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들기자세 유형별 L₄-L?의 근전도 분석 : At the Base Knee Angle 무릎각도를 중심으로
서국웅,노석규,윤양진,정미라,이훈식,박승범 釜山大學校 附設 體育科學硏究所 1998 體育科學硏究所 論文集 Vol.14 No.-
This research is to find out the most suitable lifting posture and to provide fundamental data for preventing usual injuries. To do this, we select five male graduates and five female graduates of P university, analyze their muscular actions in terms of posture types, measure the limit value of weight lifting by comparing each lifting posture type(knee angle 40˚, 80˚, 180˚) with action amplitudes of two parts of erector spinae muscle, and draw our conclusion as follow ; 1. In case of every lifting posture(that is, knee angle 40˚, 80˚, 180˚), females have higher muscular conductivity value in L⁴-L? of right erector spinae muscle than males(p<.001), but in L⁴-L? of left erector spinae males has higher muscular conductivity value than females(p<.001). 2. Males show lower degree of change in muscular conductivity value from 10kg to 25kg weight lifting. 3. Females show gradually increasing degree of change in muscular conductivity value according as weight lifting is heavier. 4. Males show the constant muscular conductivity action of average 50∼110㎶ in the L⁴-L? in case of each lifting posture, knee angle 40˚, 80˚, and 180˚. 5. Females also show the constant muscular conductivity action of average 100∼200㎶ in the L⁴-L? in case of each lifting posture, knee angle 40˚, 80˚, and 180˚. But they show more active muscular conductivity in more than 15kg weight lifting, IOSHIC permission load value. In short, in case of males, weight lifting up to 25kg has little effect on erector spinae muscle but in case of females, weight lifting from more than 15kg has gradual effect on erector spinae muscle. Therefore, the muscular conductivity values of various posture types(by knee angle)are to be identified according to weight lifting steps.
Noh, Mi Ra,Woo, Chang-Hoon,Park, Mae-Ja,In Kim, Jee,Park, Kwon Moo Elsevier 2018 Biochimica et biophysica acta. Molecular basis of Vol.1864 No.5
<P><B>Abstract</B></P> <P>Fibrosis is an undesirable consequence of injury and a critical problem in many diseases. Recent studies have demonstrated an association of C/EBP homologous protein (CHOP) with fibrosis. We investigated the mechanism of CHOP in kidney fibrosis progression after unilateral ureteral obstruction (UUO) using <I>Chop</I> gene-deleted (<I>Chop</I> <SUP>−/−</SUP>) mice and their wild-type littermates (<I>Chop</I> <SUP>+/+</SUP>). UUO-induced kidney fibrosis was reduced in the <I>Chop</I> <SUP>−/−</SUP> than <I>Chop</I> <SUP>+/+</SUP> mice. After UUO, CHOP expression was detected in the cytosol and nucleus of distal tubule cells and collecting duct cells of the kidney. UUO formed the autophagosome and increased the expression of autophagy proteins, Beclin-1, LC3-I and II, and p62 in the kidneys. These UUO-induced changes were significantly reduced in <I>Chop</I> <SUP>−/−</SUP> mice. Furthermore, <I>Chop</I> gene deletion attenuated mitochondrial fragmentation with lower expression of Fis-1, a mitochondrial fission protein, but higher expression of Opa-1, a mitochondrial fusion protein, than that seen in the wild-type mice. UUO disrupted the microtubule, which is involved in autophagosome formation, and this disruption was milder in the <I>Chop</I> <SUP>−/−</SUP> than <I>Chop</I> <SUP>+/+</SUP> mouse kidney, with less reduction of histone deacetylase 6 and α‑tubulin acetyl transferase, which acetylates tubulin, a component of the microtubule. After UUO, apoptosis, a consequence of autophagy and mitochondrial damage, was reduced in the <I>Chop</I> <SUP>−/−</SUP> mouse kidney cells than in <I>Chop</I> <SUP>+/+</SUP> mice. Thus, the ablation of <I>Chop</I> attenuates renal fibrosis, accompanied by reduced autophagy, mitochondrial fragmentation, microtubule disruption, and apoptosis. Overall, these results suggest that CHOP plays a critical role in the progression of kidney fibrosis, likely through regulation of autophagy and apoptosis.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Unilateral ureteral obstruction (UUO) induces kidney fibrosis with CHOP expression. </LI> <LI> <I>Chop</I> gene deletion attenuates UUO-induced autophagy, apoptosis, and fibrosis. </LI> <LI> <I>Chop</I> gene deletion mitigates UUO-induced disruption of the microtubule. </LI> <LI> CHOP plays a critical role on fibrosis likely through autophagy regulation. </LI> </UL> </P>
Neuroprotective effect of topiramate on hypoxic ischemic brain injury in neonatal rats
Noh, Mi-Ra,Kim, Sung Koo,Sun, Woong,Park, Soon Kwon,Choi, Hyung Chol,Lim, Ji Hyae,Kim, Il Hwan,Kim, Hyun-Ju,Kim, Hyun,Eun, Baik-Lin Elsevier 2006 Experimental neurology Vol.201 No.2
<P><B>Abstract</B></P><P>Perinatal hypoxia–ischemia is one of the most common risk factors for neonatal mortality and permanent neurodevelopmental disability. Topiramate [2,3:4,5-bis-<I>o</I>-(1-methylethylidene) β-<SMALL>D</SMALL>-fructo-pyranose sulfamate; TPM] is widely used as an antiepileptic agent with multiple targets. In the present study, we found that treatment with TPM reduced the neuronal damage induced by oxygen–glucose deprivation in vitro with strong inhibition of the alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) receptor. Because perinatal hypoxia is mediated, at least in part, by aberrant glutamatergic excitation, we tested whether treatment with TPM was effective against perinatal brain hypoxia–ischemia. Intraperitoneal or oral pretreatment with TPM was found to reduce the brain damage and subsequent cognitive impairments induced by transient hypoxia–ischemia in perinatal rats. A potent neuroprotective effect of TPM was also observed in a post-treatment regime although post-treatment window appears to be relatively narrow (<2?h). These results suggest that TPM treatment may be beneficial for perinatal hypoxia–ischemia and related damage.</P>
Noh, Mi Ra,Jang, Hee-Seong,Song, Dae-Kyu,Lee, Seong-Ryong,Lipschutz, Joshua H.,Park, Kwon Moo,Kim, Jee In Elsevier 2018 Biochemical and biophysical research communication Vol. No.
