Hepatocellular carcinoma (HCC) comprises a major subtype of primary liver cancer that could be diagnosed earlier using computed tomography (CT) examination. Video compression reduces the size of multi-frame data and induces blocking effect. This study aims to examine if the blocking effect alters the performances of HCC tumor detection and hepatic lesion classification in CT images. H.264 is considered in this study because it can compress 14-bit grayscale multi-frame data that is compatible with the image requirement of CT. A range of quantization parameters (QP) was determined in a phantom study. With this QP range, the trained support vector machines (SVM) based on image features were applied to test 20 HCC cases and 21 normal cases. The SVM performed significantly better than the random classification for detecting HCC in images compressed with the QP levels of interest. Images compressed with QP1 yielded the best performance. The same range of QP levels was applied to 15 lesion-bearing images. The image quality indices of these images were calculated to form the feature vectors. The clustering of these feature vectors identified at least six clusters. The association of the lesion classes with the identified clusters was found significant for all QP levels of interest. QP5 and QP9 yielded higher association than QP-3 and QP1. The findings proved a novel application of H.264 compression for enhancing the hepatic lesion detection classification in CT images. Keywords: Computed tomography, hepatic lesion, Hepatocellular carcinoma, video compression.
Abstract : This thesis describes several topological reduction and decomposition techniques developed to decrease the complexity of computing K-terminal reliability of an acyclic directed network with independent component failures. A program using these techniques has been coded in FORTRAN and tested on complete acyclic graphs and street networks with up to 100 vertices.
Adiponectin (Ad) is linked to various disease states and mediates antidiabetic and anti-inflammatory effects. While it was originally thought that Ad expression was limited to adipocytes, we demonstrate here that Ad is expressed in mouse skeletal muscles and within differentiated L6 myotubes, as assessed by RT-PCR, Western blot, and immunohistochemical analyses. Serial muscle sections stained for fiber type, lipid content, and Ad revealed that muscle fibers with elevated intramyocellular Ad expression were consistently type IIA and IID fibers with detectably higher intramyocellular lipid (IMCL) content. To determine the effect of Ad on muscle phenotype and function, we used an Ad-null [knockout (KO)] mouse model. Body mass increased significantly in 24-wk-old KO mice [+5.5 ± 3% relative to wild-type mice (WT)], with no change in muscle mass observed. IMCL content was significantly increased (+75.1 ± 25%), whereas epididymal fat mass, although elevated, was not different in the KO mice compared with WT (+35.1 ± 23%; P = 0.16). Fiber-type composition was unaltered, although type IIB fiber area was increased in KO mice (+25.5 ± 6%). In situ muscle stimulation revealed lower peak tetanic forces in KO mice relative to WT (−47.5 ± 6%), with no change in low-frequency fatigue rates. These data demonstrate that the absence of Ad expression causes contractile dysfunction and phenotypical changes in skeletal muscle. Furthermore, we demonstrate that Ad is expressed in skeletal muscle and that its intramyocellular localization is associated with elevated IMCL, particularly in type IIA/D fibers.
158 Background: PD-L1 inhibitor in combination with anti-angiogenic drug has become the first-line treatment strategy for unresectable hepatocellular carcinoma (HCC). However, PD-L1 inhibitor resistance remains an essential issue in treating HCC. It has been proved in the tumor microenvironment that hypoxia-induced increase in PD-L1 expression makes a significant impact on drug resistance. Methods: Two public datasets of gene expression profiles (GSE 14520 and GSE 41666) from the Gene Expression Omnibus (GEO) database were analyzed using bioinformatics: (1) HCC tumor versus adjacent normal tissue (N = 214) and (2) normoxia versus anoxia of HepG2 cells (N = 6). HCC-signature and hypoxia-related genes were identified as the differentially expressed genes (DEGs). Gene set enrichment analyses (GSEA) were performed on the DEGs. Furthermore, multiple regression analysis on the TCGA-LIHC dataset (N=371) and construction of the protein-protein interaction (PPI) network were performed to investigate potential PD-L1 regulatory genes and hub genes. Results: A total of 52 genes overlapped in HCC-signature and hypoxia-related DEGs. Five genes were identified by GSEA as being concurrently associated with the PD-L1 expression pathways. Multiple regression analysis results showed 14 potential PD-L1 regulatory genes. Ten hub genes were identified in the PPI network. Finally, three genes (DLGAP5, KIF20A, and TPX2) were found in common and may be regulatory genes affecting PD-L1 expression. Conclusions: In conclusion, our study provides new insights into the potential hypoxia-related mechanisms of PD-L1 inhibitor resistance and contributes to exploring new therapeutic strategies for treating unresectable HCC.
Non-small cell lung cancer (NSCLC) represents about 85% of the reported cases of lung cancer. Acquired resistance to targeted therapy with epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs), such as gefitinib, is not uncommon. It is thus vital to explore novel strategies to restore sensitivity to gefitinib. Provided that microRNAs (miRNAs) negatively regulate their gene targets at the transcriptional level, it is speculated that miRNA mimetics may reduce the expression, activity and signal transduction of EGFR so that sensitization of tumour sites to gefitinib-induced cytotoxicity can be achieved. Indeed, a growing body of evidence has shown that the manipulation of endogenous levels of miRNA not only attenuates the EGFR/PI3K/Akt phosphorylation cascade, but also restores apoptotic cell death in in vitro models of experimentally-induced gefitinib resistance and provoked tumour regression/shrinkage in xenograft models. These data are in concordant with the clinical data showing that the differential expression profiles of miRNA in tumour tissues and blood associate strongly with drug response and overall survival. Furthermore, another line of studies indicate that the chemopreventive effects of a variety of natural compounds may involve miRNAs. The present review aims to discuss the therapeutic capacity of miRNAs in relation to recent discoveries on EGFR-TKI resistance, including chronic drug exposure and mutations.
Omentin is an adipokine preferentially produced by visceral adipose tissue with insulin-sensitizing effects. Its expression is reduced in obesity, insulin resistance and type 2 diabetes. Omentin is also positively related with adiponectin, high-density lipoprotein levels and negatively related with body mass index, waist circumference, insulin resistance, triglyceride and leptin levels. Lower plasma omentin levels contribute to the pathogenesis of insulin resistance, type 2 diabetes and cardiovascular diseases in obese or overweight patients. Omentin has anti-inflammatory, antiatherogenic, anti-cardiovascular disease and antidiabetic properties. With respect to vascular biology, omentin causes vasodilatation of blood vessels and attenuates C-reactive protein-induced angiogenesis. The ability of omentin to reduce insulin resistance in conjunction with its anti-inflammatory and anti-atherogenic properties makes it a promising therapeutic target. Thus, omentin may have beneficial effects on the metabolic syndrome and could potentially be used as a biologic marker and/or pharmacologic agent/target in this respect. Keywords: Cardiovascular diseases, diabetes, inflammation, metabolic syndrome, omentin.
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