Community-engaged Research Partnerships as Healing Spaces for Health Professionals and Researchers.

Drawing from collective experiences in our capacity building project: Health Equity Activation Research Team for Inclusion Health, we argue that while community-engaged partnerships tend to focus on understanding health inequities and developing solutions, they can be healing spaces for health professionals and researchers. Data were obtained from a 15-month participatory ethnography, including focus groups and interviews. Ethnographic notes and transcripts were coded and analyzed using both deductive and inductive coding.

The Radical Welcome Engagement Restoration Model and Assessment Tool for Community-Engaged Partnerships.

People experiencing addiction, houselessness, or who have a history of incarceration have worse health outcomes compared with the general population. This is due, in part, to practices and policies of historically White institutions that exclude the voices, perspectives, and contributions of communities of color in leadership, socio-economic development, and decision-making that matters for their wellbeing. Community-based participatory research (CBPR) approaches hold promise for addressing health inequities.

COVID-19 and practice transformation: Building an office-based opioid treatment program in a family medicine residency practice.

Introduction: This brief report describes how a family medicine residency practice (FMRP) leveraged a resident-led quality improvement project and a grant-funded Addiction Integrated Care Team (AICT) to initiate an office-based opioid treatment (OBOT) program to provide medications for opioid use disorder during the COVID-19 pandemic.

Method: In 2020, the practice experienced four disruptors that shifted motivation for practice development: (a) The COVID-19 pandemic demanded rapid change in primary care processes/staffing, including pivoting to telehealth/remote practice. (b) The practice's transition to a federally qualified community health center model meant a shift in organizational priorities that required offering OBOT services.

The Emergence of Family Medicine Identity Among First-Year Residents: A Qualitative Study.

Background And Objectives: As part of a national pilot, the Lehigh Valley Family Medicine Residency Program implemented curricular changes to emphasize family medicine identity. These changes included limiting first-year inpatient experiences, adding "interval" outpatient weeks, and increasing family physician mentorship. This study explores how postgraduate learners describe their professional identities within the context of their chosen specialty, as defined by Family Medicine for America's Health (FMAHealth).

Using Telemedicine Technology to Assess Physician Outpatient Teaching.

Background And Objectives: Video conferencing technology (telemedicine) can be applied to many settings within the medical community; we assessed the feasibility of its use in conducting observations of faculty at remote family medicine teaching sites.

Methods: We deployed seven telemedicine units to five family medicine residency sites and two observation stations within our division. Practice managers and physician faculty members received on-site training on the basic functionality of the technology, as well as "best practices" and minor troubleshooting techniques.

Patients with disabilities as teachers.

Background And Objectives: Medical schools and residencies lack training in communication skills with patients with disabilities, thereby creating potential barriers to care. To address this shortcoming, the Department of Family Medicine at Lehigh Valley Health Network developed an innovative program in which the patients themselves serve as medical educators. The P-DAT (Patients With Disabilities as Teachers) program is designed to teach basic communication skills and disability etiquette to promote sensitivity to issues unique to this patient population.

RAFT (Resident Assessment Facilitation Team): supporting resident well-being through an integrated advising and assessment process.

Background And Objectives: During medical residency, indicators of well-being decline while rates of burnout increase. As part of a Preparing the Personal Physician for Practice (P4) innovation, this residency program used a relationship-centered periodic resident assessment process to reinforce values of adult learning within the curriculum. It was predicted that the revised assessment process would contribute to an improved educational climate for residents as reflected in global scores of well-being either remaining at the same level or improving throughout residency.

Generating developmentally appropriate competency assessment at a family medicine residency.

Background And Objectives: Ten years after the Accreditation Council for Graduate Medical Education's (ACGME) mandate that residency programs evaluate learners' competency, research is needed to guide efforts to meet this challenge. During an innovative residency redesign, the authors developed a process to effectively measure "competence." This particular family medicine residency admits six residents per class year and is sponsored by an academic community hospital.

