Inactivation of blaNDM-1-positive and blaNDM-1-negative Escherichia coli strains and their differential gene expression upon solar irradiation
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB13888 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Bacteriophages To Sensitize A Pathogenic New Delhi Metallo β-lactamase-positive Escherichia coli To Solar Disinfection
| PRJEB25811 | ENA
Project description:Inactivation of blaNDM-1-positive and blaNDM-1-negative Escherichia coli strains and their differential gene expression upon solar irradiation
| PRJEB13897 | ENA
Project description:Solar radiation is one of the biggest threats to the skin, eliciting a specific protective cellular response. To descipt the underlying mechanisms, we have chosen to study in vivo, epidermis gene expression of surface solar radiation (SSR)-irradiated skin using whole genome microarray (Agilent 44K).
2011-01-20 | GSE20062 | GEO
Project description:Solar radiation is one of the biggest threats to the skin, eliciting a specific protective cellular response. To descipt the underlying mechanisms, we have chosen to study in vivo, epidermis gene expression of surface solar radiation (SSR)-irradiated skin using whole genome microarray (Agilent 44K). We studied epidermis samples from five healthy Caucasian patients, with phototype II or III, using two different doses (2J/m2 and 4J/m2) and sham-irradiated.
2011-01-20 | E-GEOD-20062 | biostudies-arrayexpress
Project description:Solar urticaria (SU) is clinically characterised by rapid onset sunlight-induced urticaria, but its cutaneous pathophysiology is not well understood. The aim of this study was to investigate cutaneous cellular and molecular events in the evolution of SU responses following solar simulated ultraviolet radiation (SSR) exposure, and compare with responses in healthy controls (HC). Cutaneous biopsies were taken from unexposed skin and from skin exposed to a single low (physiological) dose of SSR, at 30 minutes, 3 hours and 24 hours post-exposure, in n=6 SU patients and n=6 HC. Biopsies were assessed by immunohistochemistry (n=6 SU, n=6 HC) and RNA-sequencing analysis (n=4 SU, n=4 HC). This dataset contains RNAseq data from the SU patients.
2024-03-18 | E-MTAB-12219 | biostudies-arrayexpress
Project description:solar evaporation pond sample Metagenome
| PRJNA437813 | ENA
Project description:Assessment of Microbial diversity of solar saltern
| PRJEB50509 | ENA
Project description:Carbaryl (1-naphthyl-methylcarbamate), a broad-spectrum insecticide, has recently been associated with the development of cutaneous melanoma in an epidemiological cohort study with U.S. farm workers also exposed to ultraviolet radiation, which is known to be the main etiologic factor for skin carcinogenesis. Although comprehensive and well designed, the agricultural epidemiological study was not sufficient to characterize the direct contribution of the insecticide and solar radiation in melanomagenesis. Several studies have explored the synergistic effect of certain chemicals with UV radiation, increasing its deleterious effects on the skin. We hypothesized that carbaryl exposure associated with UV solar radiation may induce melanocyte transformation. This study aimed to characterize human melanocytes after individual or combined exposure to carbaryl (100 μM) and solar radiation (375 mJ/cm2). In a microarray analysis, carbaryl, but not solar radiation, induced an important oxidative stress response, evidenced by the upregulation of antioxidant genes, such as Hemeoxygenase-1 (HMOX1), and downregulation of Microphtalmia-associated Transcription Factor (MITF), the main regulator of melanocytic activity; results were confirmed by qRT-PCR. Carbaryl and solar radiation induced a gene response suggestive of DNA damage and cell cycle alteration. The expression of genes in these categories was notably more intense in the combined treatment group, in a synergistic manner, for CDKN1A, BRCA1/2 and MDM2 genes. Likewise, flow cytometry assays demonstrated S-phase cell cycle arrest, reduced apoptosis levels and faster induction of cyclobutane pyrimidine dimers (CPD) lesions in carbaryl treated groups. Our data suggests that carbaryl is genotoxic to human melanocytes, especially when associated with solar radiation.
2017-03-15 | GSE79579 | GEO
Project description:The selection of specific miRNAs by exosomes and their release from cultured melanocytes after exposure to solar UVR (UVA+UVB) have activities in inducing these cells into a premature senescence.
2020-06-01 | GSE141618 | GEO
Project description:We here present a novel subtype of fibroblasts isolated from sun-exposed skin of elderly donors and characterized by its prominent and stable myo-chondrocyte-type differentiation. As we depict a similar chondrocyte-type expression pattern at sites of solar elastosis in human skin, we propose that this fibroblasts phenotype develops in the course of massive and perseverative UV-dependent damage as part of the process terminating in the most severe appearance of photoaging - solar elastosis. Along with the abnormal expression profile, these “old” fibroblasts generate a chondrocyte-type matrix with a layer of myofibroblast-differentiation in close vicinity to the epidermis, when propagated as skin equivalents (SEs) in 3D organotypic cultures. Importantly, these fibroblasts are strongly reduced in their ability to support epidermal growth and differentiation, allowing for rapid/premature epidermal atrophy. Having identified TGFß as an important player in this scenario, we show that the addition of TGFß to normal young fibroblast induces while inhibition of TGFß to the old fibroblast abolishes the myo-chondrogenic expression profile. Accordingly, inhibiting TGFß in the in vivo-like SEs, not only abrogates the aberrant phenotype but allows these fibroblasts to regain their normal mutual interaction with the epidermal keratinocytes and to support epidermal regeneration and longevity. Further, we provide evidence for a role of chronic solar UV radiation in initiating chondrogenic gene expression in young fibroblasts. Concomitantly, we show however, that the same UV treatment abolishes myofibroblast differentiation in the SEs with the “old” chondrogenic fibroblasts, and that this selective inhibition is already sufficient to restore the fibroblasts’ ability for successfully supporting epidermal growth and differentiation. From this it is tempting to suggest, that besides all damaging potential, “mild” solar UV radiation may exert also beneficial effects, e.g. in promoting activation of photoaged skin.
2023-03-22 | GSE200002 | GEO