• 제목/요약/키워드: MAP1B

검색결과 532건 처리시간 0.022초

The Effect of Scalp Acupuncture and rTMS on Neuromotor Function in Photothrombotic Stroke Rat Model

  • Jong-Seong Park;Eun-Jong Kim;Min-Keun Song;Jung-Kook Kim;Ganbold Selenge;Sam-Gyu Lee
    • 대한의생명과학회지
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    • 제29권4호
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    • pp.263-273
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    • 2023
  • This study aimed to investigate effect of scalp acupuncture (SA) and repetitive transcranial magnetic stimulation (rTMS) intervention on neuromotor function in photothrombotic cerebral infarction (PCI) rat model. Sixty male SD rats were used. PCI was induced on M1 cortex of right frontal lobe. SA was performed at the Qianding (GV21), Xuanli (GB6) acupoints of ipsilesional M1. Low-frequency rTMS was delivered to contralesional M1. All rats were randomly divided into 4 groups: group A, normal (n, 15); group B, PCI without any stimulation intervention (n, 15); group C, PCI with SA (n, 15); group D, PCI with rTMS (n, 15). Rota-rod test and Ladder rung walking test (LWT) were done weekly for 8 weeks after PCI. SA or rTMS was started from post-PCI 4th day as protocol for 8 weeks. H/E stain and IHC were done. Western blot and qRT-PCR study were performed for MAP2 and BDNF from ipsilesional M1 peri-infarction tissue. Brain MRI study was conducted to quantify the volume of cerebral infarction. As a result, left forelimb and hindlimb function significantly improved more in group C and D than control group, with expressed more BDNF and MAP2. And brain MRI showed focal infarction of right M1 after PCI, and infarction volume progressively decreased in group C and D than group B from post-PCI 5th to 8th week. SA or rTMS was more effective than no intervention group on neuromotor function of PCI rat model. The functional recovery was associated with stimulation intervention-related neurogenesis.

인간 신체를 자율적으로 보조하고 보호하는 지능형 소프트 슈트(엑소스킨) (Intelligent Soft Suit That Can Autonomously Augment Strength and Protect the Human Body (Exoskin))

  • 손용기;정준영;진한빛;구자범;김배선;이동우;김혜진;신형철
    • 전자통신동향분석
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    • 제36권1호
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    • pp.32-42
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    • 2021
  • Innovative developments in wearable and artificial intelligence technologies are accelerating the emergence of a soft suit that can autonomously augment a body's own strength and protect the human body. In this paper, we define the concept of "Exoskin," a new concept specifically derived from the "Road to an Intelligent Information Society" (Technology Development Map 2035) as predicted by the Electronics and Telecommunications Research Institute. In addition, we analyze the development status of each element of this technology and forecast its future development.

Tier 4 Interim 배기규제 만족을 위한 56kW급 오프로드 차량 EGR 적용에 관한 연구 (Exhaust Gas Recirculation System Applied to 56 kW Off-Road Vehicle to Satisfy the Tier 4 Interim Emission Regulation)

  • 강정호;한준섭;정재우;정건우;조규백;임중호;표수강
    • 대한기계학회논문집B
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    • 제36권2호
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    • pp.217-224
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    • 2012
  • 비도로용 차량의 경우 대부분 디젤엔진을 사용하여 엔진의 특성상 PM과 NOx의 배출이 많은 단점이 있다. 승용 및 상용 디젤 차량의 경우 CRDI 및 후처리 장치를 적용하였고 후처리 장치로 DOC/DPF를 장착함으로써 PM은 약 90% 이상 저감 가능하다. 상반관계인 NOx는 EGR 사용을 통해 1차적으로 NOx 배출량을 감소시키고 LNT, LNC, Urea-SCR 등의 DeNOx 시스템으로 NOx의 배출량을 보다 현저히 저감시켜 배기규제를 만족시키고 있다. 본 연구에서는 tier 4 interim 배기규제를 만족하기 위해 56kW급 오프로드 차량으로 연구를 진행하였다. NOx의 감소를 위해 WGT와 전자 제어방식의 HPL EGR 시스템을 적용하였고 CO와 THC, PM 배출가스를 줄이기 위해 DOC와 DPF를 사용하였다. EGR 시스템을 적용하기 위해 각 조건에 대한 기본 실험을 실시하여 EGR map을 작성하였다. 작성된 map을 NRTC 모드에서 시험하여 map의 적용성을 검증하고 tier 4 interim 배기규제 만족여부를 파악하였다.

