• Journal of the Korean Crystal Growth and Crystal Technology
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• v.11 no.5
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• pp.203-206
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• 2001

The applicability of shaped growth of yttrium orthovanadate was approved by successful growth of rod-like single crystals with the rectangular shape. Nd-doped single crystals with content of $Nd^{3+}$ ions of 1,2,3,5 atomic % in the starting melt were grown by the EFG technique with the size up to $10^{*}10mm$ in section and up to 85 mm in length. For the testing of the multiple growth of the orthovanadates, two and three Nd-and Yb-doped $YVO_{4}$ single crystals were grown by the EFG technique simultaneously up to 110 mm in length.

• BMB Reports
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• v.45 no.5
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• pp.317-322
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• 2012

2-deoxy-D-glucose(2DG)-caused endoplasmic reticulum (ER) stress inhibits protein phosphorylation at tyrosine residues. However, the accurate regulatory mechanisms, which determine the inflammatory response of chondrocytes to ER stress via protein tyrosine phosphorylation, have not been systematically evaluated. Thus, in this study, we examined whether protein phosphorylation at tyrosine residues can modulate the expression and glycosylation of COX-2, which is reduced by 2DG-induced ER stress. We observed that protein tyrosine phosphatase (PTP) inhibitors, sodium orthovanadate (SOV), and phenylarsine oxide (PAO) significantly decreased expression of ER stress inducible proteins, glucose-regulated protein 94 (GRP94), and CCAAT/ enhancer-binding-protein- related gene (GADD153), which was induced by 2DG. In addition, we demonstrated that SOV and PAO noticeably restored the expression and glycosylation of COX-2 after treatment with 2DG. These results suggest that protein phosphorylation of tyrosine residues plays an important role in the regulation of expression and glycosylation during 2DG-induced ER stress in rabbit articular chondrocytes.

• Medical Lasers
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• v.10 no.2
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• pp.82-89
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• 2021

Background and Objectives Due to changes in diet and lifestyle, the number of obese people worldwide is steadily increasing. Obesity has an adverse effect on a healthy life, so it needs treatment and improvement. Research related to this is continuously being conducted. Materials and Methods The laser system to compact designed using 808 nm laser diode and Neodymium Yttrium orthovanadate generates a 1064 nm wavelength, the periodically polarized nonlinear crystal pumping laser beam. The pulsed 1064 nm wavelength beam passing through the AO Q-switch is used as the pumping light of the nonlinear optical crystal and is irradiated to the periodic polarized nonlinear optical crystal with a quasi-phase matching period. Nonlinear optical crystals use an oven to control the temperature to generate the desired 1980 nm and 2300 nm wavelengths. Results The 1980 nm and 2300 nm wavelengths generated by temperature control of nonlinear optical crystals are effective for lipolysis. A fiber catheter was used so that the laser could be directly irradiated to the fat cells. In particular, the new wavelength (1980 nm, 2300 nm) can increase the fat reduction effect with low energy (1.3 W). When a laser with a combination wavelength of 1980 nm and 2300 nm was used, an average lipolysis effect of 20% was obtained. Conclusion A mid-infrared lipolysis laser system with excellent absorption of fat and water has been developed. We conducted a princlinical study to confirm the efficacy and safety of the lipolysis laser system, and obtained good results for lipolysis with low energy.

• The Korean Journal of Physiology and Pharmacology
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• v.10 no.5
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• pp.243-249
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• 2006

The effect of genistein, widely used as a specific tyrosine kinase inhibitor, on rat brain Kv1.5 channels which were stably expressed in Chinese hamster ovary cells was investigated using the whole-cell patch-clamp technique. Genistein inhibited Kv1.5 currents at +50 mV in a concentration-dependent manner, with an $IC_{50}$ of $54.7{\pm}8.2\;{\mu}M$ and a Hill coefficient of $1.1{\pm}0.2$. Pretreatment of Kv1.5 with protein tyrosine kinase inhibitors ($10\;{\mu}M$ lavendustin A and $100\;{\mu}M$ AG1296) and a tyrosine phosphatase inhibitor ($500\;{\mu}M$ sodium orthovanadate) did not block the inhibitory effect of genistein. The inhibition of Kv1.5 by genistein showed voltage-independence over the full activation voltage range positive to 0 mV. The activation (at +50 mV) kinetics was significantly delayed by genistein: time constant for an activation of $1.4{\pm}0.2$ msec under control conditions and $10.0{\pm}1.5$ msec in the presence of $60\;{\mu}M$ genistein. Genistein also slowed the deactivation of the tail currents, resulting in a crossover phenomenon: a time constant of $11.4{\pm}1.3$ msec and $40.0{\pm}4.2$ msec under control conditions and in the presence of $60\;{\mu}M$ genistein, respectively. Inhibition was reversed by the application of repetitive depolarizing pulses, especially during the early part of the activating pulse. These results suggest that genistein directly inhibits Kv1.5 channels, independent of phosphotyrosine-signaling pathway.

• The Korea Journal of Herbology
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• v.22 no.3
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• pp.27-37
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• 2007

Objectives: Hepatocellular carcinoma is the most common primary malignant tumor of the liver worldwide. In-Jin-Ho-Tang(IJHT) has been used as a traditional Chinese herbal medicine since ancient time. and today it is widely applied as a medication for jaundice which is associated with inflammation in liver. In this study, I investigated whether methanol extract of IJHT induced HepG2 cancer cell death. Methods: Cytotoxic activity of IJHT on HepG2 cells was using XTT assay. Apoptosis induction by Ros A in HCT116 cells was verified by the induction of cleavage of poly ADP-ribose polymerase (PARP). and activation of caspase-3, -8 and -9. The release of cytochrome c from mitochondria to cytosol. the level of Bcl-2 and Bax and the expression of p53 and p21 were examined by western blotting analysis. Furthermore, MAPKs activation was analyzed by western blotting analysis. Results: IJHT induced apoptosis in HepG2 cells. And treatment of IJHT resulted in the release of cytochrome c into cytosol, decreased anti-apoptotic Bcl-2, and increased pri-apoptotic Bax expression. IJHT markedly inactivated extracellular signal-regulated kinase (ERK1/2), and activated p38 mitogen-activated protein (MAP) kinase. Sodium orthovanadate (SOV), a phosphatase inhibitor, to reverse IJHT-induced ERK1/2 inactivation and SB203580, a specific p38 MAP Kinase inhibitor efficiently blocked apoptosis of HepG2. Thus, IJHT induces apoptosis in HepG2 cells via MAP kinase modulation. Conclusion: These results indicated that IJHT has some potential for use as an anti-cancer agent.