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Perception-based and objective food access measures are often examined as factors influencing individuals' shopping decisions and dietary habits, but the relative influence of these two factors on behaviors needs further examination. This study sought to (a) determine if perception-based and objective measures of fruit and vegetable (F&V) access were related and (b) examine perception-based and objective access measures as predictors of F&V consumption. Participants were recruited as part of a larger intervention study from 12 sites across three urban North Carolina counties. Perception-based food access measured included self-reported perceptions of convenience, variety, and quality of F&V within a neighborhood. Food outlet density was used as the objective measure. This was derived by summing the total number of geocoded convenience stores, grocery stores, supermarkets, and supercenters located within 1 road network mile of participants' home address. Associations between perception-based and objective measures were examined using Pearson's correlations, and associations of F&V access and intake were examined using linear regression models. Pearson correlations between perception-based and objective measures revealed that F&V variety was associated with supermarkets. Regression results show that perception-based barriers to F&V access were not significantly associated with intake, but supercenter density within 1 mile was significantly associated with decreased F&V intake. Common measures of perception-based and objective measures of food access may not be the best predictor of F&V intake. Understanding the relationships of these factors for lower-income populations can offer guidance for future policies and programs.

Coronavirus Disease 2019 (COVID‐19) is responsible for a worldwide pandemic, with a high rate of morbidity and mortality. The increasing evidence of an associated relevant prothrombotic coagulopathy has resulted in an increasing use of antithrombotic doses higher than usual in COVID‐19 patients. Information on the benefit/risk ratio of this approach is still lacking.

We previously reported that Herpes simplex virus type‐1 (HSV‐1) infection of cultured neurons triggered intracellular accumulation of amyloid‐β protein (Aβ) markedly impinging on neuronal functions. Here, we demonstrated that HSV‐1 affects in vitro and in vivo adult hippocampal neurogenesis by reducing neural stem/progenitor cell (NSC) proliferation and their neuronal differentiation via intracellular Aβ accumulation. Specifically, cultured NSCs were more permissive for HSV‐1 replication than mature neurons and, once infected, they exhibited reduced proliferation (assessed by 5′‐bromo‐deoxyuridine incorporation, Ki67 immunoreactivity, and Sox2 mRNA expression) and impaired neuronal differentiation in favor of glial phenotype (evaluated by immunoreactivity for the neuronal marker MAP2, the glial marker glial fibrillary astrocyte protein, and the expression of the proneuronal genes Mash1and NeuroD1). Similarly, impaired adult neurogenesis was observed in the subgranular zone of hippocampal dentate gyrus of an in vivo model of recurrent HSV‐1 infections, that we recently set up and characterized, with respect to mock‐infected mice. The effects of HSV‐1 on neurogenesis did not depend on cell death and were due to Aβ accumulation in infected NSCs. Indeed, they were: (a) reverted, in vitro, by the presence of either β/γ‐secretase inhibitors preventing Aβ production or the specific 4G8 antibody counteracting the action of intracellular Aβ; (b) not detectable, in vivo, in HSV‐1‐infected amyloid precursor protein knockout mice, unable to produce and accumulate Aβ. Given the critical role played by adult neurogenesis in hippocampal‐dependent memory and learning, our results suggest that multiple virus reactivations in the brain may contribute to Alzheimer's disease phenotype by also targeting NSCs. Stem Cells2019;37:1467–1480 Herpes simplex virus type‐1 infection of adult hippocampal neural stem cells triggers cleavage of amyloid precursor protein with consequent intracellular accumulation of amyloid‐β protein. Following infection, neural stem cells exhibit reduced proliferation and impaired neuronal differentiation in favor of glial phenotype with respect to mock‐infected neural stem cells.

