Severity: Warning
Message: file_get_contents(https://...@gmail.com&api_key=61f08fa0b96a73de8c900d749fcb997acc09&a=1): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
Filename: helpers/my_audit_helper.php
Line Number: 197
Backtrace:
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 197
Function: file_get_contents
File: /var/www/html/application/helpers/my_audit_helper.php
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Function: simplexml_load_file_from_url
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 3165
Function: getPubMedXML
File: /var/www/html/application/controllers/Detail.php
Line: 597
Function: pubMedSearch_Global
File: /var/www/html/application/controllers/Detail.php
Line: 511
Function: pubMedGetRelatedKeyword
File: /var/www/html/index.php
Line: 317
Function: require_once
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Background: Airborne fine particulate matter (PM) is associated with chronic obstructive pulmonary disease (COPD); however, the precise mechanism remains unclear. Here, we examined distinct gene and pathway characteristics across varying personal and ambient PM exposure durations within a prospective COPD cohort and the associations between differentially expressed genes (DEGs) and clinical phenotypes.
Methods: Blood samples for RNA-sequencing were collected from 50 patients with COPD who underwent spirometry and quantitative computed tomography. We estimated personal and ambient PM exposure levels using hybrid and land use regression models. Associations between DEGs and PM exposure were examined in relation to lung function indicators (FEV, FVC, and FEV/FVC ratio) using Pearson correlation analysis adjusted for factors such as hospitalization, age, sex, season, Charlson Comorbidity Index score, and smoking status.
Results: We analyzed DEGs across three cumulative PM exposure periods using personal and ambient exposure assessments. Gene ontology annotation and biological pathway analysis of the identified DEGs using the individual air pollution exposure prediction model revealed significant associations with gas transport, cellular processes related to cell cycle, cell proliferations, and neuron projection morphogenesis. The ambient air pollution prediction model revealed significant biological responses related to purine metabolism and antigen processing and presentation. EDAR, NKILA, HSD11B2, LOC100130027, LOC105378367, SENCR, CAMP, CEACAM6, CHIT1, EREG, HSD17B3, NPPA-AS1, and TRPV4 showed increased expression with higher PM, correlating with reduced lung function.
Conclusions: Our findings offer insights into the role of gene expression in patients with COPD in response to personal and ambient PM exposure, suggesting strategies to enhance respiratory conditions linked to air pollution.
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http://dx.doi.org/10.1016/j.envres.2025.122377 | DOI Listing |