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Aromatic Hydrocarbon Receptor(AhR)⅐AhR NuclearTranslocator-and p53-mediated Induction of theMurine Multidrug Resistance mdr1Gene by3-Methylcholanthrene and Benzo(a)pyrene in Hepatoma Cells*Received for publication,September18,2000,and in revised form,November10,2000Published,JBC Papers in Press,November28,2000,DOI10.1074/jbc.M008495200Marie-Claude Mathieu,Isabelle Lapierre,Karine Brault‡,and Martine Raymond§From the Institut de Recherches Cliniques de Montre´al,Montre´al,Que´bec H2W1R7,CanadaThe mouse multidrug resistance gene family consists of three genes(mdr1,mdr2,and mdr3)encoding P-gly-coprotein.We show that the expression of mdr1is in-creased at the transcriptional level upon treatment of the hepatoma cell line Hepa-1c1c7with the polycyclic aromatic hydrocarbon3-methylcholanthrene(3-MC). This increase is not observed in the aromatic hydrocar-bon receptor(AhR)-defective TAOc1BP r c1and the AhR nuclear translocator(Arnt)-defective BP r c1variants, demonstrating that the induction of mdr1by3-MC re-quires AhR⅐Arnt.We show that the mdr1promoter (؊1165to؉84)is able to activate the expression of a reporter gene in response to3-MC in Hepa-1c1c7but not in BP r c1cells.Deletion analysis indicated that the re-gion from؊245to؊141contains cis-acting sequences mediating the induction,including a potential p53bind-ing sequence.3-MC treatment of the cells increased the levels of p53and induced p53binding to the mdr1pro-moter in an AhR⅐Arnt-dependent manner.Mutations in the p53binding site abrogated induction of mdr1by 3-MC,indicating that p53binding to the mdr1promoter is essential for the induction.Benzo(a)pyrene,a polycy-clic aromatic hydrocarbon and AhR ligand,which,like 3-MC,is oxidized by metabolizing enzymes regulated by AhR⅐Arnt,also activated p53and induced mdr1tran-scription.2,3,7,8-Tetrachlorodibenzo-p-dioxin,an AhR ligand resistant to metabolic breakdown,had no effect. These results indicate that the transcriptional induc-tion of mdr1by3-MC and benzo(a)pyrene is directly mediated by p53but that the metabolic activation of these compounds into reactive species is necessary to trigger p53activation.The ability of the anticancer drug and potent genotoxic agent daunorubicin to induce mdr1independently of AhR⅐Arnt further supports the proposition that mdr1is transcriptionally up-regulated by p53in response to DNA damage.Multidrug resistance(MDR)1is characterized by cross-resis-tance of the cells to a large number of structurally and func-tionally unrelated cytotoxic agents used in chemotherapy.In cultured cells,MDR is frequently caused by the overexpression of P-glycoprotein(Pgp),an integral membrane protein belong-ing to the ATP-binding cassette superfamily of transporters and which functions as an energy-dependent efflux pump of cytotoxic drugs(1,2).Pgp is encoded by a small family of genes with two members in humans(MDR1and MDR2/MDR3)and three in rodents(mdr1/mdr1b,mdr2,and mdr3/mdr1a)(1,2). Only one human gene(MDR1)and two rodent genes(mdr1/ mdr1b and mdr3/mdr1a)can confer MDR upon overexpression in drug-sensitive cells(1,2).The different mdr genes and Pgp isoforms are expressed in a tissue-specific manner(1,2).In the mouse,mdr1is expressed mostly in the adrenal cortex,kidney,and pregnant uterus, mdr2in the liver at the canalicular face,and mdr3in the intestine and to a lesser extent in the heart,liver,lung,and capillaries of the brain(3).Pgps are localized on the apical membrane of epithelial cells lining luminal spaces,suggesting that they function in normal tissues as transporters of toxic substances and/or specific endogenous cellular products(4). Knockout mice experiments have demonstrated a role for the mdr3gene in the maintenance of the blood-brain barrier and drug elimination and for the mdr2gene in the transport of phospholipids in the bile(5,6).No physiological function has been attributed to the mouse mdr1gene so far,since knockout mdr1(Ϫ/Ϫ)mice display no obvious physiological abnormali-ties(7).However,different experimental evidence indicates that Pgp encoded by mdr1can serve in the transport of steroids(8).A number of factors have been found to modulate the level of mdr gene expression in the liver.For example,high levels of MDR1RNA have been found in human hepatocarcinomas,and overexpression of the mdr1isoforms has also been observed in rodent liver during cholestasis,during regeneration following partial hepatectomy,during chemically induced hepatocarcino-genesis,and following administration of various natural and synthetic xenobiotics(1,2).In particular,it has been shown that expression of the rat mdr1b gene is increased in liver cells in response to treatment with various polycyclic aromatic hy-*This work was supported by a research grant from the Cancer Research Society Inc.(to M.R).The costs of publication of this article were defrayed in part by the payment of page charges.This article must therefore be hereby marked“advertisement”in accordance with18 U.S.C.Section1734solely to indicate this fact.‡Supported by a studentship from the Medical Research Council ofCanada.Present address:Dept.of Biological Sciences,Bio-Mega Re-search Division,Boehringer Ingelheim(Canada)Ltd.,Laval,Que´bec H7S2G5,Canada.§Supported by a scholarship from Le Fonds de la recherche en sante´du Que´bec.To whom correspondence should be addressed:Institut de recherches cliniques de Montre´al,110Pine Ave.W.,Montre´al,Que´bec H2W1R7,Canada.Tel.:514-987-5770;Fax:514-987-5764;E-mail: raymonm@ircm.qc.ca.1The abbreviations used are:MDR,multidrug resistance;Pgp,P-glycoprotein;3-MC,3-methylcholanthrene;B(a)P,benzo(a)pyrene; TCDD,2,3,7,8-tetrachlorodibenzo-p-dioxin;DN,daunorubicin;CAT, chloramphenicol acetyl transferase;AhR,aromatic hydrocarbon recep-tor;Arnt,AhR nuclear translocator;EMSA,electrophoretic mobility shift assay;DME,drug metabolizing enzymes;PAH polycyclic aromatic hydrocarbon;XRE,xenobiotic response element;bp,base pair(s);kb, kilobase pair(s).T HE J OURNAL OF B IOLOGICAL C HEMISTRY Vol.276,No.7,Issue of February16,pp.4819–4827,2001©2001by The American Society for Biochemistry and Molecular Biology,Inc.Printed in U.S.A.This paper is available on line at 4819 at ZHEJIANG UNIVERSITY, on November 21, Downloaded fromdrocarbon(PAH)compounds,including3-methylcholanthrene (3-MC),and that this increased expression occurs at the tran-scriptional level(9–11).However,the precise molecular mech-anisms involved in mdr1b regulation in response to3-MC are still unknown.PAHs are carcinogenic compounds arising from the incom-plete combustion of organic matter and are widespread in the environment,including tobacco smoke and tar.PAHs such as 3-MC and benzo(a)pyrene(B(a)P)as well as halogenated aro-matic hydrocarbons such as2,3,7,8-tetrachlorodibenzo-p-di-oxin(TCDD)are specific inducers of genes coding for drug-metabolizing enzymes(DME),including cyp1a1and cyp1a2, that code for cytochromes P450involved in metabolic oxidation (12).PAHs and TCDD bind in the cytoplasm to the aromatic hydrocarbon receptor(AhR),a member of the bHLH-PAS(basic helix-loop-helix Per-Arnt-Sim)family of transcription factors (12,13).The ligand-bound AhR translocates to the nucleus, where it binds as a heterodimer with the AhR nuclear trans-locator(Arnt;another bHLH-PAS protein)to specific cis-acting regulatory DNA sequences located in the promoter of its tar-gets(known as AH-,dioxin-,or xenobiotic-responsive elements (or AHRE,DRE,or XRE,respectively))to enhance their tran-scription(12,13).Given that mdr1b expression is increased in liver cells in response to treatment with various PAHs,it was postulated that mdr1b may be under the control of the AhR(9). However,studies failing to show mdr1induction in the liver of mice treated with TCDD,one of the most potent agonists of the AhR,suggested that mdr1expression was not regulated by AhR(14).The involvement of AhR in the regulation of mdr1 has so far remained controversial.The mouse hepatoma cell lines Hepa-1c1c7(wild type), TAOc1BP r c1(AhR-defective),and BP r c1(Arnt-defective)con-stitute a powerful experimental system to investigate the tran-scriptional regulation of different AhR⅐Arnt targets in response to xenobiotics(12).The two mutant cell lines were derived as B(a)P-resistant variants of Hepa-1c1c7and were identified based on their inability to induce aryl hydrocarbon hydroxylase activity in response to TCDD treatment(15).TAOc1BP r c1cells have a decreased level of AhR(ϳ10%of wild-type cells)and therefore decreased induction of the cyp1a1promoter and lower aryl hydrocarbon hydroxylase activity in response to TCDD and other AhR ligands(15–18).BP r c1cells have a nor-mal cytosolic AhR,which fails to accumulate in the nucleus because of a defective Arnt(15).They have virtually no basal or inducible levels of cyp1a1expression and aryl hydrocarbon hydroxylase activity(15–17).In the present report,we have used this panel of cell lines to investigate the transcriptional regulation of the murine mdr1 gene by3-MC and other xenobiotic compounds.Our results demonstrate that mdr1is transcriptionally induced by3-MC and B(a)P and that this induction is mediated by p53but also requires AhR⅐Arnt.A model for the AhR⅐Arnt-and p53-medi-ated transactivation of mdr1in response to genotoxic stress is proposed.EXPERIMENTAL PROCEDURESCell Culture—Wild-type Hepa-1c1c7and Hepa1–6,AhR-defective TAOc1BP r c1,and Arnt-defective BP r c1cells were obtained from the American Type Culture Collection(ATCC;Manassas,VA)and main-tained in culture under the conditions recommended by the ATCC. Chinese hamster ovary LR73cell lines stably transfected with plasmid constructs carrying full-length cDNAs for the mouse mdr1,mdr2,or mdr3genes(LR73mdr1,LR73mdr2,and LR73mdr3,respectively;a gift from Dr.Philippe Gros,McGill University,Montre´al,Canada)were grown as described elsewhere(19,20).For inductions,cells atϳ50% confluence were exposed to different concentrations of xenobiotics for various periods of time(the exact conditions for each experiment are indicated in the figure legends).3-MC,B(a)P,and daunorubicin were obtained from Sigma,and TCDD was obtained from the Centre d’expertise en analyze environnementale du Que´bec(Laval,Canada).Stock solutions of3-MC(5m M)and B(a)P(25m M)were prepared in Me2SO,and the stock solutions of daunorubicin(1mg/ml)were pre-pared in water.TCDD was obtained in n-nonane at a concentration of 50␮g/ml and was stored at room temperature.Stock solutions of3-MC, B(a)P,and daunorubicin were stored atϪ80°C.RNA Preparation—Total RNA was prepared from3-MC-treated and untreated hepatocytes as well as from the LR73mdr1,LR73mdr2,and LR73mdr3cell lines by homogenizing the cells in a solution containing guanidium hydrochloride(6M)followed by sequential ethanol precipi-tation,as described previously(21).RNase Protection Assay—The plasmid constructed to detect the mdr1 RNA consisted of a165-bp Bam HI fragment isolated from the mdr1 cDNA(positions1926–2090relative to the ATG initiation codon(22)), blunt-ended with T4DNA polymerase,and cloned into plasmid pGEM-7Z(Promega,Madison,WI)at the Sma I site,giving plasmid pmdr1-G7.This plasmid was linearized with Eco RI and used as a template to synthesize an antisense mdr1probe using SP6RNA polym-erase(Amersham Pharmacia Biotech).The pKX10–3Z plasmid consist-ing of an Xba I–Kpn I mouse␤-actin cDNA fragment(positions724–969 in the␤-actin cDNA)cloned into pGEM-3Z at the Xba I and Kpn I sites (kindly provided by Dr.Rashmi Kothary,Institut du cancer de Mon-tre´al,Montre´al,Canada)was used to generate a control actin probe. pKX10–3Z was linearized with Xba I and used to synthesize an anti-sense actin RNA probe with T7RNA polymerase.The riboprobes were synthesized in the presence of[␣-32P]UTP,and the RNase protection assay was performed according to standard protocols(23).Nuclear Run-on Transcription Assay—The run-on experiment was performed essentially as described by Fisher et al.(24).Nuclei wereisolated from Hepa-1c1c7cells treated with Me2SO or with3-MC(5␮M) for48h and were used to label nascent RNAs with[␣-32P]UTP.Plas-mids pVT101-U/mdr1,carrying the full-length mouse mdr1cDNA(25); pmP1450–3Ј,carrying a1.2-kb Pst I cDNA fragment overlapping part of the mouse cyp1a1cDNA(26)(obtained from the ATCC);and pKX10–3Z were linearized with Stu I,Bam HI,and Xba I,respectively.The linear-ized plasmids were denatured,immobilized in duplicate onto a nylon membrane,and hybridized with the[␣-32P]UTP-labeled RNAs for48h at65°C.The membranes were washed and exposed for7days with two intensifying screens.Slot Blot Analyses—Slot blotting was performed as previously de-scribed(21).RNA samples(10␮g)were denatured in7ϫSSC-7.5% formaldehyde for15min at65°C and applied to a nylon membrane (Zeta-Probe).Detection of specific RNAs was performed by hybridiza-tion at65°C in0.5M NaPO4,pH7.2,1m M EDTA,7%SDS,1%bovine serum albumin,and100␮g/ml salmon sperm DNA with32P-labeled DNA probes.The mdr1probe was a4.2-kb Sph I–Eco RI fragment over-lapping the full-length mouse mdr1cDNA,isolated from plasmid pGEM7/mdr1(a gift from Dr.Philippe Gros,McGill University,Mon-tre´al);the cyp1a1probe was a 1.2-kb Pst I fragment isolated from plasmid pmP1450–3Ј;and the actin probe was a245-bp Xba I–Kpn I fragment isolated from pKX10–3Z.The membranes were washed twiceat65°C with a solution containing40m M NaPO4,pH7.2,5%SDS,1 m M EDTA,0.5%bovine serum albumin and twice with a solutioncontaining40m M NaPO4,pH7.2,5%SDS,and1m M EDTA before autoradiography.Chloramphenicol Acetyl Transferase(CAT)Expression Plasmids—Plasmid pMcat5.9consists of a482-bp DNA fragment containing the dioxin-responsive elements of the cyp1a1gene cloned upstream of the mouse mammary tumor virus promoter and the CAT gene(24)(kindly provided by Dr.Allan Okey,University of Toronto).Plasmids pmdr1, p-452,p-245,p-141,and p-93(previously referred to as pSacICAT, pExo6CAT,pExo2CAT,pExo1CAT,and pAluCAT,respectively)have been described elsewhere(27).The mdr1promoter sequence in these constructs ends at positionϩ84with respect to the transcription start site(27).To produce the p53mutant constructs,pM1and pM2,plasmid pSBM13was used.This plasmid consists of a1.2-kb Sac I–Hin dIII mdr1 promoter fragment(positionsϪ1165toϩ84)cloned into M13mp18. Single-stranded DNA was prepared from pSBM13and used as a tem-plate to perform site-directed mutagenesis of the p53binding site,using the mutant oligonucleotides M15Ј-TACCTGAA T AC A TAAAGACA and M25Ј-CGTAAAGA T AA A TCTATGTA(the base changes are shown in boldface type).The resulting M1and M2mdr1promoter fragments were then excised from pSBM13with Sac I and Hin dIII,blunt-ended with T4DNA polymerase,and cloned into plasmid pCAT at the Hin dIII site also blunt-ended with T4DNA polymerase,yielding plasmids pM1 and pM2.The presence of the mutations in the resulting constructs was confirmed by DNA sequencing.Transient Transfections and CAT Assays—Cells were plated at aInduction of the Mouse mdr1Gene by PAHs4820at ZHEJIANG UNIVERSITY, on November 21, Downloaded fromdensity of 8ϫ105/60-mm plate and transfected on the following day with 10␮g of plasmid DNA,using a standard calcium phosphate pre-cipitation method (28).After incubation with the DNA precipitate for 16h,the cells were washed twice with phosphate-buffered saline and supplied with fresh medium containing the different xenobiotics.After 48h,the cells were collected.Cell extracts were prepared,and protein concentrations were determined by the Bradford method (29).CAT activities were assayed by standard protocols as described previously,using 2␮g of proteins (27).Preparation of Nuclear Extracts—Nuclear extracts were prepared according to Schreiber et al .