• Korean Journal of Biological Psychiatry
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• v.8 no.1
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• pp.3-19
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• 2001

Recent basic and clinical studies demonstrate a major role for neural plasticity in the etiology and treatment of depression and stress-related illness. The neural plasticity is reflected both in the birth of new cell in the adult brain(neurogenesis) and the death of genetically healthy cells(apoptosis) in the response to the individual's interaction with the environment. The neural plasticity includes adaptations of intracellular signal transduction pathway and gene expression, as well as alterations in neuronal morphology and cell survival. At the cellular level, repeated stress causes shortening and debranching of dendrite in the CA3 region of hippocampus and suppress neurogenesis of dentate gyrus granule neurons. At the molecular level, both form of structural remodeling appear to be mediated by glucocorticoid hormone working in concert with glutamate and N-methyl-D-aspartate(NMDA) receptor, along with transmitters such as serotonin and GABA-benzodiazepine system. In addition, the decreased expression and reduced level of brain-derived neurotrophic factor(BDNF) could contribute the atrophy and decreased function of stress-vulnerable hippocampal neurons. It is also suggested that atrophy and death of neurons in the hippocampus, as well as prefrontal cortex and possibly other regions, could contribute to the pathophysiology of depression. Antidepressant treatment could oppose these adverse cellular effects, which may be regarded as a loss of neural plasticity, by blocking or reversing the atrophy of hippocampal neurons and by increasing cell survival and function via up-regulation of cyclic adenosine monophosphate response element-binding proteins(CREB) and BDNF. In this article, the molecular and cellular mechanisms that underlie stress, depression, and action of antidepressant are precisely discussed.

• Korean Journal of Veterinary Pathology
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• v.6 no.1
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• pp.41-48
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• 2002

Oval cell is considered as facultative precursor cells for both hepatocytes and biliary cells, as well as origin of hepatocellar and cholangiocellular carcinoma (CCC) during carcinogenesis or toxic liver injury. To clarify the cellular origin or differentiation of cholagiocarcinogensis, the fate of carcinogen-induced oval cells was pathologically and phenotypically chased in Syrian golden hamster liver after Clonorchis sinensis (CS) infection which would give rise to a promoting effect. Two week treatment of hamsters with 0.005% diethylnitrosamine (DEN) followed by 2 week treatment of 1% 2-acetylaminofluorene (AAF) under choline deficient diet resulted in massive proliferation of BrdU labeleed and PCNA positive oval cells showing various distinct morphology, histochemical and immunohistochemical phenotypes for GGT, cytokeratin 19 and OV-6. Oval cells also frequently form ductular-like structures or phenotypically show hepatocyte-like characteristics. After CS infection, the oval cells showed sequential morphological changes to atypicl proliferating bile ductules and all hamsters thereafter developed well differentiated and anaplastic CCC at 16 week after CS infection. In electron microscopy, some bile ductules were constructed by intermediate oval cells and bile ductular cells surrounded by basement membrane. The results of this study strongly suggest that CCC developed in the present study were originated from hepatic stem-like oval cells, supporting the theory of stem cell origin of cancers. In addition, this hamster model would be valuable for the molecular mechanistic study during chemical-triggered cholangiocarcinogenesis.

• Reproductive and Developmental Biology
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• v.36 no.1
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• pp.55-64
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• 2012

Peroxiredoxin II (Prdx II; a typical 2-Cys Prdx) has been originally isolated from erythrocytes, and its structure and peroxidase activity have been adequately studied. Prdx II has been reported to protect a wide range of cellular environments as antioxidant enzyme, and its dysfunctions may be implicated in a variety of disease states associated with oxidative stress, including cancer and aging-associated pathologies. But, the precise mechanism is still obscure in various aspects of aging containing ovarian aging. Identification and relative quantification of the increased proteins affected by Prdx II deficiency may help identify novel signaling mechanisms that are important for oxidative stress-related diseases. To identify the increased proteins in Prdx $II^{-/-}$ mice, we performed RBC comparative proteome analysis in membrane fraction and cytosolic fractions by nano-UPLC-$MS^E$ shotgun proteomics. We found the increased 86 proteins in membrane (32 proteins) and cytosolic (54 proteins) fractions, and analyzed comparative expression pattern in healthy RBCs of Prdx $II^{+/+}$ mice, healthy RBCs of Prdx $II^{-/-}$ mice, and abnormal RBCs of Prdx $II^{-/-}$ mice. These proteins belonged to cellular functions related with RBC lifespan maintain, such as cellular morphology and assembly, cell-cell interaction, metabolism, and stress-induced signaling. Moreover, protein networks among the increased proteins were analyzed to associate with various diseases. Taken together, RBC proteome may provide clues to understand the clue about redox-imbalanced diseases.

