Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1055055 | ENA |
REPOSITORIES: ENA
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Project description:Radiation therapy for malignancies in the pelvic region leads to a crucial complication called radiation proctopathy(RP) with acute changes in bowel habits or long-term morbidity. We used microarrays to detail the genome-wide profiles of mice with different genotypes (Pdgfc+/+ and Pdgfc-/- ) under irradiation treatment or not.
2021-08-24 | GSE145131 | GEO
Project description:This study aimed to analyze changes in gut microbiota composition in mice after transplantation of fecal microbiota (FMT, N = 6) from the feces of NSCLC patients by analyzing fecal content using 16S rRNA sequencing, 10 days after transplantation. Specific-pathogen-free (SPF) mice were used for each experiments (N=4) as controls.
2023-07-01 | E-MTAB-12812 | biostudies-arrayexpress
Project description:Exposure to high-dose radiation causes life-threatening serious intestinal damage. Histological analysis is the most accurate method for judging the extent of intestinal damage after death. However, it is difficult to predict the extent of intestinal damage to body samples. Here we focused on extracellular microRNAs (miRNAs) released from cells and investigated miRNA species that increased or decreased in serum and feces using a radiation-induced intestinal injury mouse model. A peak of small RNA of 25–200 nucleotides was detected in mouse serum and feces 72 h after radiation exposure, and miRNA presence in serum and feces was inferred. MiRNAs expressed in the small intestine and were increased by more than 2.0-fold in serum or feces following a 10 Gy radiation exposure were detected by microarray analysis and were 4 in serum and 19 in feces. In this study, miR-375-3p, detected in serum and feces, was identified as the strongest candidate for a high-dose radiation biomarker in serum and/or feces using a radiation-induced intestinal injury model.
2023-12-15 | GSE247876 | GEO
Project description:Colorectal cancer (CRC) is closely related to gut dysbiosis. We investigated the effects of imbalanced gut microbiota on the progression of intestinal adenoma in Apcmin/+ mice model using fecal microbiota transplantation (FMT). Administration of feces from CRC patients increased tumor proliferation and decreased apoptosis in tumor cells. Abnormal expression of genes related to Wnt-protein binding and lipid metabolic process was observed.
2019-09-16 | GSE136682 | GEO
Project description:<p>In this study, we investigated the role of the gut microbiota on the development of complications in kidney transplant recipients. We collected serial fecal specimens from 168 kidney transplant recipients within the first 3 months after transplantation. We performed 16S rRNA gene sequencing of the V4-V5 hypervariable region and examined whether the relative gut abundance of pathogenic bacteria was associated with future development of complications like bacteriuria and urinary tract infections. In a subset of samples, we performed metagenomic sequencing of stool and urine supernatant specimens to determine strain level analysis. </p>
| phs001879 | dbGaP
Project description:To further identify the fecal miRNAs generated in HE, we conducted an miRNA microarray analysis on feces collected from patients with HE and CHB. The microarray analysis of miRNA expression profiles revealed that the abundance of 10 miRNAs was significantly increased in feces from patients with HE, as compared with that from patients with CHB, whereas the abundance of 8 miRNAs was decreased.
2023-04-19 | GSE228731 | GEO
Project description:Primary graft dysfunction (PGD) is the leading cause of early mortality after lung transplantation. Anti-collagen type-V (col(V)) immunity has been observed in animal models of ischemia-reperfusion injury (IRI) and in PGD. We hypothesized that collagen type-V is an innate danger signal contributing to PGD pathogenesis. Methods: Anti-col(V) antibody production was detected by flow cytometric assay following cultures of murine CD19+ splenic cells with col(V). Responding murine B cells were phenotyped using surface markers. RNA-Seq analysis was performed on murine CD19+ cells. Levels of anti-col(V) antibodies were measured in 188 recipients from the Lung Transplant Outcomes Group (LTOG) after transplantation. Results: Col(V) induced rapid production of anti-col(V) antibodies from murine CD19+ B cells. Subtype analysis demonstrated innate B-1 B cells bound col(V). Col(V) induced a specific transcriptional signature in CD19+ B cells with similarities to, yet distinct from, B cell receptor (BCR) stimulation. Rapid de novo production of anti-col(V) Abs was associated with an increased incidence of clinical PGD after lung transplant. Conclusions: This study demonstrated that col(V) is an rapidly recognized by B cells and has specific transcriptional signature. In lung transplants recipients the rapid seroconversion to anti-col(V) Ab is linked to increased risk of grade 3 PGD.
