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[연구목적] 본 연구에서는 경영전략을 차별화 전략과 원가우위 전략으로 구분하여 미래성과에 미치는 영향을 확인하고 이러한 관계에 경영자 능력이 미치는 영향을 확인하고자 한다. [연구방법] 기업의 경영전략으로서 적극적인 투자활동과 신시장 개척 및 연구 활동을 활발히 수행해 성장 수준이 높은 차별화 전략과 규모의 경제나 학습효과를 높여 원가를 절감하여 기업의 성과를 유지하는 원가우위 전략은 기업의 미래 성과에 영향을 미칠 가능성이 높으며 궁극적으로 이러한 전략을 추구하는 경영자의 특성에 따라 차이가 존재할 수 있다. 본 연구에서는 경영자 특성 중에서 Demerjian et al.(2012, 2013) 연구 등에서 측정한 경영자 능력을 바탕으로 원자연과 유상열(2016) 연구에서 이용한 차별화 전략과 원가우위 전략을 구분하여 미래 성과에 미치는 영향을 검증하였다. [연구결과] 전략 중에서 원가우위 전략만이 미래 성과와 유의적인 영향을 미치며 부정적인 관계에 있는 것으로 나타났다. 또한 경영자 능력은 경영전략 중에서 원가우위 전략 수준과 미래 성과의 관계에 유의적인 양(＋)의 관계를 가져왔다. 이러한 결과는 경영자 능력수준이 높을수록 원가우위 전략이 미래 성과에 긍정적으로 기여함을 확인할 수 있었다. [연구의 시사점] 본 연구에서 미래 성과를 향후에는 확대하여 기간을 연장하여 미래 성과를 분석할 필요성이 존재할 것으로 보인다. 또한 당기순이익을 성과의 대체적 측정치로 이용하였으나 차별화 전략을 수행하는 기업은 적극적인 투자활동을 하는 기업으로 비용지출 수준이 높기 때문에 성과로 연결되기 어려울 수 있다. 따라서 성과를 매출액, 기업가치등 다양한 지표를 활용하여 추가적인 분석을 향후에는 보완적으로 필요할 것으로 보인다.

Although sodium glucose cotransporter 2 (SGLT2) inhibitors have many beneficial effects for type 2 diabetes, including decreased cardiovascular death, recent reports that they increased glucagon through SGLT2 inhibition raised some concern. Troglitazone, Peroxisome proliferator-activated receptor γ (PPAR-γ) agonist, was reported to increase SGLT2 in renal proximal tubule cells, but its role on pancreatic alpha cells have not been reported. We investigated the effect of troglitazone on SGLT2 expression in alpha cells and subsequent glucagon regulation in hyperglycemia. An Alpha TC1-6 cell line was cultured in control (5 mM) or hyperglycemia (HG, 15 mM) for 72 h. We applied troglitazone with or without PPARγ antagonist (GW9662 10 μM). To investigate the involvement of PI3K/Akt pathway, we applied troglitazone with or without Wortmanin. We measured sodium glucose transporter 2 (SGLT2) and glucagon (GCG) mRNA and protein expression. PPAR gamma, PI3K and Akt protein were also measured. Exposure of alpha TC cells to HG for 72 h increased glucagon mRNA and protein expression. HG decreased SGLT2 mRNA and protein expression. Troglitazone significantly reversed HG-induced reduction of SGLT2 expression and increase of glucagon secretion. PPARγ antagonist (GW9662 10 μM) decreased the expression of SGLT2 and increased glucagon as HG did. Hyperglycemia increased PI3K and pAkt expression in alpha cells. Wortmanin (PI3K inhibitor, 1 μM) reversed HG-induced SGLT2 decrease and glucagon increase. Troglitazone treatment decreased PI3K and pAkt expression in HG. In conclusion, PPARγ agonist, troglitazone improved glucose transport SGLT2 dysfunction and subsequent glucagon dysregulation in alpha cell under hyperglycemia. Those effects were through the involvement of PI3K/pAkt signaling pathway. This study may add one more reason for the ideal combination of PPARγ agonist and SGLT2 inhibitor in clinical practice.

The purpose of this study was to assess the physical activity and energy balance of weekdays and weekend in male high school students. Fifty healthy male high school students participated in this study. Anthropometric data were collected. Physical activity level (PAL) and energy intake for weekdays and weekend were calculated from a physical activity diary and food diary using the 24-hour recall method and interview. The resting metabolic rate (RMR) and estimated energy requirement (EER) were calculated from the prediction equations suggested in 2015 KDRIs. Total energy expenditure (TEE) was calculated by multiplying RMR by PAL. Mean age of subjects was 15.9±0.33 years. The daily pedometer counts were significantly higher in the weekdays (12,837 steps) than in weekend (6,661 steps) (P

The modification of proteins by small ubiquitin-like modifier (SUMO) is crucial for the regulation of diverse cellular processes. Protein SUMOylation is reversed by isopeptidases, collectively known as deSUMOylases. Only one family of SUMO-specific proteases has been described so far: the sentrin-specific proteases (SENP). Here, we identify and characterize a new deSUMOylase, which we have named DeSI-1 (DeSumoylating Isopeptidase 1). We describe BZEL—a new transcriptional repressor—as substrate of DeSI-1. DeSI-1 catalyses the deSUMOylation, but not the deubiquitination, of BZEL. Furthermore, the SENP substrates PML and ΔNp63 are not deSUMOylated by DeSI-1, suggesting that SENP and DeSI enzymes recognize different sets of substrates. Together, these data identify a second class of SUMO proteases.

Objectives: Metabolic syndrome components, insulin resistance and central obesity cause type 2 diabetes and hypertension. This will increase the risk of cardiovascular disease. Women after menopause are at increased risk of metabolic syndrome. Several researchers studied that in menopause, metabolic syndrome increased cardiovascular mortality. We studied the impact on cardiovascular mortality of postmenopausal women with metabolic syndrome in the Republic of Korea. Methods: Twenty four thousand nine hundred forty nine postmenopausal women aged 40 years or older were enrolled at health promotion centers of national university hospital located in 18 regions during 1994-2004. Age, weights, height, body mass index (BMI), systolic blood pressure (SBP), diastolic blood pressure (DBP), fasting blood glucose (FBG), cholesterol, triglyceride (TG), high-density lipoprotein were evaluated and history taking about alcohol consumption, smoking, and exercise was performed. In addition, subjects who died of cardiac disease were analyzed from January 1995 to December 2009. Results: Metabolic syndrome was higher in postmenopausal women with increased in age, BMI, blood pressure (BP), FBG, cholesterol, TG. Thirty cardiac deaths occurred during the observation period. Factors affecting cardiac death were age, smoking, FBG and when age and smoking were controlled. FBG was an important factor affecting cardiovascular mortality in our study. When controlling age, smoking, and alcohol consumption, metabolic syndrome caused an increased relative risk of cardiovascular mortality. Survival rate was much lower in postmenopausal women with metabolic syndrome than those without metabolic syndrome. Conclusion: Metabolic syndrome in Korean postmenopausal women increased cardiovascular mortality.