• The Journal of the Korean bone and joint tumor society
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• v.10 no.1
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• pp.29-33
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• 2004

A giant cell tumor (GCT) of the distal radius is not common. Curettage with bone cementation is considered as a treatment of choice but, in the case of recurrence, marked cortical disruption, or articular invasion, en bloc excision and reconstruction with proximal fibular bone graft is usual procedure. In reconstruction of en bloc resected distal radius which had recurred GCT after conservative operation, we used the ultrahigh molecular weight polyethylene (UHMWPE) liner with intramedullary rod and bone cement, because the contamination was extent in previous operation and recurrence after fibular bone graft was fearful. This article introduce our new surgical procedure.

• Toxicological Research
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• v.31 no.4
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• pp.331-337
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• 2015

Synthetic pyrethroids (SPs) are the most common pesticides which are recently used for indoor pest control. The widespread use of SPs has resulted in the increased exposure to wild animals and humans. Recently, some SPs are suspected as endocrine disrupting chemicals (EDCs) and have been assessed for their potential estrogenicity by adopting various analyzing assays. In this study, we examined the estrogenic effects of lambda-cyhalothrin (LC) and cypermethrin (CP), the most commonly used pesticides in Korea, using BG-1 ovarian cancer cells expressing estrogen receptors (ERs). To evaluate the estrogenic activities of two SPs, LC and CP, we employed MTT assay and reverse-transcription polymerase chain reaction (RT-PCR) in LC or CP treated BG-1 ovarian cancer cells. In MTT assay, LC ($10^{-6}M$) and CP ($10^{-5}M$) significantly induced the growth of BG-1 cancer cells. LC or CP-induced cell growth was antagonized by addition of ICI 182,720 ($10^{-8}M$), an ER antagonist, suggesting that this effect appears to be mediated by an ER-dependent manner. Moreover, RT-PCR results showed that transcriptional level of cyclin D1, a cell cycle-regulating gene, was significantly up-regulated by LC and CP, while these effects were reversed by co-treatment of ICI 182,780. However, p21, a cyclin D-ckd-4 inhibitor gene, was not altered by LC or CP. Moreover, $ER{\alpha}$ expression was not significantly changed by LC and CP, while down-regulated by E2. Finally, in xenografted mouse model transplanted with human BG-1 ovarian cancer cells, E2 significantly increased the tumor volume compare to a negative control, but LC did not. Taken together, these results suggest that LC and CP may possess estrogenic potentials by stimulating the growth of BG-1 ovarian cancer cells via partially ER signaling pathway associated with cell cycle as did E2, but this estrogenic effect was not found in in vivo mouse model.

• Biomolecules & Therapeutics
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• v.12 no.1
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• pp.25-33
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• 2004

In this study we investigated whether ATP loss was involved in the potentiated death of immunostimulated rat primary astrocytes in glucose-deprived condition. Rat primary astrocytes immunostimulated with LPS plus IFN-${\gamma}$ for 48 h underwent death upon glucose deprivation, which dependent on the production of peroxynitrite. Intracellular ATP level synergistically decreased by glucose deprivation in immunostimulated astrocytes but not in control cells, and the loss of ATP occurred well ahead of the LDH release. The synergistic cell death and ATP loss by immunostimulation and glucose deprivation were inhibited by iNOS inhibitor (L-NAME and L-NNA) or peroxynitrite decomposition catalyst (also a superoxide anion scavenger), Mn(III)tetrakis(N-methyl-4'-pyridyl)porphyrin (MnTMPyP). Exogenous addition of peroxynitrite generator, SIN-l timedependently induced ATP loss and cell death in the glucose-deprived astrocytes. Depletion of intracellular glutathione (GSH) and dis겨ption of mitochondrial transmembrane potential (MTP) were also observed under same conditions. Supply cellular ATP by the addition of exogenous adenosine or ATP during glucose deprivation inhibited ATP depletion, GSH depletion, MTP disruption and cell death in SIN-l treated or immunostimulated astrocytes. This study showed that perturbation in the regulation of intracellular ATP level in immunostimulated astrocytes might make them more vulnerable to energy challenging stimuli.