• Journal of Veterinary Science
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• v.21 no.3
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• pp.44.1-44.10
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• 2020

Background: Congenital portosystemic shunt (cPSS) is one of the most common congenital disorders diagnosed in dogs. Hepatic encephalopathy (HE) is a frequent complication in dogs with a cPSS and is a major cause of morbidity and mortality. Despite HE been a major cause of morbidity in dogs with a cPSS, little is known about the cellular changes that occur in the central nervous system of dogs with a cPSS. Objectives: The objective of this study was to characterise the histological changes in the cerebral cortex and cerebellum of dogs with cPSS with particular emphasis on astrocyte morphology. Methods: Eight dogs with a confirmed cPSS were included in the study. Results: Six dogs had substantial numbers of Alzheimer type II astrocytes and all cases had increased immunoreactivity for glial fibrillary acidic protein in the cerebral cortex, even if there were minimal other morphological changes. Conclusions: This study demonstrates that dogs with a cPSS have marked cellular changes in the cerebral cortex and cerebellum. The cellular changes that occur in the cerebral cortex and cerebellum of dogs with spontaneously arising HE are similar to changes which occur in humans with HE, further validating dogs with a cPSS as a good model for human HE.

• Journal of the Microelectronics and Packaging Society
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• v.15 no.3
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• pp.27-33
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• 2008

With increasing use of portable appliances such as PDA and cellular phone, changing environment of applications requires higher solder joint reliability. The ENIG (Electroless Nickel Immersion Gold) process has been widely used for fine pitch SMT (Surface Mount Technology) and BGA (Ball Grid Array) packaged devices due to its benefits including excellent solderability, high uniformity and substantial legibility throughout the packaging process. Its brittle fracture of solder, however, has received increasingly attentions. It was Down that fracture brittleness is mainly related with black pad resulting from galvanic nickel corrosion and P-enriched layer formation between the IMC (Intermetallic Compounds) and electroless nickel layer. Theoretically, smooth electroless Ni layer was blown to have a advantages in minimizing the black pad phenomenon by uniform solution exchange during immersion gold plating. Nevertheless, how to control the surface morphology of electroless Ni layer has been hardly blown. This study investigates an effect of surface morphology of Cu underlayer on surface morphology of electroless Ni layer. To obtain various kinds of surface morphology of Cu layer, two types of Cu etching chemical and a number of Cu etching treatment were applied.

• Reproductive and Developmental Biology
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• v.34 no.3
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• pp.143-151
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• 2010

Pluripotency of human embryonic stem cell (hESC) is one of the most valuable ability of hESCs for applying cell therapy field, but also showing side effect, for example teratoma formation. When transplant multipotent stem cell, such as mesnchymal stem cell (MSC) which retains similar differentiation ability, they do not form teratoma in vivo, but there exist limitation of cellular source supply. Accordingly, differentiation of hESC into MSC will be promising cellular source with strong points of both hESC and MSC line. In this study, we described the derivation of MSC like cell population from feeder free cultured hESC (hESC-MSC) using direct differentiation system. Cells population, hESC-MSC and bone marrow derived MSC (BM-MSC) retained similar characteristics in vitro, such as morphology, MSC specific marker expression and differentiation capacity. At the point of differentiation of both cell populations, differentiation rate was slower in hESC-MSC than BM-MSC. As these reason, to verify differentially expressed molecular condition of both cell population which bring out different differentiation rate, we compare the molecular condition of hESC-MSC and BM-MSC using 2-D proteomic analysis tool. In the proteomic analysis, we identified 49 differentially expressed proteins in hESC-MSC and BM-MSC, and they involved in different biological process such as positive regulation of molecular function, biological process, cellular metabolic process, nitrogen compound metabolic process, macromolecule metabolic process, metabolic process, molecular function, and positive regulation of molecular function and regulation of ubiquitin protein ligase activity during mitotic cell cycle, cellular response to stress, and RNA localization. As the related function of differentially expressed proteins, we sought to these proteins were key regulators which contribute to their differentiation rate, developmental process and cell proliferation. Our results suggest that the expressions of these proteins between the hESC-MSC and BM-MSC, could give to us further evidence for hESC differentiation into the mesenchymal stem cell is associated with a differentiation factor. As the initial step to understand fundamental difference of hESC-MSC and BM-MSC, we sought to investigate different protein expression profile. And the grafting of hESC differentiation into MSC and their comparative proteomic analysis will be positively contribute to cell therapy without cellular source limitation, also with exact background of their molecular condition.

