Calepitrimerus vitis (Nalepa) is a grapevine pest and distributed worldwide. This study was conducted to identify grapevine damage related to density of C. vitis and to suggest an effective control time. The damaged flower buds displayed retarded growth and became dried up, and symptoms of damaged leaves such as malformed and bronzed leaves were observed. Flower cluster and leaves were collected and density of the grape rust mite were observed by using a washing and sieving method. The highest mean density (±SE) of C. vitis was found to be 672.6±112.9 per flower cluster with mid-level damage, and 450.1±66.5 per 2 leaves was found on the damaged leaves. These severe damage symptoms were observed in the early spring, and the density of the grape rust mite was significantly higher as 80 times in damaged vineyard than in the undamaged at the early growth stages of the grapevine. To determine the emergence time of the grape rust mite from lower part of a winter bud the ratio of density of C. vitis on upper-bud to lower-bud was observed. On 13 April 2015, 80% of the grape rust mites were observed on upper-bud where the mite could feed at the bud burst stage. Therefore, once the symptoms of damaged flower clusters and leaves are observed, acaricides should be sprayed before inflorescence emergence, and at the early growth stage between bud burst and leaf development in following year. This would allow the decrease of the density of C. vitis in early spring, and the progression of severe damage could be prevented.

Urbanization is one of the leading causes of habitat loss, habitat degradation, and fragmentation. Urban development negatively affects biodiversity. This study aimed to clarify the change of butterfly communities on effect of urbanization in urban green areas. Butterfly survey was conducted using the line transect methods from April to October in 2012. A total of 59 species and 1,465 individuals of butterflies were observed in four urban green areas: Namsan Park (NS), Ewha Womans University (EW), Bukseoul Dream Forest (BD), and Hongneung Forest (HF), and natural forest: Gwangneung Forest (GF). The category of land use around study site was determined based on GIS data. Species richness and abundance of niche breadth and habitat type in urban green areas differed significantly from those in GF. Estimated species richness and species diversity (H’) in four urban green areas were significantly lower than those in GF. Species richness and abundance of forest interior species and specialist were positively correlated with paddy, field, and forest, whereas those of forest interior species and specialist were negatively correlated with urban area and road. Butterfly communities in four urban green area differed from that in GF. The result suggests that the decrease of paddy, field, and forest associated with increase of urban area and road negatively influences species composition and changes butterfly communities.

에멀션 기반의 계면활성제를 이용한 주형합성법을 이용하여 산촉매로서 염산과 실리카의 전구체인 테 트라에톡시실란을 사용함으로써 메조다공성 실리카 마이크로스피어를 합성하였다. 테트라에톡시실란의 농도 증가에 의해 구형의 입자 형태가 파괴되었고, 기공구조도 크게 변하였다. 산촉매 농도 증가에 의한 구형의 입자형태 파괴 현상은 적었지만 상대적으로 작은 크기의 구형의 마이크로입자가 더 많이 생성되 었다. 하지만, 산성조건에서 입자들 간의 강한 응집현상이 나타남에 따라 낱개의 분리되어 있는 단일입자 를 얻기 위해서는 초음파 등의 후처리 과정이 필요하였다.

Considering the great potential of iron chelators at inhibiting the proliferation of tumor cells, in order to determine the molecular and biological basis for the effects of iron chelator in oral cancer, we investigated the effects of iron chelator, desferrioxamine (DFO), on the gene profiling analysis of immortalized human oral keratinocytes (IHOK), and oral cancer cells (HN12), using the cDNA microarray. We identified 46 clones cDNA exhibiting more than 2 fold overexpression in DFO treated IHOK and HN12 cells, and 94 cDNA reveal more than 2 fold down-regulated expression. Examination of gene expression that differs between DFO treated vs. control IHOK and HN12 cells apprear to be related to : cell cycle regulator, cell growth and apoptosis, signal transduction and stress. p21 for cell cell cycle factor was upregualted, and cyclin-cdk gene was decreased expression, so we observed cell cycle arrest in DFO treated IHOK and HN12 cells. In tumor growth, we have identified downregulation of hemidesmosomal protein (bullous pemphigoid antigen 1) and epiregulin expression in DFO treated IHOK and oral cancer cells. Signal transducers including mitogen-activated protein kinase-activated protein kinase 5, serine/thereonine kinase 6 were downregulated with DFO treated cells, suggesting the DFO regulates the p38 MAP kianse pathway in immortalized and maignant oral keratincytes. In conclusion, we have demonstrated the high-throughput utility of cDNA array hybridization in parallel to the gene expression analysis to identify genes that are expressed differentially in DFO treated with immortalized and malignant oral keratinocytes. The differentially expressed genes identified here should be informative in DFO-induced anti-cancer effects.

