Liver transplantation is the most effective treatment for end-stage liver disease, and early graft dysfunction often occurs after surgery. Early liver dysfunction after liver transplantation has become one of the complications after liver transplantation, which seriously affects the graft and patient survival. Therefore, reducing its occurrence can be an important means to improve the prognosis of recipients after liver transplantation. This paper discusses the research progress on the definition, influencing factors, and prognosis and prediction model in order to provide better prevention and effective reference for improving the success rate and prognosis of early liver dysfunction in recipients after liver transplantation.

AIM: To investigate whether the expression of integrin ?_3 and the activation of focal adhesion kinase(FAK) are involved in neointima formation after de-endothelium.METHODS: The model of intima hyperplasia was prepared by balloon injury.The levels of osteopontin(OPN),integrin ?_3 and FAK in vascular tissue were detected by Western blotting and immunohistochemistry.RESULTS: There were similar expression patterns in OPN,integrin ?_3 and FAK following balloon injury.The levels of three proteins were markedly increased 3 days after operation and reached the peak at 7th day.The increased FAK was mainly the phosphorylated form.The migration and proliferation of vascular smooth muscle cells was associated with the increase in the expression of integrin ?_3 and FAK,and was parallel with rapid turnover of extracellular matrix(ECM).CONCLUSION: The interaction of cells with ECM mediated by OPN and integrin ?_3 is essential for migration.The integrin ?_3-FAK pathway is involved in neointima formation.

AIM: To determine the relationship between the changes of SM ?-actin and SM22? expression and vascular tone. METHODS: The expression of SM ?-actin and SM22? during restenosis after de-endothelialization were detected by Western blotting and immunohistochemistry. The structure of myofilaments was observed by transmission electron microscopy. The vascular contraction induced by phenylephrine was measured by a force transducer. RESULTS: The levels of SM ?-actin and SM22? expression in vascualar wall declined after de-endothelialization. The myofilaments in VSMC were modulated from well arranged and dense bundles to discrete network. However, the vascular tone and reactivity to agonist were much higher than that in control (P

Objective: Buyinqianzheng Formula (BYQZF) is clinically employed in traditional Chinese medicine to treat Parkinson's disease (PD) by improving mitochondrial dysfunction. However, the underlying mechanisms by which BYQZF affects mitochondrial morphology remain unknown. Therefore, we observed the effects of BYQZF on mitochondria from the perspective of the PINK1/Parkin pathway. Methods: Cell survival rates were assessed by Cell Counting Kit-8 assay. Expression levels of PINK1 and Parkin mRNA were examined by qRT-PCR. Protein expression levels of PINK1, PINK1-Ser228, Parkin, Parkin-Ser65, Drp1, and Drp1-Ser637 were examined by western blotting. PINK1, Parkin, and Mito-Tracker? Red CMXRos (MTR) were stained by triple-labeled immunofluorescence, and observed under laser confocal microscopy. Results: Cell survival rate, mitochondrial form factor, mean length and number of mitochondrial network branches, mitochondrial activity, mRNA expression levels of PINK1 and Parkin, and protein expression levels of PINK1, Parkin, and Drp1-Ser637 were reduced after 1-methyl-4-phenylpyridinium (MPP+) intervention. In contrast, Pearson's correlation coefficients between PINK1 and Parkin, and between Parkin and MTR, as well as protein expression levels of PINK1-Ser228, Parkin-Ser65, and Drp1 increased significantly after MPP+intervention. Treatment with BYQZF increased cell survival rate, mitochondrial form factor, mean length and number of mitochondrial network branches, mitochondrial activity, mRNA expression levels of PINK1 and Parkin, and expression of PINK1, Parkin, and Drp1-Ser637 proteins. Pearson's correlation coefficients between PINK1 and Parkin, and between Parkin and MTR, as well as protein expression levels of PINK1-Ser228, Parkin-Ser65, and Drp1 decreased after BYQZF treatment. Conclusion: These results demonstrate that BYQZF has a protective effect on mitochondrial molecular mechanisms in the PD cell model, and the mechanism is related to the PINK1/Parkin pathway.