(30),with some modifications.Cells were harvested in cold phosphate-buffered saline,0.6m M EDTA and col-lected by centrifugation.The cell pellets were resuspended in 400␮l of ice-cold buffer A (10m M Tris,pH 8.0,10m M KCl,0.1m M EDTA,0.1m M EGTA,1m M dithiothreitol)containing 0.5m M phenylmethylsulfonyl fluoride,10␮g/ml aprotinin,1␮g/ml pepstatin,and 5␮g/ml leupeptin and swelled on ice for 15min.Subsequently,25␮l of 10%Nonidet P-40were added,and the tubes were vortexed vigorously.The nuclear pellets were collected by centrifugation and resuspended in 100␮l of cold buffer C (20m M Tris,pH 8.0,400m M NaCl,1m M EDTA,1m M EGTA,1m M dithiothreitol)in the presence of protease inhibitors.The suspen-sions were shaken vigorously at 4°C for 1h and centrifuged for 15min at 4°C,and the supernatants were frozen in aliquots at Ϫ80°C.Proteinconcentrations were determined by the Bradford method (29).ElectrophoreticMobility Shift Assay—Oligonucleotides overlapping the potential p53binding site in the mdr1promoter (5Ј-GAACACGTA-AAGACAAGTCTAT)and the p53consensus sequence in the p21waf1/cip1promoter (5Ј-GAACATGTCCCAACATGTTGAG)(31)were end-labeled with ␥-32P using T4polynucleotide kinase and annealed to their respec-tive in a M M 2.5m M dithiothreitol,4%Ficoll,1␮g of poly(dI-dC),and 20,000cpm of radiolabeled probe.The binding reactions were carried out at room temperature for 15min.Where needed,1␮g of the monoclonal anti-p53antibody pAb421(32)(Calbiochem)or of the polyclonal anti-Jun or anti-Skn-1antibodies (Santa Cruz Biotechnology,Inc.,Santa Cruz,CA)was added,and the incubation was continued for an additional 15min.The complexes were separated on 5%nondenaturing polyacrylamide gels in 1ϫTBE (90m M Tris,65m M boric acid,2.5m M EDTA,pH 8.0)at 200V.The gels were exposed to XAR films (Eastman Kodak Co.)for 16h with two intensifying screens at Ϫ80°C.Western Blotting—Total proteins from 3-MC-or Me 2SO-treated Hepa-1c1c7and BP r c1cells were extracted in ice-cold buffer (10m M Tris-HCl,pH 8.0,150m M NaCl,1m M EDTA,1%Nonidet P-40,and 1%sodium deoxycholate)containing 10␮g/ml leupeptin,10␮g/ml aproti-nin,1␮M sodium orthovanadate,and 1m M phenylmethylsulfonyl flu-oride.Total proteins (75␮g/sample)or nuclear extracts (30␮g/sample)were separated by SDS-polyacrylamide gel electrophoresis on a 10%acrylamide gel,transferred to a nitrocellulose membrane,and analyzed with the monoclonal anti-p53antibody pAb421(32)(Calbiochem)at a concentration of 5␮g/ml.Immune complexes were revealed by incuba-tion with a goat anti-mouse IgG antibody coupled to alkaline phospha-tase (Bio-Rad)and developed with 5-bromo-4-chloro-3-indolylphosphate p -toluidine salt and nitro blue tetrazolium chloride substrates as rec-ommended by the manufacturer (Life Technologies,Inc.).RESULTSTranscriptional Induction of the Mouse mdr1Gene by 3-MC in Hepatoma Cells—We have used an RNase protection assay to study the expression of mdr1in the hepatoma cell line Hepa-1c1c7upon exposure to 3-MC (Fig.1).An mdr1-specific riboprobe was prepared by cloning into pGEM7-Zf a mouse mdr1cDNA fragment overlapping the linker region of the protein,this domain displaying the lowest sequence homology among the three mouse mdr cDNAs (21).When tested with RNA prepared from LR73stable transfectants expressing each of the three mouse mdr cDNAs,the mdr1riboprobe was found to recognize the mdr1RNA but not the mdr2or mdr3RNA,thus confirming its specificity (Fig.1,top right ).The mdr1probe was then used with RNA from Hepa-1c1c7cells treated or not with 3-MC (Fig.1,top left ).This experiment showed that the amount of mdr1RNA detected is very low in untreated cells but is strongly increased in 3-MC-treated cells,demonstrating that expression of the mouse mdr1gene is induced by 3-MCtreatment.The use of an actin probe confirmed that equal quantities of RNA were used in the assay (Fig.1,bottom ).A similar experiment performed with mdr2-and mdr3-specific riboprobes showed that the expression of these genes is not induced under such conditions,demonstrating that the induc-tion of mdr1expression by 3-MC is isoform-specific (data not shown).A nuclear run-on experiment was performed to determine whether mdr1induction by 3-MC occurs at the transcriptional level (Fig.2).In addition to the mouse mdr1cDNA,cDNAs for the mouse cyp1a1gene (known to be transcriptionally regu-lated by 3-MC (12))and for the actin gene were also included as positive and negative controls,respectively.The data in Fig.2show that 3-MC induces an increase in the rate of mdr1mRNA synthesis,indicating that 3-MC acts at the transcriptional level to induce mdr1gene expression in Hepa-1c1c7cells.AhR ⅐Arnt-dependent Induction of mdr1Expression by 3-MC—To determine whether the increase in mdr1expression in response to 3-MC exposure is AhR ⅐Arnt-mediated,we ana-lyzed the mdr1RNA levels upon 3-MC treatment in two wild-type hepatoma cell lines Hepa-1c1c7and Hepa 1–6and in two variant cell lines derived from Hepa-1c1c7,TAOc1BP r c1(AhR-defective)and BP r c1(Arnt-defective)(15)(Fig.3).As controls,we also analyzed the level of cyp1a1and actin expression under the same conditions (Fig.3,middle and right ,respectively).This experiment showed that mdr1is expressed at low levels in the four cell lines in the absence of 3-MC induction (Fig.3,left panel ).Upon 3-MC treatment,the expression of mdr1is in-duced in the two wild-type hepatoma cell lines (by ϳ5-fold),this induction being completely abrogated in the AhR-defective or in the Arnt-defective variants (Fig.3,left panel ).The actin control probe confirmed that equal amounts of RNA had been applied to the membrane (Fig.3,right panel ).These data clearly demonstrate that the induction of mdr1in response to 3-MC requires an intact AhR ⅐Arnt complex,like cyp1a1(Fig.3,middle )(12).The Mouse mdr1Promoter Confers 3-MC-regulated Expres-sion in an AhR ⅐Arnt-dependent Manner—To determine if reg-ulatory sequences responsible for mdr1induction by 3-MC are present in the promoter region of the gene,plasmid pmdr1,consisting of a 1.2-kb Sac I–Hin dIII DNA fragment overlapping the mdr1promoter region (positions Ϫ1165to ϩ84with respect to the transcription start site (27))fused to the CAT reporter gene,was analyzed in transient transfection experiments.Plasmid pMcat5.9,which consists of a 482-bp fragment derived from the cyp1a1promoter fused to the mouse mammary tumorF IG .1.Increased mdr1expression in Hepa-1c1c7upon 3-MC treatment.The expression of mdr1was analyzed by RNase protection assay.Total RNAs (45␮g)from Hepa-1c1c7cells treated with 5␮M 3-MC (ϩMC )or with Me 2SO (ϪMC )for 56h and from the control cell lines LR73/mdr1,LR73/mdr2,and LR73/mdr3were analyzed with an mdr1riboprobe,which protects a 169-nt fragment within the mdr1transcript,or with a ␤-actin riboprobe,which protects a 245-nt actin transcript fragment.Autoradiography was for 15h with two intensify-ing screens (mdr1)or for 5h without intensifying screens (actin ).Induction of the Mouse mdr1Gene by PAHs4821at ZHEJIANG UNIVERSITY, on November 21, 2012 Downloaded fromvirus promoter and to the CAT gene (24),as well as the empty pCAT vector were also included as positive and negative con-trols,respectively.The three plasmids were transiently trans-fected into Hepa-1c1c7and BP r c1cells.The cells were treated with 3-MC or with Me 2SO for 48h,and the cellular extracts were prepared and assayed for CAT activity.This experiment showed that the mdr1promoter is transcriptionally active in Hepa-1c1c7cells and BP r c1cells,since it can drive the expres-sion of the CAT gene in both cell lines,albeit at low levels (Fig.4).This result is consistent with the basal level of expression of mdr1detected by slot blot analysis in these cells (Fig.3).3-MC treatment of the Hepa-1c1c7cells transfected with pmdr1re-sulted in a 10-fold induction in CAT activity as compared with untreated cells,reaching levels of CAT activity similar to those detected in the Hepa-1c1c7pMcat5.9transfectants upon 3-MC treatment.However,this induction was completely abrogated in BP r c1cells (Fig.4),consistent with the lack of mdr1induc-tion at the RNA level observed in the slot blot assay (Fig.3).Similar results were obtained upon transfection in TAOc1BP r c1cells (data not shown).These results,showing that the mdr1promoter is able to activate the expression of the reporter gene in response to 3-MC in Hepa-1c1c7but not in BP r c1and TAOc1BP r c1cells,demonstrate that (i)the mdr1promoter is able to confer 3-MC-mediated transcriptional acti-vation;(ii)this activation requires a functional AhR ⅐Arnt com-plex;and (iii)the sequences mediating this induction are lo-cated between positions Ϫ1165and ϩ84in the mdr1promoter.Two Putative XREs Located in the mdr1Promoter Are Dis-pensable for the Induction of mdr1by 3-MC—The AhR ⅐Arnt transcriptional complex binds to a specific DNA sequence,5Ј-(A/T)NGCGTG,known as an XRE to activate transcription (12).XREs render heterologous promoters responsive to xeno-biotics and function in a position-and orientation-independent manner (33,34).Examination of the mdr1promoter sequence indicated the presence of two potential XREs in an inverted orientation in the distal portion of the promoter at positionsϪ1129and Ϫ620(5Ј-CACGCAT and 5Ј-CACGCAA,respective-ly).To identify the cis -acting sequences responsible for the induction of mdr1by 3-MC and to investigate the possible involvement of these putative XREs,we analyzed the tran-scriptional activity of a series of mdr1promoter 5Ј-deletion CAT constructs after transient transfection into Hepa-1c1c7and treatment of the resulting transfectants with 3-MC (Fig.5A ).3-MC treatment of Hepa-1c1c7cells transfected with plas-mids p-452or p-245resulted in a level of CAT induction similar to that observed in cells transfected with plasmid pmdr1car-rying the full-length promoter,indicating that sequences lo-cated within positions Ϫ1165to Ϫ245are dispensable for the induction of mdr1by 3-MC,including the two putative XREs as well as a potential AP-1binding site (5Ј-TGACTCA;positions Ϫ265to Ϫ255(35))(Fig.5,B and C ).However,further deletion of a 104-bp region down to position Ϫ141(p Ϫ141)was found to greatly diminish the induction of CAT activity by 3-MC (Fig.5,B and C ),demonstrating that sequences important for the induction are located between positions Ϫ245and Ϫ141.CAT activity in the absence of 3-MC was reduced in the p Ϫ141transfectants when compared with the p Ϫ245transfectants,indicating that sequences between positions Ϫ245and Ϫ141are also involved in the basal transcriptional activity of the mdr1promoter in hepatoma cells.Finally,we found that alowF IG .2.Nuclear run-on experiment.Nuclei were isolated from Hepa-1c1c7cells treated with 5␮M 3-MC (ϩMC )or with Me 2SO (ϪMC )for 48h.Nascent RNAs were radiolabeled with [␣-32P]UTP and used to probe duplicate nylon membranes on which denatured cDNAs for mdr1,cyp1a1,and actin had been immobilized.The membranes were washed and exposed for 7days with two intensifyingscreens.F IG .3.AhR ⅐Arnt-dependent induction of mdr1expression by 3-MC.Total RNAs (10␮g)from wild-type Hepa-1c1c7and Hepa 1–6,AhR-defective TAOc1BP r c1,and Arnt-defective BP r c1cells treated (ϩMC )or not treated (ϪMC )with 3-MC at 5␮M for 56h were applied onto a nylon membrane.The membrane was hybridized sequentially with an mdr1(left ),a cyp1a1(middle ),and a ␤-actin (right )probe.Autoradiography was for 18h (mdr1and cyp1a1)or for 2h (actin)with two intensifyingscreens.F IG .4.AhR ⅐Arnt-dependent induction of the mdr1promoter by 3-MC.Plasmids pCAT (no promoter),pmdr1(mdr1promoter from position Ϫ1165to ϩ84),and pMcat5.9(pMcat;482-bp fragment from the cyp1a1promoter fused to the mouse mammary tumor virus pro-moter)were transiently transfected into Hepa-1c1c7and BP r c1cells by the calcium phosphate method.The cells were then treated with 3-MC (5␮M )or Me 2SO for 48h.Total cellular extracts were prepared,and equal quantities of proteins (2␮g)were assayed for CAT activity.A ,autoradiogram of a representative CAT assay,showing the activity of plasmids pCAT,pmdr1and pMcat in Hepa-1c1c7and BP r c1cells treated (ϩ)or not treated (Ϫ)with 3-MC (MC ).The position of the [14C]chloramphenicol (CM )and of its acetylated products (AcCM )is indicated on the left .B ,quantitative analysis of CAT activities.The percentage of conversion of [14C]chloramphenicol to its acetylated de-rivatives was quantitated by liquid scintillation counting.Open bars ,ϪMC ;filled bars ,ϩMC .The results presented are the averages of three independent transfections performed in duplicate.S.D.values are rep-resented by the bars .Induction of the Mouse mdr1Gene by PAHs4822 at ZHEJIANG UNIVERSITY, on November 21, 2012 Downloaded from。

