• BMB Reports
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• v.56 no.2
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• pp.90-95
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• 2023

Mitochondria are important organelles that regulate adenosine triphosphate production, intracellular calcium buffering, cell survival, and apoptosis. They play therapeutic roles in injured cells via transcellular transfer through extracellular vesicles, gap junctions, and tunneling nanotubes. Astrocytes can secrete numerous factors known to promote neuronal survival, synaptic formation, and plasticity. Recent studies have demonstrated that astrocytes can transfer mitochondria to damaged neurons to enhance their viability and recovery. In this study, we observed that treatment with mitochondria isolated from rat primary astrocytes enhanced cell viability and ameliorated hydrogen peroxide-damaged neurons. Interestingly, isolated astrocytic mitochondria increased the number of cells under damaged neuronal conditions, but not under normal conditions, although the mitochondrial transfer efficiency did not differ between the two conditions. This effect was also observed after transplanting astrocytic mitochondria in a rat middle cerebral artery occlusion model. These findings suggest that mitochondria transfer therapy can be used to treat acute ischemic stroke and other diseases.

• Journal of the Korean Ceramic Society
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• v.40 no.5
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• pp.455-459
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• 2003

Tunneling spectra of B $i_2$S $r_2$Ca(C $u_{1-x}$ N $i_{x}$ )$_2$ $O_{8+}$$\delta$/ film by LPE method have been measured using break junctions. The energy gap 2$\Delta$ and 2$\Delta$/ $k_{B}$ $T_{c}$ $^{zero}$ increased with increase of ft. We obtained the energy gap Parameter 2$\Delta$(4.2 K) = 54.4~64 meV, and corresponding1y $\Delta$/ $k_{B}$ $T_{c}$ $^{zero}$=7.36~10.14, larger than the BCS value. The lattice constant c and critical temperature $T_{c}$ $^{zero}$ decrease with increase of $\chi$$_{L}$.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.18
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• pp.8271-8279
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• 2016

Background: Hepato-carcinogenesis is multifaceted in its molecular aspects. Among the interplaying agents are altered gap junctions, the proteasome/autophagy system, and mitochondria. The present experimental study was designed to outline the roles of these players and to investigate the tumor suppressive effects of curcumin with or without mesenchymal stem cells (MSCs) in hepatocellular carcinoma (HCC). Materials and Methods: Adult female albino rats were divided into normal controls and animals with HCC induced by diethyl-nitrosamine (DENA) and $CCl_4$. Additional groups treated after HCC induction were: Cur/HCC which received curcumin; MSCs/HCC which received MSCs; and Cur+MSCs/HCC which received both curcumin and MSCs. For all groups there were histopathological examination and assessment of gene expression of connexin43 (Cx43), ubiquitin ligase-E3 (UCP-3), the autophagy marker LC3 and coenzyme-Q10 (Mito.Q10) mRNA by real time, reverse transcription-polymerase chain reaction, along with measurement of LC3II/LC3I ratio for estimation of autophagosome formation in the rat liver tissue. In addition, the serum levels of ALT, AST and alpha fetoprotein (AFP), together with the proinflammatory cytokines $TNF{\alpha}$ and IL-6, were determined in all groups. Results: Histopathological examination of liver tissue from animals which received DENA-$CCl_4$ only revealed the presence of anaplastic carcinoma cells and macro-regenerative nodules. Administration of curcumin, MSCs; each alone or combined into rats after induction of HCC improved the histopathological picture. This was accompanied by significant reduction in ${\alpha}$-fetoprotein together with proinflammatory cytokines and significant decrease of various liver enzymes, in addition to upregulation of Cx43, UCP-3, LC3 and Mito.Q10 mRNA. Conclusions: Improvement of Cx43 expression, nonapoptotic cell death and mitochondrial function can repress tumor growth in HCC. Administration of curcumin and/or MSCs have tumor suppressive effects as they can target these mechanisms. However, further research is still needed to verify their effectiveness.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.7
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• pp.2987-2991
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• 2014

