Overall, median (25th, 75th percentile) serum 25-hydroxyvitamin D concentrations were 19.9 (14.7, 26.7) ng/mL. Serum 25(OH)D was positively associated with FEV1 (p = .03), FVC (p = .18), and
FEV1/FVC (p = .04) in multivariable linear regression models adjusting Stattic clinical trial for age, race, education, smoking, height, physical activity, cognition, interleukin-6, chronic diseases, and other potential confounders. In the same models, serum parathyroid hormone was not significantly associated with FEV1, FVC, or FEV1/FVC.
These findings support the idea that vitamin D deficiency is independently associated with poor pulmonary function in older disabled women.”
“A hallmark of Alzheimer’s disease (AD) is the aggressive appearance of plaques of amyloid beta (A beta) peptides, which result from the sequential cleavage of amyloid precursor protein (APP) by the beta- and gamma-secretases. A beta production Selleck SHP099 is evaded by alternate cleavage of APP by the alpha- and gamma-secretases. Carnosic acid (CA) has been proven to activate the transcription factor Nrf2, a main regulator of the antioxidant response. We investigated the effects of CA on the production of A beta 1-42 peptide (A beta 42) and on the expressions of the related
genes in SH-SY5Y human neuroblastoma cells. The treatment of cells with CA suppressed A beta 42 secretion (61% suppression at 30 mu M). CA treatment enhanced the mRNA expressions of an alpha-secretase TACE (tumor necrosis factor-alpha-converting enzyme, also called a disintegrin and metalloproteinase-17, ADAM17) significantly and another alpha-secretase ADAM10 marginally; however, the beta-secretase BACE1 (beta-site APP-cleaving enzyme-1) was not increased by CA.
Knockdown of TACE by siRNA reduced soluble-APP alpha secretion enhanced by CA and partially recovered the CA-suppressed A beta 42 secretion. PIK-5 These results suggest that CA reduces A beta 42 production by activating TACE without promoting BACE1 in human neuroblastoma cells. The use of CA may have a potential in the prevention of A beta-mediated diseases, particularly AD. (C) 2012 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved.”
“Lifestyle and nutritional factors have been recognized to influence breast cancer survival, irrespective of genomic alterations that are the hallmarks of the disease. The biological and molecular mechanisms involved in the effects of dietary polyunsaturated fatty acids and breast cancer response to treatments in clinical and preclinical studies have been reviewed.