Replication origins oriGNAI3 and oriB of the mammalian AMPD2 locus nested in a region of straight DNA flanked by intrinsically bent DNA sites

  • Balani, Valerio Americo;De Lima Neto, Quirino Alves;Takeda, Karen Izumi;Gimenes, Fabricia;Fiorini, Adriana;Debatisse, Michelle;Fernandez, Maria Aparecida
    • BMB Reports
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    • 제43권11호
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    • pp.744-749
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    • 2010
  • The aim of this work was to determine whether intrinsically bent DNA sites are present at, or close to, the mammalian replication origins oriGNAI3 and oriB in the Chinese hamster AMPD2 locus. Using an electrophoretic mobility shift assay and in silico analysis, we located four intrinsically bent DNA sites (b1 to b4) in a fragment that contains the oriGNAI3 and one site (b5) proximal to oriB. The helical parameters show that each bent DNA site is curved in a left-handed superhelical writhe. A 2D projection of 3D fragment trajectories revealed that oriGNAI3 is located in a relatively straight segment flanked by bent sites b1 and b2, which map in previously identified Scaffold/Matrix Attachment Region. Sites b3 and b4 are located approximately 2 kb downstream and force the fragment into a strong closed loop structure. The b5 site is also located in an S/MAR that is found just downstream of oriB.

Nuclear Factor-${\kappa}B$ Dependent Induction of TNF-${\alpha}$ and IL-$1{\beta}$ by the Aggregatibacter actinomycetemcomitans Lipopolysaccharide in RAW 264.7 Cells

  • Na, Hee Sam;Jeong, So Yeon;Park, Mi Hee;Kim, Seyeon;Chung, Jin
    • International Journal of Oral Biology
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    • 제39권1호
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    • pp.15-22
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    • 2014
  • Aggregatibacter actinomycetemcomitans is an important pathogen in the development of localized aggressive periodontitis. Lipopolysaccharide (LPS) is a virulent factor of periodontal pathogens that contributes to alveolar bone loss and connective tissue degradation in periodontal disease. Our present study was designed to investigate the cytokine expression and signaling pathways regulated by A. actinomycetemcomitans LPS (Aa LPS). Cytokine gene expression profiling in RAW 264.7 cells was performed by microarray analyses. The cytokine mRNA and protein levels and related signaling pathways induced by Aa LPS were measured by RT-PCR, ELISA and western blotting. Microarray results showed that Aa LPS strongly induced the expression of NF-${\kappa}B$, NF-${\kappa}B$-related genes, inflammatory cytokines, TNF-${\alpha}$ and IL-$1{\beta}$ in RAW 264.7 cells. NF-${\kappa}B$ inhibitor pretreatment significantly reduced the levels of TNF-${\alpha}$ and IL-$1{\beta}$ mRNA and protein. In addition, the Aa LPS-induced TNF-${\alpha}$ and IL-$1{\beta}$ expression was inhibited by p38/JNK MAP kinase inhibitor pretreatment. These results show that Aa LPS stimulates TNF-${\alpha}$ and IL-$1{\beta}$ expression through NF-${\kappa}B$ and p38/JNK activation in RAW 264.7 cells, suggesting the essential role of this pathway in the pathogenesis of localized aggressive periodontitis.

