Give It to Me Straight Doc: A Medical Student Perspective on Effective Goal-Oriented Clinical Education.

The clinical years of medical school are a time when students navigate a new learning environment. Due to inexperience, discordance may exist between veteran attendings and students who do not have their bearings in this new setting. We propose a solution to strengthen the clinician-student relationship by promoting a culture of goal-oriented clinical education via a two-pronged approach.

Neurological Complications After Transcatheter Aortic Valve Replacement: A Review.

Transcatheter aortic valve replacement (TAVR) has become the dominant procedural modality for aortic valve replacement in the United States. The reported rates of neurological complications in patients undergoing TAVR have changed over time and are dependent on diagnostic definitions and modalities. Most strokes after TAVR are likely embolic in origin, and the incidence of stroke has decreased over time.

A Case of Life-Threatening Postpartum Necrotizing Pancreatitis Requiring Gastrocystostomy With Serial Pancreatic Necrosectomies.

We present a life-threatening case of postpartum acute necrotizing pancreatitis. The patient is a 37-year-old female with no past medical history who delivered a healthy baby boy via cesarean section. Twenty days later, she presented to the emergency department with acute onset of nausea, non-bloody vomiting, abdominal bloating, and epigastric pain radiating to the back.

Call it as it is - Why medical education should reconsider disease eponyms.

Medical disease names should be reflective of the pathophysiologic processes underlying them. Medical education has propagated the use of outdated eponyms when referring to diseases named after individuals who discovered or described the diseases in question. This is confusing and harmful to medical students learning about these diseases and can present a seemingly insurmountable barrier to understanding complex pathologies.

TMEM65 regulates NCLX-dependent mitochondrial calcium efflux.

The balance between mitochondrial calcium (Ca) uptake and efflux regulates ATP production, but if perturbed causes energy starvation or Ca overload and cell death. The mitochondrial sodium-calcium exchanger, NCLX, is a critical route of Ca efflux in excitable tissues, such as the heart and brain, and animal models support NCLX as a promising therapeutic target to limit pathogenic Ca overload. However, the mechanisms that regulate NCLX activity remain largely unknown.

MCU gain- and loss-of-function models define the duality of mitochondrial calcium uptake in heart failure.

Background: Mitochondrial calcium (Ca) uptake through the mitochondrial calcium uniporter channel (mtCU) stimulates metabolism to meet acute increases in cardiac energy demand. However, excessive Ca uptake during stress, as in ischemia-reperfusion, initiates permeability transition and cell death. Despite these often-reported acute physiological and pathological effects, a major unresolved controversy is whether mtCU-dependent Ca uptake and long-term elevation of cardiomyocyte Ca contributes to the heart's adaptation during sustained increases in workload.

Enhanced NCLX-dependent mitochondrial Ca efflux attenuates pathological remodeling in heart failure.

Mitochondrial calcium (Ca) uptake couples changes in cardiomyocyte energetic demand to mitochondrial ATP production. However, excessive Ca uptake triggers permeability transition and necrosis. Despite these established roles during acute stress, the involvement of Ca signaling in cardiac adaptations to chronic stress remains poorly defined.