Publications by authors named "P J Castaldi"
Background: Chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrosis (IPF) are debilitating diseases associated with divergent histopathological changes in the lungs. At present, due to cost and technical limitations, profiling cell types is not practical in large epidemiology cohorts (n > 1000). Here, we used computational deconvolution to identify cell types in COPD and IPF lungs whose abundances and cell type-specific gene expression are associated with disease diagnosis and severity.
View Article and Find Full Text PDFThe role of compost and biochar in the recovery of As and Sb-polluted soils is poorly investigated, as well as the influence of their application rates on soil health and quality. In this study, we therefore investigated the effectiveness over time (2, 4, and 6 months, M) of a municipal solid waste compost (MSWC) and a biochar (BC), applied at 10 and 30% rates, and of selected mixtures (MIX; applied at 10 and 30% total rates, 1:1 ratio of MSWC and BC), on labile As and Sb in a polluted soil from an abandoned Sb mine (Djebel Hamimat, Algeria). At the same timepoints, the amendment impact on soil chemistry was also monitored, while the activity and diversity of the resident microbial communities were investigated at 6 M.
View Article and Find Full Text PDFArticle Synopsis
- Fibrosis contributes to serious damage in organs, but treatments targeting specific activators have often failed, leading researchers to focus on the leukemia inhibitory factor receptor (LIFR) as a key player in fibrotic diseases like idiopathic pulmonary fibrosis (IPF).
- In IPF, myofibroblasts highly express LIF, and fibroblasts in key fibrotic areas coexpress LIF and LIFR, demonstrating LIFR's role in amplifying signals from other fibrotic drivers like TGFβ1, IL-4, and IL-13.
- Blocking LIFR reduces the activation of profibrotic genes and highlights LIFR's function as a master amplifier of harmful signals
Background: The clinical and pathological features of asthma and chronic obstructive pulmonary disease (COPD) can converge in smokers and elderly individuals as asthma-COPD overlap (ACO). This overlap challenges the diagnosis and treatment of the distinct aetiologies underlying these conditions.
Methods: We analysed 2453 smokers (≥10 pack-years), aged 45-80 years, from the Genetic Epidemiology of COPD (COPDGene) Study, stratified as Control, Asthma, COPD, and ACO based on Global Initiative for Chronic Obstructive Lung Disease (GOLD) criteria.
Background: Genetic variants and gene expression predict risk of chronic obstructive pulmonary disease (COPD), but their effect on COPD heterogeneity is unclear. We aimed to define high-risk COPD subtypes using genetics (polygenic risk score, PRS) and blood gene expression (transcriptional risk score, TRS) and assess differences in clinical and molecular characteristics.
Methods: We defined high-risk groups based on PRS and TRS quantiles by maximising differences in protein biomarkers in a COPDGene training set and identified these groups in COPDGene and ECLIPSE test sets.