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Increased unedited Alu RNA patterns found in cortex extracellular vesicles in Alzheimer's disease resemble hippocampus vasculature Alu RNA editing patterns but not cortex Alu RNA editing patterns.
J Alzheimers Dis
January 2025
Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA.
Background: Endogenous Alu RNAs form double-stranded RNAs recognized by double-stranded RNA sensors and activate IRF and NF-kB transcriptional paths and innate immunity. Deamination of adenosines to inosines by the ADAR family of enzymes, a process termed A-to-I editing, disrupts double-stranded RNA structure and prevents innate immune activation. Innate immune activation is observed in Alzheimer's disease, the most common form of dementia.
View Article and Find Full Text PDFMetagenomic insight into the diffusion signal factor mediated social traits of anammox consortia after starvation.
J Environ Manage
January 2025
School of Engineering, Hangzhou Normal University, Hangzhou, 311121, China; School of Life and Environmental Sciences, Hangzhou Normal University, Hangzhou, 311121, China. Electronic address:
Biomass starvation is common in biological wastewater treatment. As a social trait of microbial community, how quorum sensing (QS) regulated bacterial trade-off through interactions after starvation remains unclear. This study deciphered the mechanism of anaerobic ammonium oxidation (anammox) consortia in response to starvation, including reducing extracellular electron transfer (EET), adenosine 5'-triphosphate (ATP) content and amino acid metabolism.
View Article and Find Full Text PDFThe Anti-Human P2X7 Monoclonal Antibody (Clone L4) Can Mediate Complement-Dependent Cytotoxicity of Human Leukocytes.
Eur J Immunol
January 2025
Molecular Horizons and School of Chemistry and Molecular Bioscience, University of Wollongong, Wollongong, Australia.
P2X7 is an extracellular adenosine 5'-triphosphate (ATP)-gated cation channel that plays various roles in inflammation and immunity. P2X7 is present on peripheral blood monocytes, dendritic cells (DCs), and innate and adaptive lymphocytes. The anti-human P2X7 monoclonal antibody (mAb; clone L4), used for immunolabelling P2X7 or blocking P2X7 activity, is a murine IgG2 antibody, but its ability to mediate complement-dependent cytotoxicity (CDC) is unknown.
View Article and Find Full Text PDFAdenosine deficiency facilitates CA1 synaptic hyperexcitability in the presymptomatic phase of a knockin mouse model of Alzheimer disease.
iScience
January 2025
Department of Neuroscience, Tufts University, Boston, MA 02111, USA.
The disease's trajectory of Alzheimer disease (AD) is associated with and negatively correlated to hippocampal hyperexcitability. Here, we show that during the asymptomatic stage in a knockin (KI) mouse model of Alzheimer disease (APP; APPKI), hippocampal hyperactivity occurs at the synaptic compartment, propagates to the soma, and is manifesting at low frequencies of stimulation. We show that this aberrant excitability is associated with a deficient adenosine tone, an inhibitory neuromodulator, driven by reduced levels of CD39/73 enzymes, responsible for the extracellular ATP-to-adenosine conversion.
View Article and Find Full Text PDFMicroglia modulate the cerebrovascular reactivity through ectonucleotidase CD39.
Nat Commun
January 2025
Department of Neuroscience, Center for Brain Immunology and Glia, University of Virginia School of Medicine, Charlottesville, VA, USA.
Microglia and the border-associated macrophages contribute to the modulation of cerebral blood flow, but the mechanisms have remained uncertain. Here, we show that microglia regulate the cerebral blood flow baseline and the responses to whisker stimulation or intra-cisternal magna injection of adenosine triphosphate, but not intra-cisternal magna injection of adenosine in mice model. Notably, microglia repopulation corrects these cerebral blood flow anomalies.
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