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Hybrid Optimization for Distribution Channel Management: A Case of Retail Location Selection
Nhu-Mai Thi NONG,Duc-Son HA 한국유통과학회 2021 유통과학연구 Vol.19 No.12
Purpose: This study aims to introduce a hybrid MCDM model to support the selection of retail store location. Research design, data, and methodology: The hybrid approach of ANP and TOPSIS was used to address the location selection problem. The ANP technique was employed to compute the weights of the selection criteria, whilst the TOPSIS was used to rank alternatives. The proposed approach was then applied into a fashion company in Vietnam to select the best alternatives to be the retail store. Results: The results showed that Candidate 1 – Hai Ba Trung street is the most appropriate selection for locating retail stores. Conclusions: The proposed approach provides the decision makers with more useful methods than traditional ones. Therefore, the model can be applied to the location selection in all industries. In terms of academic contribution, the selection criteria proposed in the research can devote to the literature in the selection of location along with the concept of distribution channels. Additionally, the research also provides insight and guidelines for firms in making decision on retail store location based on limited resources to avoid the waste of funds. However, the results only answer to the context of Vietnam - a developing country. Thus, future research may be extended to developed countries where have better conditions.
Protein kinase Cδ knockout mice are protected from cocaine-induced hepatotoxicity
Mai, Huynh Nhu,Lee, Sung Hoon,Sharma, Garima,Kim, Dae-Joong,Sharma, Naveen,Shin, Eun-Joo,Pham, Duc Toan,Trinh, Quynh Dieu,Jang, Choon-Gon,Nah, Seung-Yeol,Jeong, Ji Hoon,Kim, Hyoung-Chun Elsevier 2019 Chemico-biological interactions Vol.297 No.-
<P><B>Abstract</B></P> <P>We investigated whether protein kinase Cδ (PKCδ) mediates cocaine-induced hepatotoxicity in mice. Cocaine treatment (60 mg/kg, i.p.) significantly increased cleaved PKCδ expression in the liver of wild-type (WT) mice, and led to significant increases in oxidative parameters (i.e., reactive oxygen species, 4-hydroxylnonenal and protein carbonyl). These cocaine-induced oxidative burdens were attenuated by pharmacological (i.e., rottlerin) or genetic depletion of PKCδ. We also demonstrated that treatment with cocaine resulted in significant increases in nuclear factor erythroid-2-related factor 2 (Nrf-2) nuclear translocation and increased Nrf-2 DNA-binding activity in wild-type (WT) mice. These increases were more pronounced in the rottlerin-treated WT or PKCδ knockout mice than in the saline-treated WT mice. Although cocaine treatment increased Nrf-2 nuclear translocation, DNA binding activity, and γ-glutamyl cysteine ligases (i.e., GCLc and GCLm) mRNA expressions, while it reduced the glutathione level and GSH/GSSG ratio. These decreases were attenuated by PKCδ depletion. Cocaine treatment significantly increased alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels in the serum of WT mice signifying the hepatic damage. These increases were also attenuated by PKCδ depletion. In addition, cocaine-induced hepatic degeneration in WT mice was evident 1 d post-cocaine. At that time, cocaine treatment decreased Bcl-2 and Bcl-xL levels, and increased Bax, cytosolic cytochrome c, and cleaved caspase-3 levels. Pharmacological or genetic depletion of PKCδ significantly ameliorated the pro-apoptotic properties and hepatic degeneration. Therefore, our results suggest that inhibition of PKCδ, as well as activation of Nrf-2, is important for protecting against hepatotoxicity induced by cocaine.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Cocaine induces hepatotoxicity via oxidative stress and activation of PKCδ. </LI> <LI> Depletion of PKCδ protects from cocaine-induced hepatotoxicity. </LI> <LI> Depletion of PKCδ exerts antioxidant activity via Nrf2-related glutathione system. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>
Mai, Huynh Nhu,Sharma, Naveen,Jeong, Ji Hoon,Shin, Eun-Joo,Pham, Duc Toan,Trinh, Quynh Dieu,Lee, Yu Jeung,Jang, Choon-Gon,Nah, Seung-Yeol,Bing, Guoying,Kim, Hyoung-Chun Elsevier 2019 Neurochemistry International Vol.124 No.-
