Objective To assess the value of susceptibility-weighted imaging (SWI) in staging hepatic fibrosis (HF) in rabbits. Methods Sixty healthy rabbits were randomly divided into HF group (n=44), control group (n=16). Rabbits in the HF group and supplementary group were injected subcutaneously with 50%CCl4 oily solution to establish hepatic fibrosis model. On the basis of preliminary test, 8 rabbits in the HF group and 4 rabbits in the control group were selected randomly at the 4th, 5th, 6th, 10th week after CCL4 injection ,respectively , to undergo liver MR scan,including conventional axial T1WI, T2WI and axial SWI, DWI scan. All rabbits were sacrificed after MR scan and the tissue of liver were sampled for pathological test and hepatic fibrosis staging. Rabbits were classified into group F0, F1-2 and F3-4 based on pathological results. Liver signal intensity (SI), and liver-to-muscle SI ratio were measured on SWI images and ADC values were measured on DWI images correspondently. One-way ANOVA analysis was performed to compare difference in liver SI, liver-to-muscle SI ratio and ADC values among group F0 (no fibrosis), F1-2 (mild-moderate fibrosis) and F3-4 (severe fibrosis) . Spearman correlation analysis was performed to correlate pathological staging and liver SI, liver-to-muscle SI ratio and ADC values. Receiver operating characteristic (ROC) curve analysis was performed to compare the diagnostic performance of SWI and DWI for staging HF. Results Two and 5 rabbits in the HF group died at the 5th and the 6th week after CCL4 injection , respectively due to acute hepatic necrosis, hepatorrhexis and systemic failure. Seven rabbits in supplementary group were used as supplement. Of the 16 rabbits in the control group, 1 was excluded from the study due to liver fibrosis. Fifteen rabbits in group F0, sixteen rabbits in group F1-2 and sixteen rabbits in group F3-4 underwent MRI and were included into this study. Liver-to-muscle SI ratio in group F0, F1-2 and F3-4 were 0.973 ± 0.020, 0.880 ± 0.090 and 0.649 ± 0.140, respectively. Liver SI were 378 ± 45, 374 ± 19 and 317 ± 34. ADC values were (1.473 ± 0.320) × 10-3, (1.311 ± 0.310) × 10-3 and (0.942 ± 0.180) × 10-3mm2/s. There were statistically significant differences in liver SI, liver-to-muscle SI ratio and ADC values among group F0, F1-2 and F3-4 (F=46.571,15.803 and 15.317, P< 0.01). Liver-to-muscle SI ratio was highly negatively correlated with HF staging (r=-0.818,P<0.01), while liver SI and ADC values were moderately correlated with HF staging (r=-0.565,-0.630;P<0.01). Area under ROC curve (AUC) of liver-to-muscle SI ratio, liver SI and ADC value for differentiating hepatic fibrosis stage F0 and stage F1-4 were 0.916, 0.695 and 0.768, while the AUC for differentiating hepatic fibrosis stage F0-2 and stage F3-4 were 0.951, 0.904 and 0.900. Conclusion Liver-to-muscle SI ratio on SWI provide added diagnostic value and could be an useful parameter for staging hepatic fibrosis.

AIM:Tostudywhe ther theangiotens in-(1-7)[Ang-(1-7)]/Mas receptor axis protects cardio-myocytes against high glucose (HG)-induced injury by inhibiting nuclear factor-κB (NF-κB) pathway.METHODS:The cell viability was measured by CCK-8 assay.The intracellular levels of reactive oxygen species ( ROS) were detected by DCFH-DA staining .The number of apoptotic cells was tested by Hoechst 33258 nuclear staining .Mitochondrial membrane potential ( MMP) was examined by JC-1 staining.The levels of NF-κB p65 subunit and cleaved caspase-3 protein were de-termined by Western blotting.RESULTS: Treatment of H9c2 cardiac cells with 35 mmol/L glucose (HG) for 30, 60, 90, 120 and 150 min significantly enhanced the levels of phosphorated ( p) NF-κB p65, peaking at 60 min.Co-treatment of the cells with 1 μmol/L Ang-(1-7) and HG for 60 min attenuated the up-regulation of p-NF-κB p65 induced by HG. Co-treatment of the cells with Ang-(1-7) at concentrations of 0.1~30μmol/L and HG for 24 h inhibited HG-induced cy-totoxicity, evidenced by an increase in cell viability .On the other hand, 1 μmol/L Ang-(1-7) ameliorated HG-induced apoptosis, oxidative stress and mitochondrial damage , indicated by decreases in the number of apoptotic cells , cleaved caspase-3 level, ROS generation and MMP loss .However, the above cardioprotective effects of Ang-(1-7) were markedly blocked by A-779, an antagonist of Ang-(1-7) receptor (Mas receptor).Similarly, co-treatment of H9c2 cardiac cells with 100 μmol/L PDTC ( an inhibitor of NF-κB) and HG for 24 h also obviously reduced the above injuries induced by HG.CONCLUSION:Ang-(1-7)/Mas receptor axis prevents the cardiomyocytes from the HG-induced injury by inhibiting NF-κB pathway .