2019-11-20 | GSE140681 | GEO
Project description:Today, swine is regarded as promising biomedical model, however, its gastrointestinal microbiome dynamics have been less investigated than that of humans or murine models . The aim of this study was to establish a high-throughput multi-omics pipeline to investigate the healthy fecal microbiome of swine and its temporal dynamics as basis for future infection studies. To this end, a homogenization protocol based on deep-frozen feces followed by integrated sample preparation for different meta-omics analyses was developed. Subsequent data integration linked microbiome composition with function, i.e. expressed proteins and secreted metabolites.
2021-02-15 | PXD020775 | Pride
Project description:Radiation provides excellent tumor control in prostate cancer yet unavoidably harms adjacent healthy tissue via the generation of reactive oxygen species (ROS). Radiation-induced ROS is known to impact fibroblasts long after radiation, resulting in radiation-induced fibrosis (RIF), which can cause incontinence and other side effects that reduce patient quality of life. BMX-001, a manganese porphyrin designed to mimic superoxide dismutase, is in clinical trials as a selective radioprotector when given before and during radiation therapy. However, there have been no studies evaluating BMX-001 when given after radiation for its impacts on RIF. Mice were given pelvic radiation (7.5 Gy for 5 consecutive days) followed by BMX-001 three weeks after radiation. Fibroblasts and tissues were isolated two months following radiation. We found that BMX-001 returned radiation-induced alterations in fibroblast morphology to normal and reversed markers of fibroblast activation and senescence. BMX-001 also decreased collagen deposition six months after radiation. We found that overall, radiation resulted in reduced methylation two months after radiation, and BMX-001 administered three weeks after radiation modulated radiation-altered methylation patterns back to normal and restored normal expression of a fibrosis-associated gene CAMK2beta. BMX-001 also decreased radiation-induced DNA adduct 8-hydroxy-2’-deoxyguanosine (8-OHdG), which is known to interfere with methylation. BMX-001 was able to prevent DNA oxidation and restore normal methylation patterns in an oligonucleotide model of DNA oxidation and methylation. This study reveals the feasibility of agents to reverse fibrosis in pelvic radiation and suggests that BMX-001 may be effective when given after radiation.
2026-01-28 | GSE309064 | GEO
Project description:Radiation provides excellent tumor control in prostate cancer yet unavoidably harms adjacent healthy tissue via the generation of reactive oxygen species (ROS). Radiation-induced ROS is known to impact fibroblasts long after radiation, resulting in radiation-induced fibrosis (RIF), which can cause incontinence and other side effects that reduce patient quality of life. BMX-001, a manganese porphyrin designed to mimic superoxide dismutase, is in clinical trials as a selective radioprotector when given before and during radiation therapy. However, there have been no studies evaluating BMX-001 when given after radiation for its impacts on RIF. Mice were given pelvic radiation (7.5 Gy for 5 consecutive days) followed by BMX-001 three weeks after radiation. Fibroblasts and tissues were isolated two months following radiation. We found that BMX-001 returned radiation-induced alterations in fibroblast morphology to normal and reversed markers of fibroblast activation and senescence. BMX-001 also decreased collagen deposition six months after radiation. We found that overall, radiation resulted in reduced methylation two months after radiation, and BMX-001 administered three weeks after radiation modulated radiation-altered methylation patterns back to normal and restored normal expression of a fibrosis-associated gene CAMK2beta. BMX-001 also decreased radiation-induced DNA adduct 8-hydroxy-2’-deoxyguanosine (8-OHdG), which is known to interfere with methylation. BMX-001 was able to prevent DNA oxidation and restore normal methylation patterns in an oligonucleotide model of DNA oxidation and methylation. This study reveals the feasibility of agents to reverse fibrosis in pelvic radiation and suggests that BMX-001 may be effective when given after radiation.
2026-01-28 | GSE308163 | GEO