QUANTitative Chest Computed Tomography UnMasking Emphysema Progression in Alpha-1 Antitrypsin Deficiency - RLDC 5701
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA189543 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:QUANTitative Chest Computed Tomography UnMasking Emphysema Progression in Alpha-1 Antitrypsin Deficiency - RLDC 5701
| PRJNA189544 | ENA
Project description:Gene expression profiling of lung tissue from undiseased (NML), 'usual' emphysema (EML), and Alpha-1 Antitrypsin Deficiency-related emphysema (ADL). Keywords = Emphysema Keywords = COPD Keywords = Alpha-1 Antitrypsin Deficiency Keywords: ordered
2004-06-01 | GSE1122 | GEO
Project description:Introduction: Lung cancer screening by computed tomography (CT) reduces mortality but exhibited high false-positive rates. We established a diagnostic classifier combining chest CT features with bronchial genomics. Materials and Methods: Patients with CT-detected suspected lung cancer were enrolled. The sample collected by bronchial brushing was used for RNA sequencing. R software was applied to build the model. Results: A total of 283 patients, including 183 with lung cancer and 100 with benign lesions, were included. When incorporating genomic data with radiological characteristics, the advanced model yielded 0.903 AUC with 81.1% NPV. Moreover, the classifier performed well regardless of lesion size, location, stage, histologic type, or smoking status. Pathway analysis showed enhanced epithelial differentiation, tumor metastasis, and impaired immunity were predominant in smokers with cancer, whereas tumorigenesis played a central role in non-smokers with cancer. Apoptosis and oxidative stress contributed critically in metastatic lung cancer; by contrast, immune dysfunction was pivotal in locally advanced lung cancer. Conclusions: We devised a minimal-to-noninvasive, efficient diagnostic classifier for smokers and non-smokers with lung cancer, which provides evidence for different mechanisms of cancer development and metastasis associated with smoking. A negative classifier result will help the physician make conservative diagnostic decisions.
2021-02-18 | GSE166926 | GEO
Project description:In this study, we sought to thoroughly characterize the liver pathophysiology of a human transgenic mouse model for alpha-1 antitrypsin deficiency (AATD) with a strong manifestation of AATD-mediated liver disease. Male and female transgenic mice for normal variant human alpha-1 antitrypsin (Pi*M) and mutant human alpha-1 antitrypsin (Pi*Z) at 3 and 6 months of age with a C57BL/6J background were subjected to study. The progression of hepatic accumulation of mutant alpha-1 antitrypsin (ZAAT), hepatocyte injury, steatosis, liver inflammation and fibrotic features of this mouse model were monitored by performing an in vivo study.
2023-03-19 | GSE206619 | GEO
Project description:Whole genome mRNA and microRNA profiling of bronchoalveolar lavage (BAL) and peripheral blood mononuclear cell (PBMC) in Alpha-1 Antitrypsin Deficiency patients with PiZZ or PiMZ alpha-1 antitrypsin genotypes
2020-11-03 | GSE109515 | GEO
Project description:BackgroundHistopathological studies on lung specimens from patients with cystic fibrosis (CF) and recent results from a mouse model indicate that emphysema may contribute to CF lung disease. However, little is known about the relevance of emphysema in patients with CF. In the present study, we used computationally generated density masks based on multidetector computed tomography (MDCT) of the chest for non-invasive characterization and quantification of emphysema in CF.MethodsVolumetric MDCT scans were acquired in parallel to pulmonary function testing in 41 patients with CF (median age 20.1 years; range 7-66 years) and 21 non-CF controls (median age 30.4 years; range 4-68 years), and subjected to dedicated software. The lung was segmented, low attenuation volumes below a threshold of -950 Hounsfield units were assigned to emphysema volume (EV), and the emphysema index was computed (EI). Results were correlated with forced expiratory volume in 1 s percent predicted (FEV1%), residual volume (RV), and RV/total lung capacity (RV/TLC).ResultsWe show that EV was increased in CF (457±530 ml) compared to non-CF controls (78±90 ml) (P<0.01). EI was also increased in CF (7.7±7.5%) compared to the control group (1.2±1.4%) (P<0.05). EI correlated inversely with FEV1% (rs=-0.66), and directly with RV (rs=0.69) and RV/TLC (rs=0.47) in patients with CF (P<0.007), but not in non-CF controls. Emphysema in CF was detected from early adolescence (~13 years) and increased with age (rs=0.67, P<0.001).ConclusionsOur results indicate that early onset emphysema detected by densitometry on chest MDCT is a characteristic pathology that contributes to airflow limitation and may serve as a novel endpoint for monitoring lung disease in CF.
