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Association of colorectal adenoma with components of metabolic syndrome.
Kim, Byung Chang,Shin, Aesun,Hong, Chang Won,Sohn, Dae Kyung,Han, Kyung Su,Ryu, Kum Hei,Park, Bum Joon,Nam, Ji Hyung,Park, Ji Won,Chang, Hee Jin,Choi, Hyo Seong,Kim, Jeongseon,Oh, Jae Hwan Rapid Communications of Oxford Ltd ; Kluwer Academ 2012 Cancer causes & control Vol.23 No.5
<P>Recently, some studies have shown that diabetes mellitus and metabolic syndrome increase the risk of colorectal neoplasms. Although the mechanism is not known, those have been proposed to contribute to this phenomenon, including insulin resistance, oxidative stress, and adipokine production. The objective of this study was to assess the association between metabolic risk factors and colorectal neoplasm.</P>
Oh, Chung-Hun,Shin, Jang-In,Mo, Sang Joon,Yun, Sung-Jo,Kim, Sung-Hoon,Rhee, Yun-Hee Rapid Communications of Oxford Ltd 2013 Blood coagulation & fibrinolysis Vol.24 No.5
<P>L-sulforaphane was identified as an anticarcinogen that could produce quinine reductase and a phase II detoxification enzyme. In recent decades, multi-effects of L-sulforaphane may have been investigated, but, to the authors' knowledge, the antiplatelet activation of L-sulforaphane has not been studied yet.In this study, 2 μg/ml of collagen, 50 μg/ml of ADP and 5 μg/ml of thrombin were used for platelet aggregations with or without L-sulforaphane. L-sulforaphane inhibited the platelet aggregation dose-dependently. Among these platelet activators, collagen was most inhibited by L-sulforaphane, which markedly decreased collagen-induced glycoprotein IIb/IIIa activation and thromboxane A2 (TxA2) formation in vitro. L-sulforaphane also reduced the collagen and epinephrine-induced pulmonary embolism, but did not affect prothrombin time (PT) in vivo. This finding demonstrated that L-sulforaphane inhibited the platelet activation through an intrinsic pathway.L-sulforaphane had a beneficial effect on various pathophysiological pathways of the collagen-induced platelet aggregation and thrombus formation as a selective inhibition of cyclooxygenase and glycoprotein IIb/IIIa antagonist. Thus, we recommend L-sulforaphane as a potential antithrombotic drug.</P>
Cho, Eunae,Choi, Jae Min,Kim, Hwanhee,Tahir, Muhammad Nazir,Choi, Youngjin,Jung, Seunho Rapid Communications of Oxford ; Kluwer Academic P 2013 Biometals Vol.26 No.2
<P>Iron is an essential nutrient for nitrogen-fixing legume root nodules, and the chelation of ferrous iron plays an important role in the mobility and availability of iron to the legume. In the present study, we investigated the iron-binding properties of low-molecular weight succinoglycans isolated from the nitrogen-fixing bacterium, Sinorhizobium meliloti. The low-molecular weight succinoglycans comprising three monomers (M1-M3), four dimers (D1-D4), and six trimers (T1-T6) of the succinoglycan repeating unit were purified by various chromatographic techniques. Interestingly, the colorimetric ferrozine method showed that the succinoglycans T6, M3, and D3 demonstrated a ferrous iron chelating ability of 83, 63, and 38 % per mg, respectively. The individual binding constants were determined as 43703, 2313, and 760 M(-1) for succinoglycans T6, M3, and D3 using ultraviolet-visible spectroscopy. The complexation of succinoglycan and ferrous iron can cause structural changes, which were analyzed by circular dichroism spectroscopy. Furthermore, the complex could provide antioxidant activity through an anti-Fenton reaction. These results demonstrate that the low-molecular weight succinoglycans can effectively modulate iron biochemistry as a novel ferrous iron-acquisition system of S. meliloti.</P>
Autonomic dysfunction in SCN9A-associated primary erythromelalgia.
