RESUMO
A novel antiferroelectric material, PbSnO3 (PSO), was introduced into a resistive random access memory (RRAM) to reveal its resistive switching (RS) properties. It exhibits outstanding electrical performance with a large memory window (>104), narrow switching voltage distribution (±2 V), and low power consumption. Using high-resolution transmission electron microscopy, we observed the antiferroelectric properties and remanent polarization of the PSO thin films. The in-plane shear strains in the monoclinic PSO layer are attributed to oxygen octahedral tilts, resulting in misfit dislocations and grain boundaries at the PSO/SRO interface. Furthermore, the incoherent grain boundaries between the orthorhombic and monoclinic phases are assumed to be the primary paths of Ag+ filaments. Therefore, the RS behavior is primarily dominated by antiferroelectric polarization and defect mechanisms for the PSO structures. The RS behavior of antiferroelectric heterostructures controlled by switching spontaneous polarization and strain, defects, and surface chemistry reactions can facilitate the development of new antiferroelectric device systems.
RESUMO
BACKGROUND: The functions of free radicals on the effects of insulin that result in protection against cerebral ischemic insult in diabetes remain undefined. This present study aims to explain the contradiction among nitric oxide (NO)/superoxide/peroxynitrite of insulin in amelioration of focal cerebral ischemia-reperfusion (FC I/R) injury in streptozotocin (STZ)-diabetic rats and to delineate the underlying mechanisms. Long-Evans male rats were divided into three groups (age-matched controls, diabetic, and diabetic treated with insulin) with or without being subjected to FC I/R injury. RESULTS: Hyperglycemia exacerbated microvascular functions, increased cerebral NO production, and aggravated FC I/R-induced cerebral infarction and neurological deficits. Parallel with hypoglycemic effects, insulin improved microvascular functions and attenuated FC I/R injury in STZ-diabetic rats. Diabetes decreased the efficacy of NO and superoxide production, but NO and superoxide easily formed peroxynitrite in diabetic rats after FC I/R injury. Insulin treatment significantly rescued the phenomenon. CONCLUSIONS: These results suggest that insulin renders diabetic rats resistant to acute ischemic stroke by arresting NO reaction with superoxide to form peroxynitrite.
Assuntos
Isquemia Encefálica/prevenção & controle , Diabetes Mellitus Experimental/tratamento farmacológico , Hipoglicemiantes/farmacologia , Insulina/farmacologia , Óxido Nítrico/metabolismo , Ácido Peroxinitroso/metabolismo , Acidente Vascular Cerebral/prevenção & controle , Superóxidos/metabolismo , Doença Aguda , Animais , Isquemia Encefálica/induzido quimicamente , Isquemia Encefálica/metabolismo , Isquemia Encefálica/patologia , Diabetes Mellitus Experimental/metabolismo , Diabetes Mellitus Experimental/patologia , Masculino , Ratos , Ratos Long-Evans , Acidente Vascular Cerebral/induzido quimicamente , Acidente Vascular Cerebral/metabolismoRESUMO
BACKGROUND: This study aimed to investigate the differential protective effect of resveratrol (RSV) on oxidative stress and metabolic signaling pathways in fast- and slow-twitch skeletal muscles of rats with diabetes. METHODS: Diabetic rats were induced by streptozotocin (STZ) for 2 weeks and then administered with RSV (1, 10 and 100 µg/kg per day) for 1 week. We determined oxidative stress and protein expression by lucigenin-mediated chemiluminescence and Western immunoblot. RESULTS: The superoxide anion production and copper-zinc superoxide dismutase (CuZnSOD) protein level were increased in fast-twitch muscle than in slow-twitch muscle of diabetes. The Akt and glycogen synthase kinase 3 (GSK-3) phosphorylations were reduced in both fast- and slow-twitch muscles of diabetes. Oxidative stress and GSK-3 dephosphorylation were corrected by RSV treatment in both fast- and slow-twitch muscles of diabetes. Furthermore, RSV treatment downregulated CuZnSOD protein level in diabetic fast-twitch muscle. In diabetic slow-twitch muscle, RSV treatment elevated manganese SOD (MnSOD) and phosphorylated Akt protein levels and reduced acetyl-CoA carboxylase (ACC) phosphorylation. CONCLUSIONS: Our results suggested that fast-twitch muscle incurred more oxidative stress, whereas slow-twitch muscle altered metabolic signaling molecules activities under diabetic status. The antidiabetic effect of RSV on fast- and slow-twitch skeletal muscles was mediated by different antioxidative and metabolic signals.