Rationale: H7N9 infection causes acute respiratory distress syndrome with high mortality. The use of glucocorticoids in the acute phase lessened inflammatory responses. Some case reports suggested that secondary organizing pneumonia (SOP) could occur at the recovery stage of the influenza virus infection, and the treatment with glucocorticoid was effective. However, the reports of organizing pneumonia after H7N9 infection are lacking. This study reported a patient with H7N9 virus infection who presented a suspected SOP during the recovery stage. Patient concern: A 68-year-old woman who was diagnosed with H7N9 viral pneumonia. After standard antiviral treatment, venous-venous extracorporeal membranous oxygenation (VV-ECMO) and other supportive treatment, the antigen in the alveolar lavage fluid turned negative, and the shadow in the lung was partially absorbed. However, the imaging manifestations were deteriorated at 3 weeks after disease onset, presented as exudation and consolidation shadow distributed under the pleura and along the bronchial vascular bundles. The oxygenation could not be improved. Repeated sputum, alveolar lavage fluid, and blood pathogen examinations showed negative results. Broad-spectrum anti-infective treatment was ineffective. However, the autoantibodies (ANA, anti-SSA/Ro60, anti-SSA/Ro52) were detected. Diagnosis: SOP was considered. Interventions: Glucocorticoid treatment begun at week 4 from the disease onset. The regimen was methylprednisolone at an initial dose of 40 mg twice a day for 1 week, tapering within 70 days until total withdrawal. Outcomes: The oxygenation was rapidly improved after initiation of methylprednisolone. The shadow in the lung gradually resolved, and the patient was discharged after improvement of the disease condition. The clinical disease course, imaging findings, and treatment effects in the previous cases of SOP after influenza virus infection were similar to those in this case, suggesting the occurrence of SOP after H7N9 virus infection. Lessons: Organizing pneumonia might occur during the recovery stage of influenza virus infection. When the clinical symptoms do not improve and the shadow in the lung shows no obvious absorption after elimination of the H7N9 influenza virus, or the clinical symptoms are aggravated again after improvement, the probability of transforming into the organizing pneumonia should be taken into consideration.
Background. Endothelial cell senescence is one of the key mechanistic factors in the pathogenesis of atherosclerosis. In terms of molecules, the phosphatidylinositol 3-kinase/protein kinase B/endothelial nitric oxide synthase (PI3K/Akt/eNOS) signaling plays an important role in the prevention and control of endothelial cell senescence, while hydrogen sulfide (H2S) improves the induced precocious senescence of endothelial cells through the PI3K/Akt/eNOS pathway. Comparatively, replicative senescence in endothelial cells is more in line with the actual physiological changes of human aging. This study aims to investigate the mechanism by which H2S improves endothelial cell replicative senescence and the involvement of the PI3K/Akt/eNOS pathway. Methods. we established a model of replicative senescence in human umbilical vein endothelial cells (HUVECs) and explored the effect of 200 μmol/L sodium hydrosulfide (NaHS; a donor of H2S) on senescence, which was determined by cell morphology, the expression level of plasminogen activator inhibitor 1 (PAI-1), and the positive rate of senescence-associated β-galactosidase (SA-β-Gal) staining. Cell viability was detected by MTT assay to evaluate the effect of NaHS and the PI3K inhibitor, LY294002. Meanwhile, the protein expression of PI3K, Akt, p-Akt, and eNOS in endothelial cells of each group was detected by Western blot. Results. the replicative senescence model was established in HUVECs at the passage of 16 cumulative cell population doubling values (CPDL). Treatment with NaHS not only significantly reduced the expression of PAI-1 and the positive rate of SA-β-Gal in HUVEC’s replicative senescence model but also notably increased the expression of PI3K, p-Akt, p-eNOS, and the content of nitric oxide(NO). However, the effects of NaHS on the expression of the pathway and the content of NO in HUVECs were abolished when LY294002 specifically inhibited PI3K. Conclusion. NaHS improves the replicative senescence of HUVECs with the contribution of the PI3K/Akt/eNOS pathway.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.