The experimental results show good agreement with the theoretical predictions and indicate the potential value of this material property for electromechanical device fabrication. (c) 2015 AIP HIF-1 pathway Publishing LLC.”
“PURPOSE To compare the choroidal thickness of children’s eyes with amblyopia due to strabismus or anisometropia to the fellow eye and age-matched controls. METHODS Forty patients with anisometropic amblyopia, 40 patients with strabismic
amblyopia, and 40 age-matched controls were included in this cross-sectional study. Choroidal thickness was measured via the enhanced-depth imaging technique of spectral domain optical coherence tomography in all patients and controls. Choroidal thickness was measured at subfoveal area and at 500 mu m intervals to the nasal and temporal to the fovea up to 2000 mu m. Measurements
were compared between the three groups. RESULTS The mean ages were 7.9 +/- 2.6 years (range, 4-13 years) in the anisometropic group, 9.0 +/- 3.7 (range 4-15 years) years in the strabismic group, and 8.4 +/- 2.6 years (range 4-15 years) in the control group. The mean subfoveal choroidal thickness in the anisometropic group was 362 +/- 82 mu m in the amblyopic eyes and 301 +/- 54 mu m in the fellow eyes; in the strabismic group, 413 +/- 82 mu m in the amblyopic eyes and 316 +/- 54 mu m in the fellow eyes. The mean subfoveal choroidal thickness was 310 +/- 78 mu m in control eyes. The subfoveal choroids of both anisometropic and strabismic amblyopic eyes were significantly thicker selleck compound than that of the fellow eyes of the corresponding groups and the control eyes (P smaller than 0.05 for all). CONCLUSIONS The subfoveal choroid of eyes with anisometropic and strabismic amblyopia is significantly thicker than that of the fellow eye and the age-matched controls.”
“Promoter CpG methylation of tumour suppressor genes (TSGs) is an epigenetic biomarker for TSG identification and molecular
diagnosis. We screened genome wide for novel methylated genes through methylation subtraction of a genetic demethylation model of colon cancer (double knockout of DNMT1 and DNMT3B in HCT116) and identified DLEC1 (Deleted in lung https://www.selleckchem.com/products/i-bet-762.html and oesophageal cancer 1), a major 3p22.3 TSG, as one of the methylated targets. We further found that DLEC1 was downregulated or silenced in most colorectal and gastric cell lines due to promoter methylation, whereas broadly expressed in normal tissues including colon and stomach, and unmethylated in expressing cell lines and immortalised normal colon epithelial cells. DLEC1 expression was reactivated through pharmacologic or genetic demethylation, indicating a DNMT1/DNMT3B-mediated methylation silencing. Aberrant methylation was further detected in primary colorectal (10 out of 34, 29%) and gastric tumours (30 out of 89, 34%), but seldom in paired normal colon (0 out of 17) and gastric (1 out of 20, 5%) samples. No correlation between DLEC1 methylation and clinical parameters of gastric cancers was found.