[Deep residual convolutional neural network for recognition of electrocardiogram signal arrhythmias].

Electrocardiogram (ECG) signals are easily disturbed by internal and external noise, and its morphological characteristics show significant variations for different patients. Even for the same patient, its characteristics are variable under different temporal and physical conditions. Therefore, ECG signal detection and recognition for the heart disease real-time monitoring and diagnosis are still difficult.

E2F1 interactive with BRCA1 pathway induces HCC two different small molecule metabolism or cell cycle regulation via mitochondrion or CD4+T to cytosol.

Breast cancer 1 (BRCA1) and E2F transcription factor 1 (E2F1) are related to metabolism and cell cycle regulation. However, the corresponding mechanism is not clear in HCC. High BRCA1 direct pathway was constructed with 11 molecules from E2F1 feedback-interactive network in HCC by GRNInfer based on 39 Pearson mutual positive corelation CC ≥0.

Low BIK outside-inside-out interactive inflammation immune-induced transcription-dependent apoptosis through FUT3-PMM2-SQSTM1-SFN-ZNF384.

Eighteen different Pearson mutual-positive-correlation BIK-activatory molecular feedback upstream and downstream networks were constructed from 79 overlapping of 376 GRNInfer and 98 Pearson under BIK CC ≥ 0.25 in low normal adjacent tissues of Taiwan compared with high lung adenocarcinoma. Our identified BIK interactive total feedback molecular network showed FUT3 [fucosyltransferase 3 (galactoside 3(4)-L-fucosyltransferase Lewis blood group)], PMM2 (phosphomannomutase 2), SQSTM1 (sequestosome 1), SFN_2 [REX2 RNA exonuclease 2 homolog (S.

High EGFR_1 Inside-Out Activated Inflammation-Induced Motility through SLC2A1-CCNB2-HMMR-KIF11-NUSAP1-PRC1-UBE2C.

48 different Pearson mutual-positive-correlation epidermal growth factor receptor (EGFR_1)-activatory molecular feedback, up- and down-stream network was constructed from 171 overlapping of 366 GRNInfer and 223 Pearson under EGFR_1 CC ≥0.25 in high lung adenocarcinoma compared with low human normal adjacent tissues. Our identified EGFR_1 inside-out upstream activated molecular network showed SLC2A1 (solute carrier family 2 (facilitated glucose transporter) member 1), CCNB2 (cyclin B2), HMMR (hyaluronan-mediated motility receptor (RHAMM)), KIF11 (kinesin family member 11), NUSAP1 (nucleolar and spindle associated protein 1), PRC1 (protein regulator of cytokinesis 1), UBE2C (ubiquitin-conjugating enzyme E2C) in high lung adenocarcinoma.

Low glucose transporter SLC2A5-inhibited human normal adjacent lung adenocarcinoma cytoplasmic pro-B cell development mechanism network.

Solute carrier family 2 (facilitated glucose/fructose transporter) member 5 (SLC2A5)-inhibited seven different molecular Pearson mutual-positive-correlation networks constructed by 24 overlapping molecules from 368 GRNInfer and 34 Pearson under SLC2A5 CC ≤-0.25 in low human normal adjacent tissues were compared with high lung adenocarcinoma. Based on GO, KEGG, GenMAPP, BioCarta, and disease databases, our result showed that low SLC2A5-inhibited network included Golgi apparatus of AP1M2_1; cell cycle of CUL7, SAC3D1; protein amino acid dephosphorylation of STYXL1; pro-B cell-cell differentiation of SOX4_3; and FAD biosynthesis of FLAD1.

AGR2-mediated lung adenocarcinoma metastasis novel mechanism network through repression with interferon coupling cytoskeleton to steroid metabolism-dependent humoral immune response.

