ObjectiveTo investigate the correlation between the expression of VEGF and the lymph node metastasis of colorectal carcinoma.MethodsVEGF was detected by immunohistochemistry in 24 cases of colorectal carcinoma with lymph node metastasis and 16 case of colorectal carcinoma without lymph node metastasis.CD34 was used as a marker to evaluate the MVD.All the data were analyzed using 10.1 statistical package.The comparison was performed by x2 test and Spearman rank correlation analysis.The level of significance is α =0.05.Resultsin the 40 cases of colorectal carcinoma,24 cases encountered lymph node metastasis with an MVD (40.65 ± 11.80) and 21 cases were VEGF positive (87.5％).In the 16 cases without metastasis,the MVD was (25.02 ± 11.52) and 4 cases were VEGF positive (25.0％).MVD and VEGF were significantly different between thecases with lymph node metastasis and those without (t =-4.138,x2 =16.00,P ＜0.01 ).In the 40 cases,there were 25 cases with positive VEGF with an MVD (41.33 ± 11.61 ) and 15 cases with negative VEGF with and MVD (22.84 ±8.88).The difference between the cases with positive VEGF and those with negative VEGF (t =5.301,P ＜0.05 ).VEGF level was positive correlated with MVD in the colon cancer ( rs =0.539,P ＜ 0.05 ).Conclusion VEGF may play a role in promoting the lymph node metastasis of colorectal carcinoma

Heart failure (HF) has become one of the severe public health problems.The detailed role of mitochondrial function in HF was still unclear. Benzoylaconine (BAC) is a traditional Chinese medicine, but its role in HF still needs to be explored.In this study, oxygen-glucose deprivation and reperfusion (OGD/R) was executed to mimic the injury of H9C2 cells in HF. The viability of H9C2 cells was assessed via MTT assay. OGD/R treatment markedly decreased the viability of H9C2 cells, but BAC treatment evidently increased the viability of OGD/R-treated H9C2 cells. The apoptosis of H9C2 was enhanced by OGD/R treatment but suppressed by BAC treatment. The mitochondrial membrane potential was evaluated via JC-1 assay. BAC improved the mitochondrial function and suppressed oxidative stress in OGD/R-treated H9C2 cells. Moreover, Western blot analysis revealed that the protein expression of p-AMPK and PGC-1α were reduced in OGD/R-treated H9C2 cells, which was reversed by BAC. Rescue assays indicated that AMPK attenuation reversed the BAC-mediated protective effect on OGD/R-treated cardiomyocytes. Moreover, BAC alleviated myocardial injury in vivo. In a word, BAC modulated the mitochondrial function in OGD/R-induced cardiomyocyte injury by activation of the AMPK/PGC-1 axis. The findings might provide support for the application of BAC in the treatment of HF.

GPCR proteins represent the largest family of signaling membrane proteins in eukaryotic cells. Their importance to basic cell biology, human diseases, and pharmaceutical interventions is well established. Many crystal structures of GPCR proteins have been reported in both active and inactive conformations. These data indicate that agonist binding alone is not sufficient to trigger the conformational change of GPCRs necessary for binding of downstream G-proteins, yet other essential factors remain elusive. Based on analysis of available GPCR crystal structures, we identified a potential conformational switch around the conserved Asp2.50, which consistently shows distinct conformations between inactive and active states. Combining the structural information with the current literature, we propose an energy-coupling mechanism, in which the interaction between a charge change of the GPCR protein and the membrane potential of the living cell plays a key role for GPCR activation.
Binding Sites ; GTP-Binding Proteins ; chemistry ; genetics ; metabolism ; Humans ; Hydrogen Bonding ; Membrane Potentials ; Models, Molecular ; Protein Conformation ; Receptors, G-Protein-Coupled ; chemistry ; genetics ; metabolism ; Signal Transduction