Creating healthy food environments through global benchmarking of government nutrition policies and food industry practices

Unhealthy processed food products are increasingly dominating over healthy foods, making food and nutrition environments unhealthier. Development and implementation of strong government healthy food policies is currently being circumvented in many countries by powerful food industry lobbying. In order to increase accountability of both governments and the private sector for their actions, and improve the healthiness of food environments, INFORMAS (the International Network for Food and Obesity/non-communicable diseases (NCDs) Research, Monitoring and Action Support) has recently been founded to systematically and comprehensively monitor food environments and policies in countries of varying size and income. This will enable INFORMAS to rank both governments and private sector companies globally according to their actions on food environments. Identification of those countries which have the healthiest food and nutrition policies and using them as international benchmarks against which national progress towards best practice can be assessed, should support reductions in global obesity and diet-related NCDs.     

Towards a physiological signal-based access solution for a non-verbal adolescent with severe and multiple disabilities

Objective: To find physiologically arousing stimuli and labile physiological channels in a non-verbal adolescent with severe and multiple congenital disabilities, who did not have a reliable means of communication.

Methods: The client was repeatedly presented with visual and audiovisual stimuli, representing variations of six contextual factors over three sessions in a one month period. For each stimulus, reactions were detected in the client’s four peripheral autonomic nervous system signals using a rule-based classification algorithm.

Results: During the presentation of audiovisual stimuli, the number of physiological reactions significantly differed from that observed in baseline (χ²?=?3.93, p?=?0.0476). Aural stimuli articulated in an unfamiliar voice, and aural stimuli containing anticipatory patterns were also physiologically arousing. Fingertip temperature was the client’s most labile physiological signal.

Conclusions: The results of this case study suggest that physiological data may complement caregiver acumen in deciphering the reactions of non-verbal clients with severe and multiple disabilities.     

Neuroprotective effect of carnosine in the olfactory bulb after vanadium inhalation in a mouse model

Carnosine (β‐alanyl‐L‐histidine) is synthesized in the olfactory system, has antioxidant activity as a scavenger of free radicals and has been reported to have neuroprotective action in diseases which have been attributed to oxidative damage. In neurodegenerative disorders, such as Parkinson's and Alzheimer's diseases, impairment of olfactory function has been described. Vanadium derivatives are environmental pollutants, and its toxicity has been associated with oxidative stress. Vanadium toxicity on the olfactory bulb was reported previously. This study investigates the neuroprotective effect of carnosine on the olfactory bulb in a mice model of vanadium inhalation. Male mice were divided into four groups: vanadium pentoxide (V₂O₅) [0.02 mol/L] inhalation for one hour twice a week; V₂O₅ inhalation plus 1 mg/kg of carnosine administered daily; carnosine only, and the control group that inhaled saline. The olfactory function was evaluated using the odorant test. Animals were sacrificed four weeks after exposure. The olfactory bulbs were dissected and processed using the rapid Golgi method; cytological and ultrastructural analysis was performed and malondialdehyde (MDA) concentrations were measured. The results showed evidence of olfactory dysfunction caused by vanadium exposure and also an increase in MDA levels, loss of dendritic spines and necrotic neuronal death in the granule cells. But, in contrast, vanadium‐exposed mice treated with carnosine showed an increase in dendritic spines and a decrease in neuronal death and in MDA levels when compared with the group exposed to vanadium without carnosine. These results suggest that dendritic spine loss and ultrastructural alterations in the granule cells induced by vanadium are mediated by oxidative stress and that carnosine may modulate the neurotoxic vanadium action, improving the olfactory function.