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1.
Journal of Forensic Medicine ; (6): 546-554, 2021.
Article in Chinese | WPRIM | ID: wpr-985247

ABSTRACT

In the field of forensic medicine, diagnosis of sudden cardiac death is limited by subjective factors and manual measurement methods, so some parameters may have estimation deviation or measurement deviation. As postmortem CT imaging plays a more and more important role in the appraisal of cause of death and cardiopathology research, the application of deep learning such as artificial intelligence technology to analyze vast amounts of cardiac imaging data has provided a possibility for forensic identification and scientific research workers to conduct precise diagnosis and quantitative analysis of cardiac diseases. This article summarizes the main researches on deep learning in the field of cardiac imaging in recent years, and proposes a feasible development direction for the application of deep learning in the virtual anatomy of sudden cardiac death at present.


Subject(s)
Humans , Artificial Intelligence , Autopsy , Death, Sudden, Cardiac/etiology , Deep Learning , Forensic Medicine
2.
Journal of Forensic Medicine ; (6): 615-620, 2021.
Article in English | WPRIM | ID: wpr-984062

ABSTRACT

OBJECTIVES@#To construct a cell line that can stably express human phospholamban(PLN) and initially explore its application in the study of myocardial toxicity mechanism.@*METHODS@#FastCloning method was used to insert the open reading frame sequence of target gene PLN into eukaryotic expression vector pcDNA5/FRT/TO(hereinafter referred to as pDFT) to construct the pDFT-PLN-Flag plasmid. The Flp-InTM T-RExTM 293 cells were generated by cotransfection of the constructed plasmid and pOG44 plasmid to express the target gene. Successfully recombined monoclonal cell lines were screened by hygromycin B resistance. Western blot and indirect immunofluorescence (IFA) were used to examine the expression of the target protein in recombinant cells. After the cell line was exposed to aconitine, it was verified by Western blot to detect changes in PLN protein phosphorylation.@*RESULTS@#After PCR amplification of the recombinant plasmid and DNA electrophoresis, the length of the amplified product is the same as the known PLN gene fragment, which is consistent with the open reading frame (ORF) sequence of the human PLN gene after sequencing. IFA and Western blot showed that the constructed proliferation cell line can stably express high levels of human PLN under induction and regulation. Preliminary results showed that the phosphorylation level of Thr17-PLN decreased after two hours of exposure to 1 μmol/L aconitine.@*CONCLUSIONS@#This human cell line can stably express PLN and can be used to study the mechanism of action of aconitine on the cell at molecular level.


Subject(s)
Humans , Calcium-Binding Proteins/metabolism , Cell Line , Myocardium/metabolism , Phosphorylation
3.
Journal of Southern Medical University ; (12): 774-776, 2010.
Article in Chinese | WPRIM | ID: wpr-355021

ABSTRACT

<p><b>OBJECTIVE</b>To detect the expression of important proteins associated with transforming growth factor-beta (TGF-beta)/Smad signaling pathway in Peutz-Jeghers syndrome (PJS) and investigate the correlation of these proteins to LKB1 gene expression.</p><p><b>METHODS</b>The expression and localization of LKB1, TGFbeta1 and pSmad2 proteins in 20 PJS polyp samples and normal intestinal mucosal tissues were detected with immunohistochemical staining.</p><p><b>RESULTS</b>The expressions of LKB1, TGFbeta1 and pSmad2 were lower in PJS polyps than in normal mucosa, and the differences in LKB1 and TGFbeta1 proteins were significantly different between them (P<0.05). In PJS polyps, positive correlations were found between LKB1 and TGFbeta1 and between TGFbeta1 and pSmad2 expressions.</p><p><b>CONCLUSION</b>TGFbeta/Smad pathway is probably subjected to the regulation by LKB1 and may play a role in the occurrence of PJS.</p>


Subject(s)
Humans , Immunohistochemistry , Peutz-Jeghers Syndrome , Metabolism , Protein Serine-Threonine Kinases , Genetics , Metabolism , Signal Transduction , Smad2 Protein , Genetics , Metabolism , Transforming Growth Factor beta , Genetics , Metabolism
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