Global food systems are broken and in need of profound change. These imbalances and vulnerabilities are particularly strong in cities, where most of the global population lives and that are at the core of the major challenges linked with food production and consumption. The food system transition needs cities as key game-changers towards more sustainable, equitable, healthier and fairer food systems.
View Article and Find Full Text PDFInt J Environ Res Public Health
January 2020
In light of the challenges that all cities face today, food is offered as a prism through which to read and intervene on various areas that affect the quality of life of the population: circular economy, urban metabolism, social relations, economies, and food quality. In the Roman context, in recent years, numerous initiatives have revitalized the debate on food and brought the discussion to the center of the interest of an ever-increasing number of citizens. However, these experiences appear unrelated and there is a lack of coordination and political coherence.
View Article and Find Full Text PDFAims: Abnormal Ca2+ release from the sarcoplasmic reticulum (SR), associated with Ca2+-calmodulin kinase II (CaMKII)-dependent phosphorylation of RyR2 at Ser2814, has consistently been linked to arrhythmogenesis and ischaemia/reperfusion (I/R)-induced cell death. In contrast, the role played by SR Ca2+ uptake under these stress conditions remains controversial. We tested the hypothesis that an increase in SR Ca2+ uptake is able to attenuate reperfusion arrhythmias and cardiac injury elicited by increased RyR2-Ser2814 phosphorylation.
View Article and Find Full Text PDFKey Points: Mice with Ca(2+) -calmodulin-dependent protein kinase (CaMKII) constitutive pseudo-phosphorylation of the ryanodine receptor RyR2 at Ser2814 (S2814D(+/+) mice) exhibit a higher open probability of RyR2, higher sarcoplasmic reticulum (SR) Ca(2+) leak in diastole and increased propensity to arrhythmias under stress conditions. We generated phospholamban (PLN)-deficient S2814D(+/+) knock-in mice by crossing two colonies, S2814D(+/+) and PLNKO mice, to test the hypothesis that PLN ablation can prevent the propensity to arrhythmias of S2814D(+/+) mice. PLN ablation partially rescues the altered intracellular Ca(2+) dynamics of S2814D(+/+) hearts and myocytes, but enhances SR Ca(2+) sparks and leak on confocal microscopy.
View Article and Find Full Text PDFAbnormal intracellular Ca(2+) cycling plays a key role in cardiac dysfunction, particularly during the setting of ischemia/reperfusion (I/R). During ischemia, there is an increase in cytosolic and sarcoplasmic reticulum (SR) Ca(2+). At the onset of reperfusion, there is a transient and abrupt increase in cytosolic Ca(2++), which occurs timely associated with reperfusion arrhythmias.
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