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NSAID Activated Gene (NAG-1), a Modulator of Tumorigenesis
Eling, Thomas E.,Baek, Seung-Joon,Shim, Min-sub,Lee, Chang-Ho Korean Society for Biochemistry and Molecular Biol 2006 Journal of biochemistry and molecular biology Vol.39 No.6
The NSAID activated gene (NAG-1), a member of the TGF-$\beta$ superfamily, is involved in tumor progression and development. The over-expression of NAG-1 in cancer cells results in growth arrest and increase in apoptosis, suggesting that NAG-1 has anti-tumorigenic activity. This conclusion is further supported by results of experiments with transgenic mice that ubiquitously express human NAG-1. These transgenic mice are resistant to the development of intestinal tumors following treatment with azoxymethane or by introduction of a mutant APC gene. In contrast, other data suggest a pro-tumorigenic role for NAG-1, for example, high expression of NAG-1 is frequently observed in tumors. NAG-1 may be like other members of the TGF-$\beta$ superfamily, acting as a tumor suppressor in the early stages, but acting pro-tumorigenic at the later stages of tumor progression. The expression of NAG-1 can be increased by treatment with drugs and chemicals documented to prevent tumor formation and development. Most notable is the increase in NAG-1 expression by the inhibitors of cyclooxygenases that prevent human colorectal cancer development. The regulation of NAG-1 is complex, but these agents act through either p53 or EGR-1 related pathways. In addition, an increase in NAG-1 is observed in inhibition of the AKT/GSK-$3{\beta}$ pathway, suggesting NAG-1 alters cell survival. Thus, NAG-1 expression is regulated by tumor suppressor pathways and appears to modulate tumor progression.
Insurance in a Digital World: Are Cyber Risks Insurable?
( Martin Eling ) 한국금융연구원 2022 금융연구 working paper Vol.2022 No.6
The aim of this paper is to review both academic literature and industry studies to better understand the insurability of cyber risks. We focus on five main research questions which are 1) the measurement of cyber risk, 2) the economic impact of cyber risk, 3) the comparison with other risks, 4) the analysis of the current cyber insurance market and 5) the discussion of current insurability limitations that limit market growth. Four specific characteristics of cyber risk help explain the underdevelopment of the cyber insurance market. Cyber risks are characterized by heavy tail marginal distributions, non-linear dependencies leading to potential accumulation risk, model/parameter risk and asymmetric information. All these properties make cyber insurance unattractive from an insurance company points of view. On top there are numerous demand side factors that hamper market growth.
신유진,문지혜,진호준,Ele Ferrannini,임수 대한내분비학회 2020 Endocrinology and metabolism Vol.35 No.2
Background: We assessed the glucose-lowering efficacy of adding empagliflozin versus dose escalating existing medications in patients with uncontrolled type 2 diabetes (T2D). Methods: This was a 6-month retrospective case-control study in subjects with uncontrolled T2D (glycated hemoglobin [HbA1c]>7%) on conventional treatment. The study group started add-on therapy with empagliflozin (10 mg once a day) while the controlgroup was up-titrated with existing medication, using either monotherapy or a combination of metformin, sulfonylurea, and a dipeptidyl peptidase-4 inhibitor. The primary endpoints included changes in HbA1c, fasting plasma glucose (FPG), and 2-hour postprandial glucose (PP2) levels. Secondary outcomes included changes in body composition, body mass index (BMI), and serum ketonebodies, and urinary excretion of sodium, potassium, chlorine, calcium, phosphorus, and glucose. Results: After treatment, the reduction in HbA1c was significantly greater in the empagliflozin group than in controls (from 8.6%±1.6% to 7.6%±1.5% vs. 8.5%±1.1% to 8.1%±1.1%; P<0.01). Similar patterns were found in FPG and PP2 levels. Empagliflozindecreased systolic and diastolic blood pressure, triglycerides, and alanine and aspartate aminotransferase levels. Body weight, BMI,waist circumference, fat mass, and abdominal visceral fat area decreased significantly while lean body mass was maintained. Totalketones, β-hydroxybutyrate, and acetoacetate levels increased significantly after empagliflozin. Conclusion: In addition to glucose lowering, an empagliflozin add-on regimen decreased blood pressure and body fat, and improvedmetabolic profiles significantly. Empagliflozin add-on is superior to dose escalation in patients with T2D who have inadequate glycemic control on standard medications.