ABSTRACT
Resistive random access memories (RRAMs) can be programmed to discrete resistive levels on demand via voltage pulses with appropriate amplitude and widths. This tuneability enables the design of various emerging concepts, to name a few: neuromorphic applications and reconfigurable circuits. Despite the wide interest in RRAM technologies there is still room for improvement and the key lies with understanding better the underpinning mechanism responsible for resistive switching. This work presents a methodology that aids such efforts, by revealing the nature of the resistive switching through assessing the transport properties in the non-switching operation regimes, before and after switching occurs. Variation in the transport properties obtained by analysing the current-voltage characteristics at distinct temperatures provides experimental evidence for understanding the nature of the responsible mechanism. This study is performed on prototyped device stacks that possess common Au bottom electrodes, identical TiO2 active layers while employing three different top electrodes, Au, Ni and Pt. Our results support in all cases an interface controlled transport due to Schottky emission and suggest that the acquired gradual switching originates by the bias induced modification of the interfacial barrier. Throughout this study, the top electrode material was found to play a role in determining the electroforming requirements and thus indirectly the devices' memristive characteristics whilst both the top and bottom metal/oxide interfaces are found to be modified as result of this process.
ABSTRACT
Inflammatory bowel disease (IBD) is a poorly understood chronic immune disorder for which there is no medical cure. Milk and colostrum are rich sources of bioactives with immunomodulatory properties. Here we compared the therapeutic effects of oral delivery of bovine milk-derived iron-saturated lactoferrin (Fe-bLF), angiogenin, osteopontin (OPN), colostrum whey protein, Modulen IBD (Nestle Healthsciences, Rhodes, Australia), and cis-9,trans-11 conjugated linoleic acid (CLA)-enriched milk fat in a mouse model of dextran sulfate-induced colitis. The CLA-enriched milk fat significantly increased mouse body weights after 24d of treatment, reduced epithelium damage, and downregulated the expression of proinflammatory cytokines and nitrous oxide. Modulen IBD most effectively decreased the clinical score at d 12, and Modulen IBD and OPN most effectively lowered the inflammatory score. Myeloperoxidase activity that denotes neutrophil infiltration was significantly lower in mice fed Modulen IBD, OPN, angiogenin, and Fe-bLF. A significant decrease in the numbers of T cells, natural killer cells, dendritic cells, and a significant decrease in cytokine expression were observed in mice fed the treatment diets compared with dextran sulfate administered mice. The Fe-bLF, CLA-enriched milk fat, and Modulen IBD inhibited intestinal angiogenesis. In summary, each of the milk components attenuated IBD in mice, but with differing effectiveness against specific disease parameters.
