Thiamine Deficiency and Neurodegeneration: The Interplay Among Oxidative Stress, Endoplasmic Reticulum Stress, and Autophagy

Thiamine (vitamin B1) is an essential nutrient and indispensable for normal growth and development of the organism due to its multilateral participation in key biochemical and physiological processes. Humans must obtain thiamine from their diet since it is synthesized only in bacteria, fungi, and plants. Thiamine deficiency (TD) can result from inadequate intake, increased requirement, excessive deletion, and chronic alcohol consumption. TD affects multiple organ systems, including the cardiovascular, muscular, gastrointestinal, and central and peripheral nervous systems. In the brain, TD causes a cascade of events including mild impairment of oxidative metabolism, neuroinflammation, and neurodegeneration, which are commonly observed in neurodegenerative diseases, such as Alzheimer’s disease (AD), Parkinson’s disease (PD), and Huntington’s disease (HD). Thiamine metabolites may serve as promising biomarkers for neurodegenerative diseases, and thiamine supplementations exhibit therapeutic potential for patients of some neurodegenerative diseases. Experimental TD has been used to model aging-related neurodegenerative diseases. However, to date, the cellular and molecular mechanisms underlying TD-induced neurodegeneration are not clear. Recent research evidence indicates that TD causes oxidative stress, endoplasmic reticulum (ER) stress, and autophagy in the brain, which are known to contribute to the pathogenesis of various neurodegenerative diseases. In this review, we discuss the role of oxidative stress, ER stress, and autophagy in TD-mediated neurodegeneration. We propose that it is the interplay of oxidative stress, ER stress, and autophagy that contributes to TD-mediated neurodegeneration

Electrolytic Corrosion Resistant Plating for Connector Pins

This disclosure describes an electroplating configuration that is resistant to electrolytic corrosion. The configuration is a stack-up of different layers that include copper (Cu) layer surrounding the substrate, a nickel (Ni) layer, and a nickel-tungsten (NiW) layer. The configuration additionally includes a gold (Au) layer utilized as an interface layer between the NiW layer and an outer rhodium-ruthenium (RhRu) layer. To impart electrolytic corrosion resistance, a rhodium-ruthenium (RhRu) layer is electroplated as an outer layer. The electroplating stack-up described in this disclosure has significantly improved anti-electrochemical corrosion capability than prior techniques

Protecting Electrical Connectors From Corrosion

This publication describes techniques and apparatuses for protecting electrical connectors from corrosion. An electrical connector may include an electrolytic plating stack-up of layers configured to minimize electrolytic corrosion. The plating stack-ups described in this publication utilize various elements applied in multiple ways to create a cost-efficient and effective solution for minimizing electrolytic corrosion in electrical connectors, thereby improving efficiency and extending the life of electrical connectors

Rich water flow, live water revitalizes the countryside–Rural water resources utilization design under the rural revitalization strategy

Revitalizing the countryside should first develop water resources. The rational use of rural water resources will greatly enhance the endogenous power of rural revitalization, help to achieve the 1strategic rural revitalization goal of rich water and longevity, and promote the sustainable revitalization of rural areas in China

Dynamic Effects of Early Adolescent Stress on Depressive-Like Behaviors and Expression of Cytokines and JMJD3 in the Prefrontal Cortex and Hippocampus of Rats

Aims: Expression of inflammatory cytokines in the brain has been reported to be involved in the pathogenesis of and susceptibility to depression. Jumonji domain-containing 3 (Jmjd3), which is a histone H3 lysine 27 (H3K27) demethylase and can regulate microglial activation, has been regarded as a crucial element in the expression of inflammatory cytokines. Furthermore, recent studies highlighted the fact that lipopolysaccharides induce depressive-like behaviors and higher Jmjd3 expression and lower H3K27me3 expression in the brain. However, whether the process of Jmjd3 mediating inflammatory cytokines was involved in the susceptibility to depression due to early-life stress remained elusive.Methods: Rats exposed to chronic unpredictable mild stress (CUMS) in adolescence were used in order to detect dynamic alterations in depressive-like behaviors and expression of cytokines, Jmjd3, and H3K27me3 in the prefrontal cortex and hippocampus. Moreover, minocycline, an inhibitor of microglial activation, was employed to observe the protective effects.Results: Our results showed that CUMS during the adolescent period induced depressive-like behaviors, over-expression of cytokines, and increased Jmjd3 and decreased H3K27me3 expression in the prefrontal cortex and hippocampus of both adolescent and adult rats. However, minocycline relieved all the alterations.Conclusion: The study revealed that Jmjd3 might be involved in the susceptibility to depressive-like behaviors by modulating H3K27me3 and pro-inflammatory cytokine expression in the prefrontal cortex and hippocampus of rats that had been stressed during early adolescence