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Poster Session 2 : Characterization of neural cell types expressing peroxiredoxins in mouse brain
( Mei Hua Jin ),( Young Ho Lee ),( Jin Man Kim ),( Hu Nan Sun ),( Eon Yi Moon ),( Min Ho Shong ),( Sun Uk Kim ),( Sang Ho Lee ),( Tae Hoon Lee ),( Dae Yeul Yu ),( Dong Seok Lee ) 한국생화학분자생물학회 (구 한국생화학회) 2005 생화학분자생물학회 춘계학술발표논문집 Vol.2005 No.-
DESIGN AND IMPLEMENTATION OF LONG-DISTANCE SERIAL COMMUNICATION BASED ON WEB
SUN Jian-mei,ZHOU Da-yong 한국멀티미디어학회 2006 한국멀티미디어학회 국제학술대회 Vol.2006 No.-
With the development of the information industry such as internet and so on, Long-distance controlling on the intelligent equipment becomes the direction of the modem people's lives, Long-distance serial communication is good for researching. The paper discusses the long-distance serial communication Based on Web, it introduces the basic structure and the process of realization of the system, analyzes and realizes the software flow of the serial communication, presents the instance of the Long-distance controlling on the manipulator, the same time, it prospects the development of the long-distance based on the embedded system.
Sun, Hu-Nan,Kim, Sun-Uk,Huang, Song Mei,Kim, Jin-Man,Park, Young-Ho,Kim, Seok-Ho,Yang, Hee-Young,Chung, Kyoung-Jin,Lee, Tae-Hoon,Choi, Hoon Sung,Min, Ju Sik,Park, Moon-Ki,Kim, Sang-Keun,Lee, Sang-Rae Blackwell Publishing Ltd 2010 Journal of Neurochemistry Vol.114 No.1
<P><I>J. Neurochem</I>. (2010) <B>114</B>, 39–50.</P><P>Abstract</P><P>Reactive oxygen species (ROS) actively participate in microglia-mediated pathogenesis as pro-inflammatory molecules. However, little is known about the involvement of specific antioxidants in maintaining the microglial oxidative balance. We demonstrate that microglial peroxiredoxin (Prx) 5 expression is up-regulated by lipopolysaccharide (LPS) through activation of the ROS-sensitive signaling pathway and is involved in attenuation of both microglial activation and nitric oxide (NO) generation. Unlike in stimulation of oxidative insults with paraquat and hydrogen peroxide, Prx V expression is highly sensitive to LPS-stimulation in microglia. Reduction of ROS level by treatment with either NADPH oxidase inhibitor or antioxidant ablates LPS-mediated Prx V up-regulation in BV-2 microglial cells and is closely associated with the activation of the c-<I>jun</I> N-terminal kinase (JNK) signaling pathway. This suggests the involvement of ROS/JNK signaling in LPS-mediated Prx V induction. Furthermore, NO induces Prx V up-regulation that is ablated by the addition of inducible nitric oxide synthase inhibitor or deleted mutation of inducible nitric oxide synthase in LPS-stimulated microglia. Therefore, these results suggest that Prx V is induced by cooperative action among the ROS, RNS, and JNK signaling cascades. Interestingly, knockdown of Prx V expression causes the acceleration of microglia activation, including augmented ROS generation and JNK-dependent NO production. In summary, we demonstrate that Prx V plays a key role in the microglial activation process through modulation of the balance between ROS/NO generation and the corresponding JNK cascade activation.</P>
Sun Hu-Nan,Fang Wan,Jin Mei-Hua,Han Ying-Hao,Kim Sun-Uk,Lee Sang-Han,Kim Nam-Soon,Kim Cheol-Hee,Lee Dong-Seok The Korean Society for Biomedical Laboratory Scien 2004 Journal of biomedical laboratory sciences Vol.10 No.4
Inflammatory factor such as Interleukin-1 play important roles in determining the fate of both acute and chronic neurological disorders. We investigated whether inhibitors of PKC or PTK can serve as pharmacological agents to reduce IL-I production and the mechanisms underlying their pharmacological effects in a mixed population of glia. Inhibitors of PKC such as H7, Go6976 and Ro31-8220 significantly reduced both the mRNA and protein levels of IL-1α and IL-β in lipopolysaccharide-activated primary glial cells. While the PTK inhibitor genistein also significantly reduced the production of these cytokines, it did not affect the expression of their mRNA. Taken together, inhibitors of PKC and PTK could serve as pharmacological agents to reduce IL-1 production. However, the mechanisms underlying their pharmacological effects are different. Our results provide evidence that inhibitors of protein kinases can serve as pharmacological agents to modulate IL-1 production in glial cell, and in turn, alleviate neuronal injury.
