP-5 leads primarily to the death of developing intestinal cells that results in embryonic lethality (Schaheen et al. 2006a). It is not known why developing intestinal cells die in C. elegans or why neurons die in MLIV patients. In C. elegans cup-5(null) mutants, the embryonic lethality is not solely due to cells undergoing apoptosis from starvation; when ATP levels are restored or when apoptosis is blocked, embryonic lethality is only partially rescued (14% of embryos hatch and arrest at the L1 larval stage) (Hersh et al. 2002;Schaheen et al. 2006a).We have shown that C. elegans CUP-5 and mammalian TRPML1 likely function in lysoso...
90provide foundational training for residency faculty. Courses cover the structure and requirements of residency education; how to be an effective and efficient faculty member; the nuts and bolts of curriculum development and teaching; and strategies for assessment, feedback, and remediation of residents.Conducted the first meeting of the Precepting Expansion Oversight Committee. This multidisciplinary, interprofessional committee is overseeing the implementation of an action plan to decrease the percentage of primary care clerkship directors who report difficulty finding clinical preceptor sites and increase the percentage of students completing clerkships at high-functioning sites. Five tactic teams began meeting in 2017 and are now implementing strategies to ensure medical, nurse practitioner, and physician assistant students receive hands-on opportunities with patients in real-world settings.Updated the Leading Change online course. The content is now delivered in shorter segments and the course includes interactivity, learning activities, and quizzes to promote understanding and retention.Implemented new submission systems for the Family Medicine Residency Curriculum Resource and the STFM National Clerkship Curriculum. Submissions are now made through the same system STFM uses for its journals, which allows for better tracking of submissions and communication with authors.Implemented digital badging on member profiles in STFM CONNECT. A digital badge is an online recognition of accomplishments, mastery of a skill, or completion of a learning experience. The goal of the badging is to recognize members, showcase their accomplishments and STFM involvement, and encourage participation in STFM programs and leadership activities.The celebration and innovation of 2017 built momentum for the many products and activities planned for 2018: a Medical School Faculty Fundamentals Certificate Program, an enhanced online presence for Family Medicine, a revamped, mobile-friendly website, a new conference submission and review system, and ongoing work to address the shortage of community preceptors.
482the innovative work by individual family physicians such as Jeff Brenner from Camden, New Jersey, who has demonstrated how health care costs can be cut by finding community "hot spots" where emergency departments are over-utilized. 9 We commend the Association of American Medical Colleges (AAMC) for publishing their report on how academic medical centers of the future must be system-based to survive. 9In a recently published report, the AAMC describes 4 options for academic medical centers to move toward a system identity, from forming a new system, to partnering, to merging, or to facing the reality of shrinking in isolation.10 Within ADFM, we are tracking how departments of family medicine (DFMs) are leading health care transformation within their academic health centers. Many of our DFMs are actively engaged in moving to team-based care, improving delivery of preventive services, and promoting more appropriate use of consultations and referrals. 11 We will continue to collaborate with others who share the goal of using population health management approaches to improve affordable health care for the nation.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.