Geographic and socioeconomic diversity of food and nutrient intakes: a comparison of four European countries.

PURPOSE: Public health policies and actions increasingly acknowledge the climate burden of food consumption. The aim of this study is to describe dietary intakes across four European countries, as baseline for further research towards healthier and environmentally-friendlier diets for Europe. METHODS: Individual-level dietary intake data in adults were obtained from nationally-representative surveys from Denmark and France using a 7-day diet record, Italy using a 3-day diet record, and Czech Republic using two replicates of a 24-h recall. Energy-standardised food and nutrient intakes were calculated for each subject from the mean of two randomly selected days. RESULTS: There was clear geographical variability, with a between-country range for mean fruit intake from 118 to 199 g/day, for vegetables from 95 to 239 g/day, for fish from 12 to 45 g/day, for dairy from 129 to 302 g/day, for sweet beverages from 48 to 224 ml/day, and for alcohol from 8 to 15 g/day, with higher intakes in Italy for fruit, vegetables and fish, and in Denmark for dairy, sweet beverages and alcohol. In all countries, intakes were low for legumes (< 20 g/day), and nuts and seeds (< 5 g/day), but high for red and processed meat (> 80 g/day). Within countries, food intakes also varied by socio-economic factors such as age, gender, and educational level, but less pronounced by anthropometric factors such as overweight status. For nutrients, intakes were low for dietary fibre (15.8-19.4 g/day) and vitamin D (2.4-3.0 µg/day) in all countries, for potassium (2288-2938 mg/day) and magnesium (268-285 mg/day) except in Denmark, for vitamin E in Denmark (6.7 mg/day), and for folate in Czech Republic (212 µg/day). CONCLUSIONS: There is considerable variation in food and nutrient intakes across Europe, not only between, but also within countries. Individual-level dietary data provide insight into the heterogeneity of dietary habits beyond per capita food supply data, and this is crucial to balancing healthy and environmentally-friendly diets for European citizens.

Modeling the behavior of Listeria monocytogenes during enrichment in half Fraser broth; impact of pooling and the duration of enrichment on the detection of L. monocytogenes in food.

A stochastic model describing the growth of Listeria monocytogenes during enrichment in half Fraser was developed for the purpose of estimating the effects of modifications to the first enrichment step of the EN ISO 11290-1 detection method. Information pertaining to the variability of growth rates, physiological state of the cell, and the behavior of individual cells contaminating the food were obtained from previously published studies. We used this model to investigate the impact of pooling enrichment broths (wet pooling) on the performance of the standard method. For validation of the model, the numbers of L. monocytogenes occurring in 88 naturally contaminated foods following pre-enrichment were compared to model-simulated microbial counts. The model was then used to perform simulations representative of the natural contamination observed for smoked salmon in the European baseline survey of 2010-2011. The model-estimated L. monocytogenes levels following individual enrichment or following the pooling of five broths where only one would be contaminated were compared. The model indicated a 10% loss of method sensitivity resulting from wet pooling. The model also predicted a 5% decrease in the sensitivity of the method when the duration of the enrichment was reduced from 24 to 22 h.

Evaluation of reduction of Fraser incubation by 24h in the EN ISO 11290-1 standard on detection and diversity of Listeria species.

The EN ISO 11290-1 method for the isolation of Listeria monocytogenes from food is carried out using a double enrichment in Fraser broths. While the method is effective it is also quite long requiring 4-7 days to process a contaminated food, and may be adversely affected by inter-strain and/or inter-species competition in samples containing mixed Listeria populations. Currently, we have little information on the impact of competition on food testing under routine conditions. Food samples (n=130) were analyzed using the standard method and the evolution of Listeria populations in 89 naturally contaminated samples followed over the entire enrichment process. In most instances, maximum increase in L. monocytogenes population occurred over the first 24h following sub-culture in Full Fraser broth and strain recovery was similar at both 24 and 48 h, indicating that the second enrichment step can be reduced by 24h without impacting the recovery of L. monocytogenes or affecting the sensitivity of the method. In approximately 6% of naturally contaminated samples the presence of competing Listeria species adversely impacted L. monocytogenes population levels. Moreover, these effects were more pronounced during the latter 24h of the Fraser enrichment, and potentially could affect or complicate the isolation of these strains.

Systemic inflammation perturbs developmental retinal angiogenesis and neuroretinal function.

