• Macromolecular Research
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• v.16 no.6
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• pp.549-554
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• 2008

Proton conducting crosslinked membranes were prepared using polymer blends of polystyrene-b-poly(hydroxyethyl acrylate)-b-poly(styrene sulfonic acid) (PS-b-PHEA-b-PSSA) and poly(vinyl alcohol) (PVA). PS-b-PHEA-b-PSSA triblock copolymer at 28:21:51 wt% was synthesized sequentially using atom transfer radical polymerization (ATRP). FT-IR spectroscopy showed that after thermal ($120^{\circ}C$, 2 h) and chemical (sulfosuccinic acid, SA) treatments of the membranes, the middle PHEA block of the triblock copolymer was crosslinked with PVA through an esterification reaction between the -OH group of the membrane and the -COOH group of SA. The ion exchange capacity (IEC) decreased from 1.56 to 0.61 meq/g with increasing amount of PVA. Therefore, the proton conductivity at room temperature decreased from 0.044 to 0.018 S/cm. However, the introduction of PVA resulted in a decrease in water uptake from 87.0 to 44.3%, providing good mechanical properties applicable to the membrane electrode assembly (MEA) of fuel cells. Transmission electron microscopy (TEM) showed that the membrane was microphase-separated with a nanometer range with good connectivity of the $SO_3H$ ionic aggregates. The power density of a single $H_2/O_2$ fuel cell system using the membrane with 50 wt% PVA was $230\;mW/cm^2$ at $70^{\circ}C$ with a relative humidity of 100%. Thermogravimetric analysis (TGA) also showed a decrease in the thermal stability of the membranes with increasing PVA concentration.

• Herbal Formula Science
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• v.25 no.2
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• pp.179-191
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• 2017

Objectives : Increased oxidative stress by reactive oxygen species (ROS) has been suggested as a major cause of muscle fatigue. Although several studies have demonstrated the various biological properties of Sophora flavescens Aiton, Glycyrrhiza uralensis Fischer and Dictamnus dasycarpus Turcz, but the antioxidative potentials have not been clearly demonstrated. The present study was designed to investigate the protective effects of their water and ethanol extract mixtures (medicinal herbal mixtures, MHMIXs) on hydrogen peroxide ($H_2O_2$)-induced cell damage and apoptosis in C2C12 myoblasts. Methods : Cytotoxicity was assessed by an MTT assay. Quantitative evaluation of apoptosis induction and ROS production was evaluated by flow cytometry analysis. Expression levels of apoptosis regulatory and DNA-damage proteins were detected by Western blotting. Result : The inhibition of $H_2O_2$-induced cell proliferation was effectively blocked in extracts of 3: 1: 1 (EMHMIXs-1) or 2: 2: 1 (EMHMIXs-2) of S. flavescens, G. uralensis and D. dasycarpus Turcz, ethanol extracts from various complex extracts in C2C12 myoblasts. EMHMIXs-1 and EMHMIXs-2 also effectively attenuated $H_2O_2$-induced C2C12 cell apoptosis, which was associated with the restoration of the upregulation of Bad and death receptor 4, and downregulation of XIAP and cIAP-1 induced by $H_2O_2$. In addition, these herbal mixtures significantly blocked the $H_2O_2$-induced ROS generation and phosphorylation of $p-{\gamma}H2A.X$, which suggests that they can prevent $H_2O_2$-induced cellular DNA damage. Conclusions : The results suggest that EMHMIXs-1 and EMHMIXs-2 could block the DAN damage and apoptosis of C2C12 myoblasts by oxidative stress through blocking ROS generation.