Lobaric Acid Inhibits VCAM-1 Expression in TNF-α-Stimulated Vascular Smooth Muscle Cells via Modulation of NF-κB and MAPK Signaling Pathways

  • Kwon, Ii-Seul;Yim, Joung-Han;Lee, Hong-Kum;Pyo, Suhkneung
    • Biomolecules & Therapeutics
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    • 제24권1호
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    • pp.25-32
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    • 2016
  • Lichens have been known to possess multiple biological activities, including anti-proliferative and anti-inflammatory activities. Vascular cell adhesion molecule-1 (VCAM-1) may play a role in the development of atherosclerosis. Hence, VCAM-1 is a possible therapeutic target in the treatment of the inflammatory disease. However, the effect of lobaric acid on VCAM-1 has not yet been investigated and characterized. For this study, we examined the effect of lobaric acid on the inhibition of VCAM-1 in tumor necrosis factor-alpha (TNF-${\alpha}$)-stimulated mouse vascular smooth muscle cells. Western blot and ELISA showed that the increased expression of VCAM-1 by TNF-${\alpha}$ was significantly suppressed by the pre-treatment of lobaric acid ($0.1-10{\mu}g/ml$) for 2 h. Lobaric acid abrogated TNF-${\alpha}$-induced NF-${\kappa}B$ activity through preventing the degradation of $I{\kappa}B$ and phosphorylation of extracellular signal-regulated kinases (ERK), c-Jun N-terminal kinases (JNK), and p38 mitogen activated protein (MAP) kinase. Lobaric acid also inhibited the expression of TNF-${\alpha}$ receptor 1 (TNF-R1). Overall, our results suggest that lobaric acid inhibited VCAM-1 expression through the inhibition of p38, ERK, JNK and NF-${\kappa}B$ signaling pathways, and downregulation of TNF-R1 expression. Therefore, it is implicated that lobaric acid may suppress inflammation by altering the physiology of the atherosclerotic lesion.

SSR Marker Linked to f Locus in Soybean

  • Nam, Ki-Chul;Kim, Myung-Sik;Jeong, Woo-Hyeun;Kim, Seok-Hyeon;Chung, Jong-Il
    • 한국작물학회지
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    • 제52권1호
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    • pp.51-54
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    • 2007
  • Soybean has a morphological type with a broadened and flattened stem. Fasciation has been suggested as a new gene for soybean research. SSR marker linked to the $\Large f$ locus that controls fasciation phenotype has not identified within 10 cM. A mapping population consisting of 94 $F_2$ progenies was derived from a cross between wild type Clark (FF) and fasciation mutant C32 (${\Large f}{\Large f}$). The phenotype of $F_2$ individual plants was recorded at R2 and R3 growth stage from field. One-thousand 10-mer oligonucleotide RAPD primers and 29 SSR primers selected from the D1b+W of the soybean molecular linkage map were used. A genetic map was constructed from the segregating 35 RAPD, four SSR markers and one phenotypic(wild type/fasciation) marker. The segregation ratios of 3 : 1 observed in the $F_2$ population and the Chi-square values strongly suggest that the fasciation trait is controlled by a single recessive gene. Satt537 marker was linked to $\Large f$ locus at a distance of 9.6 cM. Assignment of the $\Large f$ locus to linkage group D1b+W and identification of markers can be used as an initial step for fine mapping of the $\Large f$ gene.

오배산가미(五倍散加味)가 점막(粘膜) 및 피부질환(皮膚疾患)에 미치는 영향 (The effects of Ohbaesangami (OBSGM) on the mucosa and skin diseases)

  • 노석선;홍석훈
    • 한방안이비인후피부과학회지
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    • 제20권2호통권33호
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    • pp.10-35
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    • 2007
  • Objectives : To investigate the effects of Ohbaesangami (OBSGM) on mucosa and skin diseases, anti-microbial and anti-inflammatory tests were performed using several in vitro test models. Results : In anti-microbial test, OBSGM showed the slight inhibitory effect against Propionibacterium acnes (P. acnes) and Staphylococcus aureus (S. aureus). In anti-oxidant test, OBSGM showed the potent radical scavenging activity. In anti-inflammatory test, OBSGM weakly inhibited the lipopolysaccharide (LPS)-induced nitric oxide(NO) release from the RAW 264.7 macrophage cells. OBSGM also inhibited the LPS-induced $interleukin-1{\beta}(IL-1{\beta})$ and cyclooxygenase-2 (COX-2) expressions. The inhibitory effects of OBSGM on macrophage activation was via the inhibition of $NF-{\kappa}B$, evidenced by transient transfection assay. Furthermore, OBSGM markedly inhibited the activation of Jun-N-terminal kinase (JNK) and p38 MAP kinase in RAW 264.7 cells. In skin wrinkle formation assay, OBSGM strongly inhibited collagnease and elastase, whose activities are tightly related with the wrinkle formation. In addition, OBSGM inhibited the activities of MMP-1, MMP-2 on the mRNA levels in RAW 264.7 cells. However, OBSGM did not show an inhibitory potential on tyrosinase activity and melanin synthesis, indicating that it could not be applicable for skin whitening. Conclusion : These results suggest that the anti-inflammatory effect of OBSGM may be due to its inhibitory potentials on the macrophage activation. And, the anti-wrinkle effects of OBSGM may be due to its inhibitory potential on the collagnease and elastase activities. Therefore, OBSGM could be applicable for the treatment of mucosa and skin diseases.

