본 연구는 파인애플로 제조한 와인의 과실주의 제조 가능성을 조사하고, 첨가당의 종류가 발효과정에 어떠한 영향을 주는지를 알아보고자 실시하였다. 발효과정이 진행되는 동안 당도와 알코올 농도의 변화는 첨가한 당의 종류에 따라 다르게 변화 하였다. 당을 첨가하지 않은 과즙의 경우 가장 먼저 알코올의 증가가 종료되었으며, 특히, 포도당을 첨가한 와인에서 가장 많은 알코올(12.8%)이 생성되어 효모의 당 이용성이 높은 것으로 나타났다. 유기산은 모든 와인에서 citric acid와, malic acid, acetic acid, succinic acid 및 lactic acid가 검출되었으며, 그 밖에 oxalic acid도 소량 존재하였다. 그 중에서 설탕을 첨가한 와인에서 citric acid (0.335 mg/mL)와 malic acid (0.127 mg/mL) 함량이 높게 나타났으며, 또한, 가장 많은 유기산이 측정되었다. 총 페놀 함량 및 항산화 활성도(DPPH 라디칼 제거능)는 파인애플 제조 와인에서 약 950 mg/L 및 약 4,900 mg/L으로 나타났다. 관능검사 결과는 비전문가 집단과 비교하여 전문가 집단에서 기호도는 당을 첨가하지 않는 와인에서 가장 높게 나타났다. 특히, 와인전문가들은 알코올 함량이 적은 당을 첨가하지 않은 와인을 더 선호하는 것으로 확인되었다. 본 연구 결과와 같이 파인애플로 제조한 와인이 가당을 하지 않고서도 과실주로서의 가능성에 대해 긍정적인 평가를 내릴 수 있었다. 이처럼, 건강에도 도움을 주고, 풍미도 좋으며, 알코올 농도가 높지 않은 와인을 제조할 수 있으며, 다양한 소비층의 소비를 유도할 수 있을 것으로 판단된다.

Inhibition of proteasome activity may reduce many types of cancer, so it's pathway is effective in cancer as well as in clinical fields. Here the author has carried out experiment targeting on the elevation of apoptosis in oral cancer cells by combination of proteasome inhibitor, lactacystin, and DNA replication inhibitor, etoposide. The growth of KB cells was measured by MTT methods and apoptosis was analyzed by DNA fragmentation and Hochest nucleus staining. The proteasome activity was analyzed by fluorescent tagged peptide and cellular protein expression was detected by Western hybridization. Though lactacystin and etoposide inhibited KB cell growth alone, but low combined doses inhibited cell growth more strongly and induced apoptosis. The proteasome activity was also seriously inhibited by the combination of both chemicals. Tumor suppressor proteins and apoptosis inducing proteins were highly increased under the combination of both chemicals. From above studies we can conclude that proteasome inhibitors may be used for the treatment of oral cancer and proteasome inhibitors with DNA replication inhibitors may be effective in clinical trials of oral cancer.

Oral squamous cell carcinoma (OSCC) is the most common malignancy and is a major cause of worldwide cancer mortality. The proto-oncogene c-myb plays an important role in regulation of cell growth and differentiation, and it is expressed at high levels in hematopoietic cells and many other types of cancers. However, the function of c-myb is not well known in OSCC. The present study aimed to reveal the function of c-myb and to test the alternation of cell growth and signaling by c-myb in OSCC. In this study, c-myb and dominant-negatibe myb(DNmyb) were expressed in an adenovirus-mediated gene delivery system to KB cells. The over-expressed c-myb brought increased cellular proliferation compared with control cells. However, DN-myb infected KB cells showed significant reduction of cell growth and enhanced induction of apoptosis to activate PARP and caspase 9. c-myb induced increase of IGF-I, -II and IGF-IR expressions while DN-myb down-regulated these expression. Activation of ERK and Akt/PKB pathway was shown only in c-myb transduced cells. These findings suggest that the role of c-myb in cell growth of oral cancer cells is partially mediated through the modulation of IGFs, ERK and Akt/PKB. From this results, DN-myb is strongly recommended as a curable gene for the treatment of c-myb dependent malignancies such as OSCC.