RESUMEN
Optical coherence tomography (OCT) is a new technique applied in cardiovascular system. It can detect vessel intimal, small structure of plaque surface and discover small lesions with its high axial resolution and quantification character. Especially with the application of OCT in characterization of coronary atherosclerotic plaque, diagnosis and treatment strategy making, optimizing percutaneous coronary intervention therapy and assessment after stent planting make the OCT become an efficient tool for cardiovascular disease diagnosis and treatment. This paper presents a novel coronary vessel intimal sequence extraction method based on prior boundary constraints in OCT image. On the basis of conventional Chan-Vese model, we modified the evolutionary weight function to control the evolutionary rate of boundary by adding local information of boundary curve. At the same time, we added the gradient energy term and intimal boundary constraint term based on priori boundary condition to further control the evolutionary of boundary curve. At last, coronary vessel intimal is extracted in a sequence way. The comparison with vessel intimal, manual segmented by clinical scientists (golden standard), indicates that our coronary vessel intimal extraction method is robust to intimal boundary blur, distortion, guide wire shadow and plaque disturbs. The results of this study can be applied to clinical aid diagnosis and precise diagnosis and treatment.
RESUMEN
OBJECTIVES: HIF2α is of vital importance in the regulation of endothelial dysfunction, cell proliferation, migration, and pulmonary vascular remodeling in pulmonary hypertension. Our previous studies demonstrated that conditional and inducible deletion of HIF2α in mouse lung endothelial cells, dramatically protected the mice against vascular remodeling and the development of pulmonary arterial hypertension (PAH). Here, we provide a novel transcriptome insight into the impact of HIF2α in PAH pathogenesis and the potential to use HIF2α-mediated gene sets to differentiate PAH human subjects. METHODS: Using transcriptome data, we first tapped the value of the difference in gene expression profile between wild type (WT) and Hif2a knockdown (KD) cell lines. We considered the deregulated genes between WT and Hif2a-KD cells as HIF2α influenced genes. By examining the lung tissue transcriptome data set with nine controls and eight PAH patients, we evaluated the HIF2α regulatory network in PAH pathogenesis to further determine the identification ability of HIF2α-mediated gene sets in human PAH subjects. On the other hand, using peripheral blood mononuclear cells (PBMCs) transcriptome data from PAH patients and healthy controls, we further validated the potential of the HIF2α-mediated PBMC gene sets as a possible diagnostic tool for PAH. To verify the ability of HIF2α-mediated gene sets for the identification of PAH, endothelial cell-specific Phd2 knockout mice with spontaneous pulmonary hypertension were used for reverse validation experiments. RESULTS: 19 identified GO biological process terms were significantly correlated with the genes down-regulated in Hif2a-KD cells, all of which are strongly related to the PAH pathogenesis. We further assessed the discriminative power of these HIF2α-mediated gene sets in PAH human subjects. We found that the expression profile of the HIF2α-mediated gene sets in lung tissues and PBMCs were differentiated both between controls and PAH patients. Further, a significant positive correlation was observed between hypoxia and Phd2 deficiency mediated gene set expression profiles. As expected, 7 of the 19 significantly down-regulated GO terms in Hif2a-KD cells were found to overlap with the up-regulated GO gene sets in Phd2 EC-/- mice compared to WT controls, suggesting opposing effects of HIF2α and PHD2 on PAH pathogenesis. CONCLUSION: HIF2α-mediated gene sets may be used to differentiate pulmonary arterial hypertension.