脱细胞基质周围神经修复膜规格

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阿昔洛韦生物粘附微球的动物胃粘膜表面粘附能力和体外缓释效果

究主要有以单纯 Polycarbop hil 胃粘附微球与氯噻嗪 mPa·s ,卡乐康辅料有限公司) ;Span280 (浙江温州清
微球混合体[3 ] ,以 Polycarbop hil , Carbomer 包衣的 , 明化工厂) ;轻质液蜡 (上海大场化工厂) ;无水乙醇
Carbomer 和 Eudragit RL100 混合包衣的小肠粘附 (上海振兴化工厂) ;石油醚 (常熟市杨园化工厂) 。
微球[4 ] , Carbomer 分散于四甘油五硬脂酸酯 ( T G2
756MC 可见紫外分光光度仪 (上海第三分析仪
clovir and deoxyacyclovir. I nt J Pharm . 1993 ,99 (1) :79.
[ 2 ] Greg EP ,Dunn P ,Vinol P ,S , et al . Acyclovir Bioavailability in
Humam Skin. J I nvest Derm atol . 1992 ,98 (6) :856 - 863. [ 3 ] 陈国珍 ,黄贤知 ,刘文远 ,等. 紫外 - 可见分光光度法. 北京 :原
47 : 365.
(收稿 :1997205224)
阿昔洛韦生物粘附微球的动物胃粘膜表面粘附能力和体外缓释效果
陆伟跃潘俊刘敏 (上海 200032 上海医科大学药学研究所药物靶向制剂研究室)
摘要目的 :研制一种具有较好生物粘附能力和药物缓释效果的阿昔洛韦 (Acv)2卡波姆 (Cb)2乙基纤维素 ( Ec) 微球。方法 :通过油包水乳剂的溶媒蒸发法制备 Acv2Cb2Ec 微球 ;以动物体内外胃粘膜表面滞留程度 ,考察 Cb 与 Ec 不同配比、Acv 含量、微球粒径对 Acv2Cb2Ec 微球生物粘附能力的影响 ;以体外释药速率评价 Cb 与 Ec 不同配比、Acv 含量、微球粒径和介质 p H 对 Acv2Cb2Ec 微球缓释效果影响。结果 :Cb 配比增加 ,Acv2Cb2Ec 微球生物粘附能力增强 ,药物缓释效果降低 ,表现为负相关性 ; Acv 含量增加 ,Acv2Cb2Ec 微球生物粘附能力和药物缓释效果均降低 ,但 Acv 含量 ≤20 %时 ,缓释效果基本接近 ; 粒径增大 , Acv2Cb2Ec 微球生物粘附能力有所减小 ,但在 500～1200μm 时 ,药物缓释效果显著提高 (12 h) ,而粘附性变化不明显 ;Acv2Cb2 Ec 微球在酸性介质中的释药速率明显快于中性或近中性介质。结论 :载药量 ≤20 % ,粒径为 500～1200 μm ,Cb 与 Ec 配比为 1∶9 的 Acv2Cb2Ec 微球在胃粘膜表面具有良好粘附特性 ,且药物缓释可达 12 h ,近中性 p H 条件下的缓释效果更佳。关键词阿昔洛韦2卡波姆2乙基纤维素微球 ;生物粘附 ;药物缓释