Low-income communities often lack access to supermarkets and healthy foods. Enhanced stocking requirements for staple foods for Supplemental Nutrition Assistance Program (SNAP)-authorized retailers may increase availability of healthy foods in smaller stores which are prevalent in low-income areas. This study aimed to evaluate the extent that small food stores located in low-income areas met the U.S. Department of Agriculture's 2016 final rule on SNAP-authorized retailer stocking requirements, which increased the minimum number of required staple food varieties from three to seven for each staple food category, required a depth of stock of three units of each variety, and increased the required number of categories with perishables from two to three. A multisite research project was conducted in 2017. Nine research teams located in seven U.S. states audited the availability of perishable and nonperishable staple foods and beverages in 351 small food stores in low-income areas. Analyses determined the extent to which stores met all or part of the stocking requirements and tested differences by store type. 30.2% of stores met all of the 2016 final rule requirements; 86.3% met the requirements for fruits and vegetables, whereas only 30.5% met requirements for dairy. 53.1% of non-chain small grocery stores met all requirements compared to 17.1% of convenience stores (p < .0001). Less than one half of the food stores audited met the U.S. Department of Agriculture's 2016 final rule that would expand SNAP-authorized retailer stocking requirements suggesting that, if implemented, the rule may generate increased offerings of staple foods in small stores in low-income areas.

A lack of access to fresh fruits and vegetables (F&Vs) is associated with consumption of fewer F&Vs and higher risk of obesity, especially for lower-income individuals. It is widely believed that the addition of new food retail opportunities could improve F&V consumption and subsequently reduce the chronic disease burden. Observational studies provide some support for these hypotheses, but contradictions exist. In this study we sought to examine if the introduction of a food retailer affects F&V consumption in lower-income communities. We used a systematic PRISMA approach to conduct this study. We searched PubMed, EMBASE, and ProQuest Dissertations & Theses for academic journal references and gray literature published before August 2018. Included studies were those looking at the effect of the introduction of a new food retailer on F&V consumption. Studies were also categorized based on which dimensions of food access were targeted by the food retailer. We identified 15 studies meeting inclusion criteria: 11 studies reported a positive increase in F&V consumption attributable to the introduction of a new food retailer, of which 6 were statistically significant. The remaining 4 studies, all of which examined the impact of introducing a new retail supermarket, showed no change or a decrease in F&V intake. Results from studies which change the food environment generally support the idea that increased access to healthy food improves diet, but more studies are needed in order to assess the differences between the various types of retailers, and to identify strategies for improving impact. Understanding which types of new food retail programs are most likely to impact diet has implications for policies which incentivize new food retail.

Adult neurogenesis plays increasingly recognized roles in brain homeostasis and repair and is profoundly affected by energy balance and nutrients. We found that the expression of Hes-1(hairy and enhancer of split 1) is modulated in neural stem and progenitor cells (NSCs) by extracellular glucose through the coordinated action of CREB (cyclic AMP responsive element binding protein) and Sirt-1 (Sirtuin 1), two cellular nutrient sensors. Excess glucose reduced CREB-activated Hes-1expression and results in impaired cell proliferation. CREB-deficient NSCs expanded poorly in vitro and did not respond to glucose availability. Elevated glucose also promoted Sirt-1-dependent repression of the Hes-1promoter. Conversely, in low glucose, CREB replaced Sirt-1 on the chromatin associated with the Hes-1promoter enhancing Hes-1 expression and cell proliferation. Thus, the glucose-regulated antagonism between CREB and Sirt-1 for Hes-1 transcription participates in the metabolic regulation of neurogenesis.

We have previously shown that intraganglionic synapse disassembly consequent on superior cervical ganglion (SCG) neuron axotomy was preceded by the loss of the dystroglycan β subunit (β-DG) localized at the postsynaptic specializations. Because DG, a transmembrane molecular complex bridging the extracellular matrix to the cortical cytoskeleton, could be a physiological target of metalloproteinases (MMPs) 2 and 9, we investigated their possible involvement in the injury-induced intraganglionic synapse disassembly. In rat SCG, only MMP-2 was present and localized in both neurons and nonneuronal cells. After ganglion neuron axotomy, both MMP-2 activity and protein level increased, whereas the level of its mRNA was unchanged, suggesting prominent MMP-2 posttranslational regulation. mRNA and protein levels of the enzymes involved in the MMP-2 activation pathway, the membrane-type 1-MMP (MT1-MMP), and the tissue inhibitor of metalloproteinase-2 (TIMP-2) also increased after injury with a time course that correlated with that of MMP-2 activation. In addition, postganglionic nerve crush induced an increase in the β-DG 30-kDa fragment produced by the MMP-dependent degradation of DG. These data suggest that MMP-2 activated during SCG neuron reaction to axotomy may degrade postsynaptic DG, contributing to the disruption of the molecular bridge between pre- and postsynaptic elements and disassembly of the intraganglionic synapses.