| S-EPMC3749290 | biostudies-literature
Project description:Gene expression profiling of lung tissue from undiseased (NML), 'usual' emphysema (EML), and Alpha-1 Antitrypsin Deficiency-related emphysema (ADL).
2007-07-19 | E-GEOD-1122 | biostudies-arrayexpress
Project description:Long term chest blast exposure can lead to mental disorders, brain inflammation and oxidative stress in soldiers. However, the underlying mechanism of brain injury caused indirectly by chest blast remains unclear. It is urgent to find additional reliable biomarkers to reveal the intimate details of the pathogenesis of this phenomenon. We used iTRAQ labeling combined with LC-MS/MS to screen potential differentially expressed proteins in rat brain after chest blast at different time points. Meanwhile, we also used GO, KEGG, David and Cytoscape to analyze the proteomic profile and explore its pathogenesis. Moreover, Western blotting was used to verify the target proteins. Our data showed that, a total of 6,931 proteins were identified. A total of 255 differentially expressed proteins were identified, of which 43, 84, 52, 97 and 49 proteins were identified from brain tissues at 12h, 24h, 48h, 72h, and 1w after chest blast exposure, respectively. Bioinformatics analysis, including GO, COG, KEGG and STRING, further proved that brain damage caused by chest blast exposure affects many important biological processes and signal pathways, such as inflammation, cell adhesion, phagocytosis, neuronal and synaptic damage, oxidative stress and apoptosis. Moreover, Western blotting further confirmed that these differentially expressed proteins and signaling pathways were associated with brain damage caused by chest blast exposure. For the first time, we screened and verified the potential protein biomarkers of brain damage caused indirectly by chest blast, and provided a new target for the treatment of this disease.
2022-02-17 | PXD026015 | Pride
Project description:Long term chest blast exposure can lead to mental disorders, brain inflammation and oxidative stress in soldiers. However, the underlying mechanism of brain injury caused indirectly by chest blast remains unclear. It is urgent to find more potential biomarkers to reveal the deeper pathogenesis of this phenomenon. We used iTRAQ labeling combined with LC-MS/MS to screen potential differentially expressed proteins in rat brain after chest blast at different time points. Meanwhile, we also used Go, KEGG, David and Cytoscape to analyze the proteomic profile and explore its pathogenesis. Moreover, Western blotting was used to verify the target proteins. Our data showed that, a total of 6,931 proteins were identified. A total of 255 differentially expressed proteins were identified, of which 43, 84, 52, 97 and 49 proteins were identified from brain tissues at 12h, 24h, 48h, 72h, and 1w after chest blast exposure. Bioinformatics analysis, including GO, COG, KEGG and STRING, further proved that brain damage caused by chest blast exposure was involved in many important biological processes and signal pathways, such as inflammation, cell adhesion, phagocytosis, neuronal and synaptic damage, oxidative stress and apoptosis. Moreover, Western blotting further confirmed that these differentially expressed proteins and signaling pathways were associated with brain damage caused by chest blast exposure. For the first time, we screened and verified the potential protein biomarkers of brain damage caused indirectly by chest blast, and provided a new target for the treatment of this disease.
2021-12-30 | PXD025204 | Pride
Project description:Alpha1-Antitrypsin Deficiency Registry (AADR-BioLINCC)
| PRJNA1296684 | ENA