Allograft versus isograft mouse heterotopic tracheal transplant grafts
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE3418 | GEO | 2005/10/08
SECONDARY ACCESSION(S): PRJNA93445
REPOSITORIES: GEO
Similar Datasets
Project description:Exploration of genes associated with acute and chronic rejection associated with obliterative airway disease Experiment Overall Design: Untransplanted trachea (controls; n=5) and trachea transplanted into MHC compatible/incompatible recipients at day 4 (n = 5 compatible/5 incompatible), day 14 (n = 5/5) or day 25 (n = 5/5)
2007-10-12 | E-GEOD-3418 | biostudies-arrayexpress
Project description:The study comprises various components: We aim to screen out different gene expression profile in acute rejection on the kidney. We aim to screen out different gene expression profile in acute tubular necrosis on the kidney. We aim to screen out different gene expression profile in borderline change on the kidney. We aim to screen out different gene expression profile in non-rejection on the kidney. We aim to screen out different gene expression profile in presumed rejection on the kidney. We aim to screen out different gene expression profile in renal recipients with stable function. Results from the various study components can help to diagnose renal allograft dysfunction with different causes by distinct gene expression profile. Keywords: acute rejection, acute tubular necrosis, borderline change, non-rejection, presumed rejection, renal recipients with stable function,
2009-11-25 | GSE19130 | GEO
Project description:The study comprises various components: We aim to screen out different gene expression profile in acute rejection on the kidney. We aim to screen out different gene expression profile in acute tubular necrosis on the kidney. We aim to screen out different gene expression profile in borderline change on the kidney. We aim to screen out different gene expression profile in non-rejection on the kidney. We aim to screen out different gene expression profile in presumed rejection on the kidney. We aim to screen out different gene expression profile in renal recipients with stable function. Results from the various study components can help to diagnose renal allograft dysfunction with different causes by distinct gene expression profile. Keywords: acute rejection, acute tubular necrosis, borderline change, non-rejection, presumed rejection, renal recipients with stable function, Samples GSM456771-GSM456800: This study has been accomplished with 15 patients of acute rejection on the kidney.Technical replicates: 2 replicates(except AR10 and AR13) Samples GSM456801-GSM456810: This study has been accomplished with 5 patients of acute tubular necrosis on the kidney. Technical replicates: 2 replicates(except ATN4) Samples GSM456811-GSM456831: This study has been accomplished with 11 patients of borderline change on the kidney.Tecnical replicates:2 replicates(except BL8 and BL11) Samples GSM456833-GSM456850: This study has been accomplished with 9 patients of non-rejection on the kidney.Technical replicates: 2 replicates Samples GSM456851-GSM456864: This study has been accomplished with 7 patients of presumed rejection on the kidney.Technical replicates: 2 replicates Samples GSM456865-GSM456894: This study has been accomplished with 15 patients of renal recipients with stable function.Technical replicates: 2 replicates
2010-06-25 | E-GEOD-19130 | biostudies-arrayexpress
Project description:MOLECULAR PROFILING IMPROVES DIAGNOSES OF REJECTION AND INFECTION IN TRANSPLANTED ORGANS. The monitoring of transplanted hearts is currently based on histological evaluation of endomyocardial biopsies, a method that is fairly insensitive and that does not always accurately discriminate between rejection and infection in the heart. Accurate diagnosis of rejection and infection is absolutely crucial, however, as the respective treatments are completely different. Using microarrays we analyzed gene expression in 76 cardiac biopsies from 40 heart recipients undergoing rejection, no rejection, or T. cruzi infection. We found a set of 98 genes whose expression patterns were typical of acute rejection, and 87 genes that discriminated between rejection and T. cruzi infection. These sets revealed acute rejection episodes up to two weeks earlier, and trypanosome infection up to two months earlier than did histological evaluation. When applied to raw data from other institutions, the two sets of predictive genes were also able to accurately pinpoint acute rejection of lung and kidney transplants, as well as bacterial infections in kidneys. In addition to their usefulness as diagnostic tools, the data suggest that there are similarities in the biology of the processes involved in rejection of different grafts and also in the tissue responses to pathogens as diverse as bacteria and protozoa. pre-rejection: GSM47949, GSM48048, GSM49625 non-rejection: GSM47957, GSM48045, GSM48049, GSM48057, GSM48072, GSM48089, GSM48092, GSM49624, GSM49654, GSM49656, GSM49657, GSM49658, GSM49661, GSM49666, GSM49748, GSM49750, GSM49751, GSM49752, GSM49754, GSM49756, GSM49757, GSM49758, GSM49762, GSM49765, GSM49766, GSM49767, GSM49769, GSM49771, GSM49773, GSM49774, GSM49781, GSM49782, GSM49783, GSM49784 acute rejection: GSM48040, GSM48043, GSM48046, GSM48047, GSM48050, GSM48053, GSM48056, GSM49655, GSM49747, GSM49749, GSM49755, GSM49759, GSM49761, GSM49763, GSM49764, GSM49780 pre-Chagas disease reactivation: GSM48089, GSM49756, GSM49757, GSM49758, GSM49767, GSM49769, GSM49771 Chagas disease reactivation: GSM49753, GSM49760, GSM49768, GSM49772, GSM49775, GSM49776, GSM49777, GSM49778 Toxoplasma myocarditis: GSM48058 first subset ("summer"): GSM47949, GSM47957, GSM48040, GSM48043, GSM48045, GSM48046, GSM48047, GSM48048, GSM48049, GSM48050, GSM48053, GSM48056, GSM48057, GSM48058, GSM48072, GSM48089, GSM48092, GSM49624, GSM49625, GSM49654, GSM49655, GSM49656, GSM49657, GSM49658, GSM49661, GSM49666, GSM49747, GSM49748, GSM49749, GSM49750, GSM49751, GSM49752 second subset ("winter"): GSM49753, GSM49754, GSM49755, GSM49756, GSM49757, GSM49758, GSM49759, GSM49760, GSM49761, GSM49762, GSM49763, GSM49764, GSM49765, GSM49766, GSM49767, GSM49768, GSM49769, GSM49770, GSM49771, GSM49772, GSM49773, GSM49774, GSM49775, GSM49776, GSM49777, GSM49778, GSM49780, GSM49781, GSM49782, GSM49783, GSM49784 Keywords = cardiac transplant Keywords = acute rejection Keywords = infection Keywords: repeat sample
2005-10-24 | GSE2596 | GEO
Project description:The molecular basis of calcineurin inhibitor toxicity (CNIT) in kidney transplantation (KT) and its contribution to chronic allograft dysfunction (CAD) with interstitial fibrosis (IF) and tubular atrophy (TA) were evaluated. Molecular signatures characterizing CNIT samples were identified. The recognized CNIT gene signature was most common in patients with decreased graft function and histological evidence of IF/TA. To test CNIT contribution to CAD progression, kidney biopsies from transplant recipients with histological diagnosis of CNIT (n=14), acute rejection (ACR, n=13), and CAD with IF/TA (n=10), including 18 Normal allografts, were analyzed using gene expression microarrays.