Connexin 43 is an important gap junction protein in vertebrates and is known for its tumor suppressive properties. Cx43 is abundantly expressed in the human intestinal epithelial cells and muscularis mucosae. To explore the role of Cx43 in the genesis of human colon cancer, we performed the expression analysis of Cx43 in 80 cases of histopathologically confirmed and clinically diagnosed human colon cancer samples and adjacent control tissue and assessed correlations with clinicopathological variables. Western blotting using anti-Cx43 antibody indicated that the expression of Cx43 was significantly down regulated (75%) in the cancer samples as compared to the adjacent control samples. Moreover, immunohistochemical analysis of the tissue samples confirmed the down regulation of the Cx43 in the intestinal epithelial cells. Cx43 down regulation showed significant association (p<0.05) with the histological type and tumor invasion properties of the cancer. Our data demonstrated that loss of Cx43 may be an important event in colon carcinogenesis and tumor progression, providing significant insights about the tumor suppressive properties of the Cx43 and its potential as a diagnostic marker for colon cancer.

• Environmental Mutagens and Carcinogens
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• v.23 no.2
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• pp.56-62
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• 2003

The liver progenitor cells could form a potential target cell population fore both tumor-initiating and -promoting chemicals. Induction of drug-metabolizing and antioxidant enzymes, including AhR-dependent CYP1A1, NQO-1 and AKR1C9, was detected in the rat liver epithelial WB-F344 "stem-like" cells. Additionally, WB-F344 cells express a functional, wild-type form of p53 protein, a biomarker of genotoxic events, and connexin 43, a basic structural unit of gap junctions forming an important type of intercellular communication. In this cellular model, two complementary assays have been established for detection of the modes of action associated with tumor promotion: inhibition of gap junctional intercellular communication (GJIC) and proliferative activity in confluent cells. We found that the PAHs and PCBs, which are AhR agonists, released WB-F344 cells from contact inhibition, increasing both DNA synthesis and cell numbers. Genotoxic effects of some PAHs that lead to apoptosis and cell cycle delay might interfere with the proliferative activity of PAHs. Contrary to that, the nongenotoxic low-molecular-weight PAHs and non-dioxin-like PCB congeners, abundant in the environment, did not significantly affect cell cycle and cell proliferation; however both groups of compounds inhibited GJIC in WB-F344 cells. The release from contact inhibiton by a mechanism that possibly involves the AhR activation, inhibition of GJIC and genotoxic events induced by environmental contaminants are three important modes of action that could play an important role in carcinogenic effects of toxic compounds. The relative potencies to inhibit GJIC, to induce AhR-mediated activity, and to release cells from contact inhibition were determined for a large series of PAHs and PCBs and their metabolites. In vitro bioassays based on detection of events on cellular level (deregulation of GJIC and/or proliferation) or determination of receptor-mediated activities in both ?$stem-like^{\circ}{\times}$ and hepatocyte-like liver cellular models are valuable tools for detection of modes of action of polyaromatic hydrocarbons. They may serve, together with concentration data, as a first step in their risk assessment.

• The Korean Journal of Physiology and Pharmacology
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• v.2 no.1
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• pp.21-30
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• 1998

The effects of GABA and glutamate on the horizontal cells were explored by an intracellular recording method to discern the mechanisms of receptive field formation by chemical coupling in the catfish outer retina. The results suggest that the horizontal cells of the catfish retina might use GABA as their transmitters and that the GABAergic system contributes to the formation of receptive fields of the horizontal cells. GABAC receptors may be involved in a chemical coupling between horizontal cells and concerned with the depolarizing actions by GABA on horizontal cells in the catfish retina. Since the chloride equilibrium potential is more positive than the dark membrane potential in horizontal cells, GABA released from a horizontal cell may depolarize the neighboring horizontal cells. Thus a chemical coupling between horizontal cells may be formed. $GABA_A$ receptors also may be involved in the negative feedback mechanism between photoreceptor and horizontal cell. And glutamate may be involved in connecting positive and negative feedback systems since it potentiated the GABA's actions. Therefore, it is presumed that large receptive fields in the catfish retina are formed not only by electrical coupling but also by chemical coupling between horizontal cells. And information travels laterally by pathways involving both electrical coupling composed of gap junctions and chemical coupling in the retinal network.

