본 연구는 수수 × 수단그라스 바이오에탄올 생산을 위한 적정 수확 시기 및 수확 후 재생과정에서 요구되는 적정 질소 시비 수준을 파악하기 위해 수행되었다. 포장 실험은 2017부터 2018년까지 실시했으며, 시험구 배치는 난괴법(RCBD)으로 여름 수확 후 질소 추비 수준을 달리하여(0, 50, 100, 150 kg N/ha; 0N, 50N, 100N, 150N) 처리하였다. 재생과정에서 canopy height은 2017년 여름 수확 후(DAT, day after summer harvest treatment) DAT23에서 DAT48로 경과함에 따라 약 3.0배, 2018년 DAT26에서 DAT48로 경과함에 따라 약 2.9배 신장하였다. 엽록소 함량은 재생과정 초기 질소 무처리구와 질소처리구간 유의한 차이가 나타났으나, DAT48 이후 처리 간 차이는 없었다. 여름 수확은 2017년 파종 후 61일 뒤, 2018년 파종 후 83일 뒤 각각 이루어졌으며 건물수량은 8.6Mg/ha, 11.0Mg/ha로 차이를 보였다. 생육시기별 2차 수확의 건물수량은 2017년의 경우 생육이 진전됨에 따라 꾸준히 증가하였으며, 2018년에는 DAT76까지 증가하였다. 2017년 DAT107에서 무처리구(9.0Mg/ha)에 비해 질소 처리구(12.3Mg/ha)에서 1.4배 높았으며, 무처리의 수량이 낮았던 2018년 DAT113에서는 무처리구(2.3Mg/ha)에 비해 질소 처리구 (5.6Mg/ha)로 2.5배 높았다. 수확물의 바이오에탄올 품질을 나타내는 바이오에탄올 수율(TEP)는 생육 후기 cellulose와 hemicellulose 비율 감소로 일부 줄어들었으나, 전체적인 TEP변화는 생육시기나 추비수준과 관계없이 5% 이내로 큰 차이는 없었다. 총 바이오에탄올 수량(total TEY)은 2017년 DAT107에서 7,944L/ha, 2018년 DAT76에서 7,163L/ha로 추정되었다. 따라서 TEY를 높이려면 수확물의 단위면적당 건물중을 증가시키는 재배방법이 필요하다. 여름 수확 후 충분한 재생을 위해서 필요한 질소 추비 수준은 100kg N/ha 이상이었으며, 2차 수확은 여름 수확 실시 후 2개월 이상 경과 한 이후 실시해야 한다.

Dental caries is the most common chronic disease in the dental field. Streptococcus mutans (S. mutans) is the most important bacteria in the formation of dental plaque and dental caries. In a previous study, we confirmed that the essential oil of Chrysanthemum boreale has antibacterial activity against S. mutans. Alpha-pinene is one of the major chemical components of Chrysanthemum boreale essential oil. In the present study, we investigated the inhibitory effects of ɑ-pinene on cariogenic properties such as growth, acid production, biofilm formation, and bactericidal activity on S. mutans. Alpha-pinene at a concentration range of 0.25-0.5 mg/mL significantly inhibited the growth of S. mutans and acid production of S. mutans. Biofilm formation was significantly inhibited at > 0.0625 mg/mL ɑ-pinene, similar to the data from scanning electronic microscopy. Under confocal laser scanning microscopy, the bacterial viability was decreased by ɑ-pinene in a dose-dependent manner. These results suggested that ɑ-pinene may be a useful agent for inhibiting the cariogenic properties of S. mutans.

Streptococcus mutans (S. mutans) is one of the most important bacteria in the formation of dental plaque and dental caries. S. mutans adheres to an acquired pellicle formed on the tooth surface, and aggregates with many oral bacteria. It initiates plaque formation by synthesizing glucan from sucrose, which is catalyzed by glucosyltransferases. Propolis is a resinous mixture produced by honeybees, by mixing saliva and beeswax with secretions gathered from wood sap and flower pollen. Bees prevent pathogenic invasions by coating the propolis to the outer and inner surface of the honeycomb. Propolis has traditionally been used for the treatment of allergic rhinitis, asthma and dermatitis. We investigated the inhibitory effects of propolis ethanol extract on biofilm formation and gene expression of S. mutans. The biofilm formation of S. mutans was determined by scanning electron microscopy (SEM) and safranin staining. We observed that the extract of propolis had an inhibitory effect on the formation of S. mutans biofilms at concentrations higher than 0.2 mg/ml. Real-time PCR analysis showed that the gene expression of biofilm formation, such as gbpB, spaP, brpA, relA and vicR of S. mutans, was significantly decreased in a dose dependent manner. The ethanol extract of propolis showed concentration dependent growth inhibition of S. mutans, and significant inhibition of acid production at concentrations of 0.025, 0.05, 0.1 and 0.2 mg/ml, compared to the control group. These results suggest that the ethanol extract of propolis inhibits gene expression related to biofilm formation in S. mutans.

Retinoic acid plays an important role in the regulation of cell growth and differentiation. In our present study, we evaluated the effects of all-trans retinoic acid (RA) on cell proliferation and on the cell cycle regulation of human gingival fibroblasts (HGFs). Cell proliferation was assessed using the MTT assay. Cell cycle analysis was performed by flow cytometry, and cell cycle regulatory proteins were determined by western blot. Cell proliferation was increased in the presence of a 0.1 nM to 1μM RA dose range, and maximal growth stimulation was observed in cells exposed to 1 nM of RA. Exposure of HGFs to 1 nM of RA resulted in an augmented cell cycle progression. To elucidate the molecular mechanisms underlying cell cycle regulation by RA, we measured the intracellular levels of major cell cycle regulatory proteins. The levels of cyclin E and cyclin-dependent kinase (CDK) 2 were found to be increased in HGFs following 1 nM of RA treatment. However, the levels of cyclin D, CDK 4, and CDK 6 were unchanged under these conditions. Also after exposure to 1 nM of RA, the protein levels of p21 WAF1/CIP1 and p16 INK4A were decreased in HGFs compared with the control group, but the levels of p53 and pRb were similar between treated and untreated cells. These results suggest that RA increases cell proliferation and cell cycle progression in HGFs via increased cellular levels of cyclin E and CDK 2, and decreased cellular levels of p21 WAF1/CIP1 and p16 INK4A.