The increasing prevalence of obesity is associated with various metabolic diseases such as diabetes, posing significant social and economic burdens to the society. While obesity is a complex disease with multiple factors contributing to its pathophysiology, altered glucose and lipid metabolism is evident in obese patients as well as in animal models. Abnormal metabolic regulation often leads to development of insulin resistance, a hallmark of obesity-induced type 2 diabetes. In this review, we provide a brief overview of altered lipid metabolism manifested in the obese state. In addition, two representative animal models, Mus musculus and Drosophila melanogaster, are presented with experimental approaches adopted for generation and utilization of these models. More specifically, Drosophila has been widely used for studying the core physiological phenomena across phyla for decades, mostly due to the ease of handling and sophisticated genetic manipulations with conserved cell signaling pathways of reduced redundancy. Considering a significant degree of homology in Drosophila for human disease-associated genes, it poses as a versatile in vivo platform to study the pathophysiology of various human diseases. With core metabolic pathways governing energy homeostasis generally conserved, Drosophila can be used as a model for studying molecular mechanisms underlying disease phenotypes manifested in obese and diabetic patients. In this review, we discuss representative Drosophila studies that investigated the effects of dysregulated core signaling pathways on metabolic signatures of obese animals.

본 논문에서는 온실 구조물의 구조 성능 검토 시 적합한 모델링 방법을 제시하기 위해 대상 온실 구조물을 선정하고 지점 및 접합부 조건 그리고 케이블 요소의 단면적을 변화시켜 가며 파라메트릭 스터디를 수행하였으며, 이들 파라메터의 변화에 따른 대상 구조물의 주요 모드 형상 및 고유진동수 변화를 조사하였다. 또한 대상 구조물에 대해 현장 가속도계 측정법을 이 용하여 상시진동을 계측하여 주요 모드 형상 및 고유진동수를 측정하여 해석 결과와 비교하였다. 이들 비교 결과로부터 대 상 온실 구조물의 해석에 적합한 모델링 기법을 제시하였다.

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.

Purpose – The purpose of this study is to explore the introduction and activation of smart training for the effective training of vocational ability development of companies in the 4th industrial revolution era, we analyze the present status of smart training introduction and related difficulties and propose concrete activation plan. Research design, data, and methodology – Through the online survey, we tried to confirm the recognition of corporate about smart training. Questionnaires include what are the benefits, expectations, and difficulties of smart training, etc. The survey was conducted from August 21, 2017 to September 4, 2017. A total of 69 companies participated in the questionnaire. The questionnaire results were analyzed through frequency analysis and contents analysis. Based on the results of the questionnaire, we found out the cause of inhibition of smart training activation and suggested activation strategies. Results – The main reason for the provision of smart training is the expectation of the training performance and the recognition that it is possible to provide training in a flexible manner. The effectiveness of smart training operation was evaluated as a high level of contribution to the development of creative training course and the capacity of training institute. As a result of checking factors that hinders the activation of smart training, the most important reason is that the time and cost burden of the training institutes is excessive. The lack of expertise in the design of smart training courses and the burden of employers and trainees. Conclusions – In order to activate smart training, it is necessary to find solutions to the obstacles at the internal or external level of training institutions. The internal barriers to the training organization are lack of internal competence for preparation and course management. In this regard, we need to consider providing consulting, best practices or guidance in the process of designing and operating smart training. On the other hand, as an external obstacle factor, it is necessary to provide incentives to participate in smart training. In addition, further research is needed on strategies that can lead to participation in smart training from the viewpoint of employers and learners.