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http://dx.doi.org/10.14503/THIJ-19-7077 | DOI Listing |
Am J Physiol Heart Circ Physiol
January 2025
Amsterdam University Medical Centers, Vrije Universiteit Amsterdam, Department of Cardiology, Amsterdam, The Netherlands.
The acute response to therapeutic afterload reduction differs between heart failure with preserved (HFpEF) versus reduced ejection fraction (HFrEF), with larger left ventricular (LV) stroke work augmentation in HFrEF compared to HFpEF. This may (partially) explain the neutral effect of HFrEF-medication in HFpEF. It is unclear whether such differences in hemodynamic response persist and/or differentially trigger reverse remodeling in case of long-term afterload reduction.
View Article and Find Full Text PDFClin Cardiol
January 2025
Second Department of Internal Medicine, University of Toyama, Toyama, Japan.
Thromb J
January 2025
Pediatric Emergency Department, St. Christopher's Hopsoital for Children, Philadelphia, PA, USA.
Background: Acute pulmonary embolism (PE) is a serious and potentially fatal condition that is relatively rare in the pediatric population. In patients presenting with massive/submassive PE, catheter-directed Therapy (CDT) presents an emerging therapeutic modality by which PE can be managed.
Methods: Electronic databases were systematically searched through May 2024.
Cell Commun Signal
January 2025
Department of Vascular & Cardiology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Purpose: Cardiomyocyte death is a major cytopathologic response in acute myocardial infarction (AMI) and involves complex inflammatory interactions. Although existing reports indicating that mixed lineage kinase domain-like protein (MLKL) is involved in macrophage necroptosis and inflammasome activation, the downstream mechanism of MLKL in necroptosis remain poorly characterized in AMI.
Methods: MLKL knockout mice (MLKL), RIPK3 knockout mice (RIPK3), and macrophage-specific MLKL conditional knockout mice (MLKL) were established.
BMC Vet Res
January 2025
Department of Veterinary Clinical Sciences, Clinic for Swine, Justus-Liebig-University, Frankfurter Strasse 112, D-35392, Giessen, Germany.
Background: The recently identified swine inflammation and necrosis syndrome (SINS) affects tail, ears, teats, coronary bands, claws and heels of affected individuals. The primarily endogenous syndrome is based on vasculitis, thrombosis, and intimal proliferation, involving defence cells, interleukins, chemokines, and acute phase proteins and accompanied by alterations in clinical chemistry, metabolome, and liver transcriptome. The complexity of metabolic alterations and the influence of the boar led to hypothesize a polygenic architecture of SINS.
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