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@#Objective To summarize the early outcomes of totally thoracoscopic minimally invasive aortic valve replacement (AVR) and double valve replacement (DVR). Methods The clinical data of patients who underwent totally thoracoscopic minimally invasive AVR or DVR in Guangdong Provincial People’s Hospital from April 2020 to January 2021 were retrospectively analyzed. The patients were divided into an AVR group and a DVR group according to the surgical method, and the clinical data of the two groups were compared. Results Finally 22 patients were enrolled, including 14 males and 8 females with an average age of 50.0±11.2 years at operation. Eight patients were degenerative disease, 8 were rheumatic heart disease combined with valvular disease, and 6 were bicuspid aortic valve. Out of the 22 patients, 16 underwent AVR alone, and 6 underwent DVR. All patients completed the operation successfully, and there was no death. Perivalvular leakage during surgery occurred in 2 patients. The average cardiopulmonary bypass time was 187.0±39.9 minutes, and aortic cross-clamping time was 117.0 (99.0, 158.0) minutes. Duration of mechanical ventilation and intensive care unit stay was 9.5 (4.8, 18.3) hours and 41.0 (34.0, 64.0) hours, respectively. The volume of chest drainage at the first 24 hours after surgery was 214.0±124.6 mL, and the postoperative hospital stay was 5.5 (4.0, 8.3) days. The cardiopulmonary bypass time and aortic cross-clamping time in the DVR group were longer than those in the AVR group, and the volume of chest drainage at 24 hours after surgery was more than that in the AVR group, with a statistical difference (P<0.05). Echocardiography before hospital discharge showed paravalvular leakage in 1 patient. There was no death during follow-up of 5.9±3.0 months. Conclusion The early outcome of totally thoracoscopic minimally invasive AVR and DVR is satisfactory, and the approach of surgery is worth exploring.
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Objective To investigate the role of TLR4/NF-κB signal pathway in pathogenesis of brain inju-ry during deep hypothermia circulatory arrest(DHCA). Methods BV2 microglia cells were subjected to oxygen-glucose deprivation/reoxygenation(OGD/R),in vitro model for DHCA. The BV2 were randomly divided into the control group(C group)and the experimental group(O group). BV2 viability was determined by CCK-8 assay. TLR4 and its downstream signaling molecules ,MyD88 and phosphorylated NF-κB (p-p65) expressions were detected by Western blotting. TLR4 mRNA expression in BV2 microglial cells were determined by RT-PCR. Level of interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α) in culture medium was detected by ELASA. Results Compared with the group C,BV2 microglia cell viability in experiment group was obviously weaker(P<0.05). Expressions of TLR4,MyD88 and phosphorylated NF-κB(p-p65)from the experiment group increased remarkedly than those from the group C (P < 0.05). TLR4 mRNA level was higher significantly in the group O than in the group C (P < 0.01). Production of IL-6 and TNF-α in the group O were up-regulated apparently compared to the group C(P<0.01). Conclusion TLR4/NF-κB signaling pathway contributed to activation of BV2 microglia cells treated by OGD/Reoxygenation ,which was probably the exactly way that involved in pathogenesis of brain injury during deep hypothermia circulatory arrest.
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Objective To investigate the role of TLR4/NF-κB signal pathway in pathogenesis of brain inju-ry during deep hypothermia circulatory arrest(DHCA). Methods BV2 microglia cells were subjected to oxygen-glucose deprivation/reoxygenation(OGD/R),in vitro model for DHCA. The BV2 were randomly divided into the control group(C group)and the experimental group(O group). BV2 viability was determined by CCK-8 assay. TLR4 and its downstream signaling molecules ,MyD88 and phosphorylated NF-κB (p-p65) expressions were detected by Western blotting. TLR4 mRNA expression in BV2 microglial cells were determined by RT-PCR. Level of interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α) in culture medium was detected by ELASA. Results Compared with the group C,BV2 microglia cell viability in experiment group was obviously weaker(P<0.05). Expressions of TLR4,MyD88 and phosphorylated NF-κB(p-p65)from the experiment group increased remarkedly than those from the group C (P < 0.05). TLR4 mRNA level was higher significantly in the group O than in the group C (P < 0.01). Production of IL-6 and TNF-α in the group O were up-regulated apparently compared to the group C(P<0.01). Conclusion TLR4/NF-κB signaling pathway contributed to activation of BV2 microglia cells treated by OGD/Reoxygenation ,which was probably the exactly way that involved in pathogenesis of brain injury during deep hypothermia circulatory arrest.