Xiang Long

Dr. Xiang Long


Research Focus & Metrics

Academic Career Length

10Years (2017-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

View All Publications
22 December 2021 in Journal of Cardiovascular Pharmacology
Verified
Journal Article
Open access
XLxinliang liu
xinliang liu
KQKai Qi
Kai Qi
YGYi Gong
Yi Gong
XLXiang Long
Xiang Long
SZShuqiang Zhu
Shuqiang Zhu
JXjianjun xu
jianjun xu
Ferroptosis, a recently discovered form of regulated cell death that is characterized by iron accumulation and excessive reactive oxygen species generation, has been favored by most researchers. Increasing evidence suggest that ferulic acid (FA) could exert marked effects to myocardial ischemia reperfusion (I/R) injury, although the understanding of its molecular mechanism is still limited. In our study, the myocardial I/R injury model was established to explore the relationship between I/R injury and ferroptosis. First, we successfully constructed myocardial I/R injury model with changes in ST segment, increased creatine phosphokinase, lactate dehydrogenase activities, and N-Terminal Pro Brain Natriuretic Peptide content, and a significantly larger infarct size. Then, the increased levels of the Ptgs2 mRNA, Fe2+ accumulation, and a decreased reduced glutathione/oxidized glutathione disulfide ratio were detected in ischemia-reperfusion-injured heart, which is highly consistent with ferroptosis. However, these effects were significantly improved after FA treatment. Based on these results, FA increased the activities of the antioxidant enzymes superoxide dismutase, catalase and glutathione peroxidase, decreased the malondialdehyde level, ameliorated the production of reactive oxygen species, and promoted the generation of adenosine triphosphate. These effects of FA are similar to those of the ferroptosis inhibitor ferrostatin-1. Upregulation of AMPKα2 and Glutathione Peroxidase 4 expression were also observed in the FA group. Compound C, a specific Adenosine 5'-monophosphate (AMP)-activated protein kinase inhibitor, significantly blocked the protective effect of FA. These findings underlined that FA inhibits ferroptosis by upregulating the expression of AMPKα2 and serves as a cardioprotective strategy.

1 August 2021 in Asian Journal of Surgery
Verified
Journal Article
Open access
FLFeng Lu
Feng Lu
SZShu-Qiang Zhu
Shu-Qiang Zhu
XLXiang Long
Xiang Long
KLKun Lin
Kun Lin
BQBai-Quan Qiu
Bai-Quan Qiu
YWYong-Bing Wu
Yong-Bing Wu
There is an increasing demand for minimally invasive aortic valve replacement. This study aimed to investigate the safety and feasibility of minimally invasive aortic valve replacement through a right parasternal second intercostal transverse incision. This was a retrospective study, and we collected information from 111 patients who underwent isolated aortic valve replacement surgery performed by the same surgeon from January 2018 to December 2019. According to the operative approach, the patients were divided into a sternotomy aortic valve replacement (SAVR) group (n = 62) and a minimally invasive aortic valve replacement (Mini-AVR) group (n = 49). We compared the intraoperative and postoperative data between the two groups. There was no difference in preoperative data between the Mini-AVR and SAVR. The postoperative ventilator-assisted time, CSICU time and postoperative hospital stay of the Mini-AVR were shorter than those of the SAVR [(15.45 ± 5.75) VS (18.51 ± 6.71) h; (1.77 ± 0.31) VS (2.04 ± 0.63) d; (8.69 ± 2.75) VS (10.77 ± 2.94) d], and the difference was statistically significant (P < 0.05). Mini-AVR had lower postoperative drainage and blood transfusion rates in the first 24 h than SAVR [(109.86 ± 125.98) VS (508.84 ± 311.70) ml; 22.4% VS 46.8%], and the differences were statistically significant (P < 0.05). The incidence of postoperative AF in the Mini-AVR group was also lower than that in the SAVR group (10.2% VS 30.6%), and the differences were statistically significant (P < 0.05). Mini-AVR has the advantages of less ventilator time, a reduced need for blood transfusion, less AF and a faster recovery. Mini-AVR is a safe and feasible surgical technique that is worthy of clinical application.

12 June 2017 in Journal of Cardiothoracic Surgery
Verified
Journal Article
Open access
PDF file
YLYunfei Liao
Yunfei Liao
XLXiang Long
Xiang Long
SZShuQiang Zhu
ShuQiang Zhu
JTJun Tu
Jun Tu
HWHua Wen
Hua Wen
YWYong-Bing Wu
Yong-Bing Wu
Minimally invasive cardiac surgical techniques are increasingly applied in the treatment and management of a variety of adult ventricular septal defects (VSDs). However, repair of adult subarterial VSDs via left anterior mini-thoracotomy is rarely reported. The present study aimed to determine the feasibility and safety of the left anterior mini-thoracotomy for the repair of adult subarterial VSDs. Twenty-seven adult patients underwent repair of subarterial VSDs via left anterior mini-thoracotomy. The approach includes two options for skin incision access, longitudinal and transverse skin incisions. The skin incision length was 4.1–6.1 cm (mean, 5.1 ± 0.6 cm). The closure of the VSDs was obtained through the main pulmonary artery under direct visualization. Successful repair of the defects was achieved in all the patients. No patients died or converted to median sternotomy. Average durations of cardiopulmonary bypass (CPB) and aortic cross-clamp were 102.5 ± 13.6 min (range, 85–127 min) and 54.6 ± 6.9 min (range, 45–66 min), respectively. No patients required blood transfusion. The average postoperative hospital stay was 5.1 ± 0.7 days (range, 4–6 days). There were no postoperative complications related to the operative procedures or peripheral cannulation. During the follow-up of 5.4–32.3 months, no patients were found to have residual shunt, wound infections, pericardial effusion, neurologic or other complications. Our experiences demonstrate that minimally invasive cardiac surgical technique via left anterior mini-thoracotomy can be served as a novel, feasible and safe alternative for the repair of adult subarterial VSDs.