<P><B>Abstract</B></P> <P>Previously we demonstrated that p53 mediates dopaminergic neurotoxicity via inducing mitochondrial burdens and proapoptotsis. However, little is known about the role of p53 in the excitotoxicity induced by psychostimulant, such as cocaine. Cocaine-induced kindling (convulsive) behaviors significantly increased p53 expression in the brain. Cocaine-induced p53 expression was more pronounced in hippocampus than in striatum or prefrontal cortex. Genetic depletion of p53 significantly attenuated cocaine-induced convulsive behaviors, followed by c-Fos immunoreactivity, and oxidative burdens in the hippocampus of mice. The antioxidant potentials mediated by genetic depletion of p53 were more pronounced in the mitochondrial-than cytosolic-fraction. Depletion of p53 significantly attenuated the changes in mitochondrial transmembrane potential, intramitochondrial Ca<SUP>2+</SUP> level, and mitochondrial oxidative burdens induced by cocaine. Consistently, depletion of p53 significantly inhibited mitochondrial p53 translocation, and cleaved-PKCδ induced by cocaine. In addition, depletion of p53 protected from cytosolic cytochrome c release, and pro-apoptotic changes induced by cocaine. Importantly, the protective/anticonvulsant potentials by genetic depletion of p53 were comparable to those by pifithrin-μ (PFT), a p53 inhibitor. Our results suggest that depletion of p53 offers anticonvulsive and neuroprotective potentials mainly via attenuating mitochondrial oxidative burdens, mitochondrial dysfunction, and pro-apoptotic signalings against cocaine-induced convulsive neurotoxicity.</P> <P><B>Highlights</B></P> <P> <UL> <LI> P53 inhibition protects against cocaine-induced kindling (convulsive) behaviors. </LI> <LI> Cocaine-induced p53 expression is most pronounced in hippocampus. </LI> <LI> Cocaine-induced oxidative stress is more evident in mitochondria than in cytosol. </LI> <LI> P53 depletion attenuates cocaine-induced mitochondrial dysfunction. </LI> <LI> P53 depletion attenuates cocaine-induced pro-apoptotic phenomena. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>
Mai, Huynh Nhu,Chung, Yoon Hee,Shin, Eun-Joo,Kim, Dae-Joong,Sharma, Naveen,Lee, Yu Jeung,Jeong, Ji Hoon,Nah, Seung-Yeol,Jang, Choon-Gon,Kim, Hyoung-Chun Elsevier 2019 Neurochemistry International Vol.124 No.-
<P><B>Abstract</B></P> <P>Converging evidence has demonstrated that oxidative burdens are associated with drug dependence induced by psychostimulants. Here, we investigated whether oxidative stress directly mediates conditioned place preference and behavioral sensitization (drug dependence) induced by cocaine and whether glutathione peroxidase-1 (GPx-1), a major GPx, modulates cocaine-induced psychotoxic changes in mice. Cocaine-induced drug dependence was followed by increases in c-Fos-immunoreactivity (c-Fos-IR) in the nucleus accumbens. Simultaneously, cocaine significantly increased oxidative parameters and nuclear factor κB (NFκB) activity (i.e. nuclear translocation and DNA binding activity) in the striatum (including nucleus accumbens). Genetic depletion of GPx-1 made mice susceptible to drug dependence induced by cocaine in mice, while genetic overexpression of GPx-1 protected the mice from drug dependence. Pyrrolidine dithiocarbamate (PDTC), a NFκB inhibitor, significantly attenuated the sensitivity induced by the genetic depletion of GPx-1 in mice. However, PDTC did not exhibit any additive effects against the protection afforded by the genetic overexpression of GPx-1. Our results suggest that drug dependence induced by cocaine requires oxidative stress and NFκB activation, and that the GPx-1 gene is a potential protective factor against cocaine-induced drug dependence through positive modulation of NFκB.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Treatment with cocaine resulted in a compensative induction of GPx-1. </LI> <LI> GPx-1 gene attenuated cocaine-induced oxidative potentials in the striatum. </LI> <LI> NFkB is a critical target for the GPx-1 activity against cocaine drug dependence. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>