7 anterior gradient homolog 2 (AGR2)-inhibited different molecular mutual positive correlation network was constructed in lung adenocarcinoma compared with human normal adjacent tissues by 17 overlapping molecules of 358 GRNInfer and 19 Pearson (AGR2 CC⩽-0.25). Based on GO, KEGG, GenMAPP, BioCarta and disease databases, we determined AGR2-mediated lung adenocarcinoma metastasis through repression with cytoskeleton of MAST1; steroid metabolism of SOAT2; humoral immune response of POU2AF1; interferon alpha-inducible of IFI6; immunoglobulin of IGKC_3, CTA_246H3.

CAMK1 phosphoinositide signal-mediated protein sorting and transport network in human hepatocellular carcinoma (HCC) by biocomputation.

We data-analyzed and constructed the high-expression CAMK1 phosphoinositide signal-mediated protein sorting and transport network in human hepatocellular carcinoma (HCC) compared with low-expression (fold change ≥ 2) no-tumor hepatitis/cirrhotic tissues (HBV or HCV infection) in GEO data set, using integration of gene regulatory network inference method with gene ontology (GO). Our result showed that CAMK1 transport subnetwork upstream KCNQ3, LCN2, NKX2_5, NUP62, SORT1, STX1A activated CAMK1, and downstream CAMK1-activated AFP, ENAH, KPNA2, SLC4A3; CAMK1 signal subnetwork upstream BRCA1, DKK1, GPSM2, LEF1, NR5A1, NUP62, SORT1, SSTR5, TBL3 activated CAMK1, and downstream CAMK1-activated MAP2K6, SFRP4, SSTR5, TSHB, UBE2C in HCC. We proposed that CAMK1 activated network enhanced endosome to lysosome transport, endosome transport via multivesicular body sorting pathway, Golgi to endosome transport, intracellular protein transmembrane transport, intracellular protein transport, ion transport, mRNA transport, plasma membrane to endosome transport, potassium ion transport, protein transport, vesicle-mediated transport, anion transport, intracellular transport, androgen receptor signaling pathway, cell surface receptor-linked signal transduction, hormone-mediated signaling, induction of apoptosis by extracellular signals, signal transduction by p53 class mediator resulting in transcription of p21 class mediator, signal transduction resulting in induction of apoptosis, phosphoinositide-mediated signaling, Wnt receptor signaling pathway, as a result of inducing phosphoinositide signal-mediated protein sorting, and transport in HCC.

Adenosylmethionine decarboxylase 1 (AMD1)-mediated mRNA processing and cell adhesion activated & inhibited transition mechanisms by different comparisons between chimpanzee and human left hemisphere.

To understand adenosylmethionine decarboxylase 1 (AMD1)-mediated mRNA processing and cell adhesion activated & inhibited transition mechanisms between chimpanzee and human left hemisphere, AMD1-activated different complete (all no positive correlation, Pearson correlation coefficient < 0.25) and uncomplete (partly no positive correlation except AMD1, Pearson < 0.25) networks were identified in higher human compared with lower chimpanzee left hemisphere from the corresponding AMD1-stimulated (Pearson ≥ 0.

Early vein graft failure leading to acute myocardial infarction, dehiscence and haemopericardium treated by percutaneous coil embolisation and balloon tamponade.

Early vein graft failure is a well-described early complication of coronary artery bypass grafting. Revascularisation with emergency percutaneous coronary intervention (PCI) may limit the extent of myocardial damage and is associated with lower procedural complications compared than with emergency redo bypass surgery. We describe a case of an early saphenous vein graft (SVG) thrombosis presenting as an inferior ST-elevation to our non-surgical PCI site, complicated by SVG graft dehiscence leading to cardiac tamponade, which we treated with coil embolisation and balloon tamponade during the patient's transfer to a surgical facility for emergent haemopericardium evacuation.

BRCA1-mediated inflammation and growth activated & inhibited transition mechanisms between no-tumor hepatitis/cirrhotic tissues and HCC.

To understand breast cancer 1 early onset (BRCA1)-mediated inflammation and growth activated and inhibited transition mechanisms between no-tumor hepatitis/cirrhotic tissues (HBV or HCV infection) and human hepatocellular carcinoma (HCC), BRCA1-activated different complete (all no positive correlation, Pearson correlation coefficient <0.25) and uncomplete (partly no positive correlation except BRCA1, Pearson <0.25) networks were identified in higher HCC compared with lower no-tumor hepatitis/cirrhotic tissues (HBV or HCV infection) from the corresponding BRCA1-stimulated (Pearson ≥0.

