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Park, S R,Kong, S-Y,Nam, B-H,Choi, I J,Kim, C G,Lee, J Y,Cho, S J,Kim, Y W,Ryu, K W,Lee, J H,Rhee, J,Park, Y-I,Kim, N K Nature Publishing Group 2011 The British journal of cancer Vol.104 No.7
<P><B>Background:</B></P><P>We evaluated the association between polymorphisms of cytochrome P450 2A6 (<I>CYP2A6</I>)/excision repair cross-complementation group 1 (<I>ERCC1</I>)/X-ray repair cross-complementing group 1(<I>XRCC1</I>) and treatment outcomes of metastatic gastric cancer (MGC) patients treated with S-1/cisplatin.</P><P><B>Methods:</B></P><P>Among MGC patients (<I>n</I>=108), who received S-1 (40 mg m<SUP>−2</SUP> b.i.d., days 1–14) and cisplatin (60 mg m<SUP>−2</SUP>, day 1) every 3 weeks, we analysed the wild-type allele (<I>W</I>) and variants (<I>V</I>) of <I>CYP2A6</I> (<I>*4</I>, <I>*7, *9, *10</I>), and the polymorphisms of <I>ERCC1</I> (rs11615, rs3212986) and <I>XRCC1</I> (rs25487).</P><P><B>Results:</B></P><P>Patients having fewer <I>CYP2A6</I> variants had better response rates (<I>W</I>/<I>W vs W</I>/<I>V</I> other than <I>*1/*4 vs V</I>/<I>V</I> or <I>*1/*4</I>=66.7 <I>vs</I> 58.3 <I>vs</I> 32.3% <I>P</I>=0.008), time to progression (TTP) (7.2 <I>vs</I> 6.1 <I>vs</I> 3.5 months, <I>P</I>=0.021), and overall survival (23.2 <I>vs</I> 15.4 <I>vs</I> 12.0 months, <I>P</I>=0.004). <I>ERCC1 19442C</I>><I>A</I> (rs3212986) was also associated with response rate (<I>C/C</I>, 46.7% <I>vs C/A</I>, 55.3% <I>vs A/A</I>, 87.5%) (<I>P</I>=0.048) and TTP (4.4 <I>vs</I> 7.6 <I>vs</I> 7.9 months) (<I>P</I>=0.012). Patients carrying both risk genotypes of <I>CYP2A6</I> (<I>V</I>/<I>V</I> or <I>1/*4</I>) and <I>ERCC1 19442C</I>><I>A</I> (<I>C/C</I>) <I>vs</I> those carrying none showed an adjusted odds ratio of 0.113 (<I>P</I>=0.004) for response, and adjusted hazard ratios of 3.748 (<I>P</I>=0.0001) for TTP and 2.961 (<I>P</I>=0.006) for death.</P><P><B>Conclusion:</B></P><P>Polymorphisms of <I>CYP2A6</I> and <I>ERCC1 19442C</I>><I>A</I> correlated with the efficacy of S-1/cisplatin.</P>
Role of the Meckel’s Cartilage in Embryonic Mandibular Development of Mice
J. W Choi,S. B Han,J. H Sung,H. I Shin 대한구강악안면병리학회 2005 대한구강악안면병리학회지 Vol.29 No.5
Mecke!'s car t ilage is one of the ea rliest structu re to appear in a mandible derived from the lï rst branchi a l a rch and serves as the primorclium I"or the formation 01‘ mandible‘ mall eus. incus. and sphenomandibular li gament However. its direct role a nd the mechanism in mandibular clevelopment a re not well elucidated. 1'0 address t his Issue‘ we observed morphol ogical and histological changes and gene expression patterns in the Mecke!'s cart ilage 01" a cleveloping mouse. I"rom E13.5 to E18.5 embryos. using skeletal preparation samples a ncl routinely prepa red s lide secti ons for light mi croscopic observation in various sectional planes. The following methods were per |‘ ormecl : H&E staining I"or general hi st이 og i cal observation ‘ Von Kossafor detection of minerali zation. TRAP activ ity staining for locali zaLion 01’ osteoclastic cell s. immunohistochemistry for !Iα@-1 a ncl -9 forevaluati on of enzy matic activity 01" osteoclasLic cell s. a ncl in situ hybricli zation for detection of collagen type 1. Il. ancl X mRNA ex presslon‘ respecLively. AL E1 3.5 Mec kel's cartilage appeared