The purpose of this study was to examine the effects of vi tamin D3 and 1'etinoic acid(RA) on the human mesenchymal stem ce!ls(MSC) g1'owth and osteogenic differentiations. Cell proliferation, mineralization, cell cycle, expression of cell cycle regu l atOJγ proteins and markers fo1' osteogenic differenatiaiton were determined by MTI assay, mineralization assay, flow cytomet1'Y‘ and Western blot analysis, respectively. Cell viability was dec1'ease by each vitamin D3 and RA added to MSC. it was more decrease by vitamin D3 and RA. Mineralized nodule formation revealed similar expression pattern with positive cont rol group at vitamin D3 and RA mixed add to MSC. At vitamin D3 and RA mixed add to MSC after 7 days of incubation was increase G1 s tage. after 21 days of incubation was inhibit cell cycle prog1'ess by inc1'ease of sub-G1 Treatment vitamin D3 to MSC inhibits p53 and p21, but inc1'ease pRb. RA inhibit p53, but increase p21 and pRb, vitamin D3 plus RA group was same as added RA group. so two vitamin was effect to inhibited cell growth each different mechanism. Expression of BMP-2 protein was prominent in osteogonic supplement treated g1'oup of MSC at 2 weeks cultivation days, but vi tamin D3 treatment decreased BMP-2 expression rather than in (+) control group. BSP protein was notably increased in the OS compa red to positive controls at 2 weeks cultivation, but similar to that of vitamin D3 group t1'eatment group and was least expressed in plus RA mixed group, at 3 weeks, BSP expression was similar to 1'esult of 2 weeks Collectively, these results shows that vitamin D3 and RA have diffe1'ential effects on the MSCs g1'owth and differ entia tion 211

We have examined the effect of NO donor, S-nitl‘ oso-N-acetyl-DL-penicillamine(SNAP) on heme oxygenase-1 (HQ-l) ex pression in human oral immortalized & malignant keratinocytes, and investigated in the control of keratinocyte proliferation evidence tha t HO-1 cou ld be involved in a low dose of NO, NO inhibitor, HOinducer, and HO inhibitor medi ated cytoprotect ion against cytotoxi city induced by a high dose of NO Oral keratinocyte growth inhibitory or anti-proliferative effects were exerted by with SNAP and hemin in a dose- and cul tivation time dependent manner The level of HQ-1 protein was increased in all cell types after exposure hernin dose, and the hemin induced HQ-1 protein achieved at higher maximum level by 12 hrs in all kind of cells , The pretreatment of cells with 0, 2 μ M SNAP reduced 1 mM SNAP-induced death in IHOK and HN4 cells , These cytoprotective effects on high dose of NO induced HQ-1 expresion and cell ular toxicity were blocked by low dose of SNAP, HCB, and ZnPP IX supporting the involvement of HQ-1 in high dose NO induced growth arrest or cell death, But these cytoprotection pattern is different from immortalized and malignant keratinocytes , These results indirectly demonstrate that HQ-1 could be involved in cytoprotection by NO priming against high dose NO induced cytotoxicity in immortalized and maigla nt oral keratinocytes, Thus, HQ-1 might be an important cellular target of NO donor, with clinical implications for the pre vention of inJlammatory di seases and anti-tumor immunity