Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.ejim.2025.03.007 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Oral SARS-CoV-2 Infection and Risk for Long Covid.
Rev Med Virol
March 2025
Department of Periodontics, University of Illinois Chicago, Chicago, Illinois, USA.
SARS-CoV-2 is an oral pathogen that infects and replicates in mucosal and salivary epithelial cells, contributing to oral post-acute sequelae COVID-19 (PASC) and other oral and non-oral pathologies. While pre-existing inflammatory oral diseases provides a conducive environment for the virus, acute infection and persistence of SARS-CoV-2 can also results in oral microbiome dysbiosis that further worsens poor oral mucosal health. Indeed, oral PASC includes periodontal diseases, dysgeusia, xerostomia, pharyngitis, oral keratoses, and pulpitis suggesting significant bacterial contributions to SARS-CoV-2 and oral tissue tropism.
View Article and Find Full Text PDFClinical characteristics and outcomes of chronic obstructive pulmonary disease patients with family history of chronic airway disease.
Ann Med
December 2025
Department of Pulmonary and Critical Care Medicine, the Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Background: Chronic Obstructive Pulmonary Disease (COPD) is a heterogeneous condition with different risk factors, including family history. This study aimed to explore association between a family history of chronic airway disease and features and outcomes of COPD.
Methods: Participants were obtained from the RealDTC study between December 2016 and December 2022.
Acute exacerbation of chronic obstructive pulmonary disease: An underestimated cardiovascular risk factor.
Eur J Intern Med
March 2025
INSERM, U1059, SAINBIOSE, Jean Monnet University, 42023, Saint-Etienne, France; Therapeutic and Vascular Medicine Department, University Hospital of Saint-Etienne, 42270, Saint-Etienne, France; INSERM, CIC 1408, 42023, Saint-Etienne, France.
p38γ modulates ferroptosis in brain injury caused by ethanol and cerebral ischemia/reperfusion by regulating the p53/SLC7A11 signaling pathway.
Cell Signal
March 2025
Department of Neurology, Northwest University School of Medicine, Xi'an 710068, China; Northwest University First Hospital, Xi'an 710043, China. Electronic address:
Ischemic stroke, a neurological condition with a complicated etiology that is accompanied by severe inflammation and oxidative stress, and ethanol (EtOH) may aggravate ischemia/reperfusion (I/R)-induced brain damage. However, the effect of prolonged alcohol intake on acute brain injury remains ambiguous. As part of the mitogen-activated protein kinase (MAPK) family, p38γ is involved in ferroptosis and inflammation in various diseases.
View Article and Find Full Text PDFItaconate restrains acute proinflammatory activation of microglia MG after traumatic brain injury in mice.
Sci Transl Med
March 2025
Clinical Neuroscience Research Center, Department of Neurosurgery and Neurology, Tulane University School of Medicine, New Orleans, LA 70112, USA.
Traumatic brain injury (TBI) rapidly triggers proinflammatory activation of microglia, contributing to secondary brain damage post-TBI. Although the governing role of energy metabolism in shaping the inflammatory phenotype and function of immune cells has been increasingly recognized, the specific alterations in microglial bioenergetics post-TBI remain poorly understood. Itaconate, a metabolite produced by the enzyme aconitate decarboxylase 1 [IRG1; encoded by immune responsive gene 1 ()], is a pivotal metabolic regulator in immune cells, particularly in macrophages.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!