Dietary Lipid Intervention in the Prevention of Brain Aging

As people live longer,the burden of aging-related brain diseases,especially dementia,is increasing.Brain aging increases the risk of cognitive impairment,which manifests as a progressive loss of neuron function caused by the impairment of synaptic plasticity via disrupting lipid homeostasis.Therefore,supplemental dietary lipids have the potential to prevent brain aging.This review summarizes the important roles of dietary lipids in brain function from both structure and mechanism perspectives.Epidemiological and animal studies have provided evidence of the functions of polyunsaturated fatty acids(PUFAs)in brain health.The results of interventions indicate that phospholipids—including phosphatidylcholine,phosphatidylserine,and plasmalogen—are efficient in alleviating cognitive impairment during aging,with plasmalogen exhibiting higher efficacy than phosphatidylserine.Plasmalogen is a recognized nutrient used in clinical trials due to its special vinyl ether bonds and abundance in the postsynaptic membrane of neurons.Future research should determine the dose-dependent effects of plasmalogen in alleviating brain-aging diseases and should develop extraction and storage procedures for its clinical application.

Experiment and simulation on degradation and burnout mechanisms of SiC MOSFET under heavy ion irradiation

Experiments and simulation studies on 283 MeV I ion induced single event effects of silicon carbide(SiC) metal–oxide–semiconductor field-effect transistors(MOSFETs) were carried out. When the cumulative irradiation fluence of the SiC MOSFET reached 5×10^(6)ion·cm^(-2), the drain–gate channel current increased under 200 V drain voltage, the drain–gate channel current and the drain–source channel current increased under 350 V drain voltage. The device occurred single event burnout under 800 V drain voltage, resulting in a complete loss of breakdown voltage. Combined with emission microscope, scanning electron microscope and focused ion beam analysis, the device with increased drain–gate channel current and drain–source channel current was found to have drain–gate channel current leakage point and local source metal melt, and the device with single event burnout was found to have local melting of its gate, source, epitaxial layer and substrate. Combining with Monte Carlo simulation and TCAD electrothermal simulation, it was found that the initial area of single event burnout might occur at the source–gate corner or the substrate–epitaxial interface, electric field and current density both affected the lattice temperature peak. The excessive lattice temperature during the irradiation process appeared at the local source contact, which led to the drain–source channel damage. And the excessive electric field appeared in the gate oxide layer, resulting in drain–gate channel damage.

Association of branched-chain amino acid intake trajectory in adulthood with the risk of type 2 diabetes and its related risk factors

To the Editor:Type 2 diabetes(T2D)showed increasing prevalence worldwide and put a huge burden on healthcare systems.[1]Branched-chain amino acids(BCAAs,including Leucine,Isoleucine,and Valine),a prominent group of essential amino acids,are important nutrition signals that have important effects on protein synthesis,glucose homeostasis,and nutrient-sensitive signaling pathways.Plasma BCAA can predict the development of T2D,whereas the studies of dietary BCAA on T2D risk showed conflicting results.[2]Most of the researches about dietary BCAAs used a single or limited number of measurements,ignoring the dynamic changes of dietary BCAA levels throughout life and their relevance to the development of diabetes.A life-course approach using multiple dietary BCAA measurements over time may shed new light on dietary BCAA trajectories and their relation to T2D risk.Therefore,in the current study,we first use latent class mixed model(LCMM)to characterize BCAA intake trajectories over 18 years in longitudinal data from China and investigate the association of BCAA intake trajectories with the risk of T2D and its biomarkers after adjusting for potential confounding factors.