Functionalized M2TiC2Tx MXenes (M = Cr and Mo; T = F, O, and OH) as high performance electrode materials for sodium ion batteries.

First-principles calculations were performed to study the electrochemical performance of M2TiC2 (M = Cr or Mo) and M2TiC2Tx (T = O, F or OH) used as anode materials for sodium ion batteries (SIBs). The O functionalized MXenes (Cr2TiC2O2 and Mo2TiC2O2) are found to be more stable than F and OH terminated systems. The diffusion performance of sodium in MXene materials is mainly affected by the functional groups. The lowest diffusion barrier of functionalized MXenes is about one order larger in magnitude than that of bare MXenes. Although the introduction of O-groups hinders the diffusion of sodium, it can greatly improve the theoretical storage capacities. Meanwhile, the diffusion paths and diffusion energy barriers of Na are affected by Na concentration effects, while the interactions between terminations have little effect. Furthermore, multiple layers of sodium atoms are found to be adsorbed between the layers of M2TiC2O2, thus significantly increasing the theoretical capacities. The theoretical sodium storage capacities of M2TiC2O2 monolayers reach 515.70 mA h g-1 (M = Cr) and 362.46 mA h g-1 (M = Mo) and the OCVs can approach 0.034 V (M = Cr) and 0.042 V (M = Mo). Therefore, Cr2TiC2O2 and Mo2TiC2O2 are expected to be promising anode materials for SIBs due to their excellent properties, such as good electronic conductivity, low sodium diffusion barrier, and high theoretical sodium storage capacity.

[Effects of bone marrow mesenchymal stem cell transplantation on the expression of stromal cell-derived factor-1α and vascular endothelial growth factor in rats with acute hepatic failure].

Objective: To investigate the curative effect of bone marrow mesenchymal stem cells (BMSCs) transplantation on the expression of stromal cell-derived growth factor (SDF-1 α) and vascular endothelial growth factor (VEGF) in rats with acute hepatic failure, and to compare the effects of two transplantation pathways. Methods: Eighty-four rats with acute liver failure (ALF) induced by D-galactosamine combined with lipopolysaccharide were randomly divided into control group, tail vein and portal vein transplantation group. The latter two groups were injected allogenic BMSCs into the tail vein and portal vein. Blood samples and liver tissue samples were collected at 24, 72, 120, and 168h after transplantation to detect serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST). The improvement of liver function before and after BMSCs transplantation was compared. The expression of VEGF and SDF-1a in liver tissue was detected by immunofluorescence and Western blot. Data measurement between two groups was performed by analysis of variance and the correlation analysis was performed by Spearman's rank correlation coefficient. Results: Serum ALT and AST levels in the tail vein and portal vein transplantation group peaked at 24 h after transplantation, which were (134.60 ± 58.08 IU/L), (179.20 ± 86.68 IU/L), and (131.00 ± 54.47 IU/L), (173.50 ± 93.10 IU/L). In addition, 168h after transplantation it decreased to (46.10 ± 8.40 IU/L), (95.67 ± 13.80 IU/L) and (19.30 ± 1.30 IU/L), (54.30 ± 6.00 IU/L). After 120 and 168 hours of BMSCs transplantation, the levels of serum ALT and AST in tail vein and portal vein transplantation group were significantly higher than control group (F ≥ 12.51, P < 0.01). The results of western blot and immunofluorescence showed that the expression levels of SDF-1α and VEGF protein in the two BMSCs transplantation groups increased with the improvement of liver function, and the difference was statistically significant at 120 and 168 hours after transplantation (F ≥ 9.069, P < 0.05). There was no significant difference in the expression of SDF-1a and VEGF between the tail vein and portal vein transplantation groups (P > 0.05). Correlation analysis showed that the expression levels of SDF-1α and VEGF in liver tissues were positively correlated (r = 0.923, P < 0.05). Conclusion: BMSCs transplantation can promote the secretion of VEGF for recovery of liver function to reduce the degree of inflammation and necrosis in rats with ALF.

Use of bone mesenchymal stem cells to treat rats with acute liver failure.

This study aimed to isolate mesenchymal stem cells from bone mesenchymal stem cells (BMSCs), determine their therapeutic potential for treating rats with acute liver failure (ALF), further explore the factors that induce liver failure mechanisms, and elucidate the role of bone marrow stem cell therapy and BMSCs on liver homing. We found that differentiation potential was present in BMSCs expressing high levels of CD29 and CD90. These cells improved liver functioning in vivo after transplantation into rat livers with D-galactosamine damage, as evidenced by the levels of alanine aminotransferase and aspartate aminotransferase returning to normal (low levels) in recipient ALF rats. A significant improvement in the liver functional test and histological findings was observed in the transplantation group after 120 and 168 h of transplantation (P < 0.05). Histological data revealed that hepatocyte cell apoptosis was lower in the transplantation group compared to the control groups (P < 0.05), and that the transplantation of BMSCs reduced liver inflammation, decreased hepatic denaturation and necrosis, and promoted liver regeneration. These ameliorations were not recorded in the control groups. The results of in situ hybridization, immunofluorescence staining, and Western blot confirmed the presence of transplanted BMSCs in recipient rat livers. Stromal cell derived factor-1 alpha and vascular endothelial growth factor were significantly upregulated after the intraportal transplantation of BMSCs, with significantly higher levels being found in the portal vein and the tail vein groups (P < 0.05). In conclusion, BMSCs have a therapeutic effect against ALF rats, evoke endogenous repair mechanisms in the liver, and may represent a novel form of therapeutic intervention for the disease. Furthermore, intraportal transplantation serves as a more effective pathway compared to tail vein transplantation.

Effect of 3,6-dimethamidodibenzopyriodonium citrate on Ca2+ in rabbit platelet in vitro.

AIM: To study the effect of 3,6-dimethamidodibenzopyriodonium citrate (I-65) on the cytoplasmic free Ca2+ ([Ca2+]i) concentration in rabbit platelet. METHODS: Measurement of the cytosolic Ca2+ of platelets in vitro by using Quin 2-AM fluorescence technique. RESULTS: In the presence of CaCl2 1 mmol.L-1, I-65 (10, 20, and 30 mumol.L-1) reduced the rise in [Ca2+]i induced by thrombin and calcimycin from 142 +/- 22 nmol.L-1 and 124 +/- 18 nmol.L-1 to 118 +/- 20, 78 +/- 12, 40 +/- 10 nmol.L-1, respectively and 108 +/- 15, 77 +/- 14, 37 +/- 14 nmol.L-1, respectively. In the presence of egtazic acid 2 mmol.L-1, I-65 (10, 20, and 30 mumol.L-1), reduced the Ca2+ release induced by thrombin from 52 +/- 11 nmol.L-1 to 34 +/- 9, 19 +/- 6, and 11 +/- 5 nmol.L-1, respectively. In addition, I-65 (10, 20, and 30 mumol.L-1) also reduced the Ca2+ influx induced by thrombin from 91 +/- 13 nmol.L-1 to 84 +/- 15, 58 +/- 15, and 28 +/- 19 nmol.L-1, respectively. CONCLUSION: I-65 inhibited not only the Ca2+ release, but also the influx of Ca2+ in activation platelet.