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| http://dx.doi.org/10.1183/23120541.00727-2023 | DOI Listing |
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Long-COVID - pathophysiology, current concepts and future directions.
J Allergy Clin Immunol
December 2024
Department of Cardiology, Angiology and Intensive Care Medicine, University Hospital, Philipps University of Marburg, Marburg, Germany.
Long-COVID, an umbrella term referring to a variety of symptoms and clinical presentations, which emerge in a subset of patients after SARS-CoV-2 infection, has a significant impact on an individual's quality of life and places a substantial burden on healthcare systems worldwide, straining financial and human resources. The pathophysiology of long-COVID remains incompletely understood, though several hypotheses have been proposed to explain different aspects of this complex condition. SARS-CoV-2 persistence, direct organ damage, innate and adaptive immune system pertubation, autoimmunity, latent viruses reactivation, endothelial dysfunction, and microbiome disturbances are among the most relevant avenues for elucidating the evolution, complexity, and mechanisms of long-COVID.
View Article and Find Full Text PDFRecurring incursions and dissemination of novel Eurasian-origin H5Nx avian influenza viruses in Atlantic Canada.
Virus Evol
December 2024
Department of Biology, Memorial University of Newfoundland, St. John's, NL A1C 5S7, Canada.
Wild birds are important hosts of influenza A viruses (IAVs) and play an important role in their ecology. The emergence of the A/goose/Guangdong/1/1996 H5N1 (Gs/GD) lineage marked a shift in IAV ecology, leading to recurrent outbreaks and mortality in wild birds from 2002 onwards. This lineage has evolved and diversified over time, with a recent important derivative being the 2.
View Article and Find Full Text PDFComparison of molecular subtype composition between independent sets of primary and brain metastatic small cell lung carcinoma and matched samples.
Lung Cancer
December 2024
Department of Pathology and Experimental Cancer Research, Semmelweis University, Üllői, út 26., H-1085 Budapest, Hungary. Electronic address:
Introduction: Recent advances in the subclassification of small cell lung carcinomas (SCLCs) may help to overcome the unmet need for targeted therapies and improve survival. However, limited information is available on how the expression of the subtype markers changes during tumour progression. Our study aimed to compare the expression of these markers in primary and brain metastatic SCLCs.
View Article and Find Full Text PDFAssociation between Driving Pressure, Systemic Inflammation and Non-pulmonary Organ Dysfunction in Patients with Acute Respiratory Distress Syndrome, a Prospective Pathophysiological Study.
Anaesth Crit Care Pain Med
December 2024
CIBER de Enfermedades Respiratorias (CIBERES), Instituto de Salud Carlos III, Madrid, Spain; Institut d'Investigacions Biomèdiques August Pi I Sunyer (IDIBAPS), Barcelona, Spain; University of Barcelona (UB), Barcelona, Spain; Respiratory Intensive Care Unit, Pneumology, Respiratory Institute, Hospital Clinic of Barcelona, Barcelona, Spain. Electronic address:
Background: Driving pressure is thought to determine the effect of low tidal ventilation on survival in patients with acute respiratory distress syndrome. The leading cause of mortality in these patients is non-pulmonary multiorgan dysfunction, which is believed to worsen due to the biological response to mechanical ventilation (biotrauma). Therefore, we aimed to analyze the association between driving pressure, biotrauma, and non-pulmonary multiorgan dysfunction.
View Article and Find Full Text PDFMutations in mexT bypass the stringent response dependency of virulence in Pseudomonas aeruginosa.
Cell Rep
December 2024
Department of Biochemistry, University of Cambridge, Cambridge CB2 1QW, UK. Electronic address:
Pseudomonas aeruginosa produces a wealth of virulence factors whose production is controlled via an intricate regulatory systems network. Here, we uncover a major player in the evolution and regulation of virulence that enhances host colonization and antibiotic resistance. By characterizing a collection of mutants lacking the stringent response (SR), a system key for virulence, we show that the loss of the central regulator MexT bypasses absence of the SR, restoring full activation of virulence pathways.
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