AR级溶剂汇总

A103451乙酸戊酯Amyl acetateAR,99.00%628-63-7500mlA103667苯乙酮AcetophenoneAR,≥98.0% (GC)98-86-2500mlA103683苯甲醚AnisoleAR，99%100-66-3500mlA104443乙腈AcetonitrileAR,99.0%75-05-8500mlA108442异丙醇胺DL-1-Amino-2-propanolAR78-96-6250mlA108662乙酰氯Acetyl chlorideAR,98.5%75-36-5500mlA110367乙酰丙酮AcetylacetoneAR，99%123-54-6500mlA112077氨水Ammonia solutionAR,25-28%1336-21-6500mlA112120苯胺AnilineAR, ≥99.5%62-53-3500mlA112148丙酮AcetoneAR,99.5%67-64-1500mlA112328丙烯腈AcrylonitrileAR107-13-1500mlA112717乙醇(95%)Ethanol (95%)AR,95.0%64-17-5500mlA11288036%乙酸AcetateAR64-19-7500mlA113186丙烯醇Allyl alcoholAR,99.0% 107-18-6500mlA116166冰乙酸AcetateAR,99.5%64-19-7500mlB100035丙烯酸丁酯n-Butyl acrylateAR,99%141-32-2500mlB100300正丁醛ButyraldehydeAR，98.5%123-72-8500mlB103866叔丁胺tert-Butylamine AR,98%75-64-9250ml1LB105169癸二酸二辛酯Bis(2-ethylhexyl) sebacateAR,97.0%122-62-3500mlB105788溴代正癸烷1-BromodecaneAR，98%112-29-8 100mlB108205苯甲醇Benzyl alcoholAR,99%100-51-6500mlB108477苄胺Benzylamine AR,99.00%100-46-9250ml1LB110440正丁酸Butyric acidAR,99%107-92-6 500mlB110460苯甲醛BenzaldehydeAR,>98.5%(GC)100-52-7500mlB110581氯化苄Benzyl chlorideAR100-44-7500mlB111571正丁醇n-ButanolAR,99%71-36-3500mlB1121552-丁酮2-ButanoneAR,99.5%78-93-3500mlB116187苯Benzene StandardAR, ≥99.5%71-43-2500mlB116225乙酸丁酯Butyl acetateAR,99.0%123-86-4500mlC100584环己烷CyclohexaneAR，99.5%110-82-7500mlC103310二硫化碳Carbon disulfideAR,99.0%75-15-0500mlC104628对氯甲苯p-Chlorotoluene AR,98.0%106-43-4100ml500mlC108164邻氯甲苯O-Chlorotoluene AR,98%95-49-8100ml500mlC110401环己醇CyclohexanolAR,98%108-93-0500mlC112043四氯化碳Carbon tetrachlorideAR,99.5%56-23-5500mlC112202三氯甲烷ChloroformAR,99.0%67-66-3500mlC112602氯磺酸Chlorosulfonic acidAR,97.0% 7790-94-5500mlC1135694-氯邻二甲苯4-Chloro-1,2-dimethylbenzeneAR,98.0%615-60-1100mlC116449环己酮CyclohexanoneAR，99.0%108-94-1500mlD100014无水乙醚Diethyl ether dehydrateAR,98%60-29-7500mlD100061N,N-二甲基苯胺N,N-DimethylanilineAR,99%121-69-7 500mlD103272二甲基亚砜Dimethyl sulfoxideAR,>99%(GC)67-68-5500mlD104730二十二烷DocosaneAR，96%629-97-0100mlD108216邻苯二甲酸二乙酯Diethy phthalateAR,99.5%84-66-2500mlD108606己二酸二乙酯Diethyl adipate AR,99.5%141-28-6100ml500mlD109191正癸酸Decanoic acidAR，99%334-48-5500mlD109648邻苯二甲酸二辛酯Di(2-ethylhexyl)phthalateAR,99%117-81-7500mlD110466二乙胺DiethylamineAR,99.0%109-89-7500mlD110645二苯醚Diphenyl etherAR,98%101-84-8250mlD111034N，N-二乙基苯胺N,N-DiethylanilineAR91-66-7500mlD111999N，N-二甲基甲酰胺N,N-DimethylformamideAR，99.5%68-12-2 500mlD112298十二醇1-DodecanolAR，97.0% 112-53-8500mlD112360二乙醇胺DiethanolamineAR，99%111-42-2500mlD116144二氯甲烷DichloromethaneAR,99.5%75-09-2500mlD1161571,4-二氧六环DioxaneAR,99.0%123-91-1500mlD1162471,2-二氯乙烷1,2-DichloroethaneAR,99%107-06-2500mlE100050庚酸乙酯Ethyl heptanoateAR,98.5%106-30-9500mlE100484二十烷EicosaneAR112-95-8100mlE101076异辛醇2-Ethyl-1-hexanolAR104-76-7500mlE103319乙二醇Ethylene glycolAR,98%107-21-1500mlE103459丙酸乙酯Ethyl propionateAR，99%105-37-3500mlE103802乙醇胺EthanolamineAR,99%141-43-5500mlE103937乙酰乙酸乙酯Ethyl acetoacetateAR,98%141-97-9500mlE104388乙二醇二甲醚Ethylene glycol dimethyl etherAR，99.5%（GC)110-71-4500mlE105166氯乙酸乙酯Ethyl chloroacetate AR,99% 105-39-5100ml500mlE105183乙二醇乙醚乙酸酯2-Ethoxyethyl acetateAR,98%111-15-9500mlE108146乙基苯EthylbenzeneAR,98.5% 100-41-4500mlE108182环氧氯丙烷(±)-EpichlorohydrinAR106-89-8500mlE110415甲酸乙酯Ethyl formateAR，98%109-94-4500mlE110827乙二醇丁醚Ethylene glycol butyl etherAR，99.0%111-76-2500mlE111989无水乙醇Ethanol absoluteAR,99.7%64-17-5500mlE112642乙二胺,无水EthylenediamineAR,99%107-15-3500mlE112943丙烯酸乙酯Ethyl acrylateAR,99.0%140-88-5500mlE116132乙酸乙酯EthylacetateAR,99%141-78-6500mlF103361甲酰胺FormamideAR,99.00%75-12-7500mlG105905戊二醛(50%)GlutaraldehydeAR,50% in H2O 111-30-8500mlG116203甘油GlycerolAR,99%56-81-5500mlH103406正十六烷Hexadecane AR,98%544-76-3100ml500mlH103519正庚酸Heptanoic acid AR,98.0%111-14-8100ml500mlH103633正己酸Hexanoic acid AR,99.0%142-62-1100ml500mlH1039091,6-己二胺1,6-HexamethylenediamineAR,99.0%124-09-4500mlH104018水合联氨Hydrazinium hydrateAR,50%溶液10217-52-4 500mlH104021水合联氨Hydrazinium hydrateAR,80%溶液10217-52-4500mlH104605氢碘酸Hydroiodic acid AR,≥47.0%10034-85-2100ml500MLH104721十七烷Heptadecane AR,95.0%629-78-7100ml500mlH106017六甲基二硅胺烷Hexamethyl disilylamine AR，98%999-97-3 100ml500mlH108105正庚烷HeptaneAR,98%142-82-5500mlH108613γ -丁内酯 -丁内酯（GBL）4-Hydroxybutanoic acid lactone AR96-48-0250ml500mlH108915二十一烷HeneicosaneAR,90%629-94-7100mlH109654正己烷n-HexaneAR，97%110-54-3500mlH112515过氧化氢溶液(30%)Hydrogen peroxide solution(30%)AR，30%7722-84-1500mlH116232氢氟酸Hydrofluoric acidAR,40.0%7664-39-3500mlH116385氢溴酸Hydrobromic acidAR,40%10035-10-6500mlI103240异辛烷IsooctaneAR,97%540-84-1500mlI103788一异丙胺Isopropylamine AR,99.0%75-31-0250ml500mlI106093亚硝酸异戊酯Isopentyl nitrite AR,90%110-46-3100ml500mlI112011异丙醇Isopropyl AlcoholAR, ≥99.5% 67-63-0500mlI112108乙酸异戊酯Isoamyl acetateAR，99%123-92-2500mlL108839DL-乳酸DL-Lactic acidAR，85-90%50-21-5500mlM100030丙烯酸甲酯Methyl acrylateAR,98.5%96-33-3500mlM100588N-甲基吡咯烷酮1-Methyl-2-pyrrolidinoneAR,99.0%872-50-4500mlM102684甲胺醇溶液Methylamine AR，33 wt. % in absoluteethanol74-89-5500mlM102702甲胺溶液Methylamine solutionAR，40%水溶液74-89-5500mlM102852乙二醇甲醚2-MethoxyethanolAR109-86-4500mlM103354乙酸甲酯Methyl acetateAR,98%79-20-9500mlM104120氯乙酸甲酯Methyl chloroacetate AR,99.0%96-34-4100ml500mlM108589苯甲酸甲酯Methyl benzoateAR,98%93-58-3500mlM108740甲基异丁基甲酮4-Methyl-2-pentanoneAR,99.0%108-10-1500mlM109062吗啡啉MorpholineAR,99%110-91-8500mlM109623甲基丙烯酸甲酯Methyl methacrylateAR,99.0%80-62-6500mlM110426水杨酸甲酯Methyl salicylateAR,99%119-36-8500mlM113155β-巯基乙醇2-Mercaptoethanol AR,99.0%60-24-2250ml500mlM116115甲醇MethanolAR，99.5%67-56-1500mlM116117甲醇MethanolAR,无水级67-56-1500mlM116196异戊醇3-Methyl-1-butanolAR，98.5%123-51-3500mlN109661硝基甲烷NitromethaneAR75-52-5 500mlN116217硝基苯NitrobenzeneAR,99%98-95-3500mlN116238硝酸Nitric acidAR7697-37-2500mlO103325正辛醇n-Octanol AR,99.0%111-87-5 100ml500mlO108279正辛酸n-Octanoic acidAR,99%124-07-2500mlO108484油酸Oleic acidAR112-80-1500mlO111525仲辛醇2-OctanolAR，98%123-96-6500mlP100053正丙醛PropionaldehydeAR,97%123-38-6 500mlP102926亚磷酸溶液Phosphorous acid solutionAR,50%溶液13598-36-2500mlP1034301,2-丙二醇1AR,99%57-55-6500mlP103883乙酸正丙酯Propyl acetateAR,99.0% 109-60-4500mlP104801液体石蜡Paraffin liquidAR8042-47-5500mlP108128正戊醇1-PentanolAR,98%71-41-0500mlP1081972-苯乙醇2-PhenylethanolAR,99%60-12-8500mlP108302多乙烯多胺Polyethyene polyamineAR29320-38-5500mlP110343正丙醇PropanolAR,99.0% 71-23-8500mlP110444丙酸Propionic acidAR,≥99.5% (GC) 79-09-4500mlP110843正戊烷n-PentaneAR,99%109-66-0500mlP111511吡啶PyridineAR110-86-1500mlP112024磷酸Phosphate standard concentrateAR，85%7664-38-2500mlP112070高氯酸Perchloric acidAR,70.0-72.0%7601-90-3500mlP112618过氧乙酸Peracetic acid solutionAR,18-20%79-21-0500mlP112662哌啶Piperidine AR,99.5%110-89-4100ml500mlP116176石油醚Petroleum etherAR,bp 60-90 °C8032-32-4500mlP116177石油醚Petroleum etherAR,bp 30-60 °C8032-32-4500mlP116178石油醚Petroleum etherAR,bp 90-120 °C8032-32-4500mlS103742水杨醛Salicylaldehyde AR,98%90-02-8250ml1LT100707磷酸三丁酯Tributyl phosphateAR，99%126-73-8500mlT100717三氯乙烯TrichloroethyleneAR,99.0%79-01-6500mlT1009761,2,3,4-四氢萘1,2,3,4-Tetrahydronaphthalene AR，97%119-64-2250ml500ml, 1LT103263四氢呋喃Tetrahydrofuran AR,99.0%109-99-9500ml4LT103285三乙胺TriethylamineAR,99.0%121-44-8500mlT103291三氟乙酸Trifluoroacetic acid AR,99.0%76-05-1100ml500mlT103366四氯乙烯TetrachloroethyleneAR，98%127-18-4500mlT103764三乙烯四胺TriethylenetetramineAR,70%112-24-3500mlT1050151,3,5-三甲苯1,3,5-Trimethylbenzene AR,97%108-67-8100ml500mlT105718四氢糠醇Tetrahydro furfuryl alcohol AR,98.0%97-99-4100ml500mlT108151三乙醇胺TriethanolamineAR,78%102-71-6500mlT1081901,1,1-三氯乙烷1,1,1-Trichloroethane AR,98%71-55-6250ml500ml。

德国拜耳PC 6555物性数据

PC 6555 德国拜耳公司物性数据①原料描述部分规格级别：--- 外观颜色：---用途概述：用于工业产品及电子电器备注说明：特性：中高粘度，完全阻燃V-0/3.0mm，注塑式挤塑②原料技术数据性能项目试验条件[状态] 测试方法测试数据数据单位基本性能熔体流动速率（体积）300℃，1.2kg ISO 1133 9.5 cm3/mm熔体流动速率（质量）300℃，1.2kg ISO 1133 10 g/10min吸水性饱和值23℃，Saturation ISO 62 0.3 %吸温性23℃/50%相对温度饱和值ISO 62 0.12 %密度--- ISO 1183 1200 KG/m3物理性能折射系数--- ISO 489 1.586 ---雾度（透明材料）3mm ISO 14782 89 %透光率（透明材料）1mm DIN 5036-1 89 %透光率（透明材料）2mm DIN 5036-1 89 %透光率（透明材料）3mm DIN 5036-1 89 %透光率（透明材料）4mm DIN 5036-1 87 %机械性能拉伸模量1mm/min ISO 527 2400 MPa屈服应力50mm/min ISO 527 65 MPa屈服应变50mm/min ISO 527 6.0 %名义断裂拉伸应变50mm/min ISO 527 ＞50 %拉伸蠕变模量1h ISO 899-1 2200 MPa拉伸蠕变模量1000h ISO 899-1 1900 MPaCHARPY冲击强度23℃ISO 179-1eU N KJ/m2CHARPY冲击强度-30℃ISO 179-1eU N KJ/m2IZOD缺口冲击强度23℃ISO 180-4A 85 KJ/m2IZOD缺口冲击强度-30℃ISO 180-4A 12 KJ/m2电气性能最大穿透力23℃/2mm ISO 6603-2 5400 N最大穿透力-30℃/2mm ISO 6603-2 6400 N穿透能量23℃/2mm ISO 6603-2 60 J穿透能量-30℃/2mm ISO 6603-2 65 J相对介电常数100Hz IEC 60250 3.1 ---相对介电常数1MHz IEC 60250 3.0 ---损耗因数100Hz IEC 60250 5 10-4损耗因数1MHz IEC 60093 90 10-4体积电阻率--- IEC 60093 1014 Ω.m表面电阻率--- IEC 60093 1016 Ω介电强度1mm IEC 60243-1 32 kv/mm抗电弧径迹性溶液A/SolutionA IEC 60112 225 等级/Rating加工性能成型收缩率流动方向垂直流动方向--- ISO 1133ISO 11330.6-0.80.6-0.8%%热性能辉光金属丝试验温度 1.0mm IEC 60695-2-12 960 ℃辉光金属丝试验温度 1.5mm IEC 60695-2-12 960 ℃辉光金属丝试验温度 2.0mm IEC 60695-2-12 960 ℃辉光金属丝试验温度 3.0mm IEC 60695-2-12 960 ℃玻璃化温度10℃/min ISO 11357-2 148 ℃热变化温度 1.80MPa ISO 75-2 125 ℃热变化温度0.45MPa ISO 75-2 137 ℃维卡软化温度50N，50℃/h ISO 306 144 ℃热膨胀系数流动方向垂直流动方向23-55℃23-55℃ISO 11359-2ISO 11359-20.60.610-4/℃10-4/℃可烧性厚度mm黄卡UL 94（ISO 1210）（ISO 10351）V-2/1.5(V-0/3.0) 类别/Class 熔体温度℃ISO 294 300 ---模具温度--- ISO 294 80 ℃其它性能粘度系数--- ISO 1628-4 59 cm3/g注射速度--- ISO 294 200 mm/s氧指数方法A/ProcedureA IEC 4589-2。