• BMB Reports
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• v.55 no.2
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• pp.81-86
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• 2022

Macrophages are a major cellular component of innate immunity and are mainly known to have phagocytic activity. In the tumor microenvironment (TME), they can be differentiated into tumor-associated macrophages (TAMs). As the most abundant immune cells in the TME, TAMs promote tumor progression by enhancing angiogenesis, suppressing T cells and increasing immunosuppressive cytokine production. N-myc downstream-regulated gene 2 (NDRG2) is a tumor suppressor gene, whose expression is down-regulated in various cancers. However, the effect of NDRG2 on the differentiation of macrophages into TAMs in breast cancer remains elusive. In this study, we investigated the effect of NDRG2 expression in breast cancer cells on the differentiation of macrophages into TAMs. Compared to tumor cell-conditioned medium (TCCM) from 4T1-mock cells, TCCM from NDRG2-over-expressing 4T1 mouse breast cancer cells did not significantly change the morphology of RAW 264.7 cells. However, TCCM from 4T1-NDRG2 cells reduced the mRNA levels of TAM-related genes, including MR1, IL-10, ARG1 and iNOS, in RAW 264.7 cells. In addition, TCCM from 4T1-NDRG2 cells reduced the expression of TAM-related surface markers, such as CD206, in peritoneal macrophages (PEM). The mRNA expression of TAM-related genes, including IL-10, YM1, FIZZ1, MR1, ARG1 and iNOS, was also downregulated by TCCM from 4T1-NDRG2 cells. Remarkably, TCCM from 4T1-NDRG2 cells reduced the expression of PD-L1 and Fra-1 as well as the production of GM-CSF, IL-10 and ROS, leading to the attenuation of T cell-inhibitory activity of PEM. These data showed that compared with TCCM from 4T1-mock cells, TCCM from 4T1-NDRG2 cells suppressed the TAM differentiation and activation. Collectively, these results suggest that NDRG2 expression in breast cancer may reduce the differentiation of macrophages into TAMs in the TME.

• Reproductive and Developmental Biology
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• v.36 no.4
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• pp.275-281
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• 2012

Embryonic stem cell-preconditioned microenvironment is important for cancer cells properitities by change cell morphology and proliferation. This microenvironment induces cancer cell reprogramming and results in a change in cancer cell properties such as differentiation and migration. The cancer microenvironment affects cancer cell proliferation and growth. However, the mechanism has not been clarified yet. Using the ES-preconditioned 3-D microenvironment model, we provide evidence showing that the ES microenvironment inhibits proliferation and reduces oncogenic gene expression. But ES microenvironment has no effect on telomerase activity, cell viability, cellular senescence, and methylation on Oct4 promoter region. Furthermore, methylation of Nanog was increase on ES-preconditioned microenvironment and supports results that no difference on RNA expression levels. Taken together, these results demonstrated that in the ES-preconditioned 3-D microenvironment is a crucial role for cancer cell proliferation not senescence.

• Environmental Analysis Health and Toxicology
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• v.14 no.1_2
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• pp.55-63
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• 1999

Endocrine disrupting chemicals probably cause the cytological or/and morphological changes of germinal cells in gonad. Accordingly, this study was aimed to make sure that the effect of hormone-mimicking chemicals on gonad morphology such as decrease of germinal cells, inhibition of cellular maturation and change in the ratio of germinal cells in the different developmental phase can be observed by histopathological procedures and can be a useful bio-indicator for the evaluation of endocrine disruption by environmental chemicals. In this experiment, female Japanese medaka were exposured to quercetin, a phytoestrogen, at the concentration of 100 $\mu\textrm{g}$/L. quercetin showed the significant decrease in the number and rate of vitellogenic follicular oocytes in the treated group for 4 and 6 weeks. The weak development of yolk could be also observed. We could conclude that quercetin has anti-estrogenic or androgen-like potency by exerting the inhibition effect on oogenesis in fish female- gonad. From the result of this study, the applied methods and techniques can be evaluated to be a useful biomonitoring means for water pollution, expecting a good result of the subsequent study on apoptosis.

• BMB Reports
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• v.51 no.11
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• pp.549-556
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• 2018

Mitochondria are ubiquitous and multi-functional organelles involved in diverse metabolic processes, namely energy production and biomolecule synthesis. The intracellular mitochondrial morphology and distribution change dynamically, which reflect the metabolic state of a given cell type. A dramatic change of the mitochondrial dynamics has been observed in early development that led to further investigations on the relationship between mitochondria and the process of development. A significant developmental process to focus on, in this review, is a differentiation of neural progenitor cells into neurons. Information on how mitochondria-regulated cellular energetics is linked to neuronal development will be discussed, followed by functions of mitochondria and associated diseases in neuronal development. Lastly, the potential use of mitochondrial features in analyzing various neurodevelopmental diseases will be addressed.