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Jong-Ryoul Kim,Sung-Hee Kim,In-Ryoung Kim,Bong-Soo Park,Yong-Deok Kim 대한구강악안면외과학회 2016 대한구강악안면외과학회지 Vol.42 No.1
Objectives: The purpose of this study was to investigate the effects of low-level laser therapy (LLLT) with a diode gallium-aluminum-arsenide (GaAl-As) low-level laser device on the healing and attachment of titanium implants in bone. Materials and Methods: Thirteen New Zealand white male rabbits weighing 3.0±0.5 kg were used for this study. Dental titanium implants (3.75 mm in diameter and 8.5 mm in length, US II RBM plus fixture; Osstem, Seoul, Korea) were implanted into both femurs of each rabbit. The rabbits were randomly divided into a LLLT group and a control group. The LLLT was initiated immediately after surgery and then repeated daily for 7 consecutive days in the LLLT group. Six weeks and 12 weeks after implantation, we evaluated and compared the osseointegration of the LLLT group and control group, using histomorphometric analysis, removal torque testing, and resonance frequency analysis (RFA). The results were statistically significant when the level of probability was 0.05 or less based on a non-parametric Mann-Whitney U-test. Results: The implant survival rate was about 96%. Histologically and histomorphometrically, we observed that the titanium implants were more strongly attached in LLLT group than in control group. However, there was no significant difference between the LLLT group and control group in removal torque or RFA. Conclusion: Histologically, LLLT might promote cell-level osseointegration of titanium implants, but there was no statistically significant effects.
Effect of low-level laser therapy on bisphosphonate-treated osteoblasts
Shin, Sang-Hun,Kim, Ki-Hyun,Choi, Na-Rae,Kim, In-Ryoung,Park, Bong-Soo,Kim, Yong-Deok,Kim, Uk-Kyu,Kim, Cheol-Hun Korean Association of Maxillofacial Plastic and Re 2016 Maxillofacial Plastic Reconstructive Surgery Vol.38 No.-
Background: This study investigates the effect of alendronate-treated osteoblasts, as well as the effect of low-level laser therapy (LLLT) on the alendronate-treated osteoblasts. Bisphosphonate decreases the osteoblastic activity. Various treatment modalities are used to enhance the bisphosphonate-treated osteoblasts; however, there were no cell culture studies conducted using a low-level laser. Methods: Human fetal osteoblastic (hFOB 1.19) cells were treated with $50{\mu}M$ alendronate. Then, they were irradiated with a $1.2J/cm^2$ low-level Ga-Al-As laser (${\lambda}=808{\pm}3nm$, 80 mW, and 80 mA; spot size, $1 cm^2$; NDLux, Seoul, Korea). The cell survivability was measured with the MTT assay. The three cytokines of osteoblasts, receptor activator of nuclear factor ${\kappa}B$ ligand (RANKL), osteoprotegerin (OPG), and macrophage colony-stimulating factor (M-CSF) were analyzed. Results: In the cells treated with alendronate at concentrations of $50{\mu}M$ and higher, cell survivability significantly decreased after 48 h (p < 0.05). After the applications of low-level laser on alendronate-treated cells, cell survivability significantly increased at 72 h (p < 0.05). The expressions of OPG, RANKL, and M-CSF have decreased via the alendronate. The RANKL and M-CSF expressions have increased, but the OPG was not significantly affected by the LLLT. Conclusions: The LLLT does not affect the OPG expression in the hFOB cell line, but it may increase the RANKL and M-CSF expressions, thereby resulting in positive effects on osteoclastogenesis and bone remodeling.