• Journal of Microbiology
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• v.44 no.6
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• pp.641-648
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• 2006

We previously reported that Skp1, a component of the Skp1-Cullin-F-box protein (SCF) complex essential for the timely degradation of cell cycle proteins by ubiquitination, physically interacts with Bfa1, which is a key negative regulator of the mitotic exit network (MEN) in response to diverse checkpoint-activating stresses in budding yeast. In this study, we initially investigated whether the interaction of Skp1 and Bfa1 is involved in the regulation of the Bfa1 protein level during the cell cycle, especially by mediating its degradation. However, the profile of the Bfa1 protein did not change during the cell cycle in skp1-11, which is a SKP1 mutant allele in which the function of Skp1 as a part of SCF is completely impaired, thus indicating that Skp1 does not affect the degradation of Bfa1. On the other hand, we found that the skp1-12 mutant allele, previously reported to block G2-M transition, showed defects in mitotic exit and cytokinesis. The skp1-12 mutant allele also revealed a specific genetic interaction with ${\Delta}bfa1$. Bfa1 interacted with Skp1 via its 184 C-terminal residues (Bfa1-D8) that are responsible for its function in mitotic exit. In addition, the interaction between Bfa1 and the Skp1-12 mutant protein was stronger than that of Bfa1 and the wild type Skp1. We suggest a novel function of Skp1 in mitotic exit and cytokinesis, independent of its function as a part of the SCF complex. The interaction of Skp1 and Bfa1 may contribute to the function of Skp1 in the mitotic exit.

• Molecules and Cells
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• v.44 no.9
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• pp.647-657
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• 2021

As a pancreatic inflammatory marker, regenerating islet-derived protein 3A (Reg3A) plays a key role in inflammation-associated pancreatic carcinogenesis by promoting cell proliferation, inhibiting apoptosis, and regulating cancer cell migration and invasion. This study aimed to reveal a novel immuno-regulatory mechanism by which Reg3A modulates tumour-promoting responses during pancreatic cancer (PC) progression. In an in vitro Transwell system that allowed the direct co-culture of human peripheral blood-derived dendritic cells (DCs) and Reg3A-overexpressing/ silenced human PC cells, PC cell-derived Reg3A was found to downregulate CD80, CD83 and CD86 expression on educated DCs, increase DC endocytic function, inhibit DC-induced T lymphocyte proliferation, reduce IL-12p70 production, and enhance IL-23 production by DCs. The positive effect of tumour-derived Reg3A-educated human DCs on PC progression was demonstrated in vivo by intraperitoneally transferring them into PC-implanted severe combined immunodeficiency (SCID) mice reconstituted with human T cells. A Reg3A-JAK2/STAT3 positive feedback loop was identified in DCs educated with Reg3A. In conclusion, as a tumour-derived factor, Reg3A acted to block the differentiation and maturation of the most important antigen-presenting cells, DCs, causing them to limit their potential anti-tumour responses, thus facilitating PC escape and progression.

• International Journal of Oral Biology
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• v.34 no.1
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• pp.7-14
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• 2009

Nitric oxide (NO) acts as an intracellular messenger at the physiological level but can be cytotoxic at high concentrations. The cells within periodontal tissues, such as gingival and periodontal fibroblasts, contain nitric oxide syntheses and produce high concentrations of NO when exposed to bacterial lipopolysaccharides and cytokines. However, the cellular mechanisms underlying NO-induced cytotoxicity in periodontal tissues are unclear at present. In our current study, we examined the NO-induced cytotoxic mechanisms in human gingival fibroblasts (HGF). Cell viability and the levels of reactive oxygen species (ROS) were determined using a MTT assay and a fluorescent spectrometer, respectively. The morphological changes in the cells were examined by Diff-Quick staining. Expression of the Bcl-2 family and Fas was determined by RT-PCR or western blotting. The activity of caspase-3, -8 and -9 was assessed using a spectrophotometer. Sodium nitroprusside (SNP), a NO donor, decreased the cell viability of the HGF cells in a dose- and time-dependent manner. SNP enhanced the production of ROS, which was ameliorated by NAC, a free radical scavenger. ODQ, a soluble guanylate cyclase inhibitor, did not block the SNP-induced decrease in cell viability. SNP also caused apoptotic morphological changes, including cell shrinkage, chromatin condensation, and DNA fragmentation. The expression of Bax, a member of the proapoptotic Bcl-2 family, was upregulated in the SNP-treated HGF cells, whereas the expression of Bcl-2, a member of the anti-apoptotic Bcl-2 family, was downregulated. SNP augmented the release of cytochrome c from the mitochondria into the cytosol and enhanced the activity of caspase-8, -9, and -3. SNP also upregulated Fas, a component of the death receptor assembly. These results suggest that NO induces apoptosis in human gingival fibroblast via ROS and the Bcl-2 family through both mitochondrial- and death receptor-mediated pathways. Our data also indicate that the cyclic GMP pathway is not involved in NO-induced apoptosis.

