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허채정,홍민영,조아름,이영희,서민아 사단법인약침학회 2011 Journal of Acupuncture & Meridian Studies Vol.4 No.3
A melanoma tumor is a representative malignant tumor. Melanoma tumor growth involves vigorous angiogenesis around the tumor and a vasculogenic-like network inside an aggressive tumor. Primo vessels (PVs) are also found on the surface of the tumor and coexist alongside blood vessels (BVs), and sometimes within the BVs. We hypothesized that the primo vessels system plays a significant role in regulating the development of a melanoma tumor, and therefore has a tight coupling with BVs and angiogenesis. To prove this hypothesis, we developed a murine melanoma model by inoculating melanoma cell lines into the abdominal region. We used a green fluorescent protein (GFP) expressing mouse as a host to distinguish the endogenous source of the tumor PVs. We found strong formation of PVs on the tumor that coexisted with BVs and expression of GFP. PVs also had a tight coupling with adipose tissues, especially with white adipose tissue. These data suggest that the PVs of an induced melanoma tumor evolve endogenously from the host body and may be highly related to BVs and adipose tissue. This model of PVs in an overexpressing GFP mouse is a useful system for observing PVs, primo nodes, and primo vessel networks, and has potential to be developed as a model for examining novel treatments for cancer metastasis.
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심정은,조아름,이소희,방오영,허채정,전길자,서민아,강복만,이영미 한국뇌신경과학회 2016 Experimental Neurobiology Vol.25 No.3
Ischemia can cause decreased cerebral neurovascular coupling, leading to a failure in the autoregulation of cerebral blood flow. This study aims to investigate the effect of varying degrees of ischemia on cerebral hemodynamic reactivity using in vivo real-time optical imaging. We utilized direct cortical stimulation to elicit hyper-excitable neuronal activation, which leads to induced hemodynamic changes in both the normal and middle cerebral artery occlusion (MCAO) ischemic stroke groups. Hemodynamic measurements from optical imaging accurately predict the severity of occlusion in mild and severe MCAO animals. There is neither an increase in cerebral blood volume nor in vessel reactivity in the ipsilateral hemisphere (I.H) of animals with severe MCAO. The pial artery in the contralateral hemisphere (C.H) of the severe MCAO group reacted more slowly than both hemispheres in the normal and mild MCAO groups. In addition, the arterial reactivity of the I.H in the mild MCAO animals was faster than the normal animals. Furthermore, artery reactivity is tightly correlated with histological and behavioral results in the MCAO ischemic group. Thus, in vivo optical imaging may offer a simple and useful tool to assess the degree of ischemia and to understand how cerebral hemodynamics and vascular reactivity are affected by ischemia.
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Effects of Nicotine on Aβ or CT_(105)-induced Toxicity
Seo, Ji-Heui,Chang, Keun-A,Kim, Hye-Sun,Park, Cheol Hyoung,Kim, Seong Han,Lee, Me Jeong,Jeong, Sung-Jin,Choi, Se Hoon,Rah, Jong-Cheol,Koo, Jawook,Kim, Eun-Mee,Xu, Yanji,--,Choi, Jun Ho,Shin, Jae Kyung 한국뇌학회 2001 한국뇌학회지 Vol.1 No.1
알츠하이머 치매의 병인기전에서 아밀로이드 베타 펩티드는 중요한 역할을 할 것이라는 연구결과가 많이 보고되어있다. 그러나 알츠하이머 치매의 진행과 아밀로이드 베타 펩티드의 생성에는 여러 가지 모순도 보고되었다. 그러므로 아밀로이드 전구단백질에서 생성된 아밀로이드 베타 펩티드 외에 여러 가지 대사물들이 알츠하이머 치매의 병인기전과 관련이 있으리라 여겨진다. 이미 본 연구팀은 니코틴이 신경보호효과가 있다고 알려진 분비형 아밀로이드 전구단백질의 발현을 시간, 농도 의존적으로 증가시킨다는 연구결과를 보고하였다. 이번 논문에서는 니코틴의 전처리로 아밀로이드 베타 펩티드 및 아밀로이드 C단 단백질에 의한 1차 신경세포에서의 세포독성 효과가 억제되며, 이러한 효과는 니코틴의 길항제인 알파붕가로톡신에 의해 상쇄된다는 연구결과를 얻었다. 뿐만 아니라 C단 단백질을 PC12세포에 유전자를 이입시켰을 때, 니코틴에 의하며 세포 독성이 억제되는 결과를 얻었다. 이러한 연구결과로 볼 때, 니코틴이나 니코틴 수용체는 콜린성 신경전달 물질 보상 뿐만 아니라 아밀로이드 베타 펩티드, 아밀로이드 C단 단백질의 독성을 저해함으로써 인지기능 향상에 영향을 줄 것으로 예상된다. Several lines of evidence indicate that Aβ may play an important role in the pathogenesis of AD. However, there are several discrepancies between the production of Aβ and the development of the disease. Thus, Aβ may not be the sole active fragment of β-amyloid precursor protein (βAPP) in the neurotoxicity associated with AD. Previously, findings from our experiments have shown that nicotine enhances the release of APPs, which has neurotrophic and neuroprotective activities in concentration and time-dependent manners. In this study, our results showed that Pretreatment of nicotine (>10μM, for 24hr) partially prevented Aβ or CT_(105)-induced cytotoxicity in primary cultured neuronal cells, and the effects of nicotine-induced protection was inhibited by the pretreatment with a nicotine receptor antagonist α-bungarotoxin. Nicotine (>10μM, for 24hr) partially inhibited CT_(105)-induced cytotoxicity when PC12 cells was transfected with CT_(105). From these results, we proposed that treatment of nicotine or nicotinic receptor agonist might improve the cognitive functions not only by supplementation of cholinergic neurotransmission but also by protecting Aβ-or CT_(105)-induced neurotoxicity probably through the increased release of APPs and the activation of nicotinic receptor.
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