[Advances in non-invasive treatment of aortic diseases].

With the further development and long-term follow-up of endovascular treatment for aortic diseases, increasing evidence shows that in many cases, there are difficulties in the diagnosis of causes, decision-making of treatment timing, and lack of effective evaluation of treatment prognosis in endovascular treatments. Therefore, it is necessary to conduct in-depth research on non-invasive treatment including prevention, diagnosis, treatment, and prediction of aortic diseases. The non-invasive treatment of aortic disease is mainly applied to high-risk populations with aortic dissection, regulating key targets and mechanisms, and adopting drug intervention in advance to achieve the goal of controlling aortic dilation and preventing the occurrence of dissection. It also conducts precise multi omics analysis to determine the optimal intervention timing and treatment strategy, and aims at complications related to aortic disease or endovascular treatment for patients with a positive family history of aortic dilation and those who have developed aortic dissection. Precise regulation can control the progression of aortic aneurysm and aortic dissection, delay or achieve long-term stable coexistence with aortic disease, and even reverse disease progression and achieve benign aortic remodeling through new intervention vectors. Ultimately achieving the ideal state of complete thrombosis and mechanized healing of the aortic aneurysm or aortic dissection false lumen.

[Transcriptome analysis of human breast cancer cell lines MCF-7 and MDA-MB- 435 by RNA-seq].

The transcriptomic profiles of human breast cancer cell lines MCF-7 and MDA-MB-435 were investigated using the next-generation RNA sequencing (RNA-Seq). The DESeq package was used to screen the differentially expressed transcripts. A total of 229 genes with a significantly differential expression in MDA-MB-435 cells as compared with MCF-7 cells were obtained. Annotation of the biological functions of these genes through the Database for Annotation, Visualization and Integrated Discovery (DAVID) v6.7 demonstrated that the 229 differentially expressed genes were mainly implicated in the biological functions related to cell adhesion and motion, antigen processing and presentation (via MHC class II), hormone response, extracellular structure organization, tissue remodeling, and cell proliferation regulation. Analysis of the individual genes demonstrated that MDA-MB-435 cells exhibited a higher tendency to metastasis and antigen processing and presentation, and lower ability to hormone response. Twenty most abundant transcripts in MDA-MB-435 cells, such as VIM, TNC, and CD74, represent its high potential for metastasis. Besides the genes previously reported to be involved in tumor metastasis and development, genes newly identified in this study could provide new clues for the diagnosis and prognosis of aggressive breast cancers.

Abnormal activation of OPN inflammation pathway in livers of children with biliary atresia and relationship to hepatic fibrosis.

OBJECTIVE: Aim of the study was to investigate the expression of OPN (osteopontin) and its upper-downstream regulating factors in the biliary atretic liver and explore the relationship to progressive intrahepatic fibro-inflammation. METHOD: OPN expression in the livers of 18 children with biliary atresia (BA), 15 children with congenital biliary dilatation (CBD) and 8 normal controls were examined by immunostaining. Masson's trichrome stain was used to evaluate the level of hepatic fibrosis in each group. Western blotting and RT-polymerase chain reaction were respectively used to semiquantitatively analyze the NF-kappaB (nuclear factor-kappaB) and the TGF-beta1mRNA (transforming growth factor-beta1) expression in each group. RESULTS: OPN expression was found in the epithelial cells of the intrahepatic bile duct in the BA group, and its intensity was 0.33 +/- 0.10, while there was only little expression of OPN in the epithelial cells of the intrahepatic bile ducts in the CBD group and normal controls. There was a positive correlation between the intensity of OPN and the level of hepatic fibrosis in BA livers (r = 0.97). The intensity of NF-kappaB expression in BA livers (0.76 +/- 0.07) was much higher than that in CBD livers (0.25 +/- 0.04) or the livers of normal controls (0.22 +/- 0.02). A positive correlation was detected between the intensity of NF-kappaB and OPN in BA livers (r = 0.94). The expression of TGF-beta1mRNA in BA livers (1.46 +/- 0.17) was much higher than that in CBD livers (0.68 +/- 0.11). Little expression of TGF-beta1mRNA was detected in the livers of normal controls. A positive correlation was detected between the expression of TGF-beta1mRNA and the intensity of OPN in BA livers (r = 0.88). CONCLUSION: The abnormal activation of the OPN inflammation pathway might play a key role in the generation of intrahepatic fibrosis in BA. This progressive fibro-inflammation might be controlled by OPN and its upper-downstream regulating factors NF-kappaB and TGF-beta1.

Invasion and metastasis of liver cancer: expression of intercellular adhesion molecule 1.

PURPOSE: To study the relationship between intercellular adhesion molecule 1 (ICAM-1) and liver cancer metastasis and to find predicting factors that could indicate the growth and metastasis of liver cancer. METHODS: ICAM-1 expression in fresh tissue of normal liver and hepatocellular cancer (HCC) was examined by immunoperoxidase staining. Serum soluble intercellular adhesion molecule 1 (sICAM-1) from patients with a benign HCC tumor, and the expression of ICAM-1 in the orthotopically transplanted LCI-D20 tumor of a nude mouse liver cancer metastasis model, and in human hepatoma, the tumor surrounding tissue and normal liver, was analyzed semiquantitatively by the immuno-dot blot method. Tissue ICAM-1 expression (mRNA level) was detected by Northern blotting. RESULTS: ICAM-1 expression in LD1-20 D metastatic liver cancer had a positive correlation with tumor size and the time after implantation. It increased suddenly as metastasis occurred being 3.03+/-0.51 before metastasis and 8.24+/-0.95 after metastasis, P < 0.01, then remained high, appending on the number of sites involved (monosite metastasis 5.48+/-0.49, multisite metastasis 10.05+/-1.17, P < 0.05). All six cases of normal liver samples were negative in anti-ICAM-1 immunohistochemical staining, 80.0% (36/45) of the HCC showed some ICAM-1 expression. The rate of positive cells was a little higher in large tumors, tumors with an intact capsule and tumors with metastasis, but there was no significant difference. It was noticed that two cancer emboli also had high ICAM-1 expression. The ICAM-1 concentration in HCC (13.43+/-0.09) was higher than that in tumor surrounding the liver (5.89+/-0.17, P < 0.01) and that in normal liver (4.27+/-0.21, P < 0.01). sICAM-1, like tissue ICAM-1, was higher in HCC patients than in patients (with benign liver tumor and normal controls. Both tissue ICAM-1 and sICAM-1 were higher in the metastasis group than in the group without metastasis (tissue ICAM-1 20.24+/-0.30 vs 10.23+/-0.12 P < 0.05; sICAM-1 12.18+/-0.25 vs 9.77+/-0.54 P < 0.05). Northern blot analysis revealed that ICAM-1 expression, as indicated by mRNA level, was also higher in HCC and in cancer emboli than in tumor surrounding liver and normal liver. CONCLUSIONS: Tissue ICAM-1 and serum sICAM-1 could indicate the stage of HCC, and the potential of hepatoma cells for invasion and metastasis. They may play an important role in the metastasis cascade.