as a V-shaped rod fused a t the micl line and thin minera li zed ma ndibular buccal plaLe was I"ormed lateral to. and at some clistance from. Meckel’s carti lage in an intramembranous ossi lïcation mocle. WiLh the progression of tooth development. t he Meckel’s in carti lage adjacent incisors revealecl hyperLrophi c chonclrocyte di ff"er entiation with minerali zation of the chondroid matrix. The Meckel’s car Li lage was replacecl with bone by o~ L eoc l asLs . showing strong immunoreact ivity for MMP- l ancl -9 from E16 5 Wi Lh ti me‘ Lhis bony replacement of Meckel's cartilage in an endochondral ossification mode was ex Lenclecl up Lo the mid-porLion of Lhe molar sockets til l EI8.5. The bony replacement of minera li zed hypertrophic chondrocyte zone expressing X collagen mHNA conLri buted to the formation of thick mandibular lingual plate . 1'hese f"i ndings suggesL LhaL mandibular formalion and development is closely relatecl with not only Mecke!'s carLi lage. buL also wiLh Lhc developing LooLh. and thaL C'erLai n in f"l uence from the developing tooth may play a role in detcrmin in g Lhe faLc of Meckel’s ca rLi lage cluring ma ndi bular development.
Effects of dextrorotatory morphinans on brain Na<sup>+</sup> channels expressed in Xenopus oocytes
Lee, J.H.,Shin, E.J.,Jeong, S.M.,Lee, B.H.,Yoon, I.S.,Lee, J.H.,Choi, S.H.,Kim, Y.H.,Pyo, M.K.,Lee, S.M.,Chae, J.S.,Rhim, H.,Oh, J.W.,Kim, H.C.,Nah, S.Y. North-Holland ; Elsevier Science Ltd 2007 european journal of pharmacology Vol.564 No.1
We previously demonstrated that dextromethorphan (DM; 3-methoxy-17-methylmorphinan) analogs have neuroprotective effects. Here, we investigated the effects of DM, three of its analogs (DF, 3-methyl-17-methylmorphinan; AM, 3-allyloxy-17-methoxymorphian; and CM, 3-cyclopropyl-17-methoxymorphinan) and one of its metabolites (HM; 3-methoxymorphinan), on Na<SUP>+</SUP> channel activity. We used the two-microelectrode voltage-clamp technique to test the effects of DM, DF, AM, CM and HM on Na<SUP>+</SUP> currents (I<SUB>Na</SUB>) in Xenopus oocytes expressing cRNAs encoding rat brain Nav1.2 α and β1 or β2 subunits. In oocytes expressing Na<SUP>+</SUP> channels, DM, DF, AM and CM, but not HM, induced tonic and use-dependent inhibitions of peak I<SUB>Na</SUB> following low- and high-frequency stimulations. The order of potency for the inhibition of peak I<SUB>Na</SUB> was AM-CM > DM=DF. The DM, DF, AM and CM-induced tonic inhibitions of peak I<SUB>Na</SUB> were voltage-dependent, dose-dependent and reversible. The IC<SUB>50</SUB> values for DM, DF, AM and CM were 116.7+/-14.9, 175.8+/-16.9, 38.6+/-15.5, and 42.5+/-8.5 μM, respectively. DM and its analogs did not affect the steady-state activation and inactivation voltages. AM and CM, but not DM and DF, inhibited the plateau I<SUB>Na</SUB> more effectively than the peak I<SUB>Na</SUB> in oocytes expressing inactivation-deficient I1485Q-F1486Q-M1487Q (IFMQ3) mutant channels; the IC<SUB>50</SUB> values for AM and CM in this system were 8.4+/-1.3 and 8.7+/-1.3 μM, respectively, for the plateau I<SUB>Na</SUB> and 43.7+/-5.9 and 32.6+/-7.8 μM, respectively, for the peak I<SUB>Na</SUB>. These results collectively indicate that DM and its analogs could be novel Na<SUP>+</SUP> channel blockers acting on the resting and open states of brain Na<SUP>+</SUP> channels.