Nationwide surveillance pilot study of carbapenemase-producing Pseudomonas aeruginosa unveils a multi-hospital clonal outbreak of VIM-2-positive ST111 in the Netherlands between 2015-2017.
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PROVIDER: PRJEB39528 | ENA |
REPOSITORIES: ENA
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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:WGS of human and foodborne VIM carbapenemase-expressing Citrobacter freundii
| PRJEB22602 | 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. 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: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:OBJECTIVE:The aim of this study is to describe the evolution of the incidence of infected and colonized patients with carbapenemase VIM-producing bacteria (CPB-VIM) at a national referral pediatric center in Madrid, Spain, between 2012 and 2015. METHODS:Descriptive epidemiological surveillance study. The surveillance system included case detection (screening for BPC colonization in all admitted patients, with periodicity according to the ward) and control measures (contact precautions, identification of previously colonized patients at admission, environmental cleaning, education, supervision of contact precautions, and patient cohort). All hospitalized patients with first positive microbiological sample for CPB-VIM in 2012-2015 were included. Colonized patients were followed through clinical history to evaluate later infection. RESULTS:We found 239 colonized and 51 infected patients with CPB-VIM (49.3% women, 47.6% were 5 months old or younger, 52.1% admitted at Intensive Care Unit). Infection and colonization incidence were, respectively, 2.6 and 6.7 cases per one thousand hospitalized patients in 2012, 1.8 and 10.0 in 2014 and 0.3 and 5.0 in 2015. Within these patients, 84.4% shared ward with other patient with previous positive sample. 13.0% (31/239) of colonized patients had a subsequent infection. CONCLUSIONS:We have shown data of pediatric patients affected by BPC-VIM, collected from an epidemiological surveillance system that included systematic screening at a national referral center. After an epidemic period, the incidence of cases went down. The surveillance and infection control measures intensification, as well as coordination with involved departments, were key in the handling of the situation.
| S-EPMC6372957 | biostudies-other
Project description:The Research Institute at Nationwide Children's Hospital Genetics of Congenital Heart Disease (CHD)
| PRJNA625349 | ENA
Project description:The Research Institute at Nationwide Children's Hospital Genetics of Congenital Heart Disease (CHD)
| PRJNA625348 | ENA
Project description:Klebsiella pneumoniae strain:PEC-VIM Genome sequencing and assembly
| PRJNA473366 | ENA
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:Carbapenems belong to the group of last resort antibiotics in human medicine. Therefore, the emergence of growing numbers of carbapenemase-producing bacteria in food-producing animals or the environment is worrying and an important concern for the public health sector. In the present study, a set of 45 Enterobacteriaceae isolated from German retail seafood (clams and shrimps), sampled in 2016, were investigated by real-time PCR for the presence of carbapenemase-producing bacteria. One Escherichia coli (ST10), isolated from a Venus clam (Ruditapes philippinarum) harvested in the Mediterranean Sea (Italy), contained the carbapenemase gene blaVIM-1 as part of the variable region of a class I integron. Whole-genome sequencing indicated that the integron was embedded in a Tn3-like transposon that also contained the fluoroquinolone resistance gene qnrS1. Additional resistance genes such as the extended-spectrum beta-lactamase blaSHV-12 and the AmpC gene blaACC-1 were also present in this isolate. Except blaACC-1, all resistance genes were located on an IncY plasmid. These results confirm previous observations that carbapenemase-producing bacteria have reached the food chain and are of increasing concern for public health.
| S-EPMC5718389 | biostudies-literature