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Inhibitory Effects of Hwao-tang on the Atherosclerosis and the Venous Thrombosis
Hong, Mun Yeob,Choi, Dall Yeong,Kim, Cherl Ho,Kim, Beob Jin,Kim, Han Geu,Ahan, Jong Chan,Lee, Soo Kyung,Chung, Tae Wook,Park, Won Hwan 대한동의생리학회,대한동의병리학회 2002 동의생리병리학회지 Vol.16 No.2
The inhibitory effects of the traditional herbal medicine Hwao-tang on the progression of the atherosclerotic lesions were studied using the spontaneous familial hypercholesterolemia (FH) model, Kurosawa and Kusanagi-hypercholesterolemic (KHC) rabbits. Hwao-tang is activate blood circulation, vital energy and regulate menstruation, etc. Now a days, Hwao-tang is mainly used for the treatment of inflammation, hyperlipemia and arteriosclerosis. However, pharmacological mechanisms of Hwao-tang on lipid metabolism and atherosclerosis formation are poorly understood. We have investigated the pharmacological effects of Hwao-tang on hypercholesterolemia and atherosclerosis using a spontaneous experimental model. In conclusion, the protection of extracts of HOT and its herbs on the ischemic infarction induced artificially might be related to their inhibitory effects on DIC, platelet coagulation and thrombic action. These suggest that Hwao-tang has inhibitory effects on the development of atheromatous plaque formation in spontaneous FH model rabbits. It is possible that the antioxidative effects of Hwao-tang on LDL led to the beneficial effects observed in this study.
동서연 ( Dong Seo Yeon ),김여홍 ( Kim Yeo Hong ),허주엽 ( Heo Ju Yeob ),양문호 ( Yang Mun Ho ) 대한산부인과학회 2003 Obstetrics & Gynecology Science Vol.46 No.11
The coexistence of mucinous ovarian and appendiceal tumors in associated with pseudomyxoma peritonei is well established. But, ovarian and appendiceal mucinous tumors occur without involvement of other organs is unusual. When the two lesions are morpholog
경호 이,Dong Min Kang,Hyung Sup Yoon,Jae Yeob Shim,Jin Hee Lee,Jin-Koo Rhee,Ju Yeon Hong,Mun Kyo Lee,Sam-Dong Kim,Sung Jin Kim,Woo Jin Chang,Young-Hoon Chun 한국물리학회 2003 THE JOURNAL OF THE KOREAN PHYSICAL SOCIETY Vol.42 No.III
This paper presents the experimental results of a line of work from MMIC design, fabrication, module packaging, and measurement, to system demonstration for the next generation 60 GHz wideband wireless communications systems. We fabricated power amplifier (PA) and up-mixer monolithic microwave integrated circuits (MMICs') and their modules for the application of 60 GHz mobile broadband system (MBS) transmitter. The device technologies for the transmitter MMICs' are ETRI's own 0.15 $\mu$m gate-length GaAs pseudomorphic high electron mobility transistor (PHEMT) for PA MMIC and 0.2 $\mu$m gate-length metamorphic HEMT (MHEMT) for up-mixer MMIC. The output power at 1-dB gain compression point, P1dB, of the 4-stage PA is higher than 16 dBm and the gain higher than 12.4 dB for 58 $\sim$ 62 GHz. For 60 GHz up-mixer the conversion gain is higher than $-$12 dB and the output P1dB is higher than $-$12.85 dBm for 57 $\sim$ 70 GHz. The modules of PA (40 $\times$ 30 $\times$ 15 mm$^3$) and up-mixer ($46 \times30 \times15$ mm$^3$) were made for the transmission test on the 60 GHz MBS test system and the 60 GHz wireless transmission test was successfully demonstrated.
Park Soonbum,Cho Eun A,Chun Jung Nyeo,Lee Da Young,Lee Sanghoon,Kim Mi Yeon,Bae Sang Mun,Jo Su In,Lee So Hee,Park Hyun Ho,김태민,So Insuk,Kim Sang-Yeob,Jeon Ju-Hong 생화학분자생물학회 2022 Experimental and molecular medicine Vol.54 No.-
Crizotinib is a clinically approved tyrosine kinase inhibitor for the treatment of patients with locally advanced or metastatic non-small cell lung cancer (NSCLC) harboring EML4-ALK fusion. Crizotinib was originally developed as an inhibitor of MET (HGF receptor), which is involved in the metastatic cascade. However, little is known about whether crizotinib inhibits tumor metastasis in NSCLC cells. In this study, we found that crizotinib suppressed TGFβ signaling by blocking Smad phosphorylation in an ALK/MET/RON/ROS1-independent manner in NSCLC cells. Molecular docking and in vitro enzyme activity assays showed that crizotinib directly inhibited the kinase activity of TGFβ receptor I through a competitive inhibition mode. Cell tracking, scratch wound, and transwell migration assays showed that crizotinib simultaneously inhibited TGFβ- and HGF-mediated NSCLC cell migration and invasion. In addition, in vivo bioluminescence imaging analysis showed that crizotinib suppressed the metastatic capacity of NSCLC cells. Our results demonstrate that crizotinib attenuates cancer metastasis by inhibiting TGFβ signaling in NSCLC cells. Therefore, our findings will help to advance our understanding of the anticancer action of crizotinib and provide insight into future clinical investigations.