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CO OBSERVATIONS AND STABILITY ANALYSIS OF B133 AND B134

  • Hong, S.S.;Kim, H.G.;Park, S.H.;Park, Y.S.;Imaoka, K.
    • 천문학회지
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    • 제24권1호
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    • pp.71-94
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    • 1991
  • With the 14 m radio telescope at DRAO and the 4 m at Nagoya University, we have made detailed maps of $^{12}CO$ and $^{13}CO$ emissions from two Barnard objects B133 and B134 in the $J=1{\rightarrow}O$ rotational transition lines. Usual LTE analyses of the CO observations led us to determine the distribution of column densities over an entire area encompassing both globules. Total gas masses estimated from the column density map are $90\;M_{\odot}$ and $20\;M_{\odot}$ for B133 and B134, respectively. The radial velocity of B133 is red shifted with respect to B134 by $0.8\;km\;s^{-1}$, which is too lagre to bind the two clouds as a binary system. We have shown that the usual stability analysis based on the simplified version of virial theorem with the second time-derivative of the moment of inertia term $\ddot{I}$ being ignored could mislead us in determining whether a given cloud eventually collapses or not. The lull version of the scalar virial theorem with the $\ddot{I}$ term is shown to be useful in following up the time-dependent variations of the cloud size R and its streaming velocity $\dot{R}$ as functions of time. Results of our stability analysis suggest that B133 will eventually collapse in $(2{\sim}4){\times}10^6$ years.

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Glutaredoxin2 isoform b (Glrx2b) promotes RANKL-induced osteoclastogenesis through activation of the p38-MAPK signaling pathway

  • Yeon, Jeong-Tae;Choi, Sik-Won;Park, Kie-In;Choi, Min-Kyu;Kim, Jeong-Joong;Youn, Byung-Soo;Lee, Myeung-Su;Oh, Jae-Min
    • BMB Reports
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    • 제45권3호
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    • pp.171-176
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    • 2012
  • Receptor activator of NF-${\kappa}B$ ligand (RANKL) triggers the differentiation of bone marrow-derived monocyte/macrophage precursor cells (BMMs) of hematopoietic origin into osteoclasts through the activation of mitogen-activated protein (MAP) kinases and transcription factors. Recently, reactive oxygen species (ROS) and antioxidant enzymes were shown to be closely associated with RANKL-mediated osteoclast differentiation. Although glutaredoxin2 (Glrx2) plays a role in cellular redox homeostasis, its role in RANKL-mediated osteoclastogenesis is unclear. We found that Glrx2 isoform b (Glrx2b) expression is induced during RANKLmediated osteoclastogenesis. Over-expression of Glrx2b strongly enhanced RANKL- mediated osteoclastogenesis. In addition, Glrx2b-transduced BMMs enhanced the expression of key transcription factors c-Fos and NFATc1, but pre-treatment with SB203580, a p38-specific inhibitor, completely blocked this enhancement. Conversely, down-regulation of Glrx2b decreased RANKL- mediated osteoclastogenesis and the expression of c-Fos and NFATc1 proteins. Also, Glrx2b down-regulation attenuated the RANKL-induced activation of p38. Taken together, these results suggest that Glrx2b enhances RANKL-induced osteoclastogenesis via p38 activation.