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Park, J. M.,Choi, M.-G.,Kim, S. W.,Chung, I.-S.,Yang, C. W.,Kim, Y. S.,Jung, C. K.,Lee, K. Y.,Kang, J.-H. Wiley (Blackwell Publishing) 2010 American journal of transplantation Vol.10 No.9
<P>This study was to evaluate the frequency of colorectal neoplasia in renal transplant recipients and to investigate the association with Epstein-Barr virus (EBV) and cytomegalovirus (CMV) infection. We compared the frequency of colorectal neoplasia among renal transplant recipients with that of the healthy subjects. Specimens of colorectal neoplasia were examined for EBV and CMV using in situ hybridization and immunohistochemistry, respectively. Of 796 renal transplantation cohorts, 315 were enrolled. The frequency of colorectal neoplasia among the patients was 22.9%. Compared with the healthy subjects, the odds ratio (OR) for advanced adenoma was 3.32 (95% CI, 1.81-6.10). The frequency of cancer among the patients was 1.9% (OR, 12.0; 95% CI, 1.45-99.7). A long interval between transplantation and colonoscopy was a significant factor in the development of advanced colorectal neoplasia. EBV positivity was detected in 30.6% of colorectal neoplasia specimens from renal transplant recipients, which was higher than that for the controls (p = 0.002). CMV was not detected in any lesions of patients or controls. In conclusion, renal transplant recipients have a significantly increased risk of advanced colorectal neoplasia. EBV was more frequently found in specimens of advanced colorectal neoplasm obtained from the renal transplant recipients.</P>
Ahn, CY,Bae, SK,Bae, SH,Kim, T,Jung, YS,Kim, YC,Lee, MG,Shin, WG Wiley (Blackwell Publishing) 2009 British journal of pharmacology Vol.156 No.6
<P>BACKGROUND AND PURPOSE: The incidence of diabetes mellitus is increased in patients with liver cirrhosis. Oltipraz is currently in trials to treat patients with liver fibrosis and cirrhosis induced by chronic hepatitis types B and C and is primarily metabolized via hepatic cytochrome P450 isozymes CYP1A1/2, 2B1/2, 2C11, 2D1 and 3A1/2 in rats. We have studied the influence of diabetes mellitus on pharmacokinetics of oltipraz and on expression of hepatic, CYP1A, 2B1/2, 2C11, 2D and 3A in rats with experimental liver cirrhosis. EXPERIMENTAL APPROACH: Oltipraz was given intravenously (10 mg x kg(-1)) or orally (30 mg x kg(-1)) to rats with liver cirrhosis induced by N-dimethylnitrosamine (LC rats) or with diabetes, induced by streptozotocin (DM rats) or to rats with both liver cirrhosis and diabetes (LCD rats) and to control rats, and pharmacokinetic variables measured. Protein expression of hepatic CYP1A, 2B1/2, 2C11, 2D and 3A was measured using Western blot analysis. KEY RESULTS: After i.v. or p.o. administration of oltipraz to LC and DM rats, the AUC was significantly greater and smaller, respectively, than that in control rats. In LCD rats, the AUC was that of LC and DM rats (partially restored towards control rats). Compared with control rats, the protein expression of hepatic CYP1A increased, that of CYP2C11 and 3A decreased, but that of CYP2B1/2 and 2D was not altered in LCD rats. CONCLUSIONS AND IMPLICATIONS: In rats with diabetes and liver cirrhosis, the AUC of oltipraz was partially restored towards that of control rats.</P>
Kim, Dong Hyun,Kim, Sunho,Jeon, Su Jin,Son, Kun Ho,Lee, Seungjoo,Yoon, Byung Hoon,Cheong, Jae Hoon,Ko, Kwang Ho,Ryu, Jong Hoon Wiley (Blackwell Publishing) 2009 British journal of pharmacology Vol.158 No.4
<P>BACKGROUND AND PURPOSE: The intracellular signalling kinase, extracellular signal-regulated kinase 1/2 (ERK1/2) is required for new memory formation, suggesting that control of ERK signalling might be a target for the treatment of cognitive dysfunction. Previously, we reported that tanshinone congeners have ameliorating effects on drug-induced memory impairment in mice. Here, we have investigated possible modes of action of tanshinone I on learning and memory, associated with ERK phosphorylation. EXPERIMENTAL APPROACH: Using immunohistochemical, Western blot techniques, and behavioural testing, we studied the effect of tanshinone I on memory impairment induced by diazepam or dizocilpine (MK-801) in mice. KEY RESULTS: Tanshinone I (2 or 4 mg.kg(-1), p.o.) increased latency times versus vehicle-treated control group in the passive avoidance task. Western blot analysis and immunohistochemical data showed that tanshinone I (4 mg.kg(-1)) increased levels of phosphorylated cAMP response element binding protein (pCREB) and phosphorylated ERK (pERK) in the hippocampus. These increases in pCREB and pERK were blocked by U0126 (inhibitor of ERK1/2), which also prevented the increase in passive avoidance task latency time after tanshinone I. In models of learning and memory impairment induced by diazepam and MK-801, tanshinone I (4 mg.kg(-1)) reversed learning and memory impairments detected by the passive avoidance test. Western blot analysis showed that tanshinone I reversed the diazepam- and MK-801-induced inhibitions of ERK and CREB activation in hippocampal tissues. These effects were also blocked by U0126. CONCLUSIONS AND IMPLICATIONS: Tanshinone I ameliorates the learning and memory impairments induced by diazepam and MK-801 through activation of ERK signalling.</P>
Rituximab-induced vasculitis: A case report and review of the medical published work
