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Aortic infection

ABSTRACT: Mycobacterium chelonae as the probable cause of acute contained rupture of a biological composite graft

PROVIDER: PRJEB39759 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR4672762_1.fastq.gz	Fastqsanger.gz
	ERR4672762_2.fastq.gz	Fastqsanger.gz
	ERR4672763_1.fastq.gz	Fastqsanger.gz
	ERR4672763_2.fastq.gz	Fastqsanger.gz
	ERR4672764_1.fastq.gz	Fastqsanger.gz

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Biofilms of non-tuberculous mycobacteria display distinct expression patterns and form an extracellular matrix

Project description:Comparison of transcriptional differences (RNA-seq) between biofilm and planktonic cultures of Mycobacterium chelonae

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Atherosclerotic Plaque Macrophages Drive Abdominal Aortic Aneurysm Formation

Project description:There is no effective pharmacotherapy to prevent the growth and rupture of abdominal aortic aneurysms (AAA), a leading cause of death. We developed a novel preclinical model showing that the interaction of bona fide risk factors (i.e., cigarette smoke (CS) and hypercholesterolemia) induced AAA formation, rupture, and death. Elastin fragmentation resulted from CS-induced exacerbation of the atherosclerotic process, significant given atherosclerosis is a disease of the inner intimal layer of the artery, with the media remaining largely intact. Importantly, arterial injury was driven by CSF-1-dependent macrophages (Mφ) accumulating within developing atherosclerotic plaques that exhibited tissue degrading proteolytic activity in vivo. Single-cell RNA sequencing further demonstrated conservation of Mφ responses in atherosclerotic plaque from murine and human AAA. Our findings advance understanding of the pathological sequelae of atherosclerosis, establishing plaque Mφ as important mediators of tissue damage and a potential target for prevention of AAA growth and rupture.

2025-03-06 | GSE284253 | GEO

Project description:Mycobacterium chelonae Skin Infection

| PRJNA643662 | ENA

Gene expression study in Positron Emission Tomography (PET) positive abdominal aortic aneurysms

Project description:This study aims at identifying genes involved in this metabolic activation potentially related to rupture. A genome-wide transcriptomic analysis was performed on biopsies collected from patients with a Fluorodeoxyglucose (FDG) uptake both in the positive spot (A+Pos) and in a distant negative site of the same aneurysm (A+Neg). These paired biopsies were further compared to samples collected from (abdominal aortic aneurysms) AAA patients with no FDG uptake (A0) in order to discriminate biological alterations associated with FDG uptake, to detect new systemic biomarkers correlated with a higher risk of rupture and to identify new pathways involved in the progression and rupture of AAA).

2015-02-09 | E-MTAB-3175 | biostudies-arrayexpress

Atherosclerotic Plaque Macrophages Drive Abdominal Aortic Aneurysm Formation [snRNAseq]

2025-03-06 | GSE284249 | GEO

Atherosclerotic Plaque Macrophages Drive Abdominal Aortic Aneurysm Formation [bulkRNA-Seq]

2025-03-06 | GSE284251 | GEO

Mycobacterium

Project description:Genomic variability of Mycobacterium chelonae

| PRJNA323571 | ENA

Project description:Whole genome sequencing of Mycobacterium chelonae chelonae, an opportunistic pathogen

| PRJDB2512 | ENA

[Mycobacterium] chelonae subsp. chelonae strain:DSM 43804

Project description:[Mycobacterium] chelonae subsp. chelonae strain:DSM 43804 Phenotype or Genotype

| PRJNA508902 | ENA

Subcellular pathways shared by afflicted patients and mutant mice identify a new drug treatment for aortic aneurysm in Marfan syndrome

Project description:We analyzed differentially expressed genes in smooth muscle cells derived from the thoracic aorta of Marfan Syndrome (MFS) patients and control subjects to identify cell biological mechanisms contributing to thoracic aoritc aneurysm (TAA) development and rupture. These mechanisms were used to identify a potential drug treatment to mitigate TAA progression. We analyzed differentially expressed genes in whole aorta of P16 MFS mice vs WT mice to identify cell biological mechanisms contributing to thoracic aoritc aneurysm (TAA) development and rupture. These mechanisms were used to identify baclofen as a potential drug treatment to mitigate TAA progression. The effect of baclofen on gene expression in WT and MFS was documented in P60 mice that received treatment since P16.

2019-11-18 | GSE128101 | GEO

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