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A 90-day Repeated-Dosed Toxicity Study of Euphorbiae kansui radix Extract in Fischer 344/N Rats
Zhong-Ze Han,Hu-Song Zhang,Ki-Hyun Gil,Joo-Young Lee,Kwang-Han Kong,Myoung-Kyu Han,Hyun-Ju Yang,Hak-Soo Kim,Do-Hyung Kim,Tae-Hwan Ahn,Jin-Sook Bae,Hyun-Kyu Ko,Jung-Woon Lee,Moon-Soon Kim,Si-Whan Song 한국실험동물학회 2008 Laboratory Animal Research Vol.24 No.4
This study was performed to evaluate repeated-dose toxicities of Euphorbiae kansui radix extract in F344/N rats. Euphorbiae kansui radix extract was administered orally to rats at dose levels of 0, 37, 111, 333, 1,000 and 2,000 ㎎/㎏/day. Each group consisted of 10 rats of each gender. The Euphorbiae Kansui, Radix extract was given once a day, 5 times a week, for 90 day repeatedly. This study was conducted in accordance with the Protocol of Korea National Toxicology Program (issued by National Institute of Toxicological Research) and The Standards of Toxicity Study for Medicinal Products (issued by Korea Food and Drug Administration). In the present study, there were no dose-related changes in mortality, clinical signs, body weights, ophthalmoscopy, urine analysis, hematological findings, estrus cycle and sperm examination of all animals treated with Euphorbiae kansui radix extract. There were increases of liver weights in 2,000 ㎎/㎏/day groups of males and in 333, 1,000 and 2,000 ㎎/㎏/day groups of females. There were decreases of alkaline phosphatase levels in 1,000 and 2,000 ㎎/㎏/day groups of both sexes. These results suggest that the oral no-observed-adverse-effect level (NOAEL) of the test item, Euphorbiae kansui radix extract, in rats is 2,000 ㎎/㎏/day in both genders; no-observed-effect level (NOEL) is 1,000 ㎎/㎏/day in male and 111 ㎎/㎏/day in female. The target organs were thought to be liver and thymus.
KOCC의 피브릴화 특성 및 라이너판지 물성에 미치는 영향
한준규(Jun Kyu Han),황임정(Im Jeong Hwang),김진모(Jin Mo Kim),최재준(Jae Jun Choi),이용규(Yong Kyu Lee),원종명(Jong Myoung Won) 한국펄프·종이공학회 2018 펄프.종이技術 Vol.50 No.5
Fibrillation was attempted to determine the suitability of KOCC for the production of nanocellulose in order to utilize it as a high value added material, and the possibility of using fibrillated KOCC obtained therefrom as a papermaking additive was evaluated. A grinder was used for the fibrillation of KOCC. In order to investigate the fibrillation characteristics of KOCC, the changes of SEM images, Brookfield viscosity and degree of polymerization were measured. Also, the handsheets were prepared and the changes of major physical properties were investigated in order to evaluate the performance and applicability of fibrillated KOCC as an additive for linerboard manufacture. The fibrillation of KOCC was significantly delayed compared to the bleached chemical pulp, and the complete fibrillation was not achieved, probably due to the residual lignin content (kappa no. 19.36). It is difficult to produce nanocellulose without proper pretreatment. The average fiber length decreased to the level of fines at 20 times of grinding because KOCC was severely aged. As the fibrillation of KOCC proceeded, the degree of Brookfield viscosity continued to increase and the degree of polymerization showed a gradual decrease. Bulk, tear index, and burst index of paper were not significantly affected by the addition of fibrillated KOCC. However, it was found that the tensile index and stiffness could be improved by the combination of retention aid and fibrillated KOCC.
Han, Myoung Sook,Chung, Kun Wook,Cheon, Hyae Gyeong,Rhee, Sang Dal,Yoon, Chang-Hwan,Lee, Moon-Kyu,Kim, Kwang-Won,Lee, Myung-Shik American Diabetes Association 2009 Diabetes Vol.58 No.2
<P><B>OBJECTIVE—</B>Imatinib has been reported to induce regression of type 2 diabetes in chronic leukemia patients. However, the mechanism of diabetes amelioration by imatinib is unknown, and it is uncertain whether imatinib has effects on type 2 diabetes itself without other confounding diseases like leukemia. We studied the effect of imatinib on diabetes in <I>db/db</I> mice and investigated possible mechanism's underlying improved glycemic control by imatinib.</P><P><B>RESEARCH DESIGN AND METHODS—</B>Glucose tolerance and insulin tolerance tests were done after daily intraperitoneal injection of 25 mg/kg imatinib into <I>db/db</I> and C57BL/6 mice for 4 weeks. Insulin signaling and endoplasmic reticulum stress responses were studied by Western blotting. β-Cell mass and apoptotic β-cell number were determined by combined terminal deoxynucleotidyl transferase–mediated dUTP nick-end labeling (TUNEL) staining and insulin immunohistochemistry. The in vitro effect of imatinib was studied using HepG2 cells.</P><P><B>RESULTS—</B>Imatinib induced remission of diabetes in <I>db/db</I> mice and amelioration of insulin resistance. Expression of endoplasmic reticulum stress markers in the liver and adipose tissues of <I>db/db</I> mice, such as phospho-PERK, phospho-eIF2α, TRB3, CHOP, and phospho–c-Jun NH<SUB>2</SUB>-terminal kinase, was reduced by imatinib. Insulin receptor substrate-1 tyrosine phosphorylation and Akt phosphorylation after insulin administration were improved by imatinib. Serum aminotransferase levels and hepatic triglyceride contents were decreased by imatinib. Pancreatic β-cell mass was increased by imatinib, accompanied by decreased TUNEL<SUP>+</SUP> β-cell and increased BrdU<SUP>+</SUP> β-cell numbers. Imatinib attenuated endoplasmic reticulum stress in hepatoma cells in vitro.</P><P><B>CONCLUSIONS—</B>Imatinib ameliorated endoplasmic reticulum stress and induced remission of diabetes in <I>db/db</I> mice. Imatinib or related compounds could be used as therapeutic agents against type 2 diabetes and metabolic syndrome.</P>