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뇌동맥류 파열의 계절적 변동과 유발인자에 대한 임상분석
김윤,전용선,이남영 충남대학교 의과대학 지역사회의학연구소 1996 충남의대잡지 Vol.23 No.2
The author investigated activities and events of the patients as well as diurnal and seasonal variation in the onset of aneurysmal rupture in 124 consecutive patients. The result showed that the onset of aneurysmal rupture was associated with nonactive state(sleep, rest) in 17.9%, working on job or house in 12.8%, bathing and/ or washing up in 7.2%. Diurnal variation of the onset of aneurysmal rupture showed two broad peak from 6 to 12 a. m. (32.2%) and from 7 to 11 p. m. (24.1%). The seasonal variation of onset of aneurysmal rupture showed the large peak in from late winter to early spring. The 22.6% patients rebleeded after initial bleeding, the first day rebleeding rate is 17.9% and rebleeding in a week is 71.4%. We concluded that onset of the aneurysmal rupture is related not only to physiol ogical circadian periodicity of blood pressure change but also to the activities or event which induced a sharp rising blood pressure and changing the venous and cerebrospinal fluid pressure.
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>
김난영(Nan-Young Kim),김영숙(Young-Sug Kim),김명길(Myung-Gil Kim),정홍래(Hong-Rae Jung),김윤성(Yun-Sung Kim),김한택(Han-Taek Kim),이선우(Sun-Woo Lee),채경석(Kyeng-Suk Chae),윤미혜(Mi-Hye Yoon) 한국농약과학회 2012 농약과학회지 Vol.16 No.1
We analysed 149 samples of Korean traditional herbal tea materials. The 156 pesticides were analyzed by GC/ECD and NPD, detected pesticides were confirmed by GC-TOF/MS. Sample preparation was performed bv multi-residue analysis method of multiclass pesticides of the Korea Food Code. The residual pesticides were detected in 22 samples(14.8%), the highest detection frequency samples are lycium and jujube. Detected pesticides in Korean traditional herbal tea materials were chlorpyrifos (5 samples), chlorothalonil (3 samples), cypermethrin (3 samples), hexaconazol (3 samples) and cyhalothrin(3 samples). The pesticide types detected in Korean traditional herbal tea materials were organophosphorus(29.2%), pyrethroids(16.7%), organochlorines (12.5%) and triazoles(12.5%). The 5 samples(lycium, jujube, chrysanthemum, balloon-flower, milk vetch root) were detected pesticides below MRLs, 2 samples(cornus fruit, cnidium) were detected pesticides unnotificated MRLs.
Novel porcine model of acute myocardial infarction using polyethylene terephthalate
Yong Sook Kim,Nan Yeol Kim,In-Ho Bae,Jun Kyu Park,Dae Sung Park,Jae Won Shim,Wan Suk Kang,Han Byul Kim,Bong-Seok Song,Bon-Sang Koo,Kang-Jin Jeong,Sun-Uk Kim,Hyun Kuk Kim,Sung Soo Kim,Min Chul Kim,Doo 충북대학교 동물의학연구소 2019 Journal of Biomedical and Translational Research Vol.20 No.2
Sun, Hu-Nan,Kim, Sun-Uk,Lee, Mi-Sook,Kim, Sang-Keun,Kim, Jin-Man,Yim, Mijung,Yu, Dae-Yeul,Lee, Dong-Seok Pharmaceutical Society of Japan 2008 Biological & pharmaceutical bulletin Vol.31 No.9
<P>The importance of microglial reactive oxygen species (ROS) signaling in neuroinflammatory processes has been well demonstrated; however, relatively little is known regarding the related mechanisms underlying these processes. Here, we show that ROS-dependent signal pathways that govern microglial phagocytosis are highly dependent upon nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (Nox) activation. Specifically, phagocytosis was greatly reduced by both antioxidant and Nox inhibitor treatments in lipopolysaccharide (LPS)-stimulated BV-2 microglia. Additionally, there was a marked reduction in intracellular ROS content. These results suggest that Nox is the main ROS source for LPS-induced microglial phagocytosis. More decisive evidence for the involvement of ROS in phagocytosis was obtained from an examination of phosphatidyl inositol 3-kinase (PI3-K) and p38 mitogen-activated protein kinase (MAPK) signal pathway activation under reduced ROS levels. These two kinases were activated by LPS treatment and inhibited by ROS neutralization and Nox inhibition. We conclude that microglial phagocytosis requires ROS-dependent PI3-K and p38 MAPK activation and that Nox-derived ROS functions as an upstream regulator of both PI3-K and p38 MAPK. These findings will provide a fundamental basis for a therapeutic modality in inflammation-mediated neurodiseases.</P>
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>