2014-06-01 | E-GEOD-53605 | biostudies-arrayexpress
Project description: Not available
| S-EPMC8691915 | biostudies-literature
Project description:MOLECULAR PROFILING IMPROVES DIAGNOSES OF REJECTION AND INFECTION IN TRANSPLANTED ORGANS. The monitoring of transplanted hearts is currently based on histological evaluation of endomyocardial biopsies, a method that is fairly insensitive and that does not always accurately discriminate between rejection and infection in the heart. Accurate diagnosis of rejection and infection is absolutely crucial, however, as the respective treatments are completely different. Using microarrays we analyzed gene expression in 76 cardiac biopsies from 40 heart recipients undergoing rejection, no rejection, or T. cruzi infection. We found a set of 98 genes whose expression patterns were typical of acute rejection, and 87 genes that discriminated between rejection and T. cruzi infection. These sets revealed acute rejection episodes up to two weeks earlier, and trypanosome infection up to two months earlier than did histological evaluation. When applied to raw data from other institutions, the two sets of predictive genes were also able to accurately pinpoint acute rejection of lung and kidney transplants, as well as bacterial infections in kidneys. In addition to their usefulness as diagnostic tools, the data suggest that there are similarities in the biology of the processes involved in rejection of different grafts and also in the tissue responses to pathogens as diverse as bacteria and protozoa. Keywords: disease state analysis
2006-03-15 | GSE4470 | GEO
Project description:The data set contains 67 array (lymphochip cDNA array), published in N Engl J Med 2003 Jul 10;349(2):125-38. PMID: 12853585. TITLE: Molecular heterogeneity in acute renal allograft rejection identified by DNA microarray profiling. BACKGROUND: The causes and clinical course of acute rejection vary, and it is not possible to predict graft outcome reliably on the basis of available clinical, pathological, and genetic markers. We hypothesized that previously unrecognized molecular heterogeneity might underlie some of the variability in the clinical course of acute renal allograft rejection and in its response to treatment. METHODS: We used DNA microarrays in a systematic study of gene-expression patterns in biopsy samples from normal and dysfunctional renal allografts. A combination of exploratory and supervised bioinformatic methods was used to analyze these profiles. : We found consistent differences among the gene-expression patterns associated with acute rejection, nephrotoxic effects of drugs, chronic allograft nephropathy, and normal kidneys. The gene-expression patterns associated with acute rejection suggested at least three possible distinct subtypes of acute rejection that, although indistinguishable by light microscopy, were marked by differences in immune activation and cellular proliferation. Since the gene-expression patterns pointed to substantial variation in the composition of immune infiltrates, we used immunohistochemical staining to define these subtypes further. This analysis revealed a striking association between dense CD20+ B-cell infiltrates and both clinical glucocorticoid resistance (P=0.01) and graft loss (P<0.001). CONCLUSIONS: Systematic analysis of gene-expression patterns provides a window on the biology and pathogenesis of renal allograft rejection. Biopsy samples from patients with acute rejection that are indistinguishable on conventional histologic analysis reveal extensive differences in gene expression, which are associated with differences in immunologic and cellular features and clinical course. The presence of dense clusters of B cells in a biopsy sample was strongly associated with severe graft rejection, suggesting a pivotal role of infiltrating B cells in acute rejection. A disease state experiment design type is where the state of some disease such as infection, pathology, syndrome, etc is studied. Disease State: normal vs disease Keywords: disease_state_design Using regression correlation
2003-07-01 | E-GEOD-343 | biostudies-arrayexpress
Project description:To further understand the early molecular events in antibody mediated chronic inflammation of the lungs, we utilized a murine Obliterative Airway Disease (OAD) model of native lungs where Abs to MHC class I induces bronchiolar obliteration and fibrosis. This study identified a unique transcriptional profile with a set of genes that were stimulated while another set of genes that were repressed in anti MHC I treated lungs compared to that of isotype treated lungs. Lung transplantation (LTx) is an accepted clinical intervention for various intractable pulmonary dysfunctions. However, de novo Abs to mismatched donor HLA (DSA) predispose lung-grafts to chronic rejection, Bronchiolitis Obliterans Syndrome (BOS). The anti-MHC induced mouse OAD model, the only available preclinical model for study of early pathogenesis following MHC ligation, produces lesions analogous to BOS.
2017-07-29 | GSE71426 | GEO
Project description: Not available
| S-EPMC8389233 | biostudies-literature