AIM:To investigate the roles of ATP-sensitive potassium ( KATP ) channels in high glucose-induced cardiac injury and the inhibitory effect of hydrogen sulfide ( H2 S) on the cardiomyocyte injury.METHODS:The expres-sion level of KATP channel protein was tested by Western blot.The cell viability was measured by CCK-8 assay.The number of apoptotic cells was observed by Hoechst 33258 nuclear staining.Mitochondrial membrane potential ( MMP) was exam-ined by JC-1 staining.RESULTS:After the H9c2 cells were treated with 35 mmol/L glucose ( high glucose, HG) for 1~24 h, the protein level of KATP channel was significantly reduced at 6 h, 9 h, 12 h and 24 h, reaching the minimum level at 12 h and 24 h.Pretreatment of the cells with 400μmol/L NaHS ( a donor of H2 S) prior to exposure to HG for 12 h con-siderably blocked the down-regulation of KATP channels induced by HG.Pretreatment of the cells with 100 μmol/L mito-chondrial KATP channel opener diazoxide, 50μmol/L non-selective KATP channel opener pinacidil or NaHS obviously inhibi-ted HG-induced injuries, leading to an increase in the cell viability, and decreases in the number of apoptotic cells and the MMP loss.Pretreatment with 100μmol/L mitochondrial KATP channel antagonist 5-hydroxydecanoic acid or 1 mmol/L non-selective KATP channel antagonist glibenclamide attenuated the above cardioprotective effects of NaHS.CONCLUSION:KATP channels mediate the inhibitory effect of H2 S on HG-induced cardiac injury.

Objective:To compare the diagnostic efficacy of MR elastography (MRE), Gd-EOB-DTPA dynamic contrast-enhanced MRI (DCE-MRI) in early quantitative evaluation of liver fibrosis (LF) staging of experimental rabbits.Methods:From April to December 2019, 200 healthy rabbits were randomly divided into LF group ( n=160) and control group ( n=40). LF group were injected subcutaneously with 50% CCl 4 oil solution, while control group were injected with normal saline solution. The LF group ( n=40) and control group ( n=10) were randomly selected at the end of the 4th, 8th, 12th and 16th weeks respectively to undergo axial MRI scan including MRE and Gd-EOB-DTPA DCE-MRI. The quantitative parameter values were obtained, including liver stiffness (LS), volume transfer constant (K trans), reflux rate constant (K ep), volume fraction of extravascular extracellular space (V e) and volume fraction of plasma (V p). Histopathological LF staging was based on Scheuer staging. One-way ANOVA analysis was used to evaluate the differences of LS, K trans, K ep, V e and V p among different LF stages. The Spearman correlation analysis was used to evaluate the correlations between pathological LF staging and quantitative parameter values. The ROC curve was used to compare the diagnositic performance of all quantitative parameter values. Results:Among the final qualified 150 rabbits, there were 32 in F0, 32 in F1, 35 in F2, 30 in F3, 21 in F4. Significant differences of LS, K trans, K ep, V e and V p were found among different LF stages. There was correlation between LS, K trans, K ep and LF stages ( r=0.832, 0.730, -0.617, all P<0.001), respectively. However, no statistically correlation was found between V e, V p and LF stages ( r=-0.074, P=0.367; r=-0.078, P=0.342). The area under the ROC curve (AUCs) of LS were the greatest (0.920 for F0 vs F1-F4, 0.900 for F0 vs F1-F2, 0.945 for F0 vs F3-F4, 0.926 for F1-F2 vs F3-F4), while the AUCs of K trans were 0.897, 0.863, 0.942, 0.809, respectively. Conclusion:The early quantitative diagnostic efficacy for LF staging by MRE was superior to Gd-EOB-DTPA DCE-MRI in rabbits.

Objective:To monitor the changes in donor gene chimerism ratio after allogeneic hematopoietic stem cell transplantation (allo-HSCT) in patients with severe beta-thalassemia using third-generation sequencing, and to explore the value of this technology in monitoring the proportion of donor genes chimerism in the early stage of postoperative allo-HSCT.Methods:Case analysis. Three beta-thalassemia patients at the First Affiliated Hospital of Guangxi Medical University during June-July 2022 who had undergone allo-HSCT with genotypes IVS-Ⅱ-654/CD41-42, IVS-Ⅱ-654/IVS-Ⅱ-654 and CD41-42/CD41-42 were included in this study. "Visual" analysis of the readouts of recipient DNA using third generation sequencing was used to monitor the genetic chimerism of the donor DNA and to compare with Sanger sequencing results. Post-transplantation follow-up was performed in the three patients to monitor the blood statistics and assess their implantation status and hematopoietic reconstitution.Results:The results of donor DNA chimerism status after allo-HSCT in the three patients detected by third generation sequencing were consistent with the Sanger sequencing results. The chimeric state of donor DNA gradually shifted to complete donor gene chimerism as the number of days after transplantation increased. Recipient 1 had 95.5% and 100% donor DNA chimerism at 10 and 20 d post-transplantation, respectively; recipient 2 had 100% donor DNA chimerism at 30 and 40 d post-transplantation; recipient 3 had 69.5% donor DNA chimerism at 1 d post-transplantation, and 100% donor DNA chimerism at 10 and 20 d post-transplantation. All patients achieved full donor gene chimerism within 30 d post-transplantation. Stable implantation of granulopoiesis, platelets, and erythropoiesis with hematopoietic reconstitution were obtained in all 3 patients within 1 month after transplantation.Conclusions:In this study, we developed a new method to detect the chimerism ratio of donor DNA using third-generation sequencing technology, enabling us to monitor the gene chimerism status of donor DNA at an early stage.