质粒图谱查询方法

3.google scholar: / 有些质粒是经过改造的，所以通过上述方法不能查询到相应信息。这时，可以在google scholar中输入质粒名称，可以直观地看哪些学者在何文章中使用了该质粒，从而可了解到质粒的来源;或者籍此向作者咨询或索取。 4.尝试从各大生物公司，例如invitrogen网站查询. 5. 这个网站收录了大量图谱： http://www.embl-hamburg.de/~geerlof/webPP/vectordb/bact_vectors/table.html
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file:///D|/中科院/Selective Serotonin Transporter/质粒信息/质粒图谱查询方法.txt
file:///D|/中科院/Selective Serotonin Transporter/质粒信息/质粒图谱查询方法.txt（第 2／6 页）[2011/8/4 18:39:52]
By
0099--pGE-1—Stratagene--RNAi载体 0100--pSUPER.p53—OligoEngine--RNAi载体 0101--palter-ex1--promega 0102--pACYCDuet-1--NOVAGEN 0103--pEX lox(+) Vector—NOVAGEN--原核表达 0104--质粒名称：pBACgus-8 Transfer Plasmid—NOVAGEN--CHUANSUO 0105--pSCREEN?-1b(+) Vector Map—novagen--筛选 0106--PGEX-2T--BD Co--pDsRed2--Clontech 0107--pbgal-Basic—Clontech--mammalian reporter vector 0108—pBI—Clontech--express two genes of interest from a bidirectional tet-responsive promoter 0109--质粒名称：pbgal-Control—Clontech--mammalian reporter vector 0110-- pGEX-5X-1--原核表达 0111--pBI-EGFP—Clontech--pBI-EGFP-- coexpress 0112--pBI-G—Clontech--pBI-G--express b-galactosidase 0113--pBI-GL—Clontech--pBI-GL --express luciferase and b-galactosidase 0114--pCMS-EGFP—Clontech--mammalian expression vector 0115--pd2EYFP-1—Clontech--启动子测定 0116--质粒名称--pd2EYFP-N1—Clontech--融合表达 0117--pd4EGFP-Bid—Clontech--融合表达 Bid 0118--pDNR-CMV—Clontech--pDNR-CMV 0119--pDNR-EGFP Vector—Clontech 0120--pDNR-LacZ –Clontech 0121--pECFP-Endo—Clontech--真核表达0122--pECFP-ER—Clontech--真核表达0123--pEGFP-Actin—Clontech--真核表达0124--pGAD GH--Clontech--酵母表达 0125--pGADT7-Rec –Clontech--酵母表达 0126--pGADT7-RecAB—Clontech--酵母表达 0127--pGADT7-Rec2—Clontech--酵母表达 0128--pGBKT7—Clontech--酵母表达 0129--pHAT 10/11/12—Clontech 0130--pHAT20—Clontech 0131—pHygEGFP—Clontech 0132—pLacZi—Clontech 0133—pM—Clontech--pM is used to generate a fusion of the GAL4 DNA-BD 0134--pPKCa-EGFP—Clontech 0135--pPKCb-EGFP—Clontec 0136--pSIREN-DNR Vector—Clontech--RNAi 0137--pSIREN-DNR-DsRed-Express Vector—Clontech--RNAi 0138--pSIREN-RetroQ—Clontech--RNAi 0139--pIRES-EYFP—Clontech--RNAi 0140--pSRE-Luc—Clontech--RNAi 0141--pTK-neo—novagen--原核表达 0142--pZsGreen Vector—Clontech--pZsGreen is a pUC19-derived prokaryotic expression vector 0143--pTandem-1—novagen--原核表达 0144--pZsGreen1-C1Vector—Clontech----真核表达 0145--质粒名称：M13mp18—novagen--原核表达 0146--pZsGreen1-DR Vector—Clontech--真核表达 0147--PZsGreen1-N1 Vector—Clontech --真核表达 0148--T7Select415-1b—novagen----真核表达 0149--pZsYellow Vector—Clontech --真核表达 0150—pTimer—Clontech --真核表达 0151--pTA-Luc—Clontech --真核表达 0152--pTAL-Luc—Clontech --真核表达 0153--pTA-SEAP—Clontech --真核表达 0154--pTAL-SEAP—Clontech --真核表达 0155--pTet-On—Clontech --真核表达 0156--pTet-Off—Clontech --真核表达 0157--pTet-ATF—Clontech --真核表达 0158--pTet-CREB—Clontech --真核表达

拜耳-艾美乐吡虫啉

德国拜耳--拜耳艾美乐70% 吡虫啉3克杀蚜虫蓟马飞虱叶蝉商品名称：艾美乐70％水分散颗粒剂，杀虫对象：蚜虫飞虱蓟马叶蝉斑潜蝇，有效成分：吡虫啉包装规格：3克，生产企业农药登记证号：PD20050011分装企业农药登记证号：PD20050011F040008产品标准证号：Q/HZ-JV032-2009，生产批准证号：HNP33121-A8289生产日期：2013年2月21日质量保证期：2年艾美乐70%水分散剂是拜耳作物科学公司开发的一种氯烟碱类杀虫剂，其内吸性强，活性高，同时具备触杀和胃毒作用，该制剂有效成分含量高，剂型先进，使用、储存安全方便，艾美乐对多种刺吸式口器害虫具有优异的防效，如：蚜虫、飞虱、小绿叶蝉等，在推荐浓度下对作物安全。

与传统杀虫剂作用机制不同，无交互抗性，适用于无公害农产品的生产。

艾美乐具有强内吸性，持效期长。

是常规药剂的1-2倍，可以减少打药1-2次。

超高活性、超低用量。

先进的剂型(水分散粒剂)，崩解迅速，有利于植物吸收，药效稳定；无粉易储藏。

拜耳独特的小包装，便于使用和运输。

通过控制蚜虫等传毒害虫，有效防治介体传毒的作物病毒病。

毒性低，对使用者和环境安全，对皮肤和眼睛无刺激作用。

作用机制具有优良无比的内吸和胃毒作用，作用于乙酰胆碱酯酶的受体，阻断昆虫正常的神经传导，使其麻痹致死。

它杀虫速度虽稍慢，但持效期长。

害虫一旦吸食本品后2-3小时内失去行动能力，48小时内达到死亡高峰。

适用作物蔬菜、果树、花卉、棉花、茶、烟草等。

防治对象各种蚜虫、稻飞虱、叶蝉、白粉虱、黑刺粉虱、梨木虱、瓜蓟马等剌吸式害虫，此外，可以防治潜叶蛾，跳甲、稻水象甲、稻负泥虫。

使用技术对蚜虫、飞虱、蓟马类每亩用药3-4.5克，对水45升喷雾。

防治粉虱7000-8000倍喷雾。

若有鳞翅目害虫与蚜虫等同时混合发生，与其它杀虫剂混使用，可适当降低剂量。

质量保证期：两年规格：3g 使用更方便每亩一袋产品说明艾美乐70%水分散粒剂为新烟碱类杀虫剂，内吸性强，活性高，作用谱广，同时具备胃毒和触杀作用。

Sigma试剂清单

1.
缓冲液
产品货号英文品名中文品名优惠价 (R M B ) 目录价 (RMB)
P6757-100G P6757-1KG P6757-25G P6757-500G PVP40-100G PVP40-1KG PVP40-500G PVP40-50G PVP40-5KG P1190-100G P1190-1KG P1190-500G P9666-100G P9666-1KG P9666-500G P5655-100G P5655-1KG P5655-500G P5629-10KG P5629-1KG P5629-25G P5629-500G S7545-1KG S7545-250G S7545-500G S3817-1KG S3817-500G S3817-5KG S7795-1KG S7795-500G S5886-10KG S5886-1KG S5886-500G S5886-5KG C8532-100G C8532-10KG C8532-1KG C8532-500G C8532-5KG S5136-100G S5136-1KG S5136-500G S5136-5KG S0751-100G S0751-1KG S0751-3KG S0751-500G T5816-100G T5816-1KG T5816-25G T5816-500G T6664-10PAK T1503-100G T1503-10KG T1503-1KG T1503-250G T1503-25G T1503-25KG T1503-500G T1503-50KG T1503-5KG
Ammonium acetate ~98% Ammonium acetate ~98% Ammonium acetate ~98% Boric acid Boric acid Carbonate-Bicarbonate Buffer Carbonate-Bicarbonate Buffer Citric acid trisodium salt Citric acid trisodium salt Citric acid trisodium salt Ethanolamine >=98% Ethanolamine >=98% Ethanolamine >=98% Ethanolamine >=98% Ethanolamine >=98% Ethylenediaminetetraacetic acid >=98.5% Ethylenediaminetetraacetic acid >=98.5% HEPES >=99.5% (titration) HEPES >=99.5% (titration) HEPES >=99.5% (titration) HEPES >=99.5% (titration) HEPES >=99.5% (titration) HEPES >=99.5% (titration) Imidazole >=98.5% (titration) Imidazole >=98.5% (titration) Imidazole >=98.5% (titration) Imidazole >=98.5% (titration) Imidazole >=98.5% (titration) Imidazole >=98.5% (titration) MES hydrate >=99.5% MES hydrate >=99.5% MES hydrate >=99.5% MES hydrate >=99.5% MOPS >=99.5% (titration) MOPS >=99.5% (titration) MOPS >=99.5% (titration) MOPS >=99.5% (titration) MOPS >=99.5% (titration) MOPS >=99.5% (titration) Phosphate buffered saline Phosphate buffered saline Phosphate-Citrate Buffer Phosphate-Citrate Buffer

植物病害诊断试剂盒

植物病害诊断试剂盒美国阿格迪agdia 公司是全球最大的植物病害诊断试剂生产商，产品品种最多，可检测项目多达200多个。

包装规格最全,不同的包装规格适合不同规模的实验室。

从中您一定能发现适合您使用的产品。

选购试剂说明，请仔细阅读。

1，kit, 订货号PSAxxxxx/xxxx 或PSPxxxxx/xxxx 为完整的试剂盒包装，包括样品提取缓冲液、包被好抗体的微孔板（可拆分）、酶标记物、稀释液、缓冲液、底物发色剂、阳性质控（如果应该供应）。

特别注明Indirect ELISA 方法的kit 包括未包被的微孔板及联接用的抗体，所含有的其他组分同上。

2， Reagent Set, 订货号SRAxxxxx/xxxx ,XRAxxxxx/xxxx或SRPxxxxx/xxxx 只含有未包被的微孔板、包被需要的抗体或联接用的抗体、酶标记物。

其他试剂如样品提取缓冲液、稀释液、缓冲液、底物发色剂、质控物需另外订购或自己配制。

我公司销售原厂的上述试剂，详见目录。

3， Bacterial Reagent Set, 订货号BRAxxxxx/xxxx 只含有未包被的微孔板、包被需要的抗体或联接用的抗体、酶标记物。

其他试剂如样品提取缓冲液、稀释液、缓冲液、底物发色剂、质控物需另外订购或自己配制。

我公司销售原厂的上述试剂，详见目录。

4， Bacterial ID订货号BIDxxxxx/xxxx 为完整的试剂盒包装，包括样品提取缓冲液、包被好抗体的微孔板（可拆分）、酶标记物、稀释液、缓冲液、底物发色剂、质控（如果应该供应）。

用于鉴定培养基中或有病症植物提取液中的细菌。

操作简便快速。

5， PS A或SR A中的A代表碱性磷酸酶标记；PS P或SR P中的P代表过氧化物酶标记。

6， Immunostrip test, 为检试纸条，操作简单，几分钟内得到结果，非常适合于现场检测。

该试条必须与相应的样品提取缓冲液配套使用。

实验室需要单独购买该样品提取缓冲液，详见目录。

生物指示剂

生物指示剂LT另外根据客户要求可提供：生孢梭菌（Clostridium sporogenes），枯草芽孢杆菌（B. subtilis），巨大芽孢杆菌（B. megaterium），蜡状芽孢杆菌（B. cereus）等的芽孢悬液。

2.工业生物指示剂工业生物指示剂是根据工业企业实际情况，按照标准要求定制加工而成，以满足企业的特殊需求，通常采用不同的载体材料和包装形式，例如钢片、钢线、纸片、棉线、塑料片和滑石粉等，它与芽孢条、自含式等标准生物指示剂相比更具优势。

CICC可按照客户要求提供定制工业生物指示剂。

染菌滑石粉CICC研制的标准专用染菌滑石粉，以符合标准要求的滑石粉为载体，选用CICC 自行生产的微生物材料萎缩芽孢杆菌ATCC 9372芽孢悬液，按标准要求精制而成，每批染菌滑石粉产品均经过芽孢含量检验，确保质量稳定。

该产品适用于评定屏障材料对携菌微粒阻穿透性的实验方法，适用于国家医药行业手术衣标准《病人、医护人员和器械用手术单、手术衣和洁净服》（YY/T 0506-2009）、国际标准ISO 22612:2005 Clothing for protection against infectious agents -- Test method for resistance to dry microbial penetration（传染介质防护服--防干微生物渗入的试验方法）。