Mai, Huynh Nhu,Sharma, Naveen,Shin, Eun-Joo,Nguyen, Bao Trong,Nguyen, Phuong Tram,Jeong, Ji Hoon,Jang, Choon-Gon,Cho, Eun-Hee,Nah, Seung-Yeol,Kim, Nam Hun,Nabeshima, Toshitaka,Kim, Hyoung-Chun Elsevier 2018 Neurochemistry International Vol.116 No.-
<P><B>Abstract</B></P> <P>We demonstrated that activation of protein kinase Cδ (PKCδ) and inactivation of the glutathione peroxidase-1 (GPx-1)-dependent systems are critical for methamphetamine (MA)-induced recognition memory impairment. We also demonstrated that exposure to far-infrared rays (FIR) causes induction of the glutathione (GSH)-dependent system, including induction of the GPx-1 gene. Here, we investigated whether exposure to FIR rays affects MA-induced recognition memory impairment and whether it modulates PKC, cholinergic receptors, and the GSH-dependent system. Because the PKC activator bryostatin-1 mainly induces PKCα, PKCε, and PKCδ, we assessed expression of these proteins after MA treatment. MA treatment selectively increased PKCδ expression and its phosphorylation. Exposure to FIR rays significantly attenuated MA-induced increases in PKCδ phosphorylation. Importantly, bryostatin-1 potentiated MA-induced phosphorylation of PKCδ. MA treatment significantly decreased M1, M3, and M4 muscarinic acetylcholine receptors (mAChRs) and β2 nicotinic acetylcholine receptor expression. Of these, the decrease was most pronounced in M1 mAChR. Exposure to FIR significantly attenuated MA-induced decreases in the M1 mAChR and phospho-ERK<SUB>1/2</SUB>, while it facilitated Nrf2-dependent GSH induction. Dicyclomine, an M1 mAChR antagonist, and <SMALL>L</SMALL>-buthionine-(S, R)-sulfoximine (BSO), an inhibitor of GSH synthesis, counteracted against the protective potentials mediated by FIR. More importantly, the memory-enhancing potential of FIR rays was significantly counteracted by bryostatin-1, dicyclomine, and BSO. Our results suggest that exposure to FIR rays attenuates MA-induced impairment in recognition memory via up-regulation of M1 mAChR, Nrf2-dependent GSH induction, and ERK<SUB>1/2</SUB> phosphorylation by inhibiting PKCδ phosphorylation by bryostatin-1.</P> <P><B>Highlights</B></P> <P> <UL> <LI> FIR attenuated MA-induced memory dysfunction via inhibition of PKCδ phosphorylation. </LI> <LI> FIR potentiated MA-induced compensative induction in Nrf2 and GCLs levels. </LI> <LI> Inhibition of PKCδ phosphorylation activated M1 mAChR/Nrf-2/ERK<SUB>1/2</SUB> signaling. </LI> <LI> Protective activity of FIR was counteracted by PKC activation, dicyclomine, and BSO. </LI> </UL> </P>
Criteria for Supplier Selection in Textile and Apparel Industry : A Case Study in Vietnam
Nhu-Mai Thi NONG,Phong Thanh HO 한국유통과학회 2019 The Journal of Asian Finance, Economics and Busine Vol.6 No.2
The study aims to investigate some criteria of supplier selection in the textile and apparel (T&A) sector in Vietnam. Most research on supplier selection criteria for T&A sector was mainly conducted based on the review of literature. Therefore, the purpose of this study is to explore these criteria based on a framework in which an integrated approach of qualitative and quantitative was employed. First, an in-depth interview was used to explore what supplier selection criteria T&A companies were utilized after the literature on supplier selection criteria had been reviewed. Next, a prequestionnaire was built and sent to some practitioners and experts for their revision. Then, a pilot survey of 31 T&A companies with numerous statistical tests was conducted to validate the questionnaire. Finally, an official study of 282 respondents was conducted to determine supplier selection criteria which are best suited for T&A companies through exploratory factor analysis. The findings of the study suggest that there are eight supplier selection criteria including Quality, Cost, Delivery, Service, Capability, Company’s image, Relationship, and Sourcing country. Each criterion comprises certain sub-criteria to make the supplier selection criteria set more comprehensive. The findings will be a contribution to the selection process of T&A companies as they can utilize these criteria to select capable suppliers.