• Journal of the Society of Naval Architects of Korea
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• v.44 no.1 s.151
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• pp.16-25
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• 2007

Studies of unsteady-airfoil flows have been motivated mostly by efforts to avoid. or reduce such undesirable effects as flutter, noise and vibrations, dynamic stall. In this paper, we carry out a computational study of viscous flows around a two-dimensional oscillating airfoil to investigate unsteady effects in these important and challenging flows. A fully implicit incompressible RANS solver has been used for calculating unsteady viscous flows around an airfoil. The cell-centered End order finite volume method is utilized to discretize governing equations. in order to ease the flow computation for fluid region changing in time, improve the qualify of solution and simplify the grid generation for an oscillating airfoil flow, the computational method adopts a moving and deforming grid generation technique based on the multi-block grid topology. The numerical method is applied for calculating viscous flows of an oscillating NACA 0012 in uniform flow. The computational results are compared with available experimental data. Computed results are compared with experimental data and flow characteristics of the experiment are reproduced well In the computed results.

• The Korean Journal of Physiology and Pharmacology
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• v.20 no.3
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• pp.315-324
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• 2016

Human cardiac fibroblasts (HCFs) have various voltage-dependent $K^+$ channels (VDKCs) that can induce apoptosis. Hydrogen peroxide ($H_2O_2$) modulates VDKCs and induces oxidative stress, which is the main contributor to cardiac injury and cardiac remodeling. We investigated whether $H_2O_2$ could modulate VDKCs in HCFs and induce cell injury through this process. In whole-cell mode patch-clamp recordings, application of $H_2O_2$ stimulated $Ca^{2+}-activated$ $K^+$ ($K_{Ca}$) currents but not delayed rectifier $K^+$ or transient outward $K^+$ currents, all of which are VDKCs. $H_2O_2-stimulated$ $K_{Ca}$ currents were blocked by iberiotoxin (IbTX, a large conductance $K_{Ca}$ blocker). The $H_2O_2-stimulating$ effect on large-conductance $K_{Ca}$ ($BK_{Ca}$) currents was also blocked by KT5823 (a protein kinase G inhibitor) and 1 H-[1, 2, 4] oxadiazolo-[4, 3-a] quinoxalin-1-one (ODQ, a soluble guanylate cyclase inhibitor). In addition, 8-bromo-cyclic guanosine 3', 5'-monophosphate (8-Br-cGMP) stimulated $BK_{Ca}$ currents. In contrast, KT5720 and H-89 (protein kinase A inhibitors) did not block the $H_2O_2-stimulating$ effect on $BK_{Ca}$ currents. Using RT-PCR and western blot analysis, three subtypes of $K_{Ca}$ channels were detected in HCFs: $BK_{Ca}$ channels, small-conductance $K_{Ca}$ ($SK_{Ca}$) channels, and intermediate-conductance $K_{Ca}$ ($IK_{Ca}$) channels. In the annexin V/propidium iodide assay, apoptotic changes in HCFs increased in response to $H_2O_2$, but IbTX decreased $H_2O_2$-induced apoptosis. These data suggest that among the VDKCs of HCFs, $H_2O_2$ only enhances $BK_{Ca}$ currents through the protein kinase G pathway but not the protein kinase A pathway, and is involved in cell injury through $BK_{Ca}$ channels.

• The Korean Journal of Physiology
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• v.26 no.2
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• pp.113-122
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• 1992

