20 research outputs found
Blind Equalization for Wireless Sensor Networks
学位記号番号 : 博理工乙第252号博士の専攻分野の名称 : 博士(工学)
学位授与年月日 : 令和元年9月20日textapplication/pdfthesi
Efficacy of rechallenge transcatheter arterial chemoembolization after lenvatinib treatment for advanced hepatocellular carcinoma
JGH Open. 2022, 6 (11), P.754-762journal articl
Formation of Peer group in Which Children Enjoy Expression and Share it : Through Course Planning to Foster Children Who Enjoy Their Life (Education Practice in the Course of a Junior High Department of Tottori University school for Children with Special Needs)
departmental bulletin pape
ASYMPTOTIC PROPERTIES OF THE SOLUTIONS OF A CLASS OF OPERATOR-DIFFERENTIAL EQUATIONS
application/pdfSome asymptotic properties of the nonoscillating solutions of operator-differential equations of arbitrary order are investigated.departmental bulletin pape
Stochastic contrasts among gene expression pathways according to diversity and number of SAGE tags
<p><b>Copyright information:</b></p><p>Taken from "Impaired expression of NER gene network in sporadic solid tumors"</p><p></p><p>Nucleic Acids Research 2007;35(6):1859-1867.</p><p>Published online 1 Mar 2007</p><p>PMCID:PMC1874609.</p><p>© 2007 The Author(s)</p> () Relative activity as defined in Equation (). () Relative diversity as defined in Equation (). The values are expressed as mean ± SEM ( = 492). Statistical analyses are carried out by Kruskal–Wallis one-way analysis of variance followed by Mann–Whitney test for comparisons. *Different from controls with < 0.001; **different from others with < 0.001
Graph of interactions among genes involved in apoptosis and DNA repair pathways generated using database STRING () with input options ‘Experimental/Biochemical Data,’ ‘Association in Curated Databases,’ and 70% confidence level
<p><b>Copyright information:</b></p><p>Taken from "Impaired expression of NER gene network in sporadic solid tumors"</p><p></p><p>Nucleic Acids Research 2007;35(6):1859-1867.</p><p>Published online 1 Mar 2007</p><p>PMCID:PMC1874609.</p><p>© 2007 The Author(s)</p> () Different pathways are represented in different colors. Nodes with more than one color represent genes participating in more than one pathway. Square nodes represent genes whose somatic mutations have been reported to be causally implicated in oncogenesis (). The group of genes of each pathway is presented in details in Supplementary Tables S9–S14, defined according to several references (). Genes without known interactions with other genes are listed in the bottom left of the figure. () Connectivity of interacting nodes, which shows the number of links that a given node has with other nodes. The color of a node indicates its pathway, as in (A); mutated genes are also indicated. Mismatch repair (MMR), nucleotide-excision repair (NER), base-excision repair (BER)
Combined Gene Expression and RNAi Screening to Identify Alkylation Damage Survival Pathways from Fly to Human
<div><p>Alkylating agents are a key component of cancer chemotherapy. Several cellular mechanisms are known to be important for its survival, particularly DNA repair and xenobiotic detoxification, yet genomic screens indicate that additional cellular components may be involved. Elucidating these components has value in either identifying key processes that can be modulated to improve chemotherapeutic efficacy or may be altered in some cancers to confer chemoresistance. We therefore set out to reevaluate our prior <i>Drosophila</i> RNAi screening data by comparison to gene expression arrays in order to determine if we could identify any novel processes in alkylation damage survival. We noted a consistent conservation of alkylation survival pathways across platforms and species when the analysis was conducted on a pathway/process level rather than at an individual gene level. Better results were obtained when combining gene lists from two datasets (RNAi screen plus microarray) prior to analysis. In addition to previously identified DNA damage responses (p53 signaling and Nucleotide Excision Repair), DNA-mRNA-protein metabolism (transcription/translation) and proteasome machinery, we also noted a highly conserved cross-species requirement for NRF2, glutathione (GSH)-mediated drug detoxification and Endoplasmic Reticulum stress (ER stress)/Unfolded Protein Responses (UPR) in cells exposed to alkylation. The requirement for GSH, NRF2 and UPR in alkylation survival was validated by metabolomics, protein studies and functional cell assays. From this we conclude that RNAi/gene expression fusion is a valid strategy to rapidly identify key processes that may be extendable to other contexts beyond damage survival.</p></div
Gene level overlap and PEA showing the cellular processes associated with RNAi hits and gene expression alterations in MMS-treated Kc167 cells.
(A) Venn diagrams showing the overlap between survival hits (from RNAi screening) and alkylation altered gene expressions (from microarrays) in MMS treated Kc167 cells. For gene level overlaps, RNAi hits were obtained from [1] and only those with matched microarray expression changes in at least one time point (8, 24 and 72 h) were used. Microarray gene numbers include both MMS up (703) and downregulated (308) genes as detailed in Results section. Pathway comparisons only show pathways associated with MMS upregulated gene expressions compared to RNAi hits. The 26 RNAi hits with downregulated expressions (S1 Table) were not included in the PEA. (B-C) Antilog P-value representation of the pathways associated with the MMS survival RNAi hits and MMS upregulated genes as predicted by PEA. Pathways are shown as grouped into major biological concepts. Detailed information of differentially expressed genes and PEA are provided in S1 and S2 Tables, respectively.</p
