Stone-age-plague-2017
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB19335 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Early Divergent strains of Yersinia pestis in Eurasia five thousands years ago
| PRJEB10885 | ENA
Project description:A Genomic and Historical Synthesis of Plague in 18th Century Eurasia.
| PRJEB27821 | ENA
Project description:We recently reported elimination of renal crystals and migration of macrophages (Mφ) around crystals in hyperoxaluric mice, suggesting Mφs might eliminate crystals. Mφs are of 2 phenotypes: inflammatory (M1) and anti-inflammatory (M2). Because M2Mφs are considered to be involved in tissue repair and regeneration, we focused attention on their suppressive role in renal crystal formation. Hence, we investigated the gene array profiling of renal macrophages in stone model mice and CSF-1-deficient stone model mice.
2013-10-22 | GSE51466 | GEO
Project description:Kidney stone disease causes significant morbidity and increases health care utilization. In this dataset, we applied a single-nucleus assay to renal papila samples in order to charachterize the cellular and molecular niches in patients with calcium oxalate (CaOx) stone disease and healthy subjects. In addition to identifying cell types important in papillary physiology, we characterize collecting duct cell subtypes and an undifferentiated epithelial cell type that was more prevalent in stone patients. Despite the focal nature of mineral deposition in nephrolithiasis, we uncover a global injury signature characterized by immune activation, oxidative stress and extracellular matrix remodeling. We also identify the association of MMP7 and MMP9 expression with stone disease and mineral deposition, respectively. MMP7 and MMP9 are significantly increased in the urine of patients with CaOx stone disease, and their levels correlate with disease activity. Our results define the spatial molecular landscape and specific pathways contributing to stone-mediated injury in the human papilla and identify associated urinary biomarkers.
2023-05-04 | GSE231569 | GEO
Project description:We recently reported elimination of renal crystals and migration of macrophages (MM-OM-^F) around crystals in hyperoxaluric mice, suggesting MM-OM-^Fs might eliminate crystals. MM-OM-^Fs are of 2 phenotypes: inflammatory (M1) and anti-inflammatory (M2). Because M2MM-OM-^Fs are considered to be involved in tissue repair and regeneration, we focused attention on their suppressive role in renal crystal formation. Hence, we investigated the gene array profiling of renal macrophages in stone model mice and CSF-1-deficient stone model mice. B6C3Fe a/a-Csf1op/J wild type/homozygous mice were admistered 80mg/kg gyyoxylate (GOX) for 6days, then the kidneys were extracted and sorted CD11b+/CD11c+ macrophages using autoMACS. The gene expression of WT- and op/op-macrophages were investigated using bone marrow derived M1/M2 macrophages as controls.
2013-10-22 | E-GEOD-51466 | biostudies-arrayexpress
Project description:OBJECTIVES: Kidney stone diseases are common in premature infants, but the underlying molecular and cellular mechanisms are not fully defined. We carried out a prospective observational study using microarray analysis to identify factors that may be crucial for the initiation and progression of stone-induced injury in the developing mouse kidney. METHODS: Mice with adenine phosphoribosyltransferase (Aprt) deficiency develop 2,8-dihydroxyadenine (DHA) nephrolithiasis. Gene expression changes between Aprt-/- and Aprt+/+ kidneys from newborn and adult mice were compared using Affymetrix gene chips. RESULTS: We observed that: (i) gene expression changes induced by Aprt deficiency are developmental stage-specific; (ii) maturation-related gene expression changes are delayed in developing Aprt-/- kidneys; and (iii) immature Aprt-deficient kidneys contain large numbers of intercalated cells blocked from terminal differentiation. CONCLUSIONS: This study presents a comprehensive picture of the transcriptional changes induced by stone injury in the developing mouse kidney. Our findings help explain growth impairment in kidneys subject to injury during the early stages of development. Total RNA were extracted from kidneys of 12 newly born and 6 adult mice (half Aprt-/- and half control). Gene expression changes between Aprt-/- and Aprt+/+ kidneys from newborn and adult mice were compared using Affymetrix gene chips.
2010-01-13 | E-GEOD-18160 | biostudies-arrayexpress
Project description:During pneumonic plague, the bacterium Yersinia pestis elicits the development of inflammatory lung lesions that continue to expand throughout infection. This lesion development and persistence is poorly understood. Here, we examine spatially distinct regions of lung lesions using laser capture microdissection and RNAseq analysis to identify transcriptional differences between lesion microenvironments. We show that cellular pathways involved in leukocyte migration and apoptosis are down regulated in the center of lung lesions compared to the periphery. Probing for the bacterial factor(s) important for the alteration in neutrophil survival, we show both in vitro and in vivo that Y. pestis increases neutrophil survival in a manner that is dependent on the type-III secretion system effector YopM. This research explores the complexity of spatially distinct host - microbe interactions and emphasizes the importance of cell relevance in assays in order to fully understand Y. pestis virulence. We examine spatially distinct regions of lung lesions using laser capture microdissection and RNAseq analysis to identify transcriptional differences between lesion microenvironments. Sample types: uninfected BM-PMN, infected BM-PMN, lesion periphery, lesion center.
2015-07-13 | E-GEOD-70819 | biostudies-arrayexpress
Project description:OBJECTIVES: Kidney stone diseases are common in premature infants, but the underlying molecular and cellular mechanisms are not fully defined. We carried out a prospective observational study using microarray analysis to identify factors that may be crucial for the initiation and progression of stone-induced injury in the developing mouse kidney. METHODS: Mice with adenine phosphoribosyltransferase (Aprt) deficiency develop 2,8-dihydroxyadenine (DHA) nephrolithiasis. Gene expression changes between Aprt-/- and Aprt+/+ kidneys from newborn and adult mice were compared using Affymetrix gene chips. RESULTS: We observed that: (i) gene expression changes induced by Aprt deficiency are developmental stage-specific; (ii) maturation-related gene expression changes are delayed in developing Aprt-/- kidneys; and (iii) immature Aprt-deficient kidneys contain large numbers of intercalated cells blocked from terminal differentiation. CONCLUSIONS: This study presents a comprehensive picture of the transcriptional changes induced by stone injury in the developing mouse kidney. Our findings help explain growth impairment in kidneys subject to injury during the early stages of development.
2010-01-13 | GSE18160 | GEO
Project description:Kidney stone disease is influenced by multiple factors, including but not limited to age, gender, genetic background, hydration status, diet and drug. Regarding the gender, epidemiologic data across the world has shown that females at the reproductive age (15-49 years) have lower incidence/prevalence of kidney stone disease approximately 1.5-2.5 folds as compared to males at the same age. However, this gap is narrower in the postmenopausal age, whereas the postmenopausal females with higher serum estrogen levels are less likely to have kidney stones. Furthermore, female stone formers (patients with kidney stones) are associated with lower estrogen levels. Therefore, estrogen has been proposed to serve as the protective hormone against kidney stone disease. However, the precise mechanisms underlying such protective effects of estrogen remain unclear and require further investigations. This study thus investigated the effects of estradiol (which is the most prevalent and potent form of estrogen in females at the reproductive age) on cellular proteome of renal tubular cells using a proteomics approach.
2019-09-09 | PXD014768 | Pride