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1.
Korean Circ J ; 53(8): 535-547, 2023 Aug.
Artículo en Inglés | MEDLINE | ID: mdl-37271752

RESUMEN

BACKGROUND AND OBJECTIVES: Veno-arterial extracorporeal membrane oxygenation (VA-ECMO) as a bridge to eventual heart transplantation (HT) is increasingly used worldwide. However, the effect of different VA-ECMO types on HT outcomes remains unclear. METHODS: This was a retrospective observational study of 111 patients receiving VA-ECMO and awaiting HT. We assessed 3 ECMO configuration groups: peripheral (n=76), central (n=12), and peripheral to central ECMO conversion (n=23). Cox proportional hazards regression and landmark analysis were conducted to analyze the effect of the ECMO configuration on HT and in-hospital mortality rates. We also evaluated adverse events during ECMO support. RESULTS: HT was performed in the peripheral (n=48, 63.2%), central (n=10, 83.3%), and conversion (n=11, 47.8%) ECMO groups (p=0.133) with a median interval of 10.5, 16, and 30 days, respectively (p<0.001). The cumulative incidence of HT was significantly lower in the conversion group (hazard ratio, 0.292, 95% confidence interval, 0.145-0.586, p=0.001). However, there was no difference in in-hospital mortality (log-rank p=0.433). In the landmark analysis, in-hospital mortality did not differ significantly among the 3 groups. Although we did note a trend toward lower HT in the conversion group, the difference was not statistically significant. Surgical site bleeding occurred mainly in the central, while limb ischemia occurred mainly in the peripheral groups. CONCLUSIONS: We suggest that if patients are being stably supported with their initial ECMO configuration, whether it is central or peripheral, it should be maintained, and ECMO conversion should only be cautiously performed when necessary.

2.
Mol Med Rep ; 13(1): 967-72, 2016 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-26647855

RESUMEN

Withaferin A (WA), a withanolide purified from Withania somnifera, has been known to exert anti-inflammatory effects. The present study sought to determine the effects of WA on Helicobacter (H.) pylori-mediated inflammation in the AGS gastric epithelial cell line. Cellular production of interleukin (IL)-8 and vascular endothelial growth factor (VEGF) was measured by ELISA. Western blot analysis was performed to determine the activation of nuclear factor (NF)-κB and mitogen-activated protein kinases (MAPKs) as well as hypoxia-inducible factor 1α stabilization. Bacterial growth was also examined by measuring the optical density. Pre-treatment or co-treatment with WA efficiently reduced IL-8 production by AGS cells in response to H. pylori infection. H. pylori-induced activation of NF-κB, but not MAPKs, was also inhibited by pre-treatment of WA in the cells. However, WA did not affect VEGF production and HIF-1α stabilization induced by H. pylori in AGS cells. In addition, WA did not influence the growth of H. pylori, suggesting that the anti-inflammatory effect of WA was not due to any bactericidal effect. These findings indicate that WA is a potential preventive or therapeutic agent for H. pylori-mediated gastric inflammation.


Asunto(s)
Infecciones por Helicobacter/tratamiento farmacológico , Helicobacter pylori/efectos de los fármacos , Inflamación/tratamiento farmacológico , Interleucina-8/biosíntesis , Witanólidos/administración & dosificación , Células Epiteliales/efectos de los fármacos , Células Epiteliales/metabolismo , Células Epiteliales/microbiología , Mucosa Gástrica/efectos de los fármacos , Mucosa Gástrica/metabolismo , Mucosa Gástrica/patología , Regulación de la Expresión Génica/efectos de los fármacos , Infecciones por Helicobacter/microbiología , Infecciones por Helicobacter/patología , Helicobacter pylori/patogenicidad , Humanos , Subunidad alfa del Factor 1 Inducible por Hipoxia/biosíntesis , Subunidad alfa del Factor 1 Inducible por Hipoxia/genética , Inflamación/genética , Inflamación/microbiología , Inflamación/patología , Interleucina-8/genética , Proteínas Quinasas Activadas por Mitógenos , FN-kappa B/biosíntesis , FN-kappa B/genética , Factor A de Crecimiento Endotelial Vascular/biosíntesis , Factor A de Crecimiento Endotelial Vascular/genética
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