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1.
Journal of Biomedical Engineering ; (6): 932-939, 2021.
Article in Chinese | WPRIM | ID: wpr-921831

ABSTRACT

Craniofacial malformation caused by premature fusion of cranial suture of infants has a serious impact on their growth. The purpose of skull remodeling surgery for infants with craniosynostosis is to expand the skull and allow the brain to grow properly. There are no standardized treatments for skull remodeling surgery at the present, and the postoperative effect can be hardly assessed reasonably. Children with sagittal craniosynostosis were selected as the research objects. By analyzing the morphological characteristics of the patients, the point cloud registration of the skull distortion region with the ideal skull model was performed, and a plan of skull cutting and remodeling surgery was generated. A finite element model of the infant skull was used to predict the growth trend after remodeling surgery. Finally, an experimental study of surgery simulation was carried out with a child with a typical sagittal craniosynostosis. The evaluation results showed that the repositioning and stitching of bone plates effectively improved the morphology of the abnormal parts of the skull and had a normal growth trend. The child's preoperative cephalic index was 65.31%, and became 71.50% after 9 months' growth simulation. The simulation of the skull remodeling provides a reference for surgical plan design. The skull remodeling approach significantly improves postoperative effect, and it could be extended to the generation of cutting and remodeling plans and postoperative evaluations for treatment on other types of craniosynostosis.


Subject(s)
Child , Humans , Infant , Computer Simulation , Cranial Sutures/surgery , Craniosynostoses/surgery , Skull/surgery
2.
Frontiers of Medicine ; (4): 697-706, 2018.
Article in English | WPRIM | ID: wpr-771274

ABSTRACT

Oxidative stress induced by free fatty acid aggravates endothelial injury, which leads to diabetic cardiovascular complications. Reduction of intracellular oxidative stress may attenuate these pathogenic processes. The dietary polyphenol resveratrol reportedly exerts potential protective effects against endothelial injury. This study determined whether resveratrol can reduce the palmitic acid (PA)-induced generation of reactive oxygen species (ROS) and further explored the underlying molecular mechanisms. We found that resveratrol significantly reduced the PA-induced endothelial ROS levels in human aortic endothelial cells. Resveratrol also induced endothelial cell autophagy, which mediated the effect of resveratrol on ROS reduction. Resveratrol stimulated autophagy via the AMP-activated protein kinase (AMPK)-mTOR pathway. Taken together, these data suggest that resveratrol prevents PA-induced intracellular ROS by autophagy regulation via the AMPK-mTOR pathway. Thus, the induction of autophagy by resveratrol may provide a novel therapeutic candidate for cardioprotection in metabolic syndrome.


Subject(s)
Animals , Humans , Male , Mice , AMP-Activated Protein Kinases , Metabolism , Antioxidants , Pharmacology , Autophagy , Cells, Cultured , Endothelial Cells , Mice, Inbred C57BL , Oxidative Stress , Reactive Oxygen Species , Metabolism , Resveratrol , Pharmacology , Signal Transduction , TOR Serine-Threonine Kinases , Metabolism
3.
Journal of Third Military Medical University ; (24)2003.
Article in Chinese | WPRIM | ID: wpr-562208

ABSTRACT

Objective To construct a RhoC-siRNA expression vector, and study its role on the biological behaviors of hepatoma carcinoma cells. Methods RhoC-siRNA gene was synthesized and cloned into the expression vector pSilencer2.1. The constructed RhoC-siRNA expression vector was stably transfected into hepatoma carcinoma cell line SK-Hep1. The inhibitory effect of RhoC-siRNA on the expression of RhoC in transfected cells was detected by Western blotting. The morphous, growth velocity and the ability of cell adhesion, cell migration, cell invasion before and after transfection was observed. Results Enzyme digestion and DNA sequencing confirmed that the RhoC specific siRNA expression vector was constructed successfully. After transfection, RhoC expression was inhibited by 60%, and no marked difference was observed in cellular morphous and growth curve, while the ability of cell adhesion, cell migration, and cell invasion were markedly decreased. Conclusion The RhoC-siRNA expression vector can effectively suppress RhoC expression in transfected hepatoma carcinoma cells. Although having no effect on the morphous and growth velocity of hepatoma carcinoma cells, it decreases the potentiality of cell invasion and cell metastasis, which may provide a novel applicable strategy for gene therapy on hepatocellular carcinoma.

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