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Background: Private equity (PE) ownership in the healthcare sector has increased, raising concerns about its impact on care quality and patient outcomes. In the U.S.

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ECM Modifications Driven by Age and Metabolic Stress Directly Promote the Vascular Smooth Muscle Cell Osteogenic Processes.

Arterioscler Thromb Vasc Biol

January 2025

British Heart Foundation Centre of Research Excellence, School of Cardiovascular and Metabolic Medicine & Sciences, King's College London, United Kingdom. (M.W., M.F., R.O., L.S., M.M., C.M.S.).

Background: The ECM (extracellular matrix) provides the microenvironmental niche sensed by resident vascular smooth muscle cells (VSMCs). Aging and disease are associated with dramatic changes in ECM composition and properties; however, their impact on the VSMC phenotype remains poorly studied.

Methods: Here, we describe a novel in vitro model system that utilizes endogenous ECM to study how modifications associated with age and metabolic disease impact the VSMC phenotype.

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Introduction: The 2022 Inflation Reduction Act is expected to result in lower drug prices for Medicare beneficiaries in the United States (US). The Centers for Medicare & Medicaid Services (CMS) released the most recent draft guidance for the medicare drug price negotiation (DPN) program in May 2024.

Areas Covered: In August 2023, the list of 10 drugs selected for the DPN were published and the first round of negotiations are now complete.

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: In heart failure (HF) with reduced ejection fraction (HFrEF), the early diagnosis and proper treatment of comorbidities (CMs) are of fundamental relevance. Our aim was to assess the prevalence of CMs among real-world patients requiring hospitalisation for HFrEF and to investigate the effect of CMs on the implementation of guideline-directed medical therapy (GDMT) and on all-cause mortality (ACM). : The data of a consecutive HFrEF patient cohort hospitalised for HF between 2021 and 2024 were analysed retrospectively.

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Over 200 point mutations in the ryanodine receptor (RyR2) of the cardiac sarcoplasmic reticulum (SR) are known to be associated with cardiac arrhythmia. We have already reported on the calcium signaling phenotype of a point mutation in RyR2 Ca binding site Q3925E expressed in human stem-cell-derived cardiomyocytes (hiPSC-CMs) that was found to be lethal in a 9-year-old girl. CRISPR/Cas9-gene-edited mutant cardiomyocytes carrying the RyR2-Q3925E mutation exhibited a loss of calcium-induced calcium release (CICR) and caffeine-triggered calcium release but continued to beat arrhythmically without generating significant SR Ca release, consistent with a remodeling of the calcium signaling pathway.

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