KIM, Min Joo,KIM, Hyung Ok,KIM, Ho Yeon,PARK, Young Min Wiley (Blackwell Publishing) 2009 The Journal of Dermatology Vol.36 No.5
<P>Rituximab is an anti-CD20 chimeric murine/human monoclonal antibody mainly used in the treatment of patients with a cutaneous lymphoid malignancy. Among the side-effects associated with rituximab administration, vasculitis has been rarely reported. There are two reported cases in the English language medical published work. We describe a 38-year-old Korean man with cutaneous vasculitis occurring 1 day after rituximab administration.</P>
Kim, Mi-Sung,Kwon, Jung Yeon,Kang, Nam Joo,Lee, Ki Won,Lee, Hyong Joo Wiley (Blackwell Publishing) 2009 Annals of the New York Academy of Sciences Vol.1171 No.1
<P>Mutations in Ras play a critical role in the development of human cancers, including breast cancer. We investigated the possible antiproliferative effects of the naturally occurring dihydrochalcone phloretin [2',4',6'-trihydroxy-3-(4-hydroxyphenyl)-propiophenone] on H-Ras-transformed MCF10A human breast epithelial (H-Ras MCF10A) cells. Phloretin suppressed H-Ras MCF10A cell proliferation in a dose-dependent manner and induced nuclear condensation in the cells, indicating that phloretin-induced cell death occurs mainly via the induction of apoptosis. Prominent upregulation of p53 and Bax and cleavage of poly (ADP)-ribose polymerase were also detected in the phloretin-treated cells. Finally, phloretin markedly increased caspase-3 activity as well as JNK and p38 mitogen-activated protein kinase signaling. Our findings suggest that the phloretin-induced apoptosis of breast tumor cells contributes to the chemopreventive potential of phloretin against breast cancer.</P>
Cloning and Expression of Vitellogenin 2 Gene from the Intertidal Copepod Tigriopus japonicus
Hwang, Dae-Sik,Lee, Kyun-Woo,Lee, Jae-Seong Wiley (Blackwell Publishing) 2009 Annals of the New York Academy of Sciences Vol.1163 No.1
<P>Vitellogenin (Vg) is the precursor of the egg yolk protein vitellin. Vg induction has been used as a biomarker of exposure to endocrine disrupting chemicals in fish. However, in copepods limited information on the Vg gene is available only from two species, the salmon louse Lepeophtheirus salmonis and the intertidal copepod Tigriopus japonicus. By differential display of RNA expression between male and female adults, we identified another Vg member, i.e., vitellogenin 2 (Vg2) gene from T. japonicus. The full cDNA sequence was 5629 bp containing 5400 bp of an open reading frame. The expression of Vg transcripts was negligible in all naupliar stages and copepodid stages 1 to 4 but was detectable in female copepods of stage 5 and 6. Female adults expressed over 270 times more Vg transcripts than male adults.</P>
Steroid Biosynthesis within the Frog Brain : A Model of Neuroendocrine Regulation
Rego, Jean-Luc Do,Seong, Jae Young,Burel, Delphine,Luu-The, Van,Larhammar, Dan,Tsutsui, Kazuyoshi,Pelletier, Georges,Tonon, Marie-Christine,Vaudry, Hubert Wiley (Blackwell Publishing) 2009 Annals of the New York Academy of Sciences Vol.1163 No.1
<P>There is now clear evidence that the brain, similar to the adrenal gland, gonads, and placenta, is a steroidogenic organ. Notably in the frog brain, the presence of various steroidogenic enzymes has been detected by immunohistochemistry in specific populations of neurons and/or glial cells. These steroidogenic enzymes are biologically active, as shown by the ability of brain tissue explants to convert [(3)H]pregnenolone into various radiolabeled steroids. The frog brain has also been extensively used as a model to study the mechanism of regulation of neurosteroidogenesis by neurotransmitters and neuropeptides. It has been demonstrated that the biosynthesis of neurosteroids is inhibited by gamma-aminobutyric acid (GABA), acting through GABA(A) receptors, and neuropeptide Y, acting through Y1 receptors, and is stimulated by the octadecaneuropeptide (ODN), acting through central-type benzodiazepine receptors, triakontatetraneuropeptide (TTN), acting through peripheral-type benzodiazepine receptors, and vasotocin, acting through V1a-like receptors. These data indicate that some of the neurophysiological effects of neurotransmitters and neuropeptides may be mediated through modulation of neurosteroid biosynthesis.</P>
Jang, Young Jin,Kim, Jong-Eun,Kang, Nam Joo,Lee, Ki Won,Lee, Hyong Joo Wiley (Blackwell Publishing) 2009 Annals of the New York Academy of Sciences Vol.1171 No.1
<P>Alzheimer's disease (AD) is an age-related neurodegenerative disorder in which apoptosis plays a potentially important role. 4-Hydroxynonenal (HNE) is a major lipid peroxidation product produced by oxidative stress, and its level is elevated in the AD brain. In the present study, piceatannol (but not resveratrol) at the concentration of 20 micromol/L inhibited HNE-induced PC12 cell death. Treatment with HNE induced nuclear condensation in PC12 cells, and this was attenuated by piceatannol treatment. HNE induced poly(ADP-ribose) polymerase cleavage and decreased Bcl-2 expression, with both of these effects being attenuated by piceatannol. Piceatannol also inhibited the phosphorylation of c-Jun N-terminal kinase, which is a key regulator of HNE-induced PC12 cell death. These results indicate that piceatannol has therapeutic potential in the prevention of AD.</P>