Lee, Jeong-Sik,Jang, Deok-Jin,Lee, Nuribalhae,Ko, Hyoung-Gon,Kim, Hyoung,Kim, Yong-Seok,Kim, Byungwoo,Son, Junehee,Kim, Sung Hyun,Chung, Heekyoung,Lee, Mun-Yong,Kim, Woon Ryoung,Sun, Woong,Zhuo, Min,A The Society 2009 The Journal of neuroscience Vol.29 No.26
<P>The cAMP cascade and vascular endothelial growth factor (VEGF) are critical modulators of depression. Here we have tested whether the antidepressive effect of the cAMP cascade is mediated by VEGF in the adult hippocampus. We used a conditional genetic system in which the Aplysia octopamine receptor (Ap oa(1)), a G(s)-coupled receptor, is transgenically expressed in the forebrain neurons of mice. Chronic activation of the heterologous Ap oa(1) by its natural ligand evoked antidepressant-like behaviors, accompanied by enhanced phosphorylation of cAMP response element-binding protein and transcription of VEGF in hippocampal dentate gyrus (DG) neurons. Selective knockdown of VEGF in these cells during the period of cAMP elevation inhibited the antidepressant-like behaviors. These findings reveal a molecular interaction between the cAMP cascade and VEGF expression, and the pronounced behavioral consequences of this interaction shed light on the mechanism underlying neuronal VEGF functions in antidepression.</P>
Acute oral toxicity of the ethyl acetate fraction of <i>Orostachys japonicus</i> in mice
Kim, Seon-Hee,Ryu, Deok-Seon,Lee, Hyeong-Seon,Shin, Hye-Ryoung,Kwon, Ji-Hye,Lee, Dong-Seok Informa Healthcare USA, Inc. 2014 PHARMACEUTICAL BIOLOGY Vol.52 No.10
<P><I>Context</I>: <I>Orostachys japonicus</I> (Crassulaceae) is referred to as Wa-song in Korea. It is used as an anti-inflammatory, antifebrile, hemostatic, and anti cancer agent, and as an antidote.</P><P><I>Objective</I>: The purpose of this study was to evaluate the acute toxicity of the ethyl acetate fraction of <I>O. japonicus</I> (OJE) after the oral administration in Balb/c mice of both sexes.</P><P><I>Materials and methods</I>: Mice were oral administered a single doses of 500, 1000, and 2000 mg/kg of body weight and were monitored for 14 d. Biochemical parameters [aspartate amino transferase (AST), alanine amino transferase (ALT), alkaline phosphatase (ALP), total protein (TP), globulin (GB), total cholesterol (TC), triglyceride (TG), blood urea nitrogen (BUN), and creatinine (CR)] and histopathological examination of liver were performed.</P><P><I>Results and conclusion</I>: No animals died and no toxic changes were observed in clinical signs, body weight, and organ weight. The LD<SUB>50</SUB> of orally administered OJE was higher than 2000 mg/kg/d in both sexes. No toxicological findings were found in biochemical parameters. In histophathological examination, neutrophilic infiltration was observed at a dose of 2000 mg/kg group in both sexes. These finding suggest that oral administration of OJE does not produce acute toxicity. Therefore, these results could provide satisfactory preclinical evidence of safety to launch clinical trials on standardized formulation of OJE to be a biohealth product.</P>
Yarishkin, Oleg V.,Hwang, Eun-Mi,Kim, Dong-Gyu,Yoo, Jae-Cheal,Kang, Sang-Soo,Kim, Deok-Ryoung,Shin, Jae-Hee-Jung,Chung, Hye-Joo,Jeong, Ho-Sang,Kang, Da-Won,Han, Jae-Hee,Park, Jae-Yong,Hong, Seong-Geun The Korean Society of Pharmacology 2009 The Korean Journal of Physiology & Pharmacology Vol.13 No.6
A non-steroidal anti-inflammatory drug (NSAID) has many adverse effects including cardiovascular (CV) risk. Diclofenac among the nonselective NSAIDs has the highest CV risk such as congestive heart failure, which resulted commonly from the impaired cardiac pumping due to a disrupted excitationcontraction (E-C) coupling. We investigated the effects of diclofenac on the L-type calcium channels which are essential to the E-C coupling at the level of single ventricular myocytes isolated from neonatal rat heart, using the whole-cell voltage-clamp technique. Only diclofenac of three NSAIDs, including naproxen and ibuprofen, significantly reduced inward whole cell currents. At concentrations higher than $3\;{\mu}M$, diclofenac inhibited reversibly the $Na^+$ current and did irreversibly the L-type $Ca^{2+}$ channels-mediated inward current $(IC_{50}=12.89\pm0.43\;{\mu}M)$ in a dose-dependent manner. However, nifedipine, a well-known L-type channel blocker, effectively inhibited the L-type $Ca^{2+}$ currents but not the $Na^+$ current. Our finding may explain that diclofenac causes the CV risk by the inhibition of L-type $Ca^{2+}$ channel, leading to the impairment of E-C coupling in cardiac myocytes.
