Publications by authors named "Beth A Whalen"

Exploration of cytokine levels in systemic sclerosis-associated interstitial lung disease (SSc-ILD) and idiopathic pulmonary fibrosis (IPF) is needed to find common and diverse biomolecular pathways. Circulating levels of 87 cytokines were compared amongst 19 healthy controls and consecutive patients with SSc-ILD (n = 39), SSc without ILD (n = 29), and IPF (n = 17) recruited from a Canadian centre using a log-linear model adjusted for age, sex, baseline forced vital capacity (FVC), and immunosuppressive or anti-fibrotic treatment at time of sampling. Also examined was annualized change in FVC.

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Background: People with human immunodeficiency virus (PWH) have an increased risk of developing chronic obstructive pulmonary disease (COPD).

Methods: We phenotyped lung macrophages in 4 subgroups-M1 (CD40+CD163-), M2 (CD40-CD163+), double positives (CD40+CD163+), and double negatives and (CD40-CD163-)-and we determined their phagocytic capacity in PWH with and without COPD.

Results: People with human immunodeficiency virus with COPD have more double-negative macrophages (84.

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The classical M1/M2 polarity of macrophages may not be applicable to inflammatory lung diseases including chronic obstructive pulmonary disease (COPD) due to the complex microenvironment in lungs and the plasticity of macrophages. We examined macrophage sub-phenotypes in bronchoalveolar lavage (BAL) fluid in 25 participants with CD40 (a M1 marker) and CD163 (a M2 marker). Of these, we performed RNA-sequencing on each subtype in 10 patients using the Illumina NextSeq 500.

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Lung macrophages are the key immune effector cells in the pathogenesis of Chronic Obstructive Pulmonary Disease (COPD). Several studies have shown an increase in their numbers in bronchoalveolar lavage fluid (BAL) of subjects with COPD compared to controls, suggesting a pathogenic role in disease initiation and progression. Although reduced lung macrophage phagocytic ability has been previously shown in COPD, the relationship between lung macrophages' phenotypic characteristics and functional properties in COPD is still unclear.

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Background: Markers of plaque destabilization and disruption may have a role in identifying non-STE- type 1 Myocardial Infarction in patients presenting with troponin elevation. We hypothesized that a plaque disruption index (PDI) derived from multiple biomarkers and measured within 24 hours from the first detectable troponin in patients with acute non-STE- type 1 MI (NSTEMI-A) will confirm the diagnosis and identify these patients with higher specificity when compared to individual markers and coronary angiography.

Methods: We examined 4 biomarkers of plaque destabilization and disruption: myeloperoxidase (MPO), high-sensitivity interleukin-6, myeloid-related protein 8/14 (MRP8/14) and pregnancy-associated plasma protein-A (PAPP-A) in 83 consecutive patients in 4 groups: stable non-obstructive coronary artery disease (CAD), stable obstructive CAD, NSTEMI-A (enrolled within 24 hours of troponin positivity), and NSTEMI-L (Late presentation NSTEMI, enrolled beyond the 24 hour limit).

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Background/aims: The ideal hemoglobin target in chronic kidney disease remains unknown. Ultimately, individualized targets may depend upon the properties of the patient's endothelial and vascular milieu, and thus the complex relationships between these factors need to be further explored.

Methods: Forty-six patients with a glomerular filtration rate (GFR) <30 ml/min/1.

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Inflammation accelerates polymorphonuclear leukocyte (PMN) release from the bone marrow, and these PMNs are implicated in inappropriate tissue injury. We have previously developed a method using 5'-bromo-2'-deoxyuridine (BrdU) to study PMN kinetics using an immunocytochemical grading system of PMN on cytospin slides. The aim of this study was to develop a flow cytometric method to quantify the number of positively stained PMN and grade the intensity of staining for the transit time calculation of PMN through the marrow.

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