• IMMUNE NETWORK
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• v.13 no.3
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• pp.102-106
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• 2013

Emerging evidence suggests that gap formation and opening of the endothelial junctions during leukocyte extravasation is actively controlled to maintain the integrity of the vascular barrier. While the role for endothelial cells to this process has been well defined, it is not clear whether leukocytes are also actively contributing to endothelial barrier function. We have recently showed that extravasating leukocytes deposit microparticles on the subendothelium during the late stages of extravasation, which is LFA-1 dependent. Using multiphotonintravital microscopy (MP-IVM) of mouse cremaster muscle vessels in the current work, we show that microparticle formation and deposition maintains the integrity of the microvascular barrier during leukocyte extravasation. Inhibition of neutrophil-derived microparticle formation resulted in dramatically increased vascular leakage. These findings suggest that deposition of microparticles during neutrophil extravasation is essential for maintaining endothelial barrier function and may result in temporal difference between neutrophil extravasation and an increase in vascular leakage.

• The Korean Journal of Pain
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• v.22 no.1
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• pp.1-15
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• 2009

Neuropathic pain is often refractory to intervention because of the complex etiology and an incomplete understanding of the mechanisms behind this type of pain. Glial cells, specifically microglia and astrocytes, are powerful modulators of pain and new targets of drug development for neuropathic pain. Glial activation could be the driving force behind chronic pain, maintaining the noxious signal transmission even after the original injury has healed. Glia express chemokine, purinergic, toll-like, glutaminergic and other receptors that enable them to respond to neural signals, and they can modulate neuronal synaptic function and neuronal excitability. Nerve injury upregulates multiple receptors in spinal microglia and astrocytes. Microglia influence neuronal communication by producing inflammatory products at the synapse, as do astrocytes because they completely encapsulate synapses and are in close contact with neuronal somas through gap junctions. Glia are the main source of inflammatory mediators in the central nervous system. New therapeutic strategies for neuropathic pain are emerging such as targeting the glial cells, novel pharmacologic approaches and gene therapy. Drugs targeting microglia and astrocytes, cytokine production, and neural structures including dorsal root ganglion are now under study, as is gene therapy. Isoform-specific inhibition will minimize the side effects produced by blocking all glia with a general inhibitor. Enhancing the anti-inflammatory cytokines could prove more beneficial than administering proinflammatory cytokine antagonists that block glial activation systemically. Research on therapeutic gene transfer to the central nervous system is underway, although obstacles prevent immediate clinical application.

• Progress in Superconductivity
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• v.3 no.1
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• pp.49-55
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• 2001

Josephson junction arrays were fabricated by DC magnetron sputtering, self-aligning and reactive ion etching technique. The Al native oxide, formed by thermal oxidation, was used as the tunneling barrier of Nb/$Al-A1_2$$O_3$Nb trilayer. The arrays have 2,000 Josephson junctions with the area of $14\mu\textrm{m}$ $\times$ $46\mu\textrm{m}$. The gap voltages were in the range of 2.5 ~2.6 mV and the spread of critical current was $\pm$11~14%. When operated at 70~94 ㎓, the arrays generated zero-crossing steps up to 2.1~2.4 V. To improve transmission of microwave power and prevent diffusion of oxygen into Nb ground-plane while depositing $SiO_2$dielectric, we applied a plasma nitridation process to the Nb ground-plane. The microwave power was well propagated in Josephson junction arrays with nitridation. The difference in microwave transmission 7an be interpreted by the surface impedance change depending on nitridation.

• Journal of the Korean Magnetics Society
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• v.20 no.6
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• pp.212-215
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• 2010

Spin polarized tunneling studies were carried out with Al-Ga bilayer as a spin detector, by Meservey-Tedrow technique. The superconductor (SC)/Insulator (I)/Ferromagnet (FM) tunnel junctions were provided by ultra high vacuum molecular beam epitaxy (UHV-MBE) technique. The analysis of interfacial properties in the Al-Ga bilayer was also carried out by Auger electron spectroscopy. It was observed that the superconducting transition temperature and energy gap were raised in comparison with that of bulk Ga and pure ultrathin Al films. Current studies clearly show how one can modify the material properties at the interface just with a few monolayers.