Pyo, Se-Jeong,Song, Won-Wook,Kim, In-Ryoung,Park, Bong-Soo,Kim, Cheul-Hong,Shin, Sang-Hun,Chung, In-Kyo,Kim, Yong-Deok Baillière Tindall ; Springer London 2013 Lasers in medical science Vol.28 No.2
<P>The aim of this study was to examine the effect of low-level laser therapy (LLLT) on the cell viability and the expression of hypoxia-inducible factor-1s (HIF-1s), bone morphogenic protein-2 (BMP-2), osteocalcin, type I collagen, transforming growth factor-β1 (TGF-β1), and Akt in hypoxic-cultured human osteoblasts. Human fetal osteoblast cells (cell line 1.19) were cultured under 1?% oxygen tension for 72?h. Cell cultures were divided into two groups. At the experimental side, low-level laser (808?nm, GaAlAs diode) was applied at 0, 24, and 48?h. After irradiation, each cell culture was incubated 24?h more under hypoxia. Total energy was 1.2, 2.4, and 3.6?J/cm(2), respectively. Non-irradiated cultures served as controls. Comparisons between the two groups were analyzed by t test; a p value <0.05 was considered statistically significant. Hypoxia resulted in a decrease in the expression of type I collagen, osteocalcin, and TGF-β1 (p?<?0.001, p?<?0.001, and p?<?0.01, respectively). Cell viability and BMP-2 expression were not decreased by hypoxic condition. On the other hand, LLLT on hypoxic-cultured osteoblast promoted the expression of BMP-2, osteocalcin, and TGF-β1 (p?<?0.05, p?<?0.01, and p?<?0.001, respectively). Cell proliferation was also increased time-dependently. However, hypoxia decreased in type I collagen expression (p?<?0.001), and LLLT did not affect type I collagen expression in hypoxic-cultured osteoblasts. Furthermore, LLLT inhibited HIF-1 and Akt expression in hypoxic conditioned osteoblasts. We concluded that LLLT induces the expression of BMP-2, osteocalcin, and TGF- β1 in 1?% hypoxic-cultured human osteoblasts.</P>
Oleg V. Yarishkin,Eun Mi Hwang,Donggyu Kim,Jae Cheal Yoo,Sang Soo Kang,Deok Ryoung Kim,Jae-Hee-Jung Shin,Hye-Joo Chung,Ho-Sang Jeong,Dawon Kang,Jaehee Han,Jae-Yong Park,Seong-Geun Hong 대한생리학회-대한약리학회 2009 The Korean Journal of Physiology & Pharmacology Vol.13 No.6
A non-steroidal anti-inflammatory drug (NSAID) has many adverse effects including cardiovascular (CV) risk. Diclofenac among the nonselective NSAIDs has the highest CV risk such as congestive heart failure, which resulted commonly from the impaired cardiac pumping due to a disrupted excitation- contraction (E-C) coupling. We investigated the effects of diclofenac on the L-type calcium channels which are essential to the E-C coupling at the level of single ventricular myocytes isolated from neonatal rat heart, using the whole-cell voltage-clamp technique. Only diclofenac of three NSAIDs, including naproxen and ibuprofen, significantly reduced inward whole cell currents. At concentrations higher than 3ՌM, diclofenac inhibited reversibly the Na<sup>+</sup> current and did irreversibly the L-type Ca<sup>2+</sup> channels-mediated inward current (IC<sub>50</sub>=12.89±0.43ՌM) in a dose-dependent manner. However, nifedipine, a well-known L-type channel blocker, effectively inhibited the L-type Ca<sup>2+</sup> currents but not the Na<sup>+</sup> current. Our finding may explain that diclofenac causes the CV risk by the inhibition of L-type Ca<sup>2+</sup> channel, leading to the impairment of E-C coupling in cardiac myocytes.