Two-Phase Individual Assessments: A Second-Chance Assessment Strategy With Individualized Feedback to Promote Assessment for Learning.

Problem: High-stakes multiple-choice question (MCQ) exams in medical education typically focus on assessment of learning at a single point without providing feedback for improvement. Educators can achieve a more balanced approach to MCQ exams by combining efficient assessment of learning with the feedback and improvement opportunities of assessment for learning.

Approach: As part of a curriculum renewal at Baylor College of Medicine's MD program, the Two-Phase Individual Assessment (TPIA) model was launched within a 4-week preclinical Foundations of Medicine course in August 2023.

Widening the Road to Health Professions Education: Expanding Access for Diverse and Underserved Populations.

The Spring 2023 Webinar Audio Seminar (WAS) of the International Association of Medical Science Educators (IAMSE), titled "Widening the Road to Health Professions Education: Expanding Access for Diverse and Underserved Populations," was designed to help health science educators explore innovative practices in recruiting and enrolling students from underserved populations into health sciences programs. From March 2, 2023, to March 30, 2023, this five-part webinar series was broadcast live to institutions and educators worldwide. This series helped participants learn about creating pathways for students to meet the unique needs of their communities.

To Infinity and Beyond: Expanding the Scope of Basic Sciences in Meeting Accreditation Standards.

Interprofessional training, social sciences curricula, service-learning, pre-clerkship integration, and self-directed learning are all cornerstones of medical education and closely align with accreditation elements for most accreditation bodies within health professions education. As a sequel to the Winter 2022 series, the Spring 2022 Webcast Audio Seminar (WAS) of the International Association of Medical Science Educators (IAMSE) continued to examine the evolving roles of basic science educators. From March 3 to March 31, 2022, the five-part webinar series was broadcast live to audiences at academic institutions worldwide; recordings are available on the IAMSE website.

Back to the Future: Maximizing Student Learning and Wellbeing in the Virtual Age.

The virtual age of learning is no longer a concern of the future. It is here. The Fall 2021 Webinar Audio Series (WAS) of the International Association of Medical Science Educators (IAMSE), titled "Back to the Future: Maximizing Student Learning and Wellbeing in the Virtual Age," was designed to help health science educators equip themselves with tools to teach the next generation of health care professionals successfully.

USMLE Step-1 is Going to Pass/Fail, Now What Do We Do?

The Winter 2021 Webinar Audio Series (WAS) of the International Association of Medical Science Educators (IAMSE), titled, "USMLE Step-1 is Going to Pass/Fail, Now what do we do?" was broadcast live to audiences at academic institutions worldwide in five weekly webinars from January 7, 2021, to February 4, 2021. Recognized experts from various stakeholder groups discussed the impact of the decision to score the United States Medical Licensing Examination (USMLE) Step 1 exam Pass/Fail (P/F). The speakers identified challenges to their respective programs and explored creative ways to address potential consequences.

TNF/Ang-II synergy is obligate for fibroinflammatory pathology, but not for changes in cardiorenal function.

Angiotensin-II (Ang-II) infusion is associated with the development of interstitial fibrosis in both heart and kidney as a result of chemokine-dependent uptake of monocytes and subsequent development of myeloid fibroblasts. This study emphasizes on the synergistic role of tumor necrosis factor (TNF) on the time course of Ang-II-induced fibrosis and inflammation in heart and kidney. In wild-type (WT) hearts, Ang-II-induced fibrosis peaked within 1 week of infusion and remained stable over a 6-week period, while the myeloid fibroblasts disappeared; TNF receptor-1-knockout (TNFR1-KO) hearts did not develop a myeloid response or cardiac fibrosis during this time.

Tumor necrosis factor: a mechanistic link between angiotensin-II-induced cardiac inflammation and fibrosis.

Background: Continuous angiotensin-II infusion induced the uptake of monocytic fibroblast precursors that initiated the development of cardiac fibrosis; these cells and concurrent fibrosis were absent in mice lacking tumor necrosis factor receptor 1 (TNFR1). We now investigated their cellular origin and temporal uptake and the involvement of TNFR1 in monocyte-to-fibroblast differentiation.