Mei-Li Lu,Jing Wang,Yang Sun,Cong Li,Tai-Ran Sun,Xu-Wei Hou,Hong-Xin Wang 고려인삼학회 2021 Journal of Ginseng Research Vol.45 No.6
Background: Ginsenoside Rg1 (Rg1) has been well documented to be effective against various cardiovasculardisease. The aim of this study is to evaluate the effect of Rg1 on mechanical stress-inducedcardiac injury and its possible mechanism with a focus on the calcium sensing receptor (CaSR)signaling pathway. Methods: Mechanical stress was implemented on rats through abdominal aortic constriction (AAC)procedure and on cardiomyocytes and cardiac fibroblasts by mechanical stretching with Bioflex CollagenI plates. The effects of Rg1 on cell hypertrophy, fibrosis, cardiac function, [Ca2þ]i, and the expression ofCaSR and calcineurin (CaN) were assayed both on rat and cellular level. Results: Rg1 alleviated cardiac hypertrophy and fibrosis, and improved cardiac decompensation inducedby AAC in rat myocardial tissue and cultured cardiomyocytes and cardiac fibroblasts. Importantly, Rg1treatment inhibited CaSR expression and increase of [Ca2þ]i, which similar to the CaSR inhibitor NPS2143. In addition, Rg1 treatment inhibited CaN and TGF-b1 pathways activation. Mechanistic analysis showedthat the CaSR agonist GdCl3 could not further increase the [Ca2þ]i and CaN pathway related proteinexpression induced by mechanical stretching in cultured cardiomyocytes. CsA, an inhibitor of CaN,inhibited cardiac hypertrophy, cardiac fibrosis, [Ca2þ]i and CaN signaling but had no effect on CaSRexpression. Conclusion: The activation of CaN pathway and the increase of [Ca2þ]i mediated by CaSR are involved incardiac hypertrophy and fibrosis, that may be the target of cardioprotection of Rg1 against myocardialinjury.
Gu, Mei-Ling,Yuan, Cai-Jun,Liu, Xiao-Mei,Zhou, Yi-Chao,Di, Shu-Huan,Sun, Fei-Fei,Qu, Quan-Ying Asian Pacific Journal of Cancer Prevention 2015 Asian Pacific journal of cancer prevention Vol.16 No.13
Purpose: To research the association between pre-treatment elevated platelet count and clinicopathologic characteristics in breast cancer (BC), as well as explore the relationship between pre-treatment elevated platelet count and HER2 status and prognosis of BC patients. Materials and Methods: A retrospective cohort of BC patients who were newly diagnosed or treated by surgery only and had pathological detection results and platelet values in the Department of Oncology, the First Affiliated Hospital of Liaoning Medical College were enrolled from 1/1/2008 until 31/12/2009, and followed up until 31/12/2014. Age, thrombocyte parameters before chemotherapy and/or radiotherapy, immunohistochemical (IHM) indexes, and regional lymph node (LN) involvement and progression-free survival (PFS) were recorded. Results: A total of 447 eligible subjects were included in this research. As we analyzed, for HER2, positive and negative, the incidence rates of elevated platelet count were 25.8% and 14.7% (P<0.05). In the Cox proportional hazards model both variables were independent risk factors for BC (for HER2, OR, 0.592, 95% confidence interval, CI, 0.355 to 0.985, P=0.044;f or PLT, OR, 0.998, 95% CI, 0.996 to 1.000, P=0.042). For ER, PR, Ki67 and LN involvement, the differences were not statistically significant (P>0.05). Conclusions: In this research, pre-treatment elevated level of platelet count demostrated a significantrelationship with HER2 amplification/overexpression, and both variables significantly influenced the prognosis of BC. However, elevated platelet count did not exhibit any association with ER, PR, Ki67 and LN involvement.
