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Alzheimer's Disease: In Vitro and In Vivo Evidence of Activation of the Plasma Bradykinin-Forming Cascade and Implications for Therapy.
Cells
December 2024
Astria Pharmaceuticals, Boston, MA 02210, USA.
The plaques associated with Alzheimer's disease are formed as a result of the aggregation of Aβ peptides, which vary in length from 38 to 43 amino acids. The 1-40 peptide is the most abundant, while the 1-42 peptide appears to be the most destructive to neurons and/or glial cells in a variety of assays. We have demonstrated that aggregated Aβ, a state prior to plaque formation, will activate the plasma bradykinin-forming pathway when tested in vitro.
View Article and Find Full Text PDFSARS-CoV-2 Productively Infects Human Hepatocytes and Induces Cell Death.
J Med Virol
January 2025
Institute of Virology, Technical University of Munich/Helmholtz Munich, Munich, Germany.
Article Synopsis
- SARS-CoV-2 can infect liver cells (hepatocytes), leading to elevated liver enzymes and more severe disease in those with pre-existing liver conditions.
- The study shows that the virus replicates and spreads in hepatocytes, with infection being dependent on two specific proteins, ACE2 and TMPRSS2, which are found on the liver cells.
- Infection causes rapid liver cell death, with the Omicron variant causing quicker but less extensive damage compared to other strains, as seen in both human liver cells and infected mice.
Bradykinin attenuates NiSO-induced autophagy in MIN6 cells and protects islet function in mice by regulating the PI3K/AKT/mTOR signaling pathway.
Biochem Biophys Res Commun
December 2024
Department of Endocrinology and Metabolism, The Second Hospital & Clinical Medical School, Lanzhou University, Lanzhou, People's Republic of China; The Second Clinical Medical College, Lanzhou University, Lanzhou, People's Republic of China. Electronic address:
Previous studies have shown that nickel sulfate (NiSO) increases autophagy in thyroid cells and tissues. As an important organ of the endocrine system, the pancreas not only contributes to the exocrine function of digestion but also has the endocrine function of regulating blood sugar. However, it remains unknown whether NiSO increases pancreatic autophagy.
View Article and Find Full Text PDFEndothelial Cell-Selective Adhesion Molecule Deficiency Exhibit Increased Pulmonary Vascular Resistance Due to Impaired Endothelial Nitric Oxide Signaling.
Am J Physiol Heart Circ Physiol
December 2024
Department of Physiology.
Endothelial cell-selective adhesion molecule (ESAM) is a member of tight junction molecules, highly abundant in the heart and the lung, and plays a role in regulating endothelial cell permeability. We previously reported that mice with genetic ESAM deficiency (ESAM) exhibit coronary microvascular dysfunction leading to the development of left ventricular diastolic dysfunction. Here, we hypothesize that ESAM mice display impairments in the pulmonary vasculature, affecting the overall pulmonary vascular resistance (PVR).
View Article and Find Full Text PDFNeprilysin-Mediated Amyloid Beta Clearance and Its Therapeutic Implications in Neurodegenerative Disorders.
ACS Pharmacol Transl Sci
December 2024
Centre for Advanced Research (CFAR), Faculty of Medicine, King George's Medical University (KGMU), Lucknow 226003, India.
Neprilysin (NEP) is a neutral endopeptidase, important for the degradation of amyloid beta (Aβ) peptides and other neuropeptides, including enkephalins, substance P, and bradykinin, in the brain, that influences various physiological processes such as blood pressure homeostasis, pain perception, and neuroinflammation. NEP breaks down Aβ peptides into smaller fragments, preventing the development of detrimental aggregates such as Aβ plaques. NEP clears Aβ plaques predominantly by enzymatic breakdown in the extracellular space.
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