Methods And Results: Within a day, angiotensin-II induced a proinflammatory environment characterized by production of inflammatory chemokines, cytokines, and TH1-interleukins and uptake of bone marrow-derived M1 cells.

Rho associated coiled-coil kinase-1 regulates collagen-induced phosphatidylserine exposure in platelets.

Background: The transbilayer movement of phosphatidylserine mediates the platelet procoagulant activity during collagen stimulation. The Rho-associated coiled-coil kinase (ROCK) inhibitor Y-27632 inhibits senescence induced but not activation induced phosphatidylserine exposure. To investigate further the specific mechanisms, we now utilized mice with genetic deletion of the ROCK1 isoform.

Th1/M1 conversion to th2/m2 responses in models of inflammation lacking cell death stimulates maturation of monocyte precursors to fibroblasts.

We have demonstrated that cardiac fibrosis arises from the differentiation of monocyte-derived fibroblasts. We present here evidence that this process requires sequential Th1 and Th2 induction promoting analogous M1 (classically activated) and M2 (alternatively activated) macrophage polarity. Our models are: (1) mice subjected to daily repetitive ischemia and reperfusion (I/R) without infarction and (2) the in vitro transmigration of human mononuclear leukocytes through human cardiac microvascular endothelium.

TNF receptor 1 signaling is critically involved in mediating angiotensin-II-induced cardiac fibrosis.

Angiotensin-II (Ang-II) is associated with many conditions involving heart failure and pathologic hypertrophy. Ang-II induces the synthesis of monocyte chemoattractant protein-1 that mediates the uptake of CD34(+)CD45(+) monocytic cells into the heart. These precursor cells differentiate into collagen-producing fibroblasts and are responsible for the Ang-II-induced development of non-adaptive cardiac fibrosis.

Origin of developmental precursors dictates the pathophysiologic role of cardiac fibroblasts.

Fibroblasts in the heart play a critical function in the secretion and modulation of extracellular matrix critical for optimal cellular architecture and mechanical stability required for its mechanical function. Fibroblasts are also intimately involved in both adaptive and nonadaptive responses to cardiac injury. Fibroblasts provide the elaboration of extracellular matrix and, as myofibroblasts, are responsible for cross-linking this matrix to form a mechanically stable scar after myocardial infarction.

Mitochondrial fission triggered by hyperglycemia is mediated by ROCK1 activation in podocytes and endothelial cells.

Several lines of evidence suggest that mitochondrial dysfunction plays a critical role in the pathogenesis of microvascular complications of diabetes, including diabetic nephropathy. However, the signaling pathways by which hyperglycemia leads to mitochondrial dysfunction are not fully understood. Here we examined the role of Rho-associated coiled coil-containing protein kinase 1 (ROCK1) on mitochondrial dynamics by generating two diabetic mouse models with targeted deletions of ROCK1 and an inducible podocyte-specific knockin mouse expressing a constitutively active (cA) mutant of ROCK1.

Monocytic fibroblast precursors mediate fibrosis in angiotensin-II-induced cardiac hypertrophy.

Angiotensin-II (Ang-II) is an autacoid generated as part of the pathophysiology of cardiac hypertrophy and failure. In addition to its role in cardiac and smooth muscle contraction and salt retention, it was shown to play a major role in the cardiac interstitial inflammatory response and fibrosis accompanying cardiac failure. In this study, we examined a model of Ang-II infusion to clarify the early cellular mechanisms linking interstitial fibrosis with the onset of the tissue inflammatory response.

Rho kinase-1 mediates cardiac fibrosis by regulating fibroblast precursor cell differentiation.

Aims: Highly proliferative, CD34+/CD45+ fibroblasts derived from monocytic, blood-borne precursor cells play a critical role in the development of fibrosis in a murine ischaemic/reperfusion cardiomyopathy (I/RC) model. The differentiation of human monocytes into fibroblasts in vitro occurs after transendothelial migration (TEM) induced by monocyte chemoattractant protein 1 (MCP-1). Because Rho-associated kinase-1 (ROCK-1) has been implicated in fibrosis and leukocyte TEM, we investigated its involvement in I/RC.