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A nurse reflects on the vital role clinical preceptors play in teaching, supporting, and inspiring the next generation of nurses.We report on a 10-year-old female who rapidly developed a left atrial (LA) mass two months after orthotopic heart transplant. Nine days prior to detection of the mass, she received high-dose corticosteroids for acute cellular rejection (grade 2). Despite negative echocardiogram five days prior to detection, a large echogenic mass was noted in the LA (18 x 12 x 24 mm); it was surgically resected after unsuccessful anticoagulation treatment. Pathogenesis of this LA thrombus remains uncertain, but immunosuppression, acute rejection, and high-dose steroid therapy may have contributed. Surgical thrombectomy is a safe and effective treatment option for LA thrombus.The estrogen-related receptor (ERR) family of orphan nuclear receptors are transcriptional activators for genes involved in mitochondrial bioenergetics and metabolism. The goal of this study was to explore the role of ERRα in lipid metabolism and the potential effect of inhibiting ERRα on the development of nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH). In the current study, three experimental mouse models high-fat diet, high-carbohydrate diet, and a genetic model of hepatic insulin resistance where the liver hyperinsulinemia signal is mimicked via hepatic deletion of Pten (phosphatase and tensin homolog deleted on chromosome 10), the negative regulator of the insulin/phosphatidylinositol 3-kinase signaling pathway, were used. A recently developed small-molecule inhibitor for ERRα was used to demonstrate that inhibiting ERRα blocked NAFLD development induced by either high-carbohydrate diet or high-fat diet feeding. ERRα inhibition also diminished lipid accumulation and attenuated NASH development in the Pten null mice. Glycerolipid synthesis was discovered as an additional mechanism for ERRα-regulated NAFLD/NASH development and glycerophosphate acyltransferase 4 was identified as a novel transcriptional target of ERRα. In summary, these results establish ERRα as a major transcriptional regulator of lipid biosynthesis in addition to its characterized primary function as a regulator for mitochondrial function. This study recognizes ERRα as a potential target for NAFLD/NASH treatment and elucidates novel signaling pathways regulated by ERRα.Pulmonary fibrosis (PF) can arise from unknown causes, as in idiopathic PF, or as a consequence of infections, including severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Current treatments for PF slow, but do not stop, disease progression. We report that treatment with a runt-related transcription factor 1 (RUNX1) inhibitor (Ro24-7429), previously found to be safe, although ineffective, as a Tat inhibitor in patients with HIV, robustly ameliorates lung fibrosis and inflammation in the bleomycin-induced PF mouse model. RUNX1 inhibition blunted fundamental mechanisms downstream pathologic mediators of fibrosis and inflammation, including transforming growth factor-β1 and tumor necrosis factor-α, in cultured lung epithelial cells, fibroblasts, and vascular endothelial cells, indicating pleiotropic effects. RUNX1 inhibition also reduced the expression of angiotensin-converting enzyme 2 and FES Upstream Region (FURIN), host proteins critical for SARS-CoV-2 infection, in mice and in vitro. A subset of human lungs with SARS-CoV-2 infection overexpress RUNX1. Selleck BI 1015550 These data suggest that RUNX1 inhibition via repurposing of Ro24-7429 may be beneficial for PF and to battle SARS-CoV-2, by reducing expression of viral mediators and by preventing respiratory complications.

To examine functional outcomes of post-acute care for coronavirus disease 2019 (COVID-19) in skilled nursing facilities (SNFs).

Retrospective cohort.

Seventy-three community-dwelling adults ≥65years of age admitted for post-acute care from 2 SNFs from March 15, 2020, to May 30,2020.

COVID-19 status was determined from chart review. Frailty was measured with a deficit accumulation frailty index (FI), categorized into nonfrail, mild frailty, and moderate-to-severe frailty. The primary outcome was community discharge. Secondary outcomes included change in functional status from SNF admission to discharge, based on modified Barthel index (mBI) and continuous functional scale scored by physical (PT) and occupational therapists (OT).

Among 73 admissions (31 COVID-19 negative, 42 COVID-19 positive), mean [standard deviation (SD)] age was 83.5 (8.8) and 42 (57.5%) were female, with mean FI of 0.31 (0.01) with no differences by COVID-19 status. The mean length of SNF stay for rehabilitation was 21.2days (SD scharge rates and functional improvement comparable to a COVID-19 negative group. However, those who are frailer at admission tended to have lower function at discharge.Three palliative care clinical trials were presented at the 2020 American Society for Clinical Oncology Annual Meeting. The heterogeneity in populations, models of care, study design, and assessment of clinical outcomes across these three studies show the broad opportunities for research into interventions for palliative care. In this Viewpoint, we summarise the characteristics of these studies, discuss their novel features and lingering questions, and offer a suggestion for further expanding the focus of clinical trials for delivery of palliative care in the future. We particularly argue that the propensity to characterise palliative care as if it was a clinical or biomedical intervention hampers the design and evaluation of complex clinical interventions that influence clinicians, systems for health-care delivery, individual patients, and their families.This Review outlines a practical approach to assessing and managing polyclonal hypergammaglobulinaemia in adults. Polyclonal hypergammaglobulinaemia is most commonly caused by liver disease, immune dysregulation, or inflammation, but can also provide an important diagnostic clue of rare diseases such as histiocyte disorders, autoimmune lymphoproliferative syndrome, Castleman disease, and IgG4-related disease. Causes of polyclonal hypergammaglobulinaemia can be divided into eight categories liver disease, autoimmune disease and vasculitis, infection and inflammation, non-haematological malignancy, haematological disorders, IgG4-related disease, immunodeficiency syndromes, and iatrogenic (from immunoglobulin therapy). Measuring serum concentrations of C-reactive protein and IgG subclasses are helpful in diagnosis. IL-6-mediated inflammation, associated with persistently elevated C-reactive protein concentrations (≥30 mg/L), is an important driver of polyclonal hypergammaglobulinaemia in some cases. Although the presence of markedly elevated serum IgG4 concentrations (>5 g/L) is around 90% specific for diagnosing IgG4-related disease, mildly elevated serum IgG4 concentrations are seen in many conditions.