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Purpose: To assess the cross-sectional association between dietary indexes (DI) that underlie, respectively, the Nutri-score (NS), the proposed Canadian 'High In' Symbol (CHIL) and the Diabetes Canada Clinical Practice Guidelines (DCCP) with food consumption, nutrient intakes and metabolic markers. Methods: 1836 adults (18–74 years) participating in the representative ESTEBAN study, conducted in mainland France in 2014–2016, were included in the analysis. Food consumption was assessed with three repeated 24 h dietary recalls. Anthropometric measurements and biomarkers of metabolic risk (cholesterol—total, LDL (Low Density Lipoprotein), HDL (High Density Lipoprotein)—triglycerides, glucose) were obtained through a clinical examination and fasting blood draw. The DI were assessed for their association with food consumption, dietary intakes and metabolic biomarkers as quintiles and continuous variables using multi-adjusted linear regression. Heathier diets were assigned to lower scores. Results: Correlations between scores ranged from + 0.62 between CHIL-DI and NS-DI to + 0.75 between NS-DI and DCCP-DI. All DIs discriminated individuals according to the nutritional quality of their diets through food consumption and nutrient intakes (healthier diets were associated with lower intakes of energy, added sugars and saturated fat; and with higher intakes of fiber, vitamins and minerals). NS-DI was associated with blood glucose (adjusted mean in Q1 = 5 vs. Q5 = 5.46 mmol/dl, ptrend = 0.001) and DCCP-DI was associated with BMI (Q1 = 24.8 kg/m2 vs. Q5 = 25.8 kg/m2, ptrend = 0.025), while CHIL showed no significant association with any anthropometric measures or biomarkers. Conclusions: This study provides elements supporting the validity of the nutrient profiling systems underlying front-of-package nutrition labellings (FOPLs) to characterize the healthiness of diets. [ABSTRACT FROM AUTHOR]

Olfactomedin 1 (OLFM1) is a secreted glycoprotein and member of the olfactomedin protein family, which is preferentially expressed in various areas throughout the central nervous system. To learn about the functional properties of OLFM1 in the eye, we investigated its localization in the mouse and pig eye. In addition, we analyzed the ocular phenotype of Olfm1 mutant mice in which 52 amino acids were deleted in the central part (M2 region) of OLFM1. OLFM1 was detected in cornea, sclera, retina, and optic nerve of both wild-type and Olfm1 mutant littermates. By immunohistochemistry and double labeling with the lectin peanut agglutinin, OLFM1 was found in the interphotoreceptor matrix (IPM) of mouse and pig retina where it was directly localized to the inner segments of photoreceptors. Western blotting confirmed the presence of the OLFM1 isoforms pancortin 1 (BMY) and pancortin 2 (BMZ) in the IPM. The retinal phenotype of Olfm1 mutant mice did not obviously differ from that of wild-type littermates. In addition, outer nuclear layer (ONL) and total retinal thickness were not different, and the same was true for the area of the optic nerve in cross sections. Functional changes were observed though by electroretinography, which showed significantly lower a- and b-wave amplitudes in Olfm1 mutant mice when compared to age-matched wild-type mice. When light damage experiments were performed as an experimental paradigm of photoreceptor apoptosis, significantly more TUNEL-positive cells were observed in Olfm1 mutant mice 30 h after light exposure. One week after light exposure, the ONL was significantly thinner in Olfm1 mutant mice than in wild-type littermates indicating increased photoreceptor loss. No differences were observed when rhodopsin turnover or ERK1/2 signaling was investigated. We conclude that OLFM1 is a newly identified IPM molecule that serves an important role for photoreceptor homeostasis, which is significantly compromised in the eyes of Olfm1 mutant mice. [ABSTRACT FROM AUTHOR]

Background: Gastroesophageal reflux disease (GERD) affects two thirds of the American population. Obesity is also a disease that affects two thirds of the population. The pathophysiology of reflux disease is reasonably understood, however, the degree to which obesity affects this disease remains poorly defined. Therefore the approach to GERD in the obese patient requires special attention and its own algorithm.Methods: A literature search was conducted to consolidate the current available literature on GERD and its management in the obese. In addition, the authors reviewed the literature and present expert opinion on controversial topics.Results: It is well established that GERD is increased in obesity and the pathophysiology is reviewed. Management options for GERD are discussed, with a focus on the obese population. Management strategies including fundoplication and gastric bypass are discussed. In addition, bariatric surgery in the setting of GERD is also reviewed.Conclusions: Currently this is an extremely controversial topic and this white paper presents a strong review of the literature to help guide the management of this challenging disease in this population. Expert recommendations are given throughout the paper based upon the current available data. [ABSTRACT FROM AUTHOR]