Cartilage oligomeric matrix protein (COMP)-mediated cell differentiation to proteolysis mechanism networks from human normal adjacent tissues to lung adenocarcinoma.

Background: To understand cartilage oligomeric matrix protein (COMP) mechanism network from human normal adjacent tissues to lung adenocarcinoma.

Methods: COMP complete different activated (all no positive correlation, Pearson CC < 0.25) and uncomplete (partly no positive correlation except COMP, Pearson CC < 0.

Activated amelogenin Y-linked (AMELY) regulation and angiogenesis in human hepatocellular carcinoma by biocomputation.

In the present study, a comparison of the biological processes and gene ontology (GO) in human hepatocellular carcinoma (HCC) with high expression (fold change ≥2) of amelogenin Y-linked (AMELY)-activated upstream regulation networks with non-tumor hepatitis/cirrhotic tissues (HBV or HCV infection) with low expression of activated networks was performed. The principle biological processes involved in non-tumor hepatitis/cirrhotic tissues include positive regulation of mismatch repair, regulation of transcription from RNA polymerase II promoters, negative regulation of cell-cell adhesion, protein ubiquitinatin and protein catabolism. The main biological processes involved in the development of HCC include positive regulation of calcium ion transport into the cytosol, cell proliferation, DNA replication, fibroblast proliferation, immune response, microtubule polymerization and protein secretion.

Activated PTHLH coupling feedback phosphoinositide to G-protein receptor signal-induced cell adhesion network in human hepatocellular carcinoma by systems-theoretic analysis.

Studies were done on analysis of biological processes in the same high expression (fold change ≥2) activated PTHLH feedback-mediated cell adhesion gene ontology (GO) network of human hepatocellular carcinoma (HCC) compared with the corresponding low expression activated GO network of no-tumor hepatitis/cirrhotic tissues (HBV or HCV infection). Activated PTHLH feedback-mediated cell adhesion network consisted of anaphase-promoting complex-dependent proteasomal ubiquitin-dependent protein catabolism, cell adhesion, cell differentiation, cell-cell signaling, G-protein-coupled receptor protein signaling pathway, intracellular transport, metabolism, phosphoinositide-mediated signaling, positive regulation of transcription, regulation of cyclin-dependent protein kinase activity, regulation of transcription, signal transduction, transcription, and transport in HCC. We proposed activated PTHLH coupling feedback phosphoinositide to G-protein receptor signal-induced cell adhesion network.

Inhibited PTHLH downstream leukocyte adhesion-mediated protein amino acid N-linked glycosylation coupling Notch and JAK-STAT cascade to iron-sulfur cluster assembly-induced aging network in no-tumor hepatitis/cirrhotic tissues (HBV or HCV infection) by systems-theoretical analysis.

We analyzed the different biological processes and occurrence numbers between low expression inhibited PTHLH downstream-mediated aging gene ontology (GO) network of no-tumor hepatitis/cirrhotic tissues (HBV or HCV infection) and the corresponding high expression (fold change ≥2) inhibited GO network of human hepatocellular carcinoma (HCC). Inhibited PTHLH downstream-mediated aging network consisted of aging, branched chain family amino acid biosynthesis, cellular metabolism, cholesterol biosynthesis, coupled to cyclic nucleotide second messenger, cytolysis, 'de novo' GDP-l-fucose biosynthesis, detection of mechanical stimulus, glucose homeostasis, G-protein signaling, leukocyte adhesion, iron-sulfur cluster assembly, JAK-STAT cascade, Notch signaling pathway, nucleotide-sugar metabolism, peptidyl-tyrosine sulfation, protein amino acid N-linked glycosylation, protein amino acid phosphorylation, response to drug, rRNA processing, translational initiation, ubiquitin-dependent protein catabolism, homophilic cell adhesion in no-tumor hepatitis/cirrhotic tissues. We proposed inhibited PTHLH downstream leukocyte adhesion-mediated protein amino acid N-linked glycosylation coupling Notch and JAK-STAT cascade to iron-sulfur cluster assembly-induced aging network.

