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Higher colonic proliferation and tumor prevalence amongst azoxymethane treated A/J mice receiving fecal microbiota transplants from old mice compared to recipients of young mice [16S rRNA-Seq]

ABSTRACT: Higher colonic proliferation and tumor prevalence amongst azoxymethane treated A/J mice receiving fecal microbiota transplants from old mice compared to recipients of young mice [16S rRNA-Seq]

PROVIDER: PRJNA994607 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25269103_1.fastq.gz	Fastqsanger.gz
	SRR25269103_2.fastq.gz	Fastqsanger.gz
	SRR25269104_1.fastq.gz	Fastqsanger.gz
	SRR25269104_2.fastq.gz	Fastqsanger.gz
	SRR25269105_1.fastq.gz	Fastqsanger.gz

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Higher colonic proliferation and tumor prevalence amongst azoxymethane treated A/J mice receiving fecal microbiota transplants from old mice compared to recipients of young mice

Project description:Higher colonic proliferation and tumor prevalence amongst azoxymethane treated A/J mice receiving fecal microbiota transplants from old mice compared to recipients of young mice

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Higher colonic proliferation and tumor prevalence amongst azoxymethane treated A/J mice receiving fecal microbiota transplants from old mice compared to recipients of young mice [RNA-Seq]

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Higher colonic proliferation and tumor prevalence amongst azoxymethane treated A/J mice receiving fecal microbiota transplants from old mice compared to recipients of young mice

Project description:This SuperSeries is composed of the SubSeries listed below.

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Higher colonic proliferation and tumor prevalence amongst azoxymethane treated A/J mice receiving fecal microbiota transplants from old mice compared to recipients of young mice [RNA-Seq]

Project description:Gut microbial dysbiosis can play a causal role of in colorectal cancer. Gut microbiota chnages with age and becomes moer pro-inflammatory. We sought to determine whether microbiota from Old donors promotes more tumor formation in recipients than meterial from young donors.

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Higher colonic proliferation and tumor prevalence amongst azoxymethane treated A/J mice receiving fecal microbiota transplants from old mice compared to recipients of young mice [16S rRNA-Seq]

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Azoxymethane induced changes in Rat proximal and distal colonic epithelium.

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Human iPSC-derived GABAergic Interneuron Transplants Attenuate Neuropathic Pain

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Project description:Microarray analysis of human kidneys with acute kidney injury (AKI) has been limited because such kidneys are seldom biopsied. However, all kidney transplants experience AKI, and early kidney transplants without rejection are an excellent model for human AKI: they are screened to exclude chronic kidney disease, frequently biopsied, and have extensive follow-up. We used histopathology and microarrays to compare indication biopsies from 28 transplants with AKI to 11 pristine protocol biopsies of stable transplants. Kidneys with AKI showed increased expression of 394 injury-repair response associated transcripts, including many known epithelial injury molecules (e.g. ITGB6, LCN2), tissue remodeling molecules (e.g. VCAN), and inflammation molecules (S100A8, ITGB3). Many other genes also predict the phenotype, depending on statistical filtering rules, including AKI biomarkers as HAVCR1 and IL18. Most mouse orthologs of the top injury-repair transcripts were increased in published mouse AKI models. Pathway analysis of the injury-repair transcripts revealed similarities to cancer, development, and cell movement. The injury-repair transcript score AKI kidneys correlated with reduced function, future recovery, brain death, and need for dialysis, but not future graft loss. In contrast, histologic features of "acute tubular injury" did not correlate with function or with the molecular changes. Thus the injury-repair associated transcripts represent a massive coordinate injury-repair response of kidney parenchyma to AKI, similar to mouse AKI models, and provide an objective measure for assessing the severity of AKI in kidney biopsies and validation for the use of many AKI biomarkers.

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