The movement of the aortic annulus after AVNeo is comparable with that of the aortic annulus of a normal aortic valve. Thus, AVNeo can be regarded as a more physiological operation in that it maintains the characteristics of the aortic valve similar to those of a normal aortic valve.
Background
Excellent results have been reported regarding pulmonary valve replacement (PVR) for pulmonary valve regurgitation (PR) after intracardiac repair (ICR) in patients with tetralogy of Fallot (TOF). However, there are apparently no reports comparing the following procedures: PVR using a bioprosthetic valve and PVR using a polytetrafluoroethylene (PTFE) bicuspid valve. Herein, we retrospectively analyzed the outcomes of PVR for PR after ICR of TOF in our institution and assessed which of the two PVR procedures was better.
Methods
From June 2008 to December 2017, we performed PVR for PR after ICR of TOF in 34 patients. Patients with the right ventricle to the pulmonary artery conduits were excluded. Preoperative and postoperative cardiac magnetic resonance imagings (cMRIs) were performed in all patients. The patients were divided into the bioprosthetic valve group (BV group, n = 17) and the PTFE bicuspid valve group (PTFE group, n = 17).
Results
There were no significant differences in the preoperative cMRI data and perioperative factors between the two groups. There were no deaths in either group. Postoperative cMRI showed that the PR fraction and the right ventricular end‐diastolic volume index (RVEDVI)/left ventricular end‐diastolic volume index ratio were significantly improved in both groups. However, RVEDVI was significantly improved only in the BV group. Re‐PVR was required in four patients in the PTFE group.
Conclusion
PVR using a bioprosthetic valve was more effective for PR treatment after ICR of TOF than PVR using a PTFE bicuspid valve.
TNF receptor–associated factor 5 (TRAF5) restrains early signaling activity of the IL-6 receptor in naive CD4+ T cells by interacting with the shared gp130 chain, although TRAF5 was initially discovered as a cytoplasmic adaptor protein to activate signaling mediated by TNF receptor family molecules. This leads to the question of whether TRAF5 limits signaling via the receptor for IL-27, which is composed of gp130 and WSX-1. The aim of this study is to clarify the role of TRAF5 in IL-27 receptor signaling and to understand the differential role of TRAF5 on cytokine receptor signaling. We found that Traf5−/− CD4+ T cells displayed significantly higher levels of phosphorylated STAT1 and STAT-regulated genes Socs3 and Tbx21, as early as 1 h after IL-27 exposure when compared with Traf5+/+ CD4+ T cells. Upon IL-27 and TCR signals, the Traf5 deficiency significantly increased the induction of IL-10 and promoted the proliferation of CD4+ T cells. Traf5−/− mice injected with IL-27 displayed significantly enhanced delayed-type hypersensitivity responses, demonstrating that TRAF5 works as a negative regulator for IL-27 receptor signaling. In contrast, IL-2 and proliferation mediated by glucocorticoid-induced TNF receptor–related protein (GITR) and TCR signals were significantly decreased in Traf5−/− CD4+ T cells, confirming that TRAF5 works as a positive regulator for cosignaling via GITR. Collectively, our results demonstrate that TRAF5 reciprocally controls signals mediated by the IL-27 receptor and GITR in CD4+ T cells and suggest that the regulatory activity of TRAF5 in gp130 is distinct from that in TNF receptor family molecules in a T cell.
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