产品参数：产品名称染菌滑石粉微生物材料萎缩芽孢杆菌（B. atrophaeus）ATCC 9372芽孢含量108 CFU/g规格0.5g+0.1 g /瓶粒度＜800目（95%＜15μm）贮藏条件2~8℃，避免阳光直射和接触灭菌剂。

有效期生产日起12个月染菌石英粉CICC研制的标准专用染菌石英粉，以符合标准要求的石英粉为载体，选用CICC 自行生产的微生物材料萎缩芽孢杆菌ATCC 9372芽孢悬液，按标准要求精制而成，每批染菌石英粉产品均经过芽孢含量检验，产品质量稳定。

染色及助剂环保标准--2009年要求

§64 LFGB B 82.02.9
邻氨基偶氮甲苯
97-56-3
４氨基联苯
92-67-1
５硝基邻甲苯胺
99-55-8
邻氨基苯甲醚
90-04-0
联苯胺
92-87-5
对氯苯胺
106-47-8
４氯邻甲苯胺
95-69-2
２甲氧基５甲基苯胺
120-71-8
２，４二氨基苯甲醚
615-05-4
４，４二氨基二苯甲烷
2682-20-4
五氯化苯酚(PCP)
87-86-5
未检出
§64 LFGB B 82.02.8(RL=0.5)
四氯苯酚(TeCP)
25167-83-3
富马酸二甲酯
624-49-7
禁止使用
溶剂萃取/GC-MS
IV) Bisphenol-A (BPA)双酚A
化学物质
CAS编号
产品最高限量
(ppm)
检检法
4,4dihydroxy2,2diphenylpropane
80-05-7
未检出
GC-MS/
LC-MS
V)抗光敏性致癌的分散染料及其它染料
化学物质
CAS编号
产品最高限量
检测法
(ppm)
分散染料
未检出
DIN54231单位：
毫克/升（RL：5）
分散蓝1
2475-45-8
分散蓝3
2475-46-9
分散蓝7
4098-71-9
游离型:1
封闭型: 100
四甲基苯二甲基二异氰酸酯
(TMXDI)
2778-42-9
游离型:1
封闭型: 100
甲苯异氰酸酯
(TDI)

EPOXY PLUS RESIN 产品说明书

14350REVISION DATE: 07/10/2008SAFETY DATA SHEETEPOXY PLUS RESINPRODUCT NO.X0152SUPPLIERITW DEVCONBAY 150SHANNON INDUSTRIAL ESTATESHANNONCO CLAREIRELANDT: +353 (0)61471299F: 353(0)61471285the aquatic environment.CLASSIFICATION Xi;R36/38. R43. N;R51/53.HUMAN HEALTHAvoid contact with skin and eyes. In case of accident or if you feel unwell, seek medical advice immediately (show label where possible). INHALATIONMove the exposed person to fresh air at once. When breathing is difficult, properly trained personnel may assist affected person by administering oxygen. Contact physician if discomfort continues.INGESTIONDo not induce vomiting. If vomiting occurs, the head should be kept low so that stomach vomit doesn't enter the lungs. Drink a few glasses of water or milk. Get medical attention.SKIN CONTACTRemove affected person from source of contamination. Wash skin thoroughly with soap and water for several minutes. Contact physician if irritation persists.EYE CONTACTPromptly wash eyes with plenty of water while lifting the eye lids. Continue to rinse for at least 15 minutes and get medical attention.EXTINGUISHING MEDIAExtinguish with foam, carbon dioxide or dry powder.EPOXY PLUS RESINSPECIAL FIRE FIGHTING PROCEDURESAvoid breathing fire vapours. Keep up-wind to avoid fumes. Avoid water in straight hose stream; will scatter and spread fire. Keep run-off water out of sewers and water sources. Dike for water control.SPECIFIC HAZARDSBy heating and fire, irritating vapours/gases may be formed.PROTECTIVE MEASURES IN FIREAvoid contact with skin and eyes. Wear protective clothing as described in Section 8 of this safety data sheet. Provide adequate ventilation. ENVIRONMENTAL PRECAUTIONSDo not allow to enter drains, sewers or watercourses. Spillages or uncontrolled discharges into watercourses must be IMMEDIATELY alerted to the Environmental Agency or other appropriate regulatory body.SPILL CLEAN UP METHODSAbsorb with sand or other inert absorbent. Transfer to covered steel drums for disposal. Containers with collected spillage must be properlyUSAGE PRECAUTIONSUse only in well-ventilated areas. Keep away from heat, sparks and open flame. Open drum carefully as content may be under pressure. Do not eat, drink or smoke when using the product. Observe good industrial hygiene practices.STORAGE PRECAUTIONSPROTECTIVE EQUIPMENTPROCESS CONDITIONSProvide eyewash, quick drench.ENGINEERING MEASURESProvide adequate general and local exhaust ventilation.RESPIRATORY EQUIPMENTIf ventilation is insufficient, suitable respiratory protection must be provided.HAND PROTECTIONUse protective gloves made of: Rubber or plastic. Butyl rubber gloves are recommended.EYE PROTECTIONWear approved chemical safety goggles where eye exposure is reasonably probable.HYGIENE MEASURESKeep away from food, drink and animal feeding stuffs. Good personal hygiene is necessary. Wash hands and contaminated areas with water and soap before leaving the work site. Do not eat, drink or smoke when using the product. Change work clothing daily before leaving work place.SKIN PROTECTIONEPOXY PLUS RESINAPPEARANCE Viscous liquidCOLOUR GreyODOUR Slight odourSOLUBILITY Slightly soluble in water.BOILING POINT (°C)>260MELTING POINT (°C)N/DRELATIVE DENSITY 1.39 25 ºC VAPOUR DENSITY (air=1)>1VAPOUR PRESSURE0.03 mmHg 77.2EVAPORATION RATE<<1 (butyl acetate =1) pH-VALUE, CONC. SOLUTION7 @ 20 ºC FLASH POINT (°C)>204.4STABILITYStable under normal temperature conditions and recommended use.CONDITIONS TO AVOIDAvoid heat, flames and other sources of ignition.HAZARDOUS POLYMERISATIONWill not polymerise.MATERIALS TO AVOIDAvoid contact with: Strong oxidising agents. Strong acids. Amines.HAZARDOUS DECOMPOSITION PRODUCTSSKIN CONTACTIrritating to skin. May cause sensitisation by skin contact.EYE CONTACTIrritating to eyes.HEALTH WARNINGSPreparation contains an epoxy resin, which may cause sensitisation and development of allergy.Avoid releasing to the environment. The product contains substances which are toxic to aquatic organisms and which may cause long term adverse effects in the aquatic environment.MOBILITYDo not discharge into drains, water courses or onto the ground.WATER HAZARD CLASSIFICATIONWGK 2Dispose of waste and residues in accordance with local authority requirements.WASTE CLASSEPOXY PLUS RESINUK ROAD CLASS9PROPER SHIPPING NAME ENVIRONMENTALLY HAZARDOUS SUBSTANCE, LIQUID, N.O.S. (EPOXY RESIN (Number averageMW <= 700 ))UK ROAD PACK GR.UN NO. ROAD III3082ADR CLASS NO.Class 9: Miscellaneous9ADR CLASSdangerous substances andarticles.ADR PACK GROUP90HAZARD No. (ADR)IIIADR LABEL NO.2XHAZCHEM CODE9RID CLASS NO.CEFIC TEC(R) NO.990GM6-IIIUN NO. SEARID PACK GROUP3082IIIIMDG CLASS9IMDG PAGE NO.9EMSIMDG PACK GR.F-A, S-FIIIMARINE POLLUTANTSee GuideMFAG No.AIR CLASSUN NO. AIR93082Irritant Dangerous for theenvironmentCONTAINS EPOXY RESIN (Number average MW <= 700 )RISK PHRASESR51/53Toxic to aquatic organisms, may cause long-term adverse effects in the aquaticenvironment.R43May cause sensitisation by skin contact.R36/38Irritating to eyes and skin.SAFETY PHRASESS26In case of contact with eyes, rinse immediately with plenty of water and seek medicaladvice.Wear suitable gloves and eye/face protection.S37/39REV. NO./REPL. SDS GENERATED5DATE18.01.2005RISK PHRASES IN FULLR36/38Irritating to eyes and skin.R43May cause sensitisation by skin contact.R51/53Toxic to aquatic organisms, may cause long-term adverse effects in the aquatic environment.EPOXY PLUS RESINDISCLAIMERThis information relates only to the specific material designated and may not be valid for such material used in combination with any other materials or in any process. Such information is, to the best of the company's knowledge and belief, accurate and reliable as of the date indicated. However, no warranty guarantee or representation is made to its accuracy, reliability or completeness. It is the user's responsibility to satisfy himself as to the suitability of such information for his own particular use.14350。

乳腺癌细胞株整理

加入10%的胎牛血清
具有CD44+/hi/CD24-
/低癌症干细胞标记
LY2
浸润性导管癌
胸腔积液
DMEM培养基，90%;优质胎牛血清，10%。气相：37C,5%CO2
ER(+);PR(-);TP53(+/-)
MCF7
乳腺腺癌细胞
浸润性导管癌
乳腺，从转移位点(胸水)处获得/上皮细胞样，
MEM培养基中加入0.01mg/ml人重组胰岛素和10%胎牛血清。
细胞角蛋白19
HCC202
腺癌
乳房，乳腺
RPMI-1640，90%;优质胎牛血清，10%。气相：37°C,5%CO2
ER(-)；PR(-)；HER2(+);
TP53-
HCC2157
腺癌
乳房，乳腺
RPMI-1640，90%;优质胎牛血清，10%。气相：37°C,5%CO2
ER(-);PR(-);TP53+
贴壁生长，三阴，转移性乳腺导管腺癌
MDA-MB-436
乳腺腺癌细胞
浸润性导管癌
乳腺腺癌胸水转移灶/
有多核成分的多形细胞
L-15培养添加10ug/ml胰岛素和16ug/ml谷胱甘肽，90%;优质胎牛血清，10%。气相：空气，100%。温度：37°C。
ER(-);PR(-);TP53-
MDA-MB-453
DMEM培养基，90%;优质胎牛血清，10%。气相：37C,5%CO2
ER(+);PR(+);P53(+/-Wt表达WNT7B表达胰岛素样生长因子结合蛋白
(IGFBP)BP-2;BP-4;BP-
5;TNF-a可以抑制MCF-7细胞的生长；
MCF-10A

罗地亚产品目录

超强的渗透力、乳化力，优异的去污能力，粘度低，寒冷季节使用方便替代NP（TX-10）、OP-10等，有3/5/6/7/9/10EO供选择
HLB：8/10.5/11.4/12.1/13.3/13.7
浊点：48-50/64-66/69-72/73-75/57-59/75-77
FentacareF08
无溶剂C9-C11烷基乙氧基化物
RhodafacRP－710
有机磷酸酯阴离子表面活性剂
微浊液体
245KG/桶
低泡,良好清洗、润湿、乳化性能;高电流忍受能力,可用于电解除油、化学除油除蜡和PCB除油整孔，也可以和低泡非离子复配，用于喷淋。
RhodocalTS-60/MX
磷酸酯类阴离子表面活性剂
粘稠液体
200KG/桶
含氨基的阴离子表面活性剂,低泡,高电流负荷稳定，常与油酸类的表活复配用于电解除油粉
产品名称
化学成分
外观
产品特点及应用
MirapolWT
阳离子聚合物
淡黄色液体
200KG/桶
无氰碱性镀锌的走位剂、整平剂，能明显缩短电镀时间，改善镀层的均匀性和深镀能力，节省锌的用量，同时提高镀层的耐腐蚀能力。
PH：7.5-8.5；添加量：1.5g/L；消耗量：40-70g/KAh
沉降剂：主用于磨削液中吸附金属屑沉降
黄色液体
200KG/桶
用于水基清洗配方表面活性剂混合物，低泡、耐酸碱，对于清除油脂类的有机油污非常有效，经常可以取代溶剂，降低成本，适用于高压和低压清洗设备。
Antarox L61/62/64
EO/PO嵌段共聚物
透明液体
204.12KG/桶
泡沫控制能力优异，适用范围广。可替代陶氏TergitolL、巴斯夫Pluronic PE、亨斯曼Surfonic POA-L系列。

安捷伦科技比利时公司BRCA HP PCR试剂盒说明书

BRCA HP*************(24小时)化学品安全技术说明书GHS product identifier 应急咨询电话（带值班时间）::供应商/ 制造商:安捷伦科技比利时公司比利时迭戈姆1831，德库里蓝大街5号，巴斯9。

