The Combination of Soft Sets and N-Structures with Applications

Using the notions of soft sets and N-structures, N-soft set theory is introduced. We apply it to both a decision making problem and a BCK/BCI algebra

Quasi-valuation maps based on positive implicative ideals in BCK-algebras

The notion of PI-quasi-valuation maps of a BCK-algebra is introduced, and related properties are investigated. The relationship between an I-quasi-valuation map and a PI-quasivaluation map is examined. Conditions for an I-quasi-valuation map to be a PI-quasi-valuation map are provided, and conditions for a real-valued function on a BCK-algebra to be a quasi-valuation map based on a positive implicative ideal are founded. The extension property for a PI-quasi-valuation map is established

Targeting IκB Kinase β in Adipocyte Lineage Cells for Treatment of Obesity and Metabolic Dysfunctions

IκB kinase β (IKKβ), a central coordinator of inflammation through activation of nuclear factor-κB, has been identified as a potential therapeutic target for the treatment of obesity-associated metabolic dysfunctions. In this study, we evaluated an antisense oligonucleotide (ASO) inhibitor of IKKβ and found that IKKβ ASO ameliorated diet-induced metabolic dysfunctions in mice. Interestingly, IKKβ ASO also inhibited adipocyte differentiation and reduced adiposity in high-fat (HF)-fed mice, indicating an important role of IKKβ signaling in the regulation of adipocyte differentiation. Indeed, CRISPR/Cas9-mediated genomic deletion of IKKβ in 3T3-L1 preadipocytes blocked these cells differentiating into adipocytes. To further elucidate the role of adipose progenitor IKKβ signaling in diet-induced obesity, we generated mice that selectively lack IKKβ in the white adipose lineage and confirmed the essential role of IKKβ in mediating adipocyte differentiation in vivo. Deficiency of IKKβ decreased HF-elicited adipogenesis in addition to reducing inflammation and protected mice from diet-induced obesity and insulin resistance. Further, pharmacological inhibition of IKKβ also blocked human adipose stem cell differentiation. Our findings establish IKKβ as a pivotal regulator of adipogenesis and suggest that overnutrition-mediated IKKβ activation serves as an initial signal that triggers adipose progenitor cell differentiation in response to HF feeding. Inhibition of IKKβ with antisense therapy may represent as a novel therapeutic approach to combat obesity and metabolic dysfunctions. Stem Cells 2016;34:1883–1895

ADAR2-dependent RNA editing of GluR2 is involved in thiamine deficiency-induced alteration of calcium dynamics

BACKGROUND: Thiamine (vitamin B1) deficiency (TD) causes mild impairment of oxidative metabolism and region-selective neuronal loss in the central nervous system (CNS). TD in animals has been used to model aging-associated neurodegeneration in the brain. The mechanisms of TD-induced neuron death are complex, and it is likely multiple mechanisms interplay and contribute to the action of TD. In this study, we demonstrated that TD significantly increased intracellular calcium concentrations [Ca2+]i in cultured cortical neurons. RESULTS: TD drastically potentiated AMPA-triggered calcium influx and inhibited pre-mRNA editing of GluR2, a Ca2+-permeable subtype of AMPA receptors. The Ca2+ permeability of GluR2 is regulated by RNA editing at the Q/R site. Edited GluR2 (R) subunits form Ca2+-impermeable channels, whereas unedited GluR2 (Q) channels are permeable to Ca2+ flow. TD inhibited Q/R editing of GluR2 and increased the ratio of unedited GluR2. The Q/R editing of GluR2 is mediated by adenosine deaminase acting on RNA 2 (ADAR2). TD selectively decreased ADAR2 expression and its self-editing ability without affecting ADAR1 in cultured neurons and in the brain tissue. Over-expression of ADAR2 reduced AMPA-mediated rise of [Ca2+]i and protected cortical neurons against TD-induced cytotoxicity, whereas down-regulation of ADAR2 increased AMPA-elicited Ca2+ influx and exacerbated TD-induced death of cortical neurons. CONCLUSIONS: Our findings suggest that TD-induced neuronal damage may be mediated by the modulation of ADAR2-dependent RNA Editing of GluR2

Modelling the impacts of climate change and air pollutants on the agricultural production yields in Malaysia using Random-Effects Error Components Regression model

The occurrence of climate change is attributable to anthropogenic emissions of greenhouse gases (GHG) which have affected the C3 plants’ agricultural production yields in past decades. Therefore, this article aims to model the linear association among these C3 plants’ agricultural production yields with several climatic and non-climatic explanatory variables using one-way random-effects error components regression model. To be congruent with the main objective of this study, the balanced longitudinal dataset period 1980 to 2018 under big data was acquired. The analysis results revealed that merely maximum temperature