Finding disease-specific coordinated functions by multi-function genes: Insight into the coordination mechanisms in diseases

AbstractWe developed an approach using multi-function disease genes to find function pairs whose co-deregulation might induce a disease. Analyzing cancer genes, we found many cancer-specific coordinated function pairs co-deregulated by dysfunction of multi-function genes and other molecular changes in cancer. Studying two subtypes of cardiomyopathy, we found they show certain consistency at the functional coordination level. Our approach can also provide important information for finding novel disease genes as well as their mechanisms in diseases

Individualized analysis reveals CpG sites with methylation aberrations in almost all lung adenocarcinoma tissues

Additional file 1: Table S1. Stable and reversal CpG site pairs identified in the samples measured by two platforms

A kognitív készségek rendszere és fejlődése

Additional file 7: Figure S1. The KEGG pathways separately enriched with hypermethylated (a) and hypomethylated (b) genes in at least 10% of the 539 TCGA lung adenocarcinoma samples

A Systematic Molecular Pathology Study of a Laboratory Confirmed H5N1 Human Case

Autopsy studies have shown that human highly pathogenic avian influenza virus (H5N1) can infect multiple human organs other than just the lungs, and that possible causes of organ damage are either viral replication and/or dysregulation of cytokines and chemokines. Uncertainty still exists, partly because of the limited number of cases analysed. In this study, a full autopsy including 5 organ systems was conducted on a confirmed H5N1 human fatal case (male, 42 years old) within 18 hours of death. In addition to the respiratory system (lungs, bronchus and trachea), virus was isolated from cerebral cortex, cerebral medullary substance, cerebellum, brain stem, hippocampus ileum, colon, rectum, ureter, aortopulmonary vessel and lymph-node. Real time RT-PCR evidence showed that matrix and hemagglutinin genes were positive in liver and spleen in addition to positive tissues with virus isolation. Immunohistochemistry and in-situ hybridization stains showed accordant evidence of viral infection with real time RT-PCR except bronchus. Quantitative RT-PCR suggested that a high viral load was associated with increased host responses, though the viral load was significantly different in various organs. Cells of the immunologic system could also be a target for virus infection. Overall, the pathogenesis of HPAI H5N1 virus was associated both with virus replication and with immunopathologic lesions. In addition, immune cells cannot be excluded from playing a role in dissemination of the virus in vivo

Early warning model for passenger disturbance due to flight delays.

Disruptive behavior by passengers delayed at airport terminals not only affects personal safety but also reduces civil aviation efficiency and passenger satisfaction. This study investigated the causal mechanisms of disruptive behavior by delayed passengers in three aspects: environmental, managerial, and personal. Data on flight delays at Shenzhen Airport in 2018 were collected and analyzed. The main factors leading to disruptive behavior by delayed passengers were identified, and an early warning model for disturbances was developed using multiple logistic regression and a back-propagation(BP) neural network. The results indicated that the proposed model and method were feasible. Compared to the logistic regression model, the BP neural network model had advantages in predicting disturbances by delayed passengers, showing higher prediction accuracy. The BP network weight analysis method was used to obtain the influence weight of each factor on behavior change of delayed passengers. The influence weight of different factors was obtained, providing an assistant decision-making method to address disruption from flight-delayed passengers

The anticancer effects of ferulic acid is associated with induction of cell cycle arrest and autophagy in cervical cancer cells

Abstract Background Ferulic acid (4-hydroxy-3-methoxycinnamic acid, FA) is a hydroxycinnamic acid derived from a rich polyphenolic compound. This study aimed to investigate the effect of ferulic acid (4-hydroxy-3-methoxycinnamic acid; FA) on cell proliferation, invasion, apoptosis, and autophagy in Hela and Caski cervical carcinoma cell lines. Methods The cell proliferation of FA in Hela and Caski cells were detected by MTT assay. The cell invasion of FA in Hela and Caski cells were detected by Transwell assay. Subsequently, MMP-9 mRNA expression for cell invasion was detected by RT-PCR. Additionally, cell cycle and apoptosis were assayed using flow cytometry. Expression levels of 7 proteins for both cell cycle and autophagy were measured by Western blot analysis. Results After treated with FA (2.0 mM) for 48 h, the inhibition rates of FA in Hela and Caski cells were 88.3 and 85.4%, respectively. In addition, FA inhibited cell invasion through reducing MMP-9 mRNA expression. FA induced arrest in G0/G1 phase of the cell cycle in Hela and Caski cells with dose dependent (P < 0.05). Meanwhile, FA induced the cell cycle-related proteins expression such as p53 and p21, and reduced Cyclin D1 and Cyclin E levels. Moreover, FA decreased the autophagy-related proteins such as LC3-II, Beclin1 and Atg12-Atg5 in a dose-dependent manner. Conclusion FA can significantly inhibit cell proliferation and invasion in Hela and Caski cells. It might be acted as an anti-cancer drug through inhibiting the autophagy and inducing cell cycle arrest in human cervical carcinoma cells

Correction to: Systematic analyses reveal long non-coding RNA (PTAF)-mediated promotion of EMT and invasion-metastasis in serous ovarian cancer

An amendment to this paper has been published and can be accessed via the original article

Systematic analyses reveal long non-coding RNA (PTAF)-mediated promotion of EMT and invasion-metastasis in serous ovarian cancer

Abstract Background A deeper mechanistic understanding of epithelial-to-mesenchymal transition (EMT) regulation is needed to improve current anti-metastasis strategies in ovarian cancer (OvCa). This study was designed to investigate the role of lncRNAs in EMT regulation during process of invasion-metastasis in serous OvCa to improve current anti-metastasis strategies for OvCa. Methods We systematically analyzes high-throughput gene expression profiles of both lncRNAs and protein-coding genes in OvCa samples with integrated epithelial (iE) subtype and integrated mesenchymal (iM) subtype labels. Mouse models, cytobiology, molecular biology assays and clinical samples were performed to elucidate the function and underlying mechanisms of lncRNA PTAF-mediated promotion of EMT and invasion-metastasis in serous OvCa. Results We constructed a lncRNA-mediated competing endogenous RNA (ceRNA) regulatory network that affects the expression of many EMT-related protein-coding genes in mesenchymal OvCa. Using a combination of in vitro and in vivo studies, we provided evidence that the lncRNA PTAF-miR-25-SNAI2 axis controlled EMT in OvCa. Our results revealed that up-regulated PTAF induced elevated SNAI2 expression by competitively binding to miR-25, which in turn promoted OvCa cell EMT and invasion. Moreover, we found that silencing of PTAF inhibited tumor progression and metastasis in an orthotopic mouse model of OvCa. We then observed a significant correlation between PTAF expression and EMT markers in OvCa patients. Conclusions The lncRNA PTAF, a mediator of TGF-β signaling, can predispose OvCa patients to metastases and may serve as a potential target for anti-metastatic therapies for mesenchymal OvCa patients