Background-To

Minimally invasive transthoracic device closure of VSD with an asymmetric or symmetric domestically made device on a beating heart is a safe and feasible alternative to conventional surgical repair. More experience in multicenter and long-term follow-up is necessary to assess the actual feasibility and safety of this procedure.

Total arch repair with open triple-branched stent graft placement is an effective technique with satisfactory early and midterm results. This technique could be an attractive alternative to conventional total arch replacement.

Extensive thoracic aorta repair of acute type I aortic dissection can be performed simply by combining ascending aorta and hemiarch replacement with modified triple-branched stent graft implantation. This technique can reduce the risk and technical difficulty of extensive thoracic aorta repair to levels close to those seen with ascending aorta and hemiarch graft replacement with open distal anastomosis.

Minimally invasive transthoracic device closure of the perimembranous VSD with an asymmetric or a symmetric domestically made device without cardiopulmonary bypass is safe and feasible. It should be considered an acceptable alternative to surgery in selected subgroups. However, it is necessary to evaluate the long-term results.

Autologous fat grafting is an effective reconstructive surgery technique; however, its success is limited by inconsistent graft retention and an environment characterized by high oxidative stress and inflammation. Adipose-derived stem cells (ADSCs) increase the survival of fat grafts, although the underlying mechanisms remain unclear. Here, TLR4−/− and Nrf2−/− mice were used to explore the effects of oxidative stress and inflammation on the viability and function of ADSCs in vitro and in vivo. Enrichment of fat grafts with ADSCs inhibited inflammatory cytokine production, enhanced growth factor levels, increased fat graft survival, downregulated NADPH oxidase (NOX)1 and 4 expression, increased vascularization and reduced ROS production in a manner dependent on toll-like receptor (TLR)-4 and nuclear factor erythroid 2-related factor 2 (Nrf2) expression. Immunohistochemical analysis showed that exposure to hypoxia enhanced ADSC growth and promoted the differentiation of ADSCs into vascular endothelial cells. Hypoxia-induced inflammatory cytokine, growth factor and NOX1/4 upregulation, as well as increased ROS production and apoptosis in ADSCs were dependent on TLR4 and Nrf2, which also modulated the effect of ADSCs on promoting endothelial progenitor cell migration and angiogenesis. Western blot analyses showed that the effects of hypoxia on ADSCs were regulated by crosstalk between Nrf2 antioxidant responses and NF-κB- and TLR4-mediated inflammatory responses. Taken together, our results indicate that ADSCs can increase the survival of fat transplants through the modulation of inflammatory and oxidative responses via Nrf2 and TLR4, suggesting potential strategies to improve the use of ADSCs for cell therapy.

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