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Toward a New SUMMIT in Heart Failure with Preserved Ejection Fraction.
N Engl J Med
January 2025
From Duke University School of Medicine, Durham, NC; and Duke Clinical Research Institute, Durham, NC.
Echocardiographic Endophenotypes of Chronic Obstructive Pulmonary Disease: A Step Towards Personalized Medicine.
Am J Respir Crit Care Med
January 2025
University of Minnesota, Medicine, Minneapolis, Minnesota, United States.
Iron Deficiency and All-Cause Hospitalization Risk in a Clinical Cohort of COPD.
Chronic Obstr Pulm Dis
January 2024
Division of Pulmonary and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States.
Background: The impact of iron deficiency on COPD morbidity independent of anemia status is unknown. Understanding the association between iron deficiency, anemia status, and risk of hospitalization in COPD may inform an approach to these comorbidities.
Study Design And Methods: Adults ≥40 years from the Johns Hopkins COPD Precision Medicine Center of Excellence data repository with an outpatient iron profile and 1 year of subsequent follow-up time were included in the study.
chitinase-like protein orchestrates cyst wall glycosylation to facilitate effector export and cyst turnover.
Proc Natl Acad Sci U S A
February 2025
Department of Molecular Microbiology, Washington University in St. Louis, School of Medicine, St. Louis, MO 63130.
bradyzoites reside in tissue cysts that undergo cycles of expansion, rupture, and release to foster chronic infection. The glycosylated cyst wall acts as a protective barrier, although the processes responsible for formation, remodeling, and turnover are not understood. Herein, we identify a noncanonical chitinase-like enzyme TgCLP1 that localizes to micronemes and is targeted to the cyst wall after secretion.
View Article and Find Full Text PDFNitroxyl protects H9C2 cells from H/R-induced damage and inhibits autophagy via PI3K/Akt/mTOR pathway.
PLoS One
January 2025
Precision Laboratory of Vascular Medicine, Shanxi Cardiovascular Hospital Affiliated Shanxi Medical University, Taiyuan, PR China.
Background: Myocardial ischemia-reperfusion injury (MIRI) is an important complication in the treatment of heart failure, and its treatment has not made satisfactory progress. Nitroxyl (HNO) showed protective effects on the heart failure, however, the effect and underlying mechanism of HNO on MIRI remain largely unclear.
Methods: MIRI model in this study was established to induce H9C2 cell injury through hypoxia/reoxygenation (H/R) in vitro.
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