电话：+32(0)2 404 90 00BRCA HP化学品的推荐用途和限制用途PCR Mix Plex 1I-0674PCR Mix Plex 2I-0675Taq DNA PolymeraseI-0676部件号:物质用途:PCR Mix Plex 1 2 x 0.125 ml（毫升）PCR Mix Plex 2 2 x 0.125 ml（毫升）Taq DNA Polymerase 0.015 ml（毫升）部件号（化学品试剂盒）:MP-0401.050安全技术说明书根据 GB/ T 16483-2008 和 GB/ T 17519-2013本安全技术说明书责任人的e-mail地址:***************************GHS化学品标识:BRCA 均聚物片段扩增试剂盒危险性类别混合物中由对水生环境毒性未知的组分组成的比率： 2.2%PCR Mix Plex 2混合物中由对水生环境毒性未知的组分组成的比率： 2.2%物质或混合物的分类根据 GB13690-2009 和 GB30000-2013皮肤腐蚀/刺激 - 类别 3H320严重眼损伤/眼刺激 - 类别 2B H402危害水生环境一急性危险 - 类别 3H412危害水生环境一长期危险 - 类别 3紧急情况概述PCR Mix Plex 1液体。

PCR Mix Plex 2液体。

Taq DNA Polymerase 液体。

[清澈。

/ 溶液]PCR Mix Plex 1无资料。

PCR Mix Plex 2无资料。

Taq DNA Polymerase 无色。

PCR Mix Plex 1无资料。

PCR Mix Plex 2无资料。

Cadox M-50a VR 红色氩酸乙醛激素产品数据表说明书

Product Data SheetCadox M-50a VRMethyl ethyl ketone peroxideHighly reactive industry standard MEKP with vanishing red cure indicator for curing promoted unsaturated polyester matrices at room temperature.CAS number1338-23-4EINECS/ELINCS No.215-661-2TSCA statuslisted on inventorySpecificationsAppearance, 20-25°C Red liquid Total active oxygen8.8-9.0 %ApplicationsCadox® M-50a VR is a special purpose catalyst for the room temperature cure of promoted unsaturated polyester resins. Unpromoted unsaturated polyester resins can be heat-cured with Cadox® M-50a VR in the temperature range of 100-127°C. Cadox® M-50a VR also has a high MEKP monomer content which may provide reduced cure times in some resin systems. Cadox® M-50a Red offers all the advantages of a red MEKP. The series of products includes a red indicator system that is there to visualize hot & cold spots, schrinkage problems, mass effects, thermal effects of core materials and dead flow zones in applications like vacuum infusion.Thermal stabilityOrganic peroxides are thermally unstable substances, which may undergo self-accelerating decomposition. The lowest temperature at which self-accelerating decomposition of a substance in the original packaging may occur is the Self-Accelerating Decomposition Temperature (SADT). The SADT is determined on the basis of the Heat Accumulation Storage Test.SADT60°C (140°F)Method The Heat Accumulation Storage Test is a recognized test method for thedetermination of the SADT of organic peroxides (see Recommendations on theTransport of Dangerous Goods, Manual of Tests and Criteria - United Nations, NewYork and Geneva).StorageDue to the relatively unstable nature of organic peroxides a loss of quality can be detected over a period of time. To minimize the loss of quality, Nouryon recommends a maximum storage temperature (Ts max. ) for each organic peroxide product.Ts Max.30°C (86°F)Note When stored under these recommended storage conditions, Cadox® M-50a VRwill remain within the Nouryon specifications for a period of at least three monthsafter delivery.Packaging and transportCadox® M-50a VR is packed in non-returnable, 5 gallon polyethylene containers of 40 lb net weight. Both packaging and transport meet the international regulations. For the availability of other packed quantities contact your Nouryon representative. Cadox® M-50a VR is classified as Organic peroxide type D; liquid; Division 5. 2; UN 3105. This product contains a component that is classified as Toxic for Reproduction, Category 1B under the Globally Harmonized System of Classification and Labelling of Chemicals (GHS). Nouryon ensures that it consistently manages hazardous substances to ensure safe use. To that end, a full risk assessment of this product has been conducted under Nouryon’s Priority Substance Program and safe use has been demonstrated throughout the supply chain.Safety and handlingKeep containers tightly closed. Store and handle Cadox® M-50a VR in a dry well-ventilated place away from sources of heat or ignition and direct sunlight. Never weigh out in the storage room. Avoid contact with reducing agents (e. g. amines), acids, alkalis and heavy metal compounds (e. g. accelerators, driers and metal soaps). Please refer to the Safety Data Sheet (SDS) for further information on the safe storage, use and handling of Cadox® M-50a VR. This information should be thoroughly reviewed prior to acceptance of this product. The SDS is available at /sds-search.Major decomposition productsCarbon dioxide, Water, Acetic acid, Formic acid, Propionic acid, Methyl ethyl ketoneAll information concerning this product and/or suggestions for handling and use contained herein are offered in good faith and are believed to be reliable.Nouryon, however, makes no warranty as to accuracy and/or sufficiency of such information and/or suggestions, as to the product's merchantability or fitness for any particular purpose, or that any suggested use will not infringe any patent. Nouryon does not accept any liability whatsoever arising out of the use of or reliance on this information, or out of the use or the performance of the product. Nothing contained herein shall be construed as granting or extending any license under any patent. Customer must determine for himself, by preliminary tests or otherwise, the suitability of this product for his purposes.The information contained herein supersedes all previously issued information on the subject matter covered. The customer may forward, distribute, and/or photocopy this document only if unaltered and complete, including all of its headers and footers, and should refrain from any unauthorized use. Don’t copythis document to a website.Cadox® is a registered trademark of Nouryon Chemicals B. V. or affiliates in one or more territories.Contact UsPolymer Specialties Americas************************Polymer Specialties Europe, Middle East, India and Africa*************************Polymer Specialties Asia Pacific************************2022-7-26© 2022Thermoset composites Cadox M-50a VR。

