Search

Objective The aim of this study was to quantitatively evaluate the relationship between short echo time pulmonary 1 H magnetic resonance imaging (MRI) signal intensity (SI) and 3 He MRI apparent diffusion coefficients (ADC), high-resolution computed tomography (CT) measurements of emphysema, and pulmonary function measurements. Materials and methods Nine healthy never-smokers and 11 COPD subjects underwent same-day plethysmography, spirometry, short echo time ((TE) = 1.2 ms) 1 H and diffusion-weighted hyperpolarized 3 He MRI ( b = 1.6 s/cm 2 ) at 3.0 T. In addition, for COPD subjects only, CT densitometry was also performed. Results Mean 1 H SI was significantly greater for never-smokers (12.1 ± 1.1 arbitrary units (AU)) compared to COPD subjects (10.9 ± 1.3 AU, p = 0.04). The 1 H SI AP-gradient was also significantly greater for never-smokers (0.40 AU/cm, R 2 = 0.94) compared to COPD subjects (0.29 AU/cm, R 2 = 0.968, p = 0.05). There was a significant correlation between 1 H SI and 3 He ADC ( r = −0.58, p = 0.008) and significant correlations between 1 H MR SI and CT measurements of emphysema (RA 950 , r = −0.69, p = 0.02 and HU 15 , r = 0.66, p = 0.03). Conclusions The significant and moderately strong relationship between 1 H SI and 3 He ADC, as well as between 1 H SI and CT measurements of emphysema suggests that these imaging methods and measurements may be quantifying similar tissue changes in COPD and that pulmonary 1 H SI may be used to monitor emphysema as a complement to CT and noble gas MRI.

Biodiesel fuels, made from renewable resources, have emerged as viable alternatives to conventional diesel fuel, but their impact on emissions is not fully understood. This study examines elemental carbon (EC), organic carbon (OC), and polycyclic aromatic hydrocarbons (PAHs) emissions from cottonseed oil biodiesel (CSO-B100). Relative to normal diesel fuel, CSO-B100 reduced EC emissions by 64% (±16%). The bulk of EC emitted from CSO-B100 was in the fine particle mode (

CCL3 is a C-C family chemokine detected at high levels in the synovial tissue and fluids of rheumatoid arthritis (RA) patients. CCL3 binds to the chemokine receptors CCR1 and CCR5, which are expressed by inflammatory leukocytes such as macrophages and T cells present in the affected joints of RA patients. The present study was undertaken to investigate whether absence of CCL3 prevented development of inflammation and joint destruction in anti-type II collagen monoclonal antibody (anti-CII mAb)-induced arthritis. "CCL3 null mice were different from wild-type control mice in terms of body weight loss". In addition, CCL3 null mice exhibited milder clinical and histopathological scores following administration of anti-CII mAb and endotoxin. Moreover, the release of TNF in response to systemic administration of endotoxin was not affected in CCL3 null mice compared to wild-type mice, indicating that the phenotype was not attributable to a defect in endotoxin response. These results indicate that CCL3 plays an essential role in the development of inflammation and joint destruction induced by anti-CII mAb.