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Gene based immune profiling of vermiform appendix GALT of adult patients with pancreatic cancer or colon diseases.

ABSTRACT: Differential immune gene expression analysis in appendix GALT between patients with pancreatic cancer versus benign or malignant colon disease using the nanostring ncounter platform.

ORGANISM(S): Homo sapiens

PROVIDER: GSE236951 | GEO | 2023/11/14

REPOSITORIES: GEO

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Appendix metagenome

Project description:Appendix Metagenome

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Transcription profiling of mouse GalT knockout recipient of GalT transducded allo-bone marrow cells after sublethal irradiation

Project description:Xenotransplantation holds the promise of providing an unlimited supply of donor organs for terminal patients with organ failure. The gal carbohydrate results in rejection of wild type pig grafts, however, chimerism established by expression of the GalT gene prior to transplantation in GalT knockout mice results in tolerance to Gal+ heart grafts. We used microarrays in order to further understand the early events that occur within grafts that demonstrate tolerance. Experiment Overall Design: The GalT BMT recipient is a GalT knockout mouse which recieved GalT gene transduced allo-bone marrow cells transplantation after sublethal irradiation. A heart of wild type C57BL/6 was heterotopically transplanted into the recipient after GalT BMT. Syngeneic Control recipient is a wild type C57BL/6 transplanted a heart of wild C57BL/6.

2008-06-15 | E-GEOD-7424 | biostudies-arrayexpress

Human Appendix

Project description:Human Appendix Microbiome

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A comparison between GalT-/-;hCD39;hCD55 and GalT-/-;hCD39;hCD46;hCD55;TBM pig kidney transplanted in non-human primates

Project description:Due to shortage of donor kidney, genetically modified kidney xenograft from pigs is considered. To select the optimal gene modification for xenotransplantation, knockout of carbohydrate genes or knockin of protective proteins have been applied. In this study, we utilized GalT- /-;hCD39;hCD55 and GalT-/-;hCD39;hCD46;hCD55;thrombomodulin (TBM) pigs for transplantation in non-human primates. NHPs survived for 4 weeks after kidney transplantation (4 WAT) from GalT-/-;hCD39;hCD55 pig and 6 WAT from GalT- /-;hCD39;hCD46;hCD55;TBM pig. However, mRNA sequencing and immunohistochemistry analysis revealed that 6 WAT kidney showed the severe apoptosis, inflammation, loss of renal function, and renal fibrosis than 4 WAT kidney. These results suggest that additional knockin of anti-complement (hCD26) and anti-coagulation (TBM) is not sufficient to inhibit the renal damage.

2023-12-31 | GSE240012 | GEO

Open chromatin in human pancreatic islets (FAIRE-seq) - Appendix to E-GEOD-17616

Project description:An appendix to the published Gaulton et al. work (PMID: 20118932; E-GEOD-17616). In the original paper, the authors note that samples 1 and 2 are not as pure as the third sample. This appendix provides FAIRE-Seq data obtained from a purified islet sample to replace the problematic published data. The goal of the original experiment was to identify active regulatory DNA in human pancreatic islets. This was accomplished using high-throughput sequencing of genomic regions isolated using FAIRE from three purified pancreatic islet samples to identify sites of open chromatin.

2014-12-23 | E-MTAB-3199 | biostudies-arrayexpress

Transcription profiling of wild type, GALT-deficient and GALT-deficient-revertant yeast grown on media with galactose or glucose

Project description:To better understand the pathophysiology of galactose-1-phosphate uridyltransferase (GALT) deficiency in humans, we studied the mechanisms by which a GALT-deficient yeast survived on galactose medium. Under normal conditions, GALT-deficient yeast cannot grow in medium that contains 0.2% galactose as the sole carbohydrate, a phenotype of Gal(-). We isolated revertants from a GALT-deficient yeast by direct selection for growth in galactose, a phenotype of Gal(+). Comparison of gene expression profiles among wild-type and revertant strains on galactose medium revealed that the revertant down-regulated genes encoding enzymes including galactokinase, galactose permease, and UDP-galactose-4-epimerase (the GAL regulon). By contrast, the revertant strain up-regulated the gene for UDP-glucose pyrophosphorylase, UGP1. There was reduced accumulation of galactose-1-phosphate in the galactose-grown revertant cells when compared to the GALT-deficient parent cells.

2008-04-10 | E-MEXP-1420 | biostudies-arrayexpress

Novel mechanisms of galactose toxicity in human galactose-1-phosphate uridyltransferase (GALT)-deficient cells

Project description:Comparison of gene expression profiles in GALT-deficient and GALT-reconstituted cells showed that cells lacking GALT activity responded to galactose challenge by activating a set of genes characteristic of endoplasmic reticulum (ER) stress. This response was specific to galactose insult, as cells grown in glucose or hexose-free media did not exhibit ER stress. Keywords: GALT infected cells

2007-11-01 | GSE4864 | GEO

Tiling microarray analysis of gene expression profile of Escherichia coli galT mutant cells under D-galactose-stressed condition

Project description:To understand the altered gene expression by D-galactose in galT cells, the cells were grown in the presence and absence of D-galactose and tiling array analysis was performed for transcriptome profiling. A galT defect causes the disease Galactosemia in human. This work helps us to study the human metabolic disease Galactosemia. Total RNAs were isolated from Escherichia coli galT strain grown in the absence and presence of D-galactose. The transcriptome profile of galT cells was figured out in the galactose-stressed condition.

2013-12-17 | E-GEOD-42821 | biostudies-arrayexpress

Epigenetic inactivation of the autophagy-lysosomal system in the Parkinson’s disease appendix (8: ChIP)

Project description:The gastrointestinal tract may be a site of origin for α-synuclein (α-syn) pathology in idiopathic Parkinson’s disease (PD), and an abundance of aggregated α-syn has recently been demonstrated in both the healthy and PD appendix. However, the molecular changes that enable gut α-syn aggregates to contribute to the development and progression of PD remain unclear. Here, our deep-sequencing of DNA methylation changes at 521 autophagy-lysosomal pathway (ALP) genes in the human appendix and brain in PD and healthy controls indicates a pattern of widespread hypermethylation in the PD appendix that is recapitulated in the PD brain. There is significant overlap in the individual ALP genes affected across the PD appendix and brain, with lysosomal genes specifically downregulated in both regions. Healthy epigenetic aging, which involves a hypermethylation of macroautophagy and selective autophagy genes in the appendix and brain, is disrupted in both areas in PD. In mice, DNA methylation changes at ALP genes induced by chronic gut inflammation are greatly exacerbated by the presence of α-syn pathology. DNA methylation changes at ALP genes induced by α-synucleinopathy are significantly associated with the ALP abnormalities observed in the PD appendix, specifically involving lysosomal genes. Our work, which constitutes an in-depth, unbiased investigation of epigenetic changes in the ALP of the PD gut and brain, identifies the epigenetic misregulation of the ALP, especially a downregulation of lysosomal genes, as a potential culprit for the initiation and spread of α-syn pathology in idiopathic PD.

2021-03-01 | GSE135750 | GEO

Epigenetic inactivation of the autophagy-lysosomal system in the Parkinson’s disease appendix (2: PD_RNASeq)

2021-02-01 | GSE135743 | GEO

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