PTHLH coupling upstream negative regulation of fatty acid biosynthesis and Wnt receptor signal to downstream peptidase activity-induced apoptosis network in human hepatocellular carcinoma by systems-theoretical analysis.

Studies were done on the analysis of biological processes in the same high expression (fold change ≥ 2) PTHLH-activated feedback negative regulation-mediated apoptosis gene ontology (GO) network of human hepatocellular carcinoma (HCC) compared with the corresponding low expression activated GO network of no-tumor hepatitis/cirrhotic tissues [hepatitis B virus (HBV) or hepatitis C virus (HCV) infection]. We proposed PTHLH-activated network that upstream included the regulation of apoptosis, signal transduction resulting in induction of apoptosis, signal transduction by p53 class mediator resulting in transcription of p21 class mediator, negative regulation of centriole replication, negative regulation of fatty acid biosynthesis, negative regulation of Wnt receptor signaling pathway, anaphase-promoting complex-dependent proteasomal ubiquitin-dependent protein catabolism, apoptosis, induction of apoptosis, and negative regulation of phosphorylation. Downstream-network negative regulation of peptidase activity, anaphase-promoting complex-dependent proteasomal ubiquitin-dependent protein catabolism, apoptosis, induction of apoptosis and negative regulation of phosphorylation, as a result of coupling upstream negative regulation of fatty acid biosynthesis and Wnt receptor signal to downstream peptidase activity-induced apoptosis in HCC.

P-glycoprotein (ABCB1) inhibited network of mitochondrion transport along microtubule and BMP signal-induced cell shape in chimpanzee left cerebrum by systems-theoretical analysis.

We constructed the significant low-expression P-glycoprotein (ABCB1) inhibited transport and signal network in chimpanzee compared with high-expression (fold change ≥2) the human left cerebrum in GEO data set, by using integration of gene regulatory activated and inhibited network inference method with gene ontology (GO) analysis. Our result showed that ABCB1 transport and signal upstream network RAB2A inhibited ABCB1, and downstream ABCB1-inhibited SMAD1_2, NCK2, SLC25A46, GDF10, RASGRP1, EGFR, LRPPRC, RASSF2, RASA4, CA2, CBLB, UBR5, SLC25A16, ITGB3BP, DDIT4, PDPN, RAB2A in chimpanzee left cerebrum. We obtained that the different biological processes of ABCB1 inhibited transport and signal network repressed carbon dioxide transport, ER to Golgi vesicle-mediated transport, folic acid transport, mitochondrion transport along microtubule, water transport, BMP signaling pathway, Ras protein signal transduction, transforming growth factor beta receptor signaling pathway in chimpanzee compared with the inhibited network of the human left cerebrum, as a result of inducing inhibition of mitochondrion transport along microtubule and BMP signal-induced cell shape in chimpanzee left cerebrum.

Tissue-specific transplantation antigen P35B (TSTA3) immune response-mediated metabolism coupling cell cycle to postreplication repair network in no-tumor hepatitis/cirrhotic tissues (HBV or HCV infection) by biocomputation.

We constructed the low-expression tissue-specific transplantation antigen P35B (TSTA3) immune response-mediated metabolism coupling cell cycle to postreplication repair network in no-tumor hepatitis/cirrhotic tissues (HBV or HCV infection) compared with high-expression (fold change ≥ 2) human hepatocellular carcinoma in GEO data set, by using integration of gene regulatory network inference method with gene ontology analysis of TSTA3-activated up- and downstream networks. Our results showed TSTA3 upstream-activated CCNB2, CKS1B, ELAVL3, GAS7, NQO1, NTN1, OCRL, PLA2G1B, REG3A, SSTR5, etc. and TSTA3 downstream-activated BAP1, BRCA1, CCL20, MCM2, MS4A2, NTN1, REG1A, TP53I11, VCAN, SLC16A3, etc.

