Objective: Asthma is a common childhood disease with strong genetic components. This study compared whole-genome expression differences between asthmatic young children and healthy controls to identify gene signatures of childhood asthma.
Methods: Total RNA extracted from peripheral blood mononuclear cells (PBMC) was subjected to microarray analysis. QRT-PCR was performed to verify the microarray results. Classification and functional characterization of differential genes were illustrated by hierarchical clustering and gene ontology analysis. Multiple logistic regression (MLR) analysis, receiver operating characteristic (ROC) curve analysis, and discriminate power were used to scan asthma-specific diagnostic markers.
Results: For fold-change>2 and p < 0.05, there were 758 named differential genes. The results of QRT-PCR confirmed successfully the array data. Hierarchical clustering divided 29 highly possible genes into seven categories and the genes in the same cluster were likely to possess similar expression patterns or functions. Gene ontology analysis presented that differential genes primarily enriched in immune response, response to stress or stimulus, and regulation of apoptosis in biological process. MLR and ROC curve analysis revealed that the combination of ADAM33, Smad7, and LIGHT possessed excellent discriminating power.
Conclusions: The combination of ADAM33, Smad7, and LIGHT would be a reliable and useful childhood asthma model for prediction and diagnosis.
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http://dx.doi.org/10.3109/02770903.2014.971967 | DOI Listing |
Background: In the brain as in other organs, complement contributes to immune defence and housekeeping to maintain homeostasis. Sources of complement may include local production by brain cells and influx from the periphery, the latter severely restricted by the blood brain barrier (BBB) in healthy brain. Dysregulation of complement leads to excessive inflammation, direct damage to self-cells and propagation of injury.
View Article and Find Full Text PDFBackground: Evidence suggests glucagon-like peptide 1 receptor agonists (GLP-1RAs) may have therapeutic potential in Alzheimer's disease (AD). Cumulative evidence has indicated a potential reduction in cognitive decline in people with AD, while real-world evidence has shown decreased dementia risk in patients with type 2 diabetes. Non-clinical data reveal that GLP-1RAs impact neuroinflammation and other biological processes believed to be involved in AD pathophysiology, including effects on central and peripheral immune cells.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of Kansas Alzheimer's Disease Research Center, Fairway, KS, USA.
Background: Aerobic exercise may positively affect brain health, although relationships with cognitive change are mixed. This likely is due to individual differences in the systemic physiological response to exercise. However, the acute effects of exercise on brain metabolism and biomarker responses are not well characterized in older adults or cognitively impaired individuals.
View Article and Find Full Text PDFBackground: Prescription for inappropriate drugs can be dangerous to very old people, due to the increased risk of adverse drug reactions.
Case Report: We report the consequences of inappropriate prescriptions in a 99-year-old woman. She had a clinical history of vascular dementia, diabetes, hypothyroidism, heart failure, osteoarthritis, chronic renal failure, and hypoacusia, and was admitted to our attention for asthenia and loss of appetite.
Curr Pharm Des
January 2025
Department of Translational Medicine and for Romagna, University of Ferrara, Via Luigi Borsari 46, 44121, Ferrara, Italy.
Amyloid beta (Aβ) dyshomeostasis is considered the main biological aberration in Alzheimer's Disease (AD) pathology. The interplay between Aβ formation and clearance is predominantly modulated by a disintegrin and a metalloproteinase 10 (ADAM10, α-secretase) and β-site APP Cleaving Enzyme 1 (BACE1), the two pivotal enzymes in both non-amyloidogenic/amyloidogenic and amyloidolytic pathways. Emerging evidence suggests that aberrations in ADAM10 and BACE1 expression, activity, and function in the brain of AD patients also manifest in peripheral fluids, suggesting their potential as blood-based biomarkers for AD diagnosis.
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