• Energy Research
• 3. Good health close
• NL close

Data from the Netherlands Cohort Study on Diet and Cancer were used to investigate the association between anthropometry, energy intake, and physical activity and risk of renal cell carcinoma (RCC). The Netherlands Cohort Study on Diet and Cancer consists of 120,852 men and women aged 55-69 years who completed a self-administered questionnaire at baseline (1986). A case-cohort approach was used. After 9.3 years of follow-up, 275 microscopically confirmed incident cases were available for analysis. Incidence rate ratios for RCC were estimated using Cox proportional hazards models. Height was associated with RCC risk only in women (per 5-cm increment, rate ratio (RR) = 1.23, 95% confidence interval (CI): 1.03, 1.46). Body mass index (weight (kg)/height (m)(2)) was associated with increased risk of RCC (per 1-kg/m(2 )increment, RR = 1.07, 95% CI: 1.02, 1.12) for men and women, as was gain in body mass index from age 20 years to baseline (per 1-kg/m(2 )increment, RR = 1.06, 95% CI: 1.01, 1.10). Energy intake was not related to RCC risk, while a possible protective effect was observed for physical activity in men. These results suggest that body mass index and gain in body mass index since age 20 are associated with increased risk of RCC.

AbstractExtra strain effects have been observed to occur as a result of cathodic polarization during the creep of Ni wires in electrolyte solutions.

Objective: Injured drivers with blood alcohol concentration (BAC) above the legal limit are rarely convicted of impaired driving. One explanation is that police may have difficulty recognizing alcohol intoxication in injured drivers. In this study we compare police documentation of alcohol involvement with BAC measured on arrival in hospital. Our objectives are to determine how often police document alcohol involvement in injured drivers with BAC > 0.05%, and identify factors that influence police documentation of alcohol involvement. Methods: We included injured drivers (1999 – 2003) who were admitted to a British Columbia (BC) trauma centre or treated in the Vancouver General Hospital emergency department. We used probabilistic linkage to obtain police collision reports. Police were considered to indicate alcohol involvement if i) police documented that alcohol contributed to the crash, ii) the driver received an administrative sanction for impaired driving, or iii) the driver was criminally convicted of impaired driving. The proportions of drivers for whom police indicated alcohol involvement was determined relative to age, gender, BAC levels, crash severity and crash characteristics. Multivariate logistic regression was used to identify factors independently associated with police indication of alcohol involvement. Results: 2410 injured drivers (73.5% male) were matched to a police report. Overall, 857 (35.6%) drivers tested positive for alcohol (BAC > 0) and 736/857 (85.9%) of alcohol positive drivers had a BAC > 0.05% (the BC legal limit). Of the 736 drivers with BAC > 0.05% at time of admission, police indicated alcohol involvement in 530 (72.0%). The criminal code conviction rate for impaired driving was 4.7% for drivers with 0.08% ≤ BAC < 0.16%, and 13.6% for drivers with BAC > 0.16%. The following factors were associated with higher odds of police indicating alcohol involvement: i) increasing blood alcohol levels, ii) a prior record of impaired driving, iii) involvement in a single vehicle crash, iv) involvement in a night time crash, and v) traffic violations or unsafe driving actions recorded by police. Conclusions: Police recognized and documented alcohol involvement in 72% of injured drivers with BAC ≥ 0.05%. Police documentation of alcohol involvement is more common at higher BAC levels, in night time or single vehicle crashes, for drivers who committed traffic violations or drove unsafely, and for drivers with a prior record of impaired driving. The low conviction rate of injured impaired drivers does not appear to be due to police inability to recognize alcohol involvement.