Understanding the role of the promotora in a Latino diabetes education program.

We explore the role of the promotora de salud (health promoter) who provided diabetes self-management education to Puerto Rican diabetics in her community. The education program was developed as a hospital and community-based organization partnership. Information from both Spanish-language focus groups with 35 class participants and an in-depth interview with the promotora indicated patients appreciated having the classes taught in Spanish by a Latina promotora from their community.

Evidence for a critical contribution of haploinsufficiency in the complex pathogenesis of Marfan syndrome.

Marfan syndrome is a connective tissue disorder caused by mutations in the gene encoding fibrillin-1 (FBN1). A dominant-negative mechanism has been inferred based upon dominant inheritance, mulitimerization of monomers to form microfibrils, and the dramatic paucity of matrix-incorporated fibrillin-1 seen in heterozygous patient samples. Yeast artificial chromosome-based transgenesis was used to overexpress a disease-associated mutant form of human fibrillin-1 (C1663R) on a normal mouse background.

Characterization of microsatellite markers flanking FBN1: utility in the diagnostic evaluation for Marfan syndrome.

Marfan syndrome (MFS) is an autosomal dominant disorder of connective tissue with marked interfamilial and intrafamilial variation in phenotype. The primary defect in affected patients resides in the gene for fibrillin-1 (FBN1) on 15q21. Linkage analysis has shown no locus heterogeneity in the classic phenotype, although substantial allelic heterogeneity exists.

Familial Tetralogy of Fallot caused by mutation in the jagged1 gene.

Tetralogy of Fallot (ToF) is the most common form of complex congenital heart disease, occurring in approximately 1 in 3000 live births. Evaluation of candidate loci in a large kindred segregating autosomal dominant ToF with reduced penetrance culminated in identification of a missense mutation (G274D) in JAG1, the gene encoding jagged1, a Notch ligand expressed in the developing right heart. Nine of eleven mutation carriers manifested cardiac disease, including classic ToF, ventricular septal defect with aortic dextroposition and isolated peripheral pulmonic stenosis (PPS).

Phenotypic alteration of vascular smooth muscle cells precedes elastolysis in a mouse model of Marfan syndrome.

Marfan syndrome is associated with early death due to aortic aneurysm. The condition is caused by mutations in the gene (FBN1) encoding fibrillin-1, a major constituent of extracellular microfibrils. Prior observations suggested that a deficiency of microfibrils causes failure of elastic fiber assembly during late fetal development.

Pathogenetic sequence for aneurysm revealed in mice underexpressing fibrillin-1.

Dissecting aortic aneurysm is the hallmark of Marfan syndrome (MFS) and the result of mutations in fibrillin-1, the major constituent of elastin-associated extracellular microfibrils. It is yet to be established whether dysfunction of fibrillin-1 perturbs the ability of the elastic vessel wall to sustain hemodynamic stress by disrupting microfibrillar assembly, by impairing the homeostasis of established elastic fibers, or by a combination of both mechanisms. The pathogenic sequence responsible for the mechanical collapse of the elastic lamellae in the aortic wall is also unknown.

Revised genomic organization of FBN1 and significance for regulated gene expression.

FBN1 encodes fibrillin-1, an extracellular matrix protein that is defective in Marfan syndrome. This gene is divided into 65 exons and was previously reported to be approximately 110 kb in length. The existence of 3 exons upstream of the exon containing the putative initiating methionine left open the possibility of alternative fibrillin-1 isoforms that vary at their N-termini.

Targetting of the gene encoding fibrillin-1 recapitulates the vascular aspect of Marfan syndrome.

Aortic aneurysm and dissection account for about 2% of all deaths in industrialized countries; they are also components of several genetic diseases, including Marfan syndrome (MFS). The vascular phenotype of MFS results from mutations in fibrillin-1 (FBN1), the major constituent of extracellular microfibrils. Microfibrils, either associated with or devoid of elastin, give rise to a variety of extracellular networks in elastic and non-elastic tissues.