• 한국측량학회지
• /
• 제28권1호
• /
• pp.83-92
• /
• 2010

고해상도 항공 디지털 사진기와 고밀도 3차원 데이터를 획득할 수 있는 항공 레이저 스캐너의 보급은 사진측량 및 공간정보 분야에 큰 발전을 가져왔다. 본 연구는 패치기반의 정사영상을 생생하여 폐색지역을 탐색하고 정사영상에서 발생하는 폐색지역을 복원하여 정밀정사영상을 생성하는 방법을 개발하는 것을 목적으로 한다. 정사영상에서 발생하는 폐색지역의 처리를 위하여 대상지역을 포함하고 있는 다중 영상들을 이용하여 상호 복원하는 방법을 개발하였다. 제시된 방법을 적용하면 폐색지역이 많이 발생하는 도심지역의 정밀정사영상을 효율적으로 생성할 수 있을 것으로 판단된다.

• 대한원격탐사학회:학술대회논문집
• /
• 대한원격탐사학회 2008년도 International Symposium on Remote Sensing
• /
• pp.371-374
• /
• 2008

In very high-spatial resolution remote sensing imagery, it is difficult to extract the feature information of various objects because of occlusion and shadows. Moreover, various and feeble information within shadows can be of use in GIS-based applications and remote sensing analysis. In this paper, we developed a radiometric restoration method for shadow areas using KOMPSAT-2 satellite image. After detecting the shadow, non-shadow pixels nearby are extracted using a morphological filter. An iterative linear regression method is applied to calculate the relationship between shadow and non-shadow pixels. The shadows are restored by the parameters of the linear regression algorithm. Tests show that recovery of shadowed areas by our method leads to improved image quality.

• 대한한의학회지
• /
• 제24권3호
• /
• pp.72-83
• /
• 2003

Objective : The goal of the present study was to investigate the protective effect of Gamiheechum-tang (Jiaweixiqian-tang; GHCT) on brain tissue damage from chemical or ischemic insults. Methods : Levels of cultured cortical neuron death caused by toxic chemicals were measured by LDH release assay. Neuroprotective effects of GHCT on brain tissues were examined in vivo by ischemic model of middle cerebral artery (MCA) occlusion. Results : Animal groups treated with GBCT showed significantly decreased hypertension, and reduced levels of aldosterone, dopamine, and epinephrine in the plasma. GHCT treatments ($l0-200\mu\textrm{g}/ml$) significantly decreased cultured cortical neuron death mediated by AMPA, kainate, BSO, or Fe2+ when measured by LDH release assay. Yet, cell death mediated by NMDA was effectively protected by GHCT at the highest concentration examined ($200\mu\textrm{g}/ml$). In the in vivo experiment examining brain damage by MCA occlusion, affected brain areas by ischemic damage and edema were significantly less in animal groups administered with GHCT compared to the non-treated control group. Neurological examinations of forelimbs and hindlimbs showed that GHCT treatment improved animals' recovery from ischemic injury. Moreover, the extent of injury in cortical and hippocampal pyramidal neurons in ischemic rats was much reduced by GHCT, whose morphological features were similarly observed in non-ischemic animals. Conclusion : The present data suggest that GBCT may play an important role in protecting brain tissues from chemical or ischemic injuries.

• The Korean Journal of Physiology and Pharmacology
• /
• 제8권2호
• /
• pp.77-81
• /
• 2004

The loss of neurons and synaptic contacts following cerebral ischemia may lead to a synaptic plastic modification, which may contribute to the functional recovery after a brain lesion. Using synapsin I and GAP-43 as markers, we investigated the neuronal cell death and the synaptic plastic modification in the rat hippocampus of a middle cerebral artery occlusion (MCAO) model. Cresyl violet staining revealed that neuronal cell damage occurred after 2 h of MCAO, which progressed during reperfusion for 2 weeks. The immunoreactivity of synapsin I and GAP-43 was increased in the stratum lucidum in the CA3 subfield as well as in the inner and outer molecular layers of dentate gyrus in the hippocampus at reperfusion for 2 weeks. The immunoreactivity of phosphosynapsin was increased in the stratum lucidum in the CA3 subfield during reperfusion for 1 week. Our data suggest that the increase in the synapsin I and GAP-43 immunoreactivity probably mediates either the functional adaptation of the neurons through reactive synaptogenesis from the pre-existing presynaptic nerve terminals or the structural remodeling of their axonal connections in the areas with ischemic loss of target cells. Furthermore, phosphosynapsin may play some role in the synaptic plastic adaptations before or during reactive synaptogenesis after the MCAO.