Signal transducer and activator of transcription 2 (STAT2) metabolism coupling postmitotic outgrowth to visual and sound perception network in human left cerebrum by biocomputation.

We constructed the high-expression signal transducer and activator of transcription 2 (STAT2) metabolism coupling postmitotic outgrowth to visual and sound perception network in human left cerebrum compared with low-expression (fold change ≥2) chimpanzee left cerebrum in GEO data set by using integration of gene regulatory network inference method with gene ontology (GO) analysis of STAT2-activated up- and downstream network. Our result showed that upstream RECQL, PDIA2, ENOSF1, THBS4, RASGRP1, PER2, PDE8A, ORC2L, DCI, OGG1_2, SMA4, GPD1, etc. activated STAT2, and downstream STAT2-activated GSTM3_1, GOSR1, SH3BGR, OSBPL8, PHYH, SAPS2, C21orf33, PDIA2, TRAPPC6A, ENOSF1, CAMTA1, GTF2I_2, etc.

Glycogen debranching enzyme 6 (AGL), enolase 1 (ENOSF1), ectonucleotide pyrophosphatase 2 (ENPP2_1), glutathione S-transferase 3 (GSTM3_3) and mannosidase (MAN2B2) metabolism computational network analysis between chimpanzee and human left cerebrum.

We identified significantly higher expression of the genes glycogen debranching enzyme 6 (AGL), enolase 1 (ENOSF1), ectonucleotide pyrophosphatase 2 (ENPP2_1), glutathione S-transferase 3 (GSTM3_3) and mannosidase (MAN2B2) from human left cerebrums versus chimpanzees. Yet the distinct low- and high-expression AGL, ENOSF1, ENPP2_1, GSTM3_3 and MAN2B2 metabolism networks between chimpanzee and human left cerebrum remain to be elucidated. Here, we constructed low- and high-expression activated and inhibited upstream and downstream AGL, ENOSF1, ENPP2_1, GSTM3_3 and MAN2B2 metabolism network between chimpanzee and human left cerebrum in GEO data set by gene regulatory network inference method based on linear programming and decomposition procedure, under covering AGL, ENOSF1, ENPP2_1, GSTM3_3 and MAN2B2 pathway and matching metabolism enrichment analysis by CapitalBio MAS 3.

Survivin (BIRC5) cell cycle computational network in human no-tumor hepatitis/cirrhosis and hepatocellular carcinoma transformation.

Survivin (BIRC5) relationship with tumor is presented in several papers. However, how the molecular network and interpretation concerning BIRC5 cell cycle between no-tumor hepatitis/cirrhosis and hepatocellular carcinoma (HCC) remains to be elucidated. Here, we constructed and analyzed significant higher expression gene BIRC5 activated and inhibited cell cycle network from HCC versus no-tumor hepatitis/cirrhosis patients (viral infection HCV or HBV) in GEO Dataset by combination of gene regulatory network inference method based on linear programming and decomposition procedure with the CapitalBio MAS 3.

CREB5 computational regulation network construction and analysis between frontal cortex of HIV encephalitis (HIVE) and HIVE-control patients.

CREB5 computational regulation network construction and analysis of frontal cortex of HIV encephalitis (HIVE) is very useful to identify novel markers and potential targets for prognosis and therapy. By integration of gene regulatory network infer and the database for annotation, visualization and integrated discovery we identified and constructed significant molecule CREB5 regulation network from 12 frontal cortex of HIVE-control patients and 16 HIVE in the same GEO Dataset GDS1726. Our result verified CREB5 biological regulation module in the upstream of frontal cortex of HIVE-control patients (MAPKAPK3 activation; DGKG, LY96, TNFRSF11B inhibition) and downstream (ATP6V0E1, CFB, DGKG, MX1, TGFBR3 activation; LGALS3BP, RASGRP3, RDX, STAT1 inhibition), whereas in the upstream of frontal cortex of HIVE (BST2, CFB, LCAT, TNFRSF11B activation; CFHR1, LY96 inhibition) and downstream (GAS1, LCAT, LGALS3BP, NFAT5, VEZF1, ZNF652 activation; DGKG, IFITM1, LY96, TNFRSF11B inhibition).

