A Rare Presentation of Myocardial Bridging With Heart Failure Symptoms.

Myocardial bridging is an under-recognized cause of angina. This congenital anomaly occurs when a segment of the epicardial coronary artery has a short intra-myocardial course. A significant intra-myocardial course may lead to ischemia, causing anginal symptoms. In this case report, we discuss a rare presentation of myocardial bridging with symptoms of heart failure. The pathology led to a marked degree of ventricular dysfunction and a significant drop in cardiac output (CO), and the patient had severe exertional dyspnea and functional limitations. The ischemic workup with diagnostic imaging and angiograms failed to explain the severity of symptoms, which were only evident in hemodynamic studies and cardiopulmonary exercise testing.

COVID-19 Unveiling Heart Failure in the Realm of Rheumatic Heart Disease.

The global coronavirus disease 2019 (COVID-19) pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has resulted in various clinical manifestations, including cardiovascular complications. This case report focuses on a unique instance where COVID-19 infection exacerbated heart failure and induced atrial fibrillation in a previously asymptomatic young male with undiagnosed rheumatic heart disease (RHD). RHD, a prevalent cause of valvular abnormalities in developing countries, poses an additional risk for severe outcomes when coexisting with COVID-19 infection, highlighting the need for prompt and tailored interventions.

Calcineurin contributes to RNAi-mediated transgene silencing and small interfering RNA production in the human fungal pathogen Cryptococcus neoformans.

Adaptation to external environmental challenges at the cellular level requires rapid responses and involves relay of information to the nucleus to drive key gene expression changes through downstream transcription factors. Here, we describe an alternative route of adaptation through a direct role for cellular signaling components in governing gene expression via RNA interference-mediated small RNA production. Calcium-calcineurin signaling is a highly conserved signaling cascade that plays central roles in stress adaptation and virulence of eukaryotic pathogens, including the human fungal pathogen Cryptococcus neoformans. Upon activation in C. neoformans, calcineurin localizes to P-bodies, membraneless organelles that are also the site for RNA processing. Here, we studied the role of calcineurin and its substrates in RNAi-mediated transgene silencing. Our results reveal that calcineurin regulates both the onset and the reversion of transgene silencing. We found that some calcineurin substrates that localize to P-bodies also regulate transgene silencing but in opposing directions. Small RNA sequencing in mutants lacking calcineurin or its targets revealed a role for calcineurin in small RNA production. Interestingly, the impact of calcineurin and its substrates was found to be different in genome-wide analysis, suggesting that calcineurin may regulate small RNA production in C. neoformans through additional pathways. Overall, these findings define a mechanism by which signaling machinery induced by external stimuli can directly alter gene expression to accelerate adaptative responses and contribute to genome defense.

Calcineurin contributes to RNAi-mediated transgene silencing and small interfering RNA production in the human fungal pathogen Cryptococcus neoformans.

Adaptation to external environmental challenges at the cellular level requires rapid responses and involves relay of information to the nucleus to drive key gene expression changes through downstream transcription factors. Here, we describe an alternative route of adaptation through a direct role for cellular signaling components in governing gene expression via RNA interference-mediated small RNA production. Calcium-calcineurin signaling is a highly conserved signaling cascade that plays central roles in stress adaptation and virulence of eukaryotic pathogens, including the human fungal pathogen Cryptococcus neoformans. Upon activation in C. neoformans, calcineurin localizes to P-bodies, membrane-less organelles that are also the site for RNA processing. Here, we studied the role of calcineurin and its substrates in RNAi-mediated transgene silencing. Our results reveal that calcineurin regulates both the onset and the reversion of transgene silencing. We found that some calcineurin substrates that localize to P-bodies also regulate transgene silencing but in opposing directions. Small RNA sequencing in mutants lacking calcineurin or its targets revealed a role for calcineurin in small RNA production. Interestingly, the impact of calcineurin and its substrates was found to be different in genome-wide analysis, suggesting that calcineurin may regulate small RNA production in C. neoformans through additional pathways. Overall, these findings define a mechanism by which signaling machinery induced by external stimuli can directly alter gene expression to accelerate adaptative responses and contribute to genome defense.

A Financial Case for a Medical-Legal Partnership: Reducing Lengths of Stay for Inpatient Care.

While Medical-Legal Partnerships (MLPs) have improved the health and well-being of the people they serve, most healthcare institutions will only invest in an MLP if they are convinced that doing so will improve its balance sheet. This article offers a detailed estimation of the cost savings that an MLP targeted toward the most acute legal needs would accrue to an academic medical center (AMC) in North Carolina.