Kim, Min-Kyeong,Yuk, Ji-Won,Kim, Hyang-Sook,Park, Ki-Jong,Kim, Dae-Seong Rapid Communications of Oxford ; Steinkopff Verlag 2013 Clinical autonomic research Vol.23 No.2
<P>Primary erythromelalgia (EM) is an autosomal dominant disorder caused by mutations of SCN9A. It is clinically characterized by reddish discoloration and episodic burning sensation of distal extremities triggered by warmth. We report a 49-year-old male with primary EM caused by SCN9A mutation (p.F216S), in whom an autonomic reflex screening test revealed a mild sudomotor dysfunction.</P>
Lee, Seoung Hee,Park, Hye Soon,Lee, Jung Ah,Song, Young Sook,Jang, Yeon Jin,Kim, Jong-Hyeok,Lee, Yeon Ji,Heo, Yoonseok Rapid Communications of Oxford 2013 Obesity surgery Vol.23 No.4
<P>Limited data are available on the in vivo expression of fibronectin, one of the main extracellular matrix components. We investigated the expression of fibronectin in abdominal visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) and the associations of leptin, adiponectin, and vaspin gene expression with metabolic parameters in obese women.</P>
Kim, Gwang-Won,Jeong, Gwang-Woo Rapid Communications of Oxford Ltd 2014 NEUROREPORT - Vol.25 No.12
<P>Residential environments are important in the daily lives of individuals, especially in terms of cognitive psychophysiology. This study compared the neural responses to two extreme residential environments: comfortable versus uncomfortable. Thirteen healthy individuals underwent a 3.0-T functional MRI while viewing images representing comfortable and uncomfortable residential environments. During exposure to the comfortable scenery, significant activation was observed in the calcarine gyrus selectively, whereas the uncomfortable scenery induced significant activation in the ventrolateral prefrontal cortex and anterior cingulate cortex, which are related to cognitive control, as well as in the medial prefrontal cortex, hippocampus, parahippocampal gyrus, amygdala, and insula, which are involved in the regulation and expression of emotion. Such differential brain activation patterns may reflect the neural networks mediating cognitive and emotional responses to residential environments. These findings would be helpful for understanding the neural mechanism associated with human comfortability for their residential environments.</P>
Kim, Byung-Su,Bae, Eunkyung,Kim, Young-Ju,Ahn, Kwang-Sung,Park, Juwon,Rhee, Ji young,Lee, Young Yiul,Kim, Youngsoo,Lee, Dongsoon,Kim, Byoung Kook,Yoon, Sung-Soo RAPID COMMUNICATIONS OF OXFORD LTD 2007 ANTICANCER DRUGS Vol.18 No.6
Although STI571 still plays a key role in the treatment of chronic myeloid leukemia, emergence of resistance to STI571 is a major obstacle to successful outcome. Therefore, new agents that increase the sensitivity of chronic myeloid leukemia cells to STI571 are urgently required. SK-7041 is a novel hybrid synthetic histone deacetylase inhibitor derived from the hydroxamic acid of trichostatin A and pyridyl ring of MS-275. Its cytotoxic effects were examined both as a single agent and in combination with STI571 in acute and chronic myeloid leukemia. SK-7041 exhibited growth inhibition of leukemia cells by downregulation of CDK4, cyclin E and cyclin B1 expression, and by upregulation of p21 expression with subsequent activation of the mitochondria-mediated caspase pathway. SK-7041 showed synergism on growth inhibition, cell cycle arrest and induction of apoptosis in chronic myeloid leukemia (K562) when combined with STI571. The synergistic effect was mediated through the same mechanism as in SK-7041 alone, involving reduction of cyclin D1 and induction of p21. Taken together, our findings suggest that SK-7041 is active against leukemia and offers new prospects for overcoming STI571 resistance in chronic myeloid leukemia.
Rho, Youn-Hwa,Lee, Byong-Won,Park, Ki-Hun,Bae, Young-Seuk RAPID COMMUNICATIONS OF OXFORD LTD 2007 ANTICANCER DRUGS Vol.18 No.9
A chloroform extract of the root bark of Cudrania tricuspidata showed an inhibitory effect on mammalian DNA topoisomerase I. The topoisomerase I inhibitory compound was purified and identified as 2S-2&vprime;,5,7-trihydroxy-4&vprime;,5&vprime;-(2,2-dimethylchromeno)-6-prenyl flavanone (cudraflavanone A). Cudraflavanone A was shown to inhibit the activity of topoisomerase I with approximately 0.4 mmol/l 50% inhibitory concentration. A concentration of 6 μmol/l cudraflavanone A caused a 50% growth inhibition of human cancer cell U937. Cudraflavanone A-induced cell death was characterized by the cleavage of poly(ADP-ribose) polymerase and pro-caspase-3. Furthermore, cudraflavanone A induced the fragmentation of DNA into multiples of 180 bp (an apoptotic DNA ladder), indicating that the inhibitor triggered apoptosis. This induction of apoptosis by cudraflavanone A was also confirmed using flow-cytometry analysis. In addition, this compound inhibited protein kinase C activity with approximately 150 μmol/l 50% inhibitory concentration. Taken together, these results suggest that cudraflavanone A may function by inhibiting oncogenic disease, at least in part, through the inhibition of protein kinase C and topoisomerase I activity.
Lipoic acid rescues DBA mice from early-onset age-related hearing impairment.
Ahn, Joong Ho,Kang, Hun Hee,Kim, Tae Yong,Shin, Jung-Eun,Chung, Jong Woo Rapid Communications of Oxford Ltd 2008 NEUROREPORT - Vol.19 No.13
<P>We fed DBA mice with alpha-lipoic acid (100 mg/kg body weight/day), beginning 2, 4, or 8 weeks after birth. Hearing thresholds were measured weekly. At 12 weeks after birth, control mice not fed with alpha-lipoic acid showed significant hearing decreases at all frequencies. In contrast, mice fed with alpha-lipoic acid beginning at 2 weeks after birth showed significantly better hearing at all frequencies. Mice fed with alpha-lipoic acid beginning at 4 and 8 weeks after birth also showed significantly better hearing than control mice after they were fed with alpha-lipoic acid. The stria vascularis of mice fed with alpha-lipoic acid showed reduced 8-oxoguanine residues in DNA and cytoplasm compared with that of control mice. Western blotting showed that the level of hypoxia-inducible factor-1alpha was lower in mice fed with alpha-lipoic acid than in control mice. From these results, we suggest that alpha-lipoic acid prevented early-onset hearing impairment in DBA mice.</P>