Description of two strains of Klebsiella pneumoniae VIM-1 isolated in an Northern Italian hospital
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB25824 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Purpose: To detect the diffirential expressed genes in LNCaP cells transfected with VIM-AS1 overexression vetor and control pcDNA3.1 vector Method: Transcriptome sequencing was sued to detect the diffirential expressed genes in LNCaP cells transfected with VIM-AS1 overexression vetor and control pcDNA3.1 vector Results :We performed transcriptome sequencing to identify the target genes in VIM-AS1 overexpressed LNCaP cells and normal control. 67 genes were found statistically up-regulated more than two-fold and 187 genes were found statistically down-regulated more than two-fold in VIM-AS1 overexpressed LNCaP cells Conclusion:Our study represents the first detailed analyasis of transcriptomes in LNCaP cells with VIM-AS1 overexpression and control cells.
2022-12-08 | GSE220250 | GEO
Project description:GFAP and vimentin deficiency alters gene expression in astrocytes and microglia in wild-type mice and changes the transcriptional response of reactive glia in mouse model for Alzheimer's disease. Reactive astrocytes with an increased expression of intermediate filament (IF) proteins Glial Fibrillary Acidic Protein (GFAP) and Vimentin (VIM) surround amyloid plaques in Alzheimer's disease (AD). The functional consequences of this upregulation are unclear. To identify molecular pathways coupled to IF regulation in reactive astrocytes, and to study the interaction with microglia, we examined WT and APPswe/PS1dE9 (AD) mice lacking either GFAP, or both VIM and GFAP, and determined the transcriptome of cortical astrocytes and microglia from 15- to 18-month-old mice. Genes involved in lysosomal degradation (including several cathepsins) and in inflammatory response (including Cxcl5, Tlr6, Tnf, Il1b) exhibited a higher AD-induced increase when GFAP, or VIM and GFAP, were absent. The expression of Aqp4 and Gja1 displayed the same pattern. The downregulation of neuronal support genes in astrocytes from AD mice was absent in GFAP/VIM null mice. In contrast, the absence of IFs did not affect the transcriptional alterations induced by AD in microglia, nor was the cortical plaque load altered. Visualizing astrocyte morphology in GFAP-eGFP mice showed no clear structural differences in GFAP/VIM null mice, but did show diminished interaction of astrocyte processes with plaques. Microglial proliferation increased similarly in all AD groups. In conclusion, absence of GFAP, or both GFAP and VIM, alters AD-induced changes in gene expression profile of astrocytes, showing a compensation of the decrease of neuronal support genes and a trend for a slightly higher inflammatory expression profile. However, this has no consequences for the development of plaque load, microglial proliferation, or microglial activation. 2 cell types from 6 conditions: cortical microglia and cortical astrocytes from 15-18 month old APPswe/PS1dE9 mice compared to wildtype littermates. Biological replicates: microglia from APPswe/PS1dE9, N=7, microglia from WT, N=7, astrocytes from APPswe/PS1dE9, N=4, microglia from WT, N=4
2015-11-04 | E-GEOD-74614 | biostudies-arrayexpress
Project description:Evolution of VIM-1 producing Klebsiella pneumoniae isolates from a hospital outbreak revealed the genetic bases of the frequent loss of the urease-positive identification character.
| PRJEB41835 | ENA
Project description:GFAP and vimentin deficiency alters gene expression in astrocytes and microglia in wild-type mice and changes the transcriptional response of reactive glia in mouse model for Alzheimer's disease. Reactive astrocytes with an increased expression of intermediate filament (IF) proteins Glial Fibrillary Acidic Protein (GFAP) and Vimentin (VIM) surround amyloid plaques in Alzheimer's disease (AD). The functional consequences of this upregulation are unclear. To identify molecular pathways coupled to IF regulation in reactive astrocytes, and to study the interaction with microglia, we examined WT and APPswe/PS1dE9 (AD) mice lacking either GFAP, or both VIM and GFAP, and determined the transcriptome of cortical astrocytes and microglia from 15- to 18-month-old mice. Genes involved in lysosomal degradation (including several cathepsins) and in inflammatory response (including Cxcl5, Tlr6, Tnf, Il1b) exhibited a higher AD-induced increase when GFAP, or VIM and GFAP, were absent. The expression of Aqp4 and Gja1 displayed the same pattern. The downregulation of neuronal support genes in astrocytes from AD mice was absent in GFAP/VIM null mice. In contrast, the absence of IFs did not affect the transcriptional alterations induced by AD in microglia, nor was the cortical plaque load altered. Visualizing astrocyte morphology in GFAP-eGFP mice showed no clear structural differences in GFAP/VIM null mice, but did show diminished interaction of astrocyte processes with plaques. Microglial proliferation increased similarly in all AD groups. In conclusion, absence of GFAP, or both GFAP and VIM, alters AD-induced changes in gene expression profile of astrocytes, showing a compensation of the decrease of neuronal support genes and a trend for a slightly higher inflammatory expression profile. However, this has no consequences for the development of plaque load, microglial proliferation, or microglial activation.
2015-11-04 | GSE74614 | GEO
Project description:We report the application of Illumina RNA sequencing for characterization and discovery of genes and transcripts in Italian Large Whtie pig backfat tissue.
2016-03-15 | GSE68007 | GEO
Project description:We report the application of Illumina short RNA sequencing for characterization and discovery of miRNAs and moRNAs in two Italian Large White pig backfat tissue.
2014-07-14 | GSE47748 | GEO
Project description:16 Genomes of KPC Klebsiella pneumoniae sequenced from isolates of an Italian hospital. Gene content analysis, phylogeny and outbreak reconstruction were performed
| PRJEB7661 | ENA
Project description:Mycobacterium bovis description isolates
| PRJEB33598 | ENA