<P><B>Abstract</B></P> <P>Migration of surviving kidney tubule cells after sub-lethal injury, for example ischemia/reperfusion (I/R), plays a critical role in recovery. Exocytosis is known to be involved in cell migration, and a key component in exocytosis is the highly-conserved eight-protein exocyst complex. We investigated the expression of a central exocyst complex member, Sec10, in kidneys following I/R injury, as well as the role of Sec10 in wound healing following scratch injury of cultured Madin-Darby canine kidney (MDCK) cells. Sec10 overexpression and knockdown (KD) in MDCK cells were used to investigate the speed of wound healing and the mechanisms underlying recovery. In mice, Sec10 decreased after I/R injury, and increased during the recovery period. In cell culture, Sec10 OE inhibited ruffle formation and wound healing, while Sec10 KD accelerated it. Sec10 OE cells had higher amounts of diacylglycerol kinase (DGK) gamma at the leading edge than did control cells. A DGK inhibitor reversed the inhibition of wound healing and ruffle formation in Sec10 OE cells. Conclusively, downregulation of Sec10 following I/R injury appears to accelerate recovery of kidney tubule cells through activated ruffle formation and enhanced cell migration.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Exocyst Sec10 decreases by I/R injury and restores with functional recovery. </LI> <LI> Sec10 inversely regulates kidney tubule cell wound healing after scratch injury. </LI> <LI> Sec10 inversely regulates ruffle formation at the leading edge during recovery. </LI> <LI> Upregulation of Sec10 increases DGKγ expression at the leading edge during recovery. </LI> <LI> DGK inhibitor reversed Sec10-mediated ruffle formation and wound healing defect. </LI> </UL> </P>
Noh, Hyun-Jin,Ha, Hun-Joo,Yu, Mi-Ra,Kim, Young-Ok,Kim, Ji-Hye,Lee, Hi-Bahl 이화여자대학교 약학연구소 2004 藥學硏究論文集 Vol.- No.14
Objective: To demonstrate the presence of an independent renin-angiotensin system (RAS) in the peritoneum and to determine the role of locally produced angiotensin (Ang) Ⅱ in high glucose-induced upregulation of transforming growth factor (TGF)-β1 and fibronectin by human peritoneal mesothelial cells (HPMC). Methods: In cultured HPMC, the expression of mRNAs for angiotensinogen, angiotensin-converting enzyme (ACE), Ang Ⅱ type 1 receptor (AT1), and TGF-β1 was evaluated by real-time polymerase chain reaction; ACE, AT1, and fibronectin proteins by Western blot analysis; and Ang Ⅰ, Ang Ⅱ, and TGF-β1 proteins by ELISA. Dichlorofluorescein (DCF) -sensitive cellular reactive oxygen species (ROS) were measured by fluorometry. Results: HPMC constitutively expressed all the components of RAS, and 50 mmol/LD-glucose (high glucose) significantly increased angiotensinogen, ACE, and AT1 mRNAs and ACE, AT1, and Ang Ⅱ proteins. Ang Ⅱ increased TGF-β1 and fibronectin protein expression and DCF-sensitive cellular ROS. Losartan prevented Ang Ⅱ-induced increase in cellular ROS. Both losartan and captopril inhibited high glucose-induced upregulation of TGF-β1 and fibronectin expression in HPMC in a dose-dependent manner. Antioxidant catalase and NADPH oxidase inhibitor diphenyleneiodinium effectively inhibited Ang Ⅱ-induced TGF-β1 and fibronectin protein expression. Conclusions: The present data demonstrate that H PMC constitutively express RAS, that AngⅡI produced by HPMC mediates high glucose-induced upregulation of TGF-β1 and fibronectin expression, and that Ang Ⅱ-induced TGF-β1 and fibronectin expression in HPMC is medicted by NADPH oxidase-dependent ROS. These data suggest that locally produced Ang Ⅱ and ROS in the peritoneum may be potential therapeutic targets in peritoneal fibrosis during long-term peritoneal dialysis.
Uremia induces functional incompetence of bone marrow-derived stromal cells.
Noh, Hyunjin,Yu, Mi Ra,Kim, Hyun Joo,Jeon, Jin Seok,Kwon, Soon Hyo,Jin, So Young,Lee, Jeeyun,Jang, Jiryeon,Park, Joon Oh,Ziyadeh, Fuad,Han, Dong Cheol,Lee, Hi Bahl Springer International ; Oxford University Press 2012 Nephrology, dialysis, transplantation Vol.27 No.1
<P>Chronic kidney disease (CKD) is associated with increased risk for cardiovascular diseases (CVD). We hypothesized that inadequate angiogenic response in uremic patients could result from dysfunction of bone marrow-derived stromal cells [mesenchymal stem cells (MSCs)].</P>