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Low individual socioeconomic status (SES) is known to be associated with a higher risk of type 2 diabetes mellitus (T2DM), but the extent to which the local context in which people live may influence T2DM rates remains unclear. This study examines whether living in a low property value neighbourhood is associated with higher rates of T2DM independently of individual SES. Research design and methodsUsing cross-sectional data from the Maastricht Study (2010-2013) and geographical data from Statistics Netherlands, multilevel logistic regression was used to assess the association between neighbourhood property value and T2DM. Individual SES was based on education, occupation and income. Of the 2,056 participants (aged 40-75 years), 494 (24%) were diagnosed with T2DM. ResultsIndividual SES was strongly associated with T2DM, but a significant proportion of the variance in T2DM was found at the neighbourhood level (VPC = 9.2%; 95% CI = 5.0%-16%). Participants living in the poorest neighbourhoods had a 2.38 times higher odds ratio of T2DM compared to those living in the richest areas (95% CI = 1.58-3.58), independently of individual SES.

The aim of our study was to investigate the changes of various biochemical parameters (concentrations of lactate, free arachidonate, cyclo- and lipoxygenase products) in rat brain after ischemia and reperfusion and the effects of pretreatment with the ganglioside derivative GM1-lactone on the same parameters. Ischemia was induced by reversible occlusion of common carotid arteries for 20 min, which included a final 5 min of respiration of 5% oxygen in nitrogen. Reperfusion was obtained by removing the occlusion. Pre-ischemic conditions were obtained on sham-operated animals. Animals were killed by microwave irradiation of their heads. Brain levels of lactate and of free arachidonate were markedly increased after ischemia and returned to normal values at 5 min of reperfusion. Levels of the cyclooxygenase metabolites prostaglandin F2 alpha, 6-keto-prostaglandin F1 alpha, and thromboxane B2 were increased after ischemia, whereas levels of the lipoxygenase metabolite leukotriene C4 (LTC4) did not change. After reperfusion, a very marked increase of the cyclooxygenase products occurred but not of LTC4. Treatment with GM1-lactone prevented the elevation of cyclo- and lipoxygenase metabolites especially during reperfusion, with limited effects on lactate and free arachidonate levels.