• Parasites, Hosts and Diseases
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• v.49 no.1
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• pp.1-8
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• 2011

The pathogenesis and pathophysiology of Acanthamoeba infections remain incompletely understood. Phospholipases are known to cleave phospholipids, suggesting their possible involvement in the host cell plasma membrane disruption leading to host cell penetration and lysis. The aims of the present study were to determine phospholipase activities in Acanthamoeba and to determine their roles in the pathogenesis of Acanthamoeba. Using an encephalitis isolate (T1 genotype), a keratitis isolate (T4 genotype), and an environmental isolate (T7 genotype), we demonstrated that Acanthamoeba exhibited phospholipase $A_2$ (PLA$_2$). and phospholipase D (PLD) activities in a spectrophotometry-based assay. Interestingly, the encephalitis isolates of Acanthamoeba exhibited higher phospholipase activities as compared with the keratitis isolates, but the environmental isolates exhibited the highest phospholipase activities. Moreover, Acanthamoeba isolates exhibited higher PLD activities compared with the PLA$_2$. Acanthamoeba exhibited optimal phospholipase activities at $37^{\circ}C$ and at neutral pH indicating their physiological relevance. The functional role of phospholipases was determined by in vitro assays using human brain microvascular endothelial cells (HBMEC), which constitute the blood-brain barrier. We observed that a PLD-specific inhibitor, i.e., compound 48/80, partially inhibited Acanthamoeba encephalitis isolate cytotoxicity of the host cells, while PLA$_2$-specific inhibitor, i.e., cytidine 5'-diphosphocholine, had no effect on parasite-mediated HBMEC cytotoxicity. Overall, the T7 exhibited higher phospholipase activities as compared to the T4. In contract, the T7 exhibited minimal binding to, or cytotoxicity of, HBMEC.

• Journal of Microbiology
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• v.39 no.4
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• pp.286-292
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• 2001

During mitosis. the proper segregation of duplicated chromosomes is corrdinated by a spindle check-point. The bifurcated spindle checkpoint blocks cell cycle progression at metaphase by monitoring unattached kinetochores and inhibits mitotic exit in response to the misorientation of the mitotic spin- dle Ibd1p/Bfa1p is a spindle checkpoint regulator of budding yeast in the Bub2p checkpoint pathway for mitotic exit and its disruption abolishes mitotic arrest when proper organization of the mitotic spin-dls inhibited. Ibd1p/Bfa1p localizes to the spindle pole body, a microtublue-organizing center in yeast, and its overexpression arrests the cell cycle in 80% of cells with an enlarged budy at mitosis and in 20 % of cells with multiple buds. In this study, we found that the C-terminus of Ibd1p/Bfa1p phys-ically interacts with Skp1p, a key component of SCF (Skp1/cullin/F-box) complex for ubiquition-medi-ated proteolysis of cel cycle regulatores as well as an evolutionally conserved kinetochore protein for cell cycle progression. A putative F-box motif was found in the C-terminus of Ibd1p/Bfa1p and its function was investigated by making mutants of conserved residues in the motif. These Ibd1p/Bfa1p mutants of a putative F-box interacted with SKp1p in vitro by two-hybrid assays as wild type Ibd1p/Bfa1p. Also these Ibd1p/Bfa1p utants displayed the overexpression phenotypes of wild type Ibd1p, when over-expressed under inducible promoters . These results suggest that a putative F-box motif of Ibd1p/Bfa1p is not essential for the interaction with SKp1p and its function in mitotic exit and cytokinesis.

• The Korean Journal of Malacology
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• v.29 no.1
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• pp.7-13
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• 2013

This study was conducted to find out biological response of Manila clam, Ruditapes philippinarum exposed to lead (Pb). Experimental period was four weeks. Experimental groups were composed of one control condition and three lead exposure conditions (0.25, 0.50 and 1.00 mg/l). The results of the study confirmed that lead induces reduction of survival rate and oxygen consumption rate and histopathology of organ structure of the bivalve. Oxygen consumption rate was observed exposure groups lower than control decline by 25%-72%. Histological analysis of organ system illustrated expansion of hemolymph sinus, disappearance of epidermal layer and degeneration of connective tissue layer of the mantle. Also, histological degenerations as epithelial necrosis and hyperplasia of mucous cells are recognized in the gill and it was observed expansion of hemolymph sinus, disruption of epithelial layer, decrease of mucous cell and degeneration of connective tissue layer in the foot. In the digestive diverticulum, it was showed atrophy of basophilic cell and degeneration of epithelial cell in the digestive tubules, and as the concentration of lead increased the accumulation of lipofuscin increased.

• Molecules and Cells
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• v.41 no.8
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• pp.733-741
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• 2018

Mutations in spliceosome components have been implicated in carcinogenesis of various types of cancer. One of the most frequently found is U2AF1 S34F missense mutation. Functional analyses of this mutation have been largely limited to hematological malignancies although the mutation is also frequently seen in other cancer types including lung adenocarcinoma (LUAD). We examined the impact of knockdown (KD) of wild type (wt) U2AF1 and ectopic expression of two splice variant S34F mutant proteins in terms of alternative splicing (AS) pattern and cell cycle progression in A549 lung cancer cells. We demonstrate that induction of distinct AS events and disruption of mitosis at distinct sub-stages result from KD and ectopic expression of the mutant proteins. Importantly, when compared with the splicing pattern seen in LUAD patients with U2AF1 S34F mutation, ectopic expression of S34F mutants but not KD was shown to result in common AS events in several genes involved in cell cycle progression. Our study thus points to an active role of U2AF1 S34F mutant protein in inducing cell cycle dysregulation and mitotic stress. In addition, alternatively spliced genes which we describe here may represent novel potential markers of lung cancer development.

