Additionally, ex vivo studies of human brain slices from an independent sample of patients who had AD were performed.\n\nSetting: Three university medical centers.\n\nPatients: Patients with mild-to-moderate AD.\n\nIntervention: Two 3 consecutive cohorts of patients received 2 to 7 infusions of intravenous gantenerumab (60 or 200 mg) or placebo every 4 weeks. Brain slices from patients who had AD were coincubated with gantenerumab at increasing concentrations and with human microglial cells.\n\nMain Outcome Measures: Percent change in the ratio of regional carbon 11-labeled Pittsburgh Compound B retention in vivo and semiquantitative assessment of gantenerumab-induced

phagocytosis ex vivo.\n\nResults: Sixteen patients with end-of-treatment positron emission tomographic scans were included in the analysis. Fer-1 The mean (95% CI) percent change from baseline difference relative to placebo (n=4) in cortical brain amyloid level was -15.6% (95% CI, -42.7 to 11.6) for the 60-mg group (n=6) and -35.7% (95% CI, -63.5 to -7.9) for the 200-mg group (n=6). Two patients in the 200-mg group showed transient and focal areas of inflammation or vasogenic edema on magnetic resonance imaging scans at sites with the highest level of amyloid reduction. Gantenerumab induced phagocytosis of human amyloid in a dose-dependent manner ex vivo.\n\nConclusion: Gantenerumab treatment resulted in a dose-dependent reduction in brain

amyloid level, possibly through an effector cell-mediated mechanism of action.”
“Many patients have been characterized harboring a mutation in thyroid hormone receptor (TR) beta. Surprisingly this website none has yet been identified carrying a mutation in TR alpha 1. To facilitate the identification of such patients,

several animal models with a mutant TR alpha 1 have been generated. While some phenotypic characteristics, such as an adult euthyroidism, are similar in the mutant mice, other aspects such as metabolism are quite variable. This review summarizes the most important consequences of a mutation in TR alpha 1 in mice focusing on the TR alpha 1-R384C mutation, and projects the selleck chemicals insights from the animal models to a putative phenotype of patients with a mutated TR alpha 1.”
“Background: We performed a meta-analysis to evaluate the value of (18)FDG PET-CT for the detection of gastric cancer recurrence after surgical resection.\n\nMethods: A systematic literature search was performed in the MEDLINE and EMBASE databases. We calculated the sensitivity, specificity, positive likelihood ratio, and negative likelihood ratio for (18)FDG PET-CT. We also constructed summary receiver operating characteristic curves for (18)FDG PET-CT.\n\nResults: Eight studies (500 patients) were included. The sensitivity, specificity, positive likelihood ratio and negative likelihood ratio of (18)FDG PET-CT were 0.86 (95% confidence interval [CI] = 0.71-0.94), 0.88 (95% CI = 0.75-0.94), 17.0 (95% CI = 3.5-14.0), and 0.16 (95% CI = 0.07-0.34), respectively.