Ya Mei Sun,Yan Gao,Feng Gao 대한소화기 기능성질환∙운동학회 2019 Journal of Neurogastroenterology and Motility (JNM Vol.25 No.4
Background/Aims Recently, esophageal mean nocturnal baseline impedance (MNBI) and post-reflux swallow-induced peristaltic wave (PSPW) index have been proposed, which can increase the diagnostic role of multichannel intraluminal impedance and pH recording (MII/pH) for differentiating patients with heartburn. Therefore, our aim is to investigate the role of esophageal proximal MNBI, distal MNBI, and PSPW index in differentiating Chinese patients with heartburn. Methods Patients with heartburn from the Beijing Anzhen Hospital, who underwent upper gastrointestinal endoscopy and 24-hour MII/pH, were enrolled in this study. Results In all, 24 erosive esophagitis (EE), 46 non-erosive reflux disease (NERD), 52 reflux hypersensitivity (RH), and 78 functional heartburn (FH) patients were recruited. The respective median values for the EE, NERD, RH, and FH groups were as follows: proximal MNBI 1858.0, 2147.5, 2374.3, and 2329.0 Ω (P = 0.053); distal MNBI 1243.4, 1506.5, 2451.2, and 2477.3 Ω (P < 0.001); and PSPWI 15.0%, 25.0%, 25.0%, and 45.0% (P < 0.001). Spearman correlation analysis showed that distal MNBI and PSPW index were significantly negatively correlated with acid and bolus exposure time and acid reflux events. Receiver operating characteristic analyses showed that distal MNBI and PSPW index significantly discriminated FH from EE, NERD, and RH (P < 0.001), with cut-off values of 1890.6 Ω and 27.5% and areas under the curve of 0.721 and 0.779, respectively. Conclusion Esophageal distal MNBI and PSPW index could increase the diagnostic role of MII/pH, especially for differentiating Chinese patients with heartburn.
Kim, Sun-Uk,Hwang, Chang Nam,Sun, Hu-Nan,Jin, Mei-Hua,Han, Ying-Hao,Lee, Hwang,Kim, Jin-Man,Kim, Sang-Keun,Yu, Dae-Yeul,Lee, Dong-Seok,Lee, Sang Ho Pharmaceutical Society of Japan 2008 Biological & pharmaceutical bulletin Vol.31 No.5
<P>Imbalance between oxidative stress and antioxidative defence system is generally known as one of mechanisms causing an oxidative stress-medieated neuropathogenesis. Peroxiredoxins (Prxs), a family of antioxidative enzymes neutralizing cellular hydroperoxides, was characterized recently, but their distributions and roles have not been resolved clearly or controversial in the central nervous system, Therefore, the present study was carried out to determine the specific cell types that express Prx I in the mouse brain and primary neural cells, and to examine its antioxidative role in the preferential cell types. Immunohistochemical reactivity for Prx I was detected dominantly in oligodendrocytes and rarely in microglia, whereas strong and specific immunoreactivity for Prx I was observed exclusively in microglia of primary neural cell culture. Further evidences for Prx I specificity were its relatively high expression in BV-2 microglial cells and its upregulated expression in microglia after lipopolysaccharide (LPS) stimulation. These results imply that Prx I can be used as an indicator of microglial activation. Inhibition of p38 MAPK ablated LPS-mediated Prx I upregulation and sensitized the microglia to H<SUB>2</SUB>O<SUB>2</SUB>-mediated cell death. These findings indicate that Prx I function as a scavenger for H<SUB>2</SUB>O<SUB>2</SUB> generated during microglial activation. The results of this study will help in unraveling the neuropathologic roles of the six Prx isoforms in neural function.</P>