Application of a Modified Extracorporeal Circulation Perfusion Method During Surgery for Acute Stanford Type A Aortic Dissection.

AIM: The aim of this study was to investigate the effect of the modified extracorporeal circulation perfusion method during surgery for acute Stanford type A aortic dissection in patients who underwent stented elephant trunk implantation and arch replacement. METHOD: A total of 69 patients with acute Stanford type A aortic dissection who underwent stented elephant trunk implantation and arch replacement were retrospectively analysed from 2017 to 2018. According to the perfusion method of extracorporeal circulation, patients were divided into a routine perfusion (RP) group and a modified perfusion (MP) group. Clinical data were collected, including the time of extracorporeal circulation and deep hypothermic circulatory arrest, incidence of acute kidney injury and neurological complications, and comparisons between the two groups were conducted by using independent sample t-tests for normally distributed qualitative data, the Mann-Whitney U-test for skewed qualitative data, and the chi square test or Fisher's exact test for categorical data. RESULTS: There were 55 (80%) males and 14 (20%) females in the entire cohort, and the mean ± standard deviation age was 50.4±9.0 years. A total of 53 (77%) patients were included in the RP group, and 16 (23%) were included in the MP group. Patients in the MP group were older (55.5±7.8 vs 48.8±8.9 years), and the difference was significant (p=0.008). Compared with the RP group, the time of extracorporeal circulation (218.0 [44.7] vs 246.0 [58.0] min; p=0.005) and deep hypothermic circulatory arrest (4.0 [2.0] vs 25.0 [10.0] min; p<0.001) was shorter, and the incidence of postoperative acute kidney injury (n=6 [37.5%] vs n=36 [67.9%]; p=0.029) was lower in the MP group; the differences were significant. Six (6) patients died in the RP group; no patients died in the MP group. The total in-hospital mortality rate was 8.7%. CONCLUSIONS: The modified extracorporeal circulation perfusion method is feasible, with satisfactory results.

SNHG16 accelerates the proliferation of primary cardiomyocytes by targeting miRNA-770-5p.

The present study aimed to clarify the influence of long non-coding RNA small nuclear host gene 16 (lncRNA SNHG16) on cardiomyocyte proliferation following ischemia/reperfusion injury (IRI) and the potential mechanism. An IRI model in mice was established by performing ligation of the anterior descending coronary artery (LAD). Primary cardiomyocytes were isolated from newborn mice and subjected to H2O2 treatment to mimic in vitro IRI. Relative levels of SNHG16 and miRNA-770-5p in both in vivo and in vitro IRI models were examined. The regulatory effects of SNHG16 and miRNA-770-5p on the proliferative ability of H2O2-treated cardiomyocytes were assessed by Cell Counting Kit-8 (CCK-8) and 5-ethynyl-2'-deoxyuridine (EdU) assay. The binding relationship between SNHG16 and miRNA-770-5p was verified through dual-luciferase reporter gene assay. It is found that SNHG16 was time-dependently downregulated in the IRI models. Overexpression of SNHG16 enhanced the proliferative ability of the cardiomyocytes. miRNA-770-5p was found to be a direct target of SNHG16. Moreover, SNHG16 was able to negatively regulate the miRNA-770-5p level. Overexpression of miRNA-770-5p partially reversed the role of SNHG16 on accelerating cardiomyocyte proliferation. Collectively, SNHG16 accelerates the proliferative ability of cardiomyocytes following IRI by negatively regulating miRNA-770-5p.

Role of MICA expression, anti-MICA antibodies and serum MICA during acute rejection in a rat-to-mouse cardiac transplantation model.

BACKGROUND AND OBJECTIVE: Human major histocompatibility complex class I-related gene A (MICA) is reportedly associated with poor transplant outcomes and a high risk of acute and chronic rejection in solid organ transplantation. However, studies on these risks have found conflicting results. In the present study, we investigate the MICA expression and serum MICA (sMICA) as well as the MICA antibodies (anti-MICA) in serum of recipients during acute rejection (AR) in a rat-to-mouse cardiac transplantation model. METHODS: Construct rat-to-mouse concordant cardiac transplantation models, histological examination of the heart in recipients during AR at 2-6 hours time point was done. We then studied the MICA gene expression of the heart in recipients during AR at 2-6 hours time point by western blot and RT-PCR assay. We latter studied the anti-MICA and sMICA levels in serum of recipients during AR at 2-6 hours time point by Flow cytometry and ELISA measurement. RESULTS: We found that Lewis rat hearts transplanted into BALB/c mice developed typical AR in 6 days. The level of severity of xenograft rejection from 2 d to 6 d was increased in a time-dependant way. MICA protein and MICA mRNA was also increased in time-dependant way and reached the highest value at 6 h. The prevalence of anti-MICA was significantly higher among those with severe acute rejection. However, sMICA was significantly increased during AR at 2 hours, then gradually decreased, and reached the lowest value at 6 h. CONCLUSIONS: MICA expression in recipients' heart and anti-MICA antibodies in recipients' sera may associated with high risk of AR in rat-to-mouse transplantation. sMICA showed a negative association with acute rejection and may be a good predictor of heart transplant outcomes.