• Advances in environmental research
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• v.3 no.4
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• pp.307-319
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• 2014

Four chickpea cultivars viz. kabuli (Pusa 1088 and Pusa 1053) and desi (Pusa 1103 and Pusa 547) differing in sensitivity to high temperature conditions were analyzed in earthern pot (30 cm) at different stages of growth and development in the year of 2010 and 2011. Pusa-1053 (kabuli type) showed maximum photosynthetic rate and least by Pusa-547 (desi type), whereas maximum cell membrane thermostability were recorded in Pusa-1103 and minimum in Pusa-1088. Among the treatments, the plants grown under elevated temperature conditions had produced 13.01% more significant data in comparison to plants grown under continuous natural conditions. Stomatal conductance were reduced 44.25% under elevated temperature conditions than natural conditions, whereas 35.56%, when plants grown under initially natural conditions upto 30DAS, then 30-60DAS elevated temperature and finally shifted to natural conditions till harvest. In case of Pusa-1103, stomatal conductance was maximum as compared to rest of 2.7% from Pusa-1053, 8.9% from Pusa-1088, and 10.3% in Pusa-547 throughout the study. Plants grown under continuous elevated temperature conditions had produced 15.30% and 15.32% more significant membrane thermostability index in comparison to continuous natural conditions at vegetative stage and 19.40% and 18.44% at flowering stage, while the better response was recorded at pod formation stage. Pusa-1053 had given 2.8% more membrane thermostability index than Pusa-1088 and Pusa-1103 had given 1.6% more membrane thermostability index than Pusa-547 in the present study. The membrane disruption caused by high temperature may alter water ion and inorganic solutes movement, photosynthesis and respiration. Thus, thermostability of the cell membrane depends on the degree of the electrolyte leakage.

• The Journal of Korean Institute of Communications and Information Sciences
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• v.36 no.6B
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• pp.697-709
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• 2011

For improvement of wireless Internet service quality at vehicle's moving speed, it is advised to reduce the service disruption time by reducing the handover frequency on vehicle's moving path. Particularly, it is advantageous to avoid the handover to cell whose dwell time is short or can be ignored in terms of service continuity and average throughput. This paper proposes the handover scheme that is suitable for vehicle in order to improve the wireless Internet service quality. In the proposed scheme, the handover process continues to be learned before being modeled to Discrete-Time Markov Chain (DTMC). This modeling reduces the handover frequency by preventing the handover to cell that could provide service sufficiently to passenger even when vehicle passed through the cell but there was no need to perform handover. In order to verify the proposed scheme, we observed the average number of handovers, the average RSSI and the average throughput on various moving paths that vehicle moved in the given urban environment. The experiment results confirmed that the proposed scheme was able to provide the improved wireless Internet service to vehicle that moved to some degree of consistency.

• The Korean Journal of Physiology and Pharmacology
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• v.23 no.2
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• pp.121-130
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• 2019

Glutamate toxicity-mediated mitochondrial dysfunction and neuronal cell death are involved in the pathogenesis of several neurodegenerative diseases as well as acute brain ischemia/stroke. In this study, we investigated the neuroprotective mechanism of dieckol (DEK), one of the phlorotannins isolated from the marine brown alga Ecklonia cava, against glutamate toxicity. Primary cortical neurons ($100{\mu}M$, 24 h) and HT22 neurons (5 mM, 12 h) were stimulated with glutamate to induce glutamate toxic condition. The results demonstrated that DEK treatment significantly increased cell viability in a dose-dependent manner ($1-50{\mu}M$) and recovered morphological deterioration in glutamate-stimulated neurons. In addition, DEK strongly attenuated intracellular reactive oxygen species (ROS) levels, mitochondrial overload of $Ca^{2+}$ and ROS, mitochondrial membrane potential (${\Delta}{\Psi}_m$) disruption, adenine triphosphate depletion. DEK showed free radical scavenging activity in the cell-free system. Furthermore, DEK enhanced protein expression of heme oxygenase-1 (HO-1), an important anti-oxidant enzyme, via the nuclear translocation of nuclear factor-like 2 (Nrf2). Taken together, we conclude that DEK exerts neuroprotective activities against glutamate toxicity through its direct free radical scavenging property and the Nrf-2/HO-1 pathway activation.