It is well known that chromaffin cells of adrenal medulla secrete catecholamine in response to sympathetic nerve activation and the influx of $Ca^{2+}$ through the voltage dependent $Ca^{2+}$ channels (VDCC) in the cell membrane do a major role in this secretory process. In this study, we explored the effect of divalent cations on VDCC of rat chromaffin cells. Rat (Sprague-Dawley rat, 150-250 gm) chromaffin cells were isolated and cultured. Standard giga seal, whole cell recording techniques were employed to study $Ca^{2+}$ current with external and internal solutions that could effectively isolate VDCC currents $(NMG\;in\;external\;and\;TEA\;and\;Cs^{2+}\;in\;internal\;solution)$. The voltage dependence and the inactivation time course of VDCC in our cells were identical to those of bovine chromaffin cells. A persistent inward current was first activated by depolarizing step pulse from the holding potential (H.P.) of -80 mV to -40 mV, increased to maximum amplitude at around +10 mV, and became smaller with progressively higher depolarizing pulses to reverse at around +60 mV. The inactivation time constant $(\tau)$, fitted from the long duration test potential (2 sec) was $1295.2{\pm}126.8$ msec $(n=20,\;1\;day\;of\;culture,\;mean\;{\pm}S.E.M.)$ and the kinetic parameters were not altered along the culture duration. Nicardipine $(10\;{\mu}M)$ blocked the current almost completely. Among treated divalent cations such as $Cd^{2+},\;Co^{2+},\;Ni^{2+},\;Zn^{2+}\;and\;,Mn^{2+},\;Cd^{2+}$ was the most potent blocker on VDCC. When the depolarizing step pulse from -80 mV to 10 mV was applied, the equilibrium dissociation constant $(K_d)$ of $Cd^{2+}\;was\;39\;{\mu}M,\;K_d\;of\;Co^{2+}\;was\;100\;{\mu}M\;and\;K_d\;of\;Ni^{2+}];was];780{\mu}M.$ The principal findings of this study are as follows. First, the majority of $Ca^{2+}$ channels in rat chromaffin cells are well classified to L-type $Ca^{2+}$ channel in the view of kinetics and pharmacology. Second, all divalent cations tested could block the $Ca^{2+}$ current and the most potent blocker among the tested was $Cd^{2+}$.

• Journal of Periodontal and Implant Science
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• v.33 no.4
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• pp.705-715
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• 2003

Procedures for treatment of molar furcation invasion defects range from open flap debridement, apically repositioned flap surgery, hemisection, tunneling or extraction, to regenerative therapies using bone grafting or guided tissue regenerative therapy, or a combination of both. Several clinical evaluations using regenerative techniques have reported the potential for osseous repair of treated furcation invasions. Regenerative treatment of maxillary molars are more difficult due to the multiple root anatomy and multiple furcation entrances therefore, purpose of this study was to evaluated histologically compomer and Ketac Silver as a barrier in the treatment of a bi-furcated maxillary premolar. Five adult beagle dogs were used in this experiment. With intrasulcular and crestal incision, mucoperiostcal flap was elevated. Following decortication with 1/2 high speed round bur, furcation defect was made on maxillary premolar. 2 month later one premolar was filled with compomer and the other premolar was filled with Ketac Silver. After 4, 8 weeks, the animals were sacrificed by vascular perfusion. Tissue block was excised including the tooth and prepared for light microscope with H-E staining. Results were as follows. 1. Compomer & Ketac Silver restoration were encapsulated fine connective tissue. 2. In 4 weeks, compomer & Ketac Silver restoration slightly infiltrated inflammatory cells but not disturb the new bone or new cementum formation. 3. In 8 weeks, compomer & Ketac Silver restoration were less infiltrated iflammatory cell and encapsulated fine connective tissue. 4. Therefore, compomer & Ketac Silver filling to the grade III maxillary furcations with multiple root anatomy and multiple furcation entrances is possible clinical method and this technique is useful method for maxillary furcation involvement but it is thought that periodic maintenance should be needed

• JSTS:Journal of Semiconductor Technology and Science
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• v.2 no.2
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• pp.111-124
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• 2002

The ferroelectric RAM (FeRAM) has a great advantage for a system on a chip (SOC) and mobile product memory, since FeRAM not only supports non-volatility but also delivers a fast memory access similar to that of DRAM and SRAM. This work develops at three levels: 1) low voltage operation with boost voltage control of bitline and plateline, 2) reducing bitline capacitance with multiple divided sub cell array, and 3) increasing chip performance with write operation sharing both active and precharge time period. The key techniques are implemented on the proposed hierarchy bitline scheme with proposed hybrid-bitline and high voltage boost control. The test chip and simulation results show the performance of sub-1.5 voltage operation with single step pumping voltage and self-boost control in a cell array block of 1024 ($64{\;}{\times}{\;}16$) rows and 64 columns.