Here, we report a method for tracking the progression of A beta accumulation in vivo using bioluminescence imaging (BLI) on two lines of Tg mice, which express luciferase (luc) under control of the Gfap promoter as well as mutant human amyloid precursor protein.
Bigenic mice exhibited an age-dependent increase in BLI signals that correlated with the deposition of A beta in the brain. Bioluminescence signals began to increase in 7-mo-old Tg(CRND8: Gfap-luc) mice and 14-mo-old Tg(APP23: Gfap-luc) mice. When Tg(APP23: Gfap-luc) mice were inoculated with brain homogenates from aged Tg(APP23) mice, BLI detected the accelerated disease onset and induced Etomoxir A beta deposition at 11 mo of age. Because of its rapid, noninvasive, and quantitative format,
BLI permits the objective repeated analysis of individual mice at multiple time points, which is likely to facilitate the testing of A beta-directed therapeutics.”
“AIM: To investigate screening makers for gastric cancer, we assessed the association between gastric cancer and serum pepsinogens (PGs).\n\nMETHODS: The subjects comprised 450 patients with gastric cancer, 111 individuals with gastric atrophy, and 961 healthy controls. Serum anti-Helicobacter pylori (H. pylon) GW4869 manufacturer immunoglobulin G (IgG), PG I and PG II were detected by enzyme-linked immunosorbent assay. Gastric atrophy and gastric cancer were diagnosed by endoscopy and histopathological examinations. Odds ratios and 95%CIs were calculated using multivariate logistic regression.\n\nRESULTS: Rates of H. pylori infection remained high in Northeastern
China. Rates of H. pylori IgG positivity were greater in the gastric cancer and gastric atrophy groups compared to the control group (69.1% and 75.7% vs 49.7%, P < 0.001). Higher this website levels of PG II (15.9 mu g/L and 13.9 mu g/L vs 11.5 mu g/L, P < 0.001) and lower PG I / PG II ratio (5.4 and 4.6 vs 8.4, P < 0.001) were found in patients with gastric cancer or gastric atrophy compared to healthy controls, whereas no correlation was found between the plasma PG I concentration and risk of gastric cancer (P = 0.537). In addition, multivariate logistic analysis indicated that H. pylori infection and atrophic gastritis were independent risk factors for gastric cancer. Lower plasma PG I /PG H ratio was associated with higher risks of atrophy and gastric cancer. Furthermore, plasma PG II level significantly correlated with H. pylori-infected gastric cancer.\n\nCONCLUSION: Serum PG II concentration and PG I /PG 11 ratio are potential biomarkers for H. pylori-infected gastric disease. PG 11 is independently associated with risk of gastric cancer. (C) 2012 Baishideng. All rights reserved.