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RISS 인기검색어
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- 저자 : Elif Ari (검색결과 2 건)
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Arie Arenst Andreas,Kristianto Hans,Cengiz Elif Ceylan,Demir-Cakan Rezan 한국탄소학회 2020 Carbon Letters Vol.30 No.2
Salacca peel-based porous carbon (SPPC) with high surface area (1945 m2 g−1) and large specifc pore volume (1.68 cm3 g−1) was prepared by pre-carbonization and K2CO3 activation method. Based on the TGA results, it can be estimated that up to 70 wt% of sulfur-active materials could be infltrated into the pores of SPPC to form SPPC/S composite cathode for LiS battery. The porous structure of SPPC could act as a bufer layer against volume expansion and minimize the shuttle efect due to the penetration of intermediate polysulfdes during cycle tests. Optimization on sulfur loading (50, 60 and 70 wt%) in SPPCC/S composite was also investigated. It was found that the SPPC/S composites with 60 wt% of sulfur loading had the best electrochemical performances. With 60 wt% of sulfur loading, SPPC/S composite electrodes showed excellent electrochemical performances in terms of high initial specifc discharge capacity of 1006 mAh g−1 at 0.5 C and capacity retention of 71% until the 100th cycle. For both cases of low and high sulfur loading, they caused much worse electrochemical performances. Based on the experimental results, it can be concluded that porous carbons derived from the salacca peel were promising materials for sulfur loading in LiS battery.
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Do Statins Counteract the Effect of Antidiabetic Drugs? Results of the SCEAD Study
Bahar Arican Tarim,Francesco Fici,Istemihan Tengiz,Saadet Avunduk,Yurdaer Ozcan,Gokhan Faikoglu,Elif Ari,Nicolás Roberto Robles,Guido Grassi 연세대학교의과대학 2023 Yonsei medical journal Vol.64 No.3
Purpose: Diabetes and dyslipidemia are leading causes of mortality and morbidity. According to international guidelines, statins are the cornerstone of treatment in patients with diabetes and/or dyslipidemia. However, statins and antidiabetic agents have op posite pharmacological effects, because statins, particularly atorvastatin and rosuvastatin, impair glucose homeostasis, increas ing the risk of new-onset diabetes, whereas antidiabetic drugs improve glycemic homeostasis. The aim of this study was to inves tigate the effect of atorvastatin, rosuvastatin, and pitavastatin on glucose homeostasis in patients with type 2 diabetes mellitus (T2DM) and dyslipidemia during stable treatment with hypoglycemic drugs. Materials and Methods: The study was conducted as a pilot, prospective, randomized, open label, parallel group with blinded endpoints (PROBE) study. Of 180 recruited patients with T2DM and dyslipidemia, 131 were randomized to atorvastatin (n=44), rosuvastatin (n=45), and pitavastatin (n=42) and treated for 6 months. Results: Fasting plasma glucose (FPG) marginally decreased in patients assigned to atorvastatin (-3.5 mg/dL, p=0.42) and rosuvas tatin (-6.5 mg/dL, p=0.17), while it decreased much more in patients treated with pitavastatin (-19.0 mg /dL, p<0.001). Mean gly cated hemoglobin A1c (HbA1c ) values remained unchanged during treatment with atorvastatin (-0.10%, p=0.53) and rosuvastatin (0.20%, p=0.40), but were significantly reduced with pitavastatin (-0.75%, p=0.01). Atorvastatin, rosuvastatin, and pitavastatin sig nificantly lowered (p<0.001) plasma levels of total cholesterol, low-density lipoprotein-cholesterol, and triglycerides, while high density lipoprotein-cholesterol (HDL-C) levels increased significantly (p=0.04) only in the pitavastatin group. Conclusion: The results of the present study suggest that pitavastatin affects FPG and HbA1c less than atorvastatin and rosuvas tatin in patients with T2DM and concomitant dyslipidemia. Lipid-lowering efficacies were not significantly different among the three statins, with the exception of HDL-C, which increased significantly with pitavastatin. Although the pharmacological mecha nism of pitavastatin on glucose homeostasis in patients with T2DM during stable antidiabetic therapy is not known, it can be as sumed that pitavastatin has less drug interaction with hypoglycemic agents or that it increases plasma levels of adiponectin.
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