PURPOSE: Perinatal inflammatory stress in preterm babies is associated with increased rates of severe retinopathy of prematurity (ROP) and adverse neurological dysfunction. In this study, we set out to determine the consequences of severe systemic inflammatory stress on developmental retinal vascularization and evaluate the subsequent outcome on retinal function in later life. METHODS: Systemic inflammatory stress was induced in C57BL/6J mouse pups by an intraperitoneal injection of lipopolysaccharide (LPS; 1 mg/kg) at postnatal day 4. In response to LPS, retinal inflammation was confirmed by quantitative RT-PCR analysis of diverse inflammatory markers. A detailed and systematic analysis of retinal microglial infiltration, retinal vascular morphology, density, and growth rate was performed at key time points throughout retinal vascularization. Retinal function in adult life was assessed by using electroretinography at 6 weeks postinjection. RESULTS: As early as 48 hours after intraperitoneal administration of LPS, a significant increase in retinal vascular density was noted throughout the retina. A pronounced increase in the number of activated microglial cell was observed in the retinal ganglion cell layer and in the outer plexiform layer just prior to their vascularization; direct physical contact between activated microglia and sprouting vessels suggested that microglia partake in promoting the aberrant retinal vascularization. With maturity, animals subjected to perinatal inflammatory stress displayed depleted retinal vascular beds and had significantly decreased retinal function as determined by electroretinography. CONCLUSIONS: Our data reveal that early severe postnatal inflammatory stress leads to abnormal retinal vascular development and increased vessel anastomosis and, ultimately, permanently compromises retinal function. The aberrant and initially exaggerated retinal vascularization observed is associated with microglial activation, providing a cellular mechanism by which perinatal sepsis predisposes to ROP.

Neuronal ER stress impedes myeloid-cell-induced vascular regeneration through IRE1α degradation of netrin-1.

In stroke and proliferative retinopathy, despite hypoxia driven angiogenesis, delayed revascularization of ischemic tissue aggravates the loss of neuronal function. What hinders vascular regrowth in the ischemic central nervous system remains largely unknown. Using the ischemic retina as a model of neurovascular interaction in the CNS, we provide evidence that the failure of reparative angiogenesis is temporally and spatially associated with endoplasmic reticulum (ER) stress. The canonical ER stress pathways of protein kinase RNA-like ER kinase (PERK) and inositol-requiring enzyme-1α (IRE1α) are activated within hypoxic/ischemic retinal ganglion neurons, initiating a cascade that results in angiostatic signals. Our findings demonstrate that the endoribonuclease IRE1α degrades the classical guidance cue netrin-1. This neuron-derived cue triggers a critical reparative-angiogenic switch in neural macrophage/microglial cells. Degradation of netrin-1, by persistent neuronal ER stress, thereby hinders vascular regeneration. These data identify a neuronal-immune mechanism that directly regulates reparative angiogenesis.

Semaphorin 3F forms an anti-angiogenic barrier in outer retina.

Semaphorins are known modulators of axonal sprouting and angiogenesis. In the retina, we identified a distinct and almost exclusive expression of Semaphorin 3F in the outer layers. Interestingly, these outer retinal layers are physiologically avascular. Using functional in vitro models, we report potent anti-angiogenic effects of Semaphorin 3F on both retinal and choroidal vessels. In addition, human retinal pigment epithelium isolates from patients with pathologic neovascularization of the outer retina displayed reduced Semaphorin 3F expression in 10 out of 15 patients. Combined, these results elucidate a functional role for Semaphorin 3F in the outer retina where it acts as a vasorepulsive cue to maintain physiologic avascularity.

Deficiency in the metabolite receptor SUCNR1 (GPR91) leads to outer retinal lesions.

Age-related macular degeneration (AMD) is a prominent cause of blindness in the Western world. To date, its molecular pathogenesis as well as the sequence of events leading to retinal degeneration remain largely ill-defined. While the invasion of choroidal neovessels in the retina is the primary mechanism that precipitates loss of sight, an earlier dry form precedes it. Here we provide the first evidence for the protective role of the Retinal Pigment Epithelium (RPE)-resident metabolite receptor, succinate receptor 1 (SUCNR1; G-Protein coupled Receptor-91 (GPR91), in preventing dry AMD-like lesions of the outer retina. Genetic analysis of 925 patients with geographic atrophy and 1199 AMD-free peers revealed an increased risk of developing geographic atrophy associated with intronic variants in theSUCNR1 gene. In mice, outer retinal expression of SUCNR1 is observed in the RPE as well as microglial cells and decreases progressively with age. Accordingly, Sucnr1-/- mice show signs of premature sub-retinal dystrophy with accumulation of oxidized-LDL, abnormal thickening of Bruch's membrane and a buildup of subretinal microglia. The accumulation of microglia in Sucnr1-deficient mice is likely triggered by the inefficient clearance of oxidized lipids by the RPE as bone marrow transfer of wild-type microglia into Sucnr1-/- mice did not salvage the patho-phenotype and systemic lipolysis was equivalent between wild-type and control mice. Our findings suggest that deficiency in SUCNR1 is a possible contributing factor to the pathogenesis of dry AMD and thus broaden our understanding of this clinically unmet need.