MYBPC1 computational phosphoprotein network construction and analysis between frontal cortex of HIV encephalitis (HIVE) and HIVE-control patients.

MYBPC1 computational phosphoprotein network construction and analysis of frontal cortex of HIV encephalitis (HIVE) was very useful to identify novel markers and potential targets for prognosis and therapy. Based on integrated gene regulatory network infer method by linear programming and a decomposition procedure with analysis of the significant function cluster using kappa statistics and fuzzy heuristic clustering from the database for annotation, visualization, and integrated discovery, we identified and constructed significant molecule MYBPC1 phosphoprotein network from 12 frontal cortex of HIVEcontrol patients and 16 HIVE in the same GEO Dataset GDS1726. Our result verified MYBPC1 phosphoprotein module only in the upstream of frontal cortex of HIVEcontrol patients (CREB5, MAPKAPK3 inhibition), whereas in the upstream of frontal cortex of HIVE (CREB5, ZC3HAV1 activation; ROR1 inhibition) and downstream (MAPKAPK3 activation; CFDP1, PDCD4, RBBP6 inhibition).

RRM2 computational phosphoprotein network construction and analysis between no-tumor hepatitis/cirrhotic liver tissues and human hepatocellular carcinoma (HCC).

RRM2 computational phosphoprotein network construction and analysis of human hepatocellular carcinoma (HCC) is very useful to identify novel markers and potential targets for prognosis and therapy. By integration of gene regulatory network infer (GRNInfer) and the database for annotation, visualization and integrated discovery (DAVID) we identified and constructed significant molecule RRM2 phosphoprotein network from 25 no-tumor hepatitis/cirrhotic liver tissues and 25 HCC patients in the same GEO Dataset GSE10140-10141. We gained the negative result of RRM2 phosphoprotein module through the net numbers of activation minus inhibition compared with no-tumor hepatitis/cirrhotic liver tissues and predicted possibly the decrease of RRM2 phosphoprotein module in HCC.

AFP computational secreted network construction and analysis between human hepatocellular carcinoma (HCC) and no-tumor hepatitis/cirrhotic liver tissues.

Alpha-fetoprotein (AFP) computational secreted network construction and analysis of human hepatocellular carcinoma (HCC) is very useful to identify novel markers and potential targets for prognosis and therapy. By integration of gene regulatory network infer and the database for annotation, visualization, and integrated discovery, we identified and constructed significant molecule AFP secreted network from 25 no-tumor hepatitis/cirrhotic liver tissues and 25 HCC patients in the same GEO Dataset GSE10140-10141. Our result verified AFP secreted module in the upstream of no-tumor hepatitis/cirrhotic liver tissues (AMELY, LCN2, and REG3A activation; DKK1, SFRP4, and SPINK1 inhibition) and its downstream (PRSS1, REG3A, and TSHB activation; AMELY and DKK1 inhibition), and also in the upstream of HCC (LCN2, REG3A, and SFRP4 activation; AMELY and DKK1 inhibition) and its downstream (AMELY activation; DKK1, LCN2, PRSS1, SEMA3B, and SPINK1 inhibition).

Secreted phosphoprotein 1 upstream invasive network construction and analysis of lung adenocarcinoma compared with human normal adjacent tissues by integrative biocomputation.

The aim of this study is to set up single molecular secreted phosphoprotein 1 (SPP1) upstream invasive network of lung adenocarcinoma. This paper proposed an integrated method based on linear programming and a decomposition procedure with integrated analysis of the significant function cluster using Kappa statistics and fuzzy heuristic clustering. Our study proved that only modules appearing in lung adenocarcinoma include cytokine module (CXCL13, GREM1_2 inhibition), cell adhesion module (COL11A1_2 activation; CDH3 inhibition), and receptor binding module (NMU activation; CXCL13, GREM1_2 inhibition), which increase the invasion of cancer cell.