Project description:The Acute Respiratory Distress Syndrome (ARDS)/Acute Lung Injury (ALI) was described 30 years ago, yet the interaction between specific sets of genes involved in this syndrome remains incompletely understood. Keywords: disease state analysis
Project description:Proteomic investigation of immune response of Lung Tissue from Lipopolysaccharide-induced Acute Respiratory Distress Syndrome in Tree Shrews
Project description:Acute respiratory distress syndrome (ARDS) is an acute inflammatory lung injury and one of the serious life-threatening forms of respiratory failure. Alveolar procoagulation and fibrinolytic inhibition constitute the core part of the pathophysiology of ARDS, RUNX1 plays an important role in this pathogenesis. We screened for AKT3, the target gene of RUNX1, using CHIP-seq and verified its binding target by a dual luciferase assay.
Project description:The Acute Respiratory Distress Syndrome (ARDS)/Acute Lung Injury (ALI) was described 30 years ago, yet the interaction between specific sets of genes involved in this syndrome remains incompletely understood. Experiment Overall Design: 13 patients with ALI + sepsis and 21 patients with sepsis alone were recruited from the Medical Intensive Care Unit of the University of Pittsburgh Medical Center between February 2005 and June 2007. Whole blood was obtained from each patient within 48 hours of admission, and RNA was extracted for gene expression profiling, and comparison analysis.
Project description:Human volunteers were exposed to endotoxin by bronchoscopic instillation, airspace and circulating neutrophils were isolated 16 hours later and compared to circulating neutrophils obtained prior to endotoxin exposure, and to circulating neutrophils exposed to endotoxin in vitro. Keywords = pulmonary inflammantion Keywords = acute lung injury Keywords = acute respiratory distress syndrome Keywords: parallel sample
Project description:Pulmonary surfactant (PS) produced by alveolar type II (ATII) cells is necessary in maintaining normal lung function, and a decrease or change in composition of PS is the main cause of alveolar collapse in acute respiratory distress syndrome (ARDS). But the mechanism of decrease or com-position change of PS is still unknown.
Project description:Sepsis is a complex syndrome associated with physiological, pathological, and biochemical abnormalities resulting from infection. Sepsis is the major cause of acute respiratory distress syndrome (ARDS). Extracellular vesicles (EVs) are serving as new messengers to mediate cell-cell communication in vivo. The function of EVs in sepsis patients are not well defined. We found sepsis EV encapsulating G6PD induced pro-inflammatory effects in the lung tissue by reprogramming purine metabolism. Most notably, guanine accumulation led to EZH2-mediated H3K27Me3 level. Finally Our study provides a novel mechanism of how EV reviried puring metabolism in lung tissue and leading to acute lung damage.
2024-04-30 | GSE230648 | GEO
Project description:Familial fatal acute respiratory distress syndrome in Dalmatians
Project description:Acute respiratory distress syndrome (ARDS) remains a common and devastating syndrome. CircRNAs are crucial in a variety of diseases and can provide new potential diagnostic and therapeutic targets for disease. The development of circular RNA (circRNA) microarray has facilitated the study of the role of circRNAs in regulating gene expression. This research was designed to explore the expression profile of circRNAs in lung tissues from rats with lipopolysaccharide-induced ARDS. Our findings indicate that the expression profiles of circRNAs has changed in ARDS as compared with normal rat lung tissue, and may provide novel insight into the molecular mechanism underlying the disease and potential novel diagnostic or therapeutic targets for ARDS.
Project description:We saw a patient who presented with respiratory distress from birth due to interstitial lung disease. Before the age of three months a diagnosis of nephrotic syndrome was made. Lung biopsy revealed pulmonary interstitial glycogenosis. Despite extensive investigations, no known genetic or infectious cause was found for the congenital nephrotic syndrome. The patient died at the age of 8 months due to respiratory failure. A 20 Mb homozygous region was identified on chromosome 17 in the patient’s DNA, revealing a novel homozygous missense variant in ITGA3 gene.