Intoxicating concentrations of ethanol inhibit N-methyl-d-aspartate (NMDA) receptor-dependent long-term potentiation, an interaction thought to underlie a major component of the central nervous system actions of ethanol. Another form of synaptic potentiation involving activation of L-type dihydropyridine-sensitive voltage-gated calcium channels (VGCCs) has been described, but very little information concerning ethanol effects on VGCC-dependent synaptic potentiation is available. Here, we assessed ethanol effects on VGCC-dependent synaptic potentiation using whole cell patch-clamp recordings of alpha-amino-3-hydroxy-5-methyl-4-soxazolepropionic acid (AMPA) receptor-mediated miniature excitatory postsynaptic currents (mEPSCs) in area CA1 of the rat hippocampus. No potentiation was observed in artificial cerebrospinal fluid containing 2 to 3 mM Ca2+, but marked potentiation of mEPSCs was consistently observed in 4 mM Ca2+ and with patch pipettes containing an ATP-regenerating system. This potentiation was insensitive to the NMDA receptor antagonist DL-2-amino-5-phosphonovaleric acid, whereas it was completely blocked the L-type VGCC antagonist nifedipine. Potentiation was also blocked dose dependently by bath application of ethanol (25-75 mM), which had no effect on baseline mEPSC amplitude or frequency. The synaptic potentiation involved enhancement of both presynaptic and postsynaptic components because significant increases in both the frequency and amplitude of AMPA mEPSCs were observed. Ethanol inhibition of VGCC-dependent synaptic potentiation seemed to occur at the induction step because both the increases in mEPSC frequency and amplitude were affected. To address that question more directly, we used fluorescent imaging of synaptically evoked dendritic calcium events, which displayed a similarly marked ethanol sensitivity. Thus, ethanol modulates fast excitatory synaptic transmission by inhibiting the induction of an NMDA receptor-independent form of synaptic potentiation observed at excitatory synapses on central neurons.

High ethanol intake is well known to induce both anxiolytic and anxiogenic effects, in correlation with chromatin remodeling in the amygdaloid brain region and deficits in cell proliferation and survival in the hippocampus of rodents. Whether only moderate but chronic ethanol intake in C57BL/6J mice could also have an impact on chromatin remodeling and neuroplasticity was addressed here. Chronic ethanol consumption in a free choice paradigm was found to induce marked changes in the expression of genes implicated in neural development and histone post-translational modifications in the mouse hippocampus. Transcripts encoding neural bHLH activators and those from Bdnf exons II, III and VI were upregulated, whereas those from Bdnf exon VIII and Hdacs were downregulated by ethanol compared with water consumption. These ethanol-induced changes were associated with enrichment in both acetylated H3 at Bdnf promoter PVI and trimethylated H3 at PII and PIII. Conversely, acetylated H3 at PIII and PVIII and trimethylated H3 at PVIII were decreased in ethanol-exposed mice. In parallel, hippocampal brain-derived neurotrophic factor (BDNF) levels and TrkB-mediated neurogenesis in the dentate gyrus were significantly enhanced by ethanol consumption. These results suggest that, in C57BL/6J mice, chronic and moderate ethanol intake produces marked epigenetic changes underlying BDNF overexpression and downstream hippocampal neurogenesis.

We report on the use of the chemostat as an optimal device to create time-invariant conditions that allow accurate sampling for various omics assays in Escherichia coli, in combination with recording of the dynamics of the physiological transition in the organism under study that accompany the initiation of glucose repression. E. coli cells respond to the addition of glucose not only with the well-known transcriptional response, as was revealed through quantitative PCR analysis of the transcript levels of key genes from the CRP (cAMP receptor protein) regulon, but also with an increased growth rate and a transient decrease in the efficiency of its aerobic catabolism. Less than half of a doubling time is required for the organism to recover to maximal values of growth rate and efficiency. Furthermore, calculations based on our results show that the specific glucose uptake rate (qs ) and the H+/e− ratio increase proportionally, up to a growth rate of 0.4 h–1, whilst biomass yield on glucose (Yx / s ) drops during the first 15 min, followed by a gradual recovery. Surprisingly, the growth yields after the recovery phase show values even higher than the maximum theoretical yield. Possible explanations for these high yields are discussed.

Climate change, rapid urbanization, war, and economic recession are key drivers of the current food systems’ disruption, which has been exacerbated by the COVID pandemic. Local, regional, and global food systems are unable to provide consumers with nutritious and affordable diets. Suboptimal diets exacerbate the triple burden of malnutrition, with micronutrient deficiencies affecting more than two billion people, two billion people suffering from overweight, and more than 140 million children who are stunted. The unaffordability of nutritious diets represents an obstacle for many, especially in low- and middle-income countries where healthy diets are five times more expensive than starchy staple diets. Food system transformations are urgently required to provide consumers with more affordable and nutritious diets that are capable of meeting social and environmental challenges. In this review, we underline the critical role of innovation within the food system transformation discourse. We aim to define principles for implementing evidence-based and long-term food system innovations that are economically, socially, and environmentally sustainable and, above all, aimed at improving diets and public health. We begin by defining and describing the role of innovation in the transformation of food systems and uncover the major barriers to implementing these innovations. Lastly, we explore case studies that demonstrate successful innovations for healthier diets.