Dako Antibody Diluent 化学品安全技术说明书

Products Containing Dako Antibody Diluent 化学品安全技术说明书GHS product identifier :Products Containing Dako Antibody Diluent化学品的推荐用途和限制用途IC002, IC004, IK001, IK002, IK004, IR002, IR051, IR052, IR053, IR054,IR055, IR056, IR057, IR058, IR059, IR060, IR061, IR062, IR066, IR067,IR068, IR069, IR072, IR074, IR075, IR076, IR077, IR079, IR080, IR082,IR084, IR085, IR086, IR087, IR088, IR089, IR091, IR092, IR093, IR094,IR600, IR750, IS051, IS052, IS053, IS054, IS055, IS056, IS057, IS059,IS060, IS062, IS067, IS068, IS069, IS072, IS074, IS075, IS077, IS079,IS080, IS082, IS084, IS600, IS750, IX018, IX019, K3954, M0617, M0630,M0633, M0634, M0635, M3501, M3502, M3503, M3504, M3505, M3512, M3515,M3517, M3525, M3528, M3539, M3556, M3562, M3563, M3567, M3568, M3569,M3571, M3575, M3612, M3614, M3615, M3616, M3617, M3619, M3620, M3621,M3623, M3624, M3625, M3626, M3627, M3628, M3631, M3632, M3636, M3638,M3639, M3640, M3641, M3642, M3643, M3646, M3647, M3649, M3651, M3653,M3666, M7019, M7020, M7191, M7235, M7237, M7240, M7271, M7310, SK310部件号:物质用途:GA051 // FLEX Monoclonal Mouse anti-Human Cytokeratin, HMW, Clone 34βE12 RTU (Omnis) // 12 mLGA052 // FLEX Monoclonal Mouse anti-Human Melanosome, Clone HMB45 RTU (Omnis) // 12 mLGA053 // FLEX Monoclonal Mouse anti-Human Cytokeratin, Clone AE1/AE3 (Omnis) // 12 mLGA054 // FLEX Monoclonal Mouse anti-Human Caldesmon, Clone h-CD (Omnis) //12 mLGA055 // /FLEX Monoclonal Mouse Anti-Human Wilms' Tumor 1 (WT1) // 12 ml Protein, Clone 6F-H2, RTU (Dako Omnis) // 12 mlGA058 // /FLEX Monoclonal Mouse Anti-Human Inhibin ¿, Clone R1, RTU (Dako Omnis) // 12 mlGA059 // FLEX Monoclonal Mouse anti-Human E-Cadherin, Clone NCH-38 (Omnis)// 12 mLGA060 // FLEX Monoclonal Rabbit anti-Human AMACR, Clone 13H4-38 (Omnis) //12 mLGA061 // FLEX Monoclonal Mouse anti-Human CD15, Clone Carb-3 (Omnis) //12 mLGA062 // /FLEX Monoclonal Mouse Anti-Human CD15, Clone Carb-3, RTU (Dako Omnis) // 12 mlGA067 // /FLEX Monoclonal Mouse Anti-Myogenin, Clone F5D, RTU (Dako Omnis)// 12 mlGA074 // /FLEX Monoclonal Mouse Anti-Human Mammaglobin, Clone 304-1A5,RTU (Dako Omnis) // 12 mlGA075 // /FLEX Monoclonal Mouse Anti-Human Renal Cell Carcinoma Marker,Clone SPM314, RTU (Dako Omnis) // 12 mlGA077 // /FLEX Monoclonal Mouse Anti-Human Gross Cystic Disease Fluid Protein-15, Clone 23A3, RTU (Dako Omnis) // 12 mlGA080 // /FLEX Monoclonal Mouse Anti-Human CDX2, Clone DAK-CDX2, RTU (Dako Omnis) // 12 mlGA083 // FLEX Monoclonal Rabbit Anti-Human Cyclin D1, Clone EP12, Ready-to-Use (Dako Omnis) // 12 mlGA084 // /FLEX Monoclonal Rabbit Anti-Human Estrogen Receptor ¿, Clone EP1, RTU (Dako Omnis) // 12 mlGA090 // FLEX Monoclonal Mouse Anti-Human Progesterone Receptor Clone PgR 1294 RTU (Dako Omnis) // 12 mlGA600 // /FLEX Universal Negative Control, Rabbit, RTU (Dako Omnis) // 12安全技术说明书根据 GB/ T 16483-2008 和 GB/ T 17519-2013GHS化学品标识:含有Dako抗体稀释液的产品GA750 // FLEX Universal Negative Control Mouse RTU // 12 mLIC001 // DuoFLEX Cocktail anti-S100 anti-Tyrosinase anti-Melan-A RTU (Link) // 6 mLIC002 // DuoFLEX Cocktail anti-CD3 anti-CD20cy RTU (Link) // 6 mLIC004 // DuoFLEX Cocktail anti-AMACR anti-Cytokeratin HMW anti-Cytokeratin 5/6 RTU (Link) // 6 mLIK001 // DuoFLEX Cocktail anti-S100 anti-Tyrosinase anti-Melan-A RTU // 6 mLIK002 // DuoFLEX Cocktail anti-CD3 anti-CD20cy RTU // 6 mLIK004 // DuoFLEX Cocktail anti-AMACR anti-Cytokeratin HMW anti-Cytokeratin 5/6 RTU // 6 mLIR002 // /FLEX Polyclonal Guinea Pig Anti-Insulin, RTU (Link) // 12 mlIR051 // /FLEX Monoclonal Mouse Anti-Human Cytokeratin, High Molecular Weight, Clone 34ßE12, RTU (Link) // 12 mlIR052 // FLEX Monoclonal Mouse anti-Human Melanosome, Clone HMB45 RTU (Link) // 12 mLIR053 // FLEX Monoclonal Mouse anti-Human Cytokeratin, Clone AE1/AE3 RTU (Link) // 12 mLIR054 // FLEX Monoclonal Mouse anti-Human Caldesmon, Clone h-CD RTU (Link) // 12 mLIR055 // FLEX Monoclonal Mouse anti-Human Wilms' Tumor 1 (WT1) Protein, Clone 6F-H2 RTU (Link) // 12 mLIR056 // FLEX Monoclonal Mouse anti-Thyroid Transcription Factor, TTF-1, Clone 8G7G3/1 RTU (Link) // 12 mLIR057 // FLEX Monoclonal Mouse anti-Human CD99, MIC2 Ewing's Sarcoma Marker, Clone 12E7 RTU (Link) // 12 mLIR059 // FLEX Monoclonal Mouse anti-Human E-Cadherin, Clone NCH-38 RTU (Link) // 12 mLIR060 // FLEX Monoclonal Rabbit anti-Human AMACR, Clone 13H4 RTU (Link) // 12 mLIR062 // FLEX Monoclonal Mouse anti-Human CD15, Clone Carb-3 RTU (Link) // 12 mLIR067 // FLEX Monoclonal Mouse anti-Myogenin, Clone F5D RTU (Link) // 12 mLIR068 // FLEX Monoclonal Mouse anti-Human Progesterone Receptor, Clone PgR 636 RTU (Link) // 12 mLIR069 // FLEX Monoclonal Mouse anti-Human CD1a, Clone 010 RTU (Link) //12 mLIR072 // FLEX Monoclonal Mouse anti-Human Podoplanin, Clone D2-40 RTU (Link) // 12 mLIR074 // FLEX Monoclonal Mouse anti-Human Mammaglobin, Clone 304-1A5 RTU (Link) // 12 mLIR075 // FLEX Monoclonal Mouse anti-Human Renal Cell Carcinoma Marker, Clone SPM314 RTU (Link) // 12 mLIR077 // FLEX Monoclonal Mouse anti-Human Gross Cystic Disease Fluid Protein-15, Clone 23A3 RTU (Link) // 12 mLIR079 // FLEX Monoclonal Mouse anti-Human MutL Protein Homolog 1, Clone ES05 RTU (Link) // 12 mLIR080 // FLEX Monoclonal Mouse anti-Human CDX2, Clone DAK-CDX2 RTU (Link) // 12 mLIR082 // FLEX Monoclonal Mouse anti-Human CD5, Clone 4C7 RTU (Link) // 12 mLIR084 // FLEX Monoclonal Rabbit anti-Human Estrogen Receptor α, Clone EP1 RTU (Link) // 12 mLIR085 // FLEX Monoclonal Mouse anti-Human MutS Protein Homolog 2, Clone FE11 RTU (Link) // 12 mLIR086 // FLEX Monoclonal Rabbit anti-Human MutS Protein Homolog 6, Clone EP49 RTU (Link) // 12 mLIR087 // FLEX Monoclonal Rabbit anti-Human Postmeitic Segregation Increased 2, Clone EP51 RTU (Link) // 12 mLIR088 // FLEX Monoclonal Mouse anti-Human Prostein, Clone 10E3 RTU (Link) // 12 mLAntigen, Clone 3E6 RTU (Link) // 12 mLIR091 // FLEX Monoclonal Mouse anti-Human ERCC1, Clone 4F9 RTU (Link) // 12 mLIR092 // FLEX Monoclonal Mouse Octamer-Binding Transcription Factor 3/4, Clone N1NK RTU (Link) // 12 mLIR093 // FLEX Monoclonal Rabbit anti-Human Terminal Deoxynucleotidyl Transferase, Clone EP266 RTU (Link) // 12 mLIR094 // FLEX Monoclonal Rabbit anti-Human Cytokeratin 8/18, CloneEP17/EP30 RTU (Link) // 12 mLIR600 // FLEX Negative Control Rabbit Immunoglobulin Fraction of Serum from Non-immunized Rabbits RTU // 12 mLIR750 // FLEX Negative Control Mouse Cocktail of Mouse, RTU (Link) / 12 mL IS051 // FLEX Monoclonal Mouse anti-Human Cytokeratin, HMW, Clone 34βE12 RTU // 6 mLIS052 // FLEX Monoclonal Mouse anti-Human Melanosome, Clone HMB45 RTU //6 mLIS053 // FLEX Monoclonal Mouse anti-Human Cytokeratin, Clone AE1/AE3 RTU // 6 mLIS054 // FLEX Monoclonal Mouse anti-Human Caldesmon, Clone h-CD RTU // 6 mLIS055 // FLEX Monoclonal Mouse anti-Human Wilms' Tumor 1 (WT1) Protein, Clone 6F-H2 RTU // 6 mLIS056 // FLEX Monoclonal Mouse anti-Thyroid Transcription Factor, TTF-1, Clone 8G7G3/1 RTU // 6 mLIS057 // FLEX Monoclonal Mouse anti-Human CD99, MIC2 Ewing's Sarcoma Marker, Clone 12E7 RTU // 6 mLIS059 // FLEX Monoclonal Mouse anti-Human E-Cadherin, Clone NCH-38 RTU // 6 mLIS060 // FLEX Monoclonal Rabbit anti-Human AMACR, Clone 13H4 RTU // 6 mL IS062 // FLEX Monoclonal Mouse anti-Human CD15, Clone Carb-3 RTU // 6 mL IS067 // /FLEX Monoclonal Mouse Anti-Myogenin, Clone F5D, RTU (Dako Autostainer/Autostainer Plus) // 6 mLIS068 // FLEX Monoclonal Mouse anti-Human Progesterone Receptor, Clone PgR 636 RTU // 6 mLIS069 // FLEX Monoclonal Mouse anti-Human CD1a, Clone 010 RTU // 6 mLIS072 // FLEX Monoclonal Mouse anti-Human Podoplanin, Clone D2-40 RTU //6 mLIS074 // FLEX Monoclonal Mouse anti-Human Mammaglobin, Clone 304-1A5 RTU // 6 mLIS075 // FLEX Monoclonal Mouse anti-Human Renal Cell Carcinoma Marker, Clone SPM314 RTU // 6 mLIS077 // FLEX Monoclonal Mouse anti-Human Gross Cystic Disease Fluid Protein-15, Clone 23A3 RTU // 6 mLIS079 // FLEX Monoclonal Mouse anti-Human MutL Protein Homolog 1, Clone ES05 RTU // 6 mLIS080 // FLEX Monoclonal Mouse anti-Human CDX2, Clone DAK-CDX2 RTU // 6 mL IS082 // FLEX Monoclonal Mouse anti-Human CD5, Clone 4C7 RTU // 6 mLIS084 // FLEX Monoclonal Rabbit anti-Human Estrogen Receptor α, Clone EP1 RTU // 6 mLIS600 // FLEX Negative Control Rabbit Immunoglobulin Fraction of Serum from Non-immunized Rabbits RTU // 6 mLIS750 // FLEX Negative Control Mouse Cocktail of Mouse, RTU // 6 mL’IX018 // Monoclonal Mouse Anti-Human Proinsulin, Clone 3B1 // 50 ml - 3 L IX019 // Monoclonal Mo a Hu Proinsulin, Clone A6C9 // 50 ml - 3 LK3954 // Biotinylation Reagent // Dako ARK (Animal Research Kit), Peroxidase // 1.5 mLK3954 // Blocking Reagent // Dako ARK (Animal Research Kit), Peroxidase // 1.5 mLM0617 // Monoclonal Mouse Anti-Thrombomodulin, Clone 1009 // 1 mLM0630 // Monoclonal Mouse Anti-Human Cytokeratin, High Molecular Weight, Clone 34βE12 // 1 mLM0633 // Monoclonal Mouse Anti-Rabbit Macrophage, Clone RAM11 // 1 mL1 mlM0635 // Monoclonal Mouse Anti-Human Muscle Actin, Clone HHF35 // 1 mLM3501 // Monoclonal Mouse Anti-Adrenocorticotropin (ACTH), Clone 02A3 //1 mLM3502 // Monoclonal Mouse Anti-Human Luteinizing Hormone (LH), Clone C93 // 1 mLM3503 // Monoclonal Mouse Anti-Human Thyroid-Stimulating Hormone (TSH), Clone 0042 // 1 mLM3504 // Monoclonal Mouse Anti-Human Follicle-Stimulating Hormone (FSH), Clone C10 // 1 mLM3505 // Monoclonal Mouse Anti-Human Mesothelial Cell, Clone HBME-1 // 1 mLM3512 // Monoclonal Mouse Anti-Human MyoD1, Clone 5.8A // 1 mLM3515 // Monoclonal Mouse Anti-Human Cytokeratin, Clone AE1 // AE3 // 0.2 ml, 1 mlM3517 // Monoclonal Mouse Anti-CA 19-9, Clone 116-NS-19-9 // 1 mLM3525 // Monoclonal Mouse Anti-Human Epithelial-Related Antigen, Clone MOC-31 // 1 mLM3528 // Monoclonal Mouse Anti-Human Papillomavirus (HPV), Clone K1H8 //1 mLM3539 // Monoclonal Mouse Anti-Human Beta-Catenin, Clone β-Catenin-1 //1 mLM3556 // Monoclonal Mouse Anti-Human Calponin, Clone CALP // 1 mLM3562 // Monoclonal Mouse Anti-Human Androgen Receptor, Clone AR441 // 1 mLM3563 // Monoclonal Mouse Anti-Human Epidermal Growth Factor Receptor, Clone H11 // 1 mLM3567 // Monoclonal Mouse Anti-Human Fascin, Clone 55K-2 // 1 mLM3568 // Monoclonal Mouse Anti-Human Progesterone Receptor, Clone PgR 1294 // 1 mLM3569 // Monoclonal Mouse Anti-Human Progesterone Receptor, Clone PgR 636 // 0.2 ml, 1 mlM3571 // Monoclonal Mouse Anti-Human CD1a, Clone O10 010 // 1 mLM3575 // Monoclonal Mouse Anti-Thyroid Transcription Factor, Clone 8G7G3 // 1 // 0.2 ml, 1 mlM3612 // Monoclonal Mouse Anti-Human E-Cadherin, Clone NCH-38 // 0.2 ml,1 mlM3614 // Monoclonal Mouse Anti-Human Thymidylate Synthase, Clone TS106 // 1 mLM3615 // Monoclonal Mouse Anti-Human P501S Prostein, Clone 10E3 // 0.2 ml, 1 mlM3616 // Monoclonal Rabbit Anti-Human P504S AMACR, Clone 13H4 // 0.2 ml,1 mlM3617 // Monoclonal Mouse Anti-Human COX-2, Clone CX-294 // 1 mLM3619 // Monoclonal Mouse Anti-Human D2-40, Clone D2-40 // 0.2 ml, 1 mlM3620 // Monoclonal Mouse Anti-Human Prostate-Specific Membrane Antigen, Clone 3E6 // 0.2 ml, 1 mlM3621 // Monoclonal Mouse Anti-Human MITF, Clone D5 // 0.2 mLM3623 // Monoclonal Mouse Anti-Human Tyrosinase, Clone T311 // 0.2 mLM3624 // Monoclonal Mouse Anti-Human Survivin, Clone 12C4 // 0.2 mLM3625 // Monoclonal Mouse Anti-Human Mammaglobin, Clone 304-1A5 // 0.2 mL M3626 // Monoclonal Mouse Anti-Human L523S Protein IMP3, Clone 69.1 //0.2 mLM3627 // Monoclonal Mouse Anti-Human PTEN, Clone 6H2.1 // 0.2 mLM3628 // Monoclonal Rabbit Anti-Human Akt-pS473, Phosphorylation Site Specific, Clone 14-5 // 1 mLM3631 // Monoclonal Mouse Anti-Human CD15, Clone Carb-3 // 0.2 ml, 1 mlM3632 // Monoclonal Mouse Anti-Human Renal Cell Carcinoma Marker, Clone SPM314 // 1 mLM3636 // Monoclonal Mouse Anti-Human CDX2, Clone DAK-CDX2 // 0.2 ml, 1 ml M3638 // Monoclonal Mouse Anti-Human Gross Cystic Disease Fluid Protein-15, Clone 23A3 // 1 mL*************(24小时)应急咨询电话（带值班时间）:供应商/ 制造商:供应商/ 制造商: Agilent Technologies, Inc.（美国安捷伦科技有限公司）住所：5301 Stevens Creek Boulevard, Santa Clara, CA, 95051, United States 联系电话：+1 800 227 9770 供应商/ 制造商: Agilent Technologies Singapore (International) Pte Ltd.（安捷伦科技新加坡（国际）私人有限公司）住所：No. 1 Yishun Avenue 7, Singapore, 768923 联系电话：(65) 6276 2622供应商/ 制造商: Agilent Technologies Denmark ApS (安捷伦科技丹麦私人有限公司)住所：Produktionsvej 42， DK-2600 Glostrup, Denmark 联系电话： +45 44859500 M3640 // Monoclonal Mouse Anti-Human MutL Protein Homolog 1, Clone ES05 //0.2 ml, 1 mlM3641 // Monoclonal Mouse Anti-Human CD5, Clone 4C7 // 1 mlM3642 // Monoclonal Rabbit Anti-Human Cyclin D1, Clone EP12 // 1 mlM3643 // Monoclonal Rabbit Anti-Human Estrogen Receptor ¿, Clone EP1 //0.2 ml, 1 mlM3646 // Monoclonal Rabbit Anti-Human MutS Protein Homolog 6, Clone EP49 // 0.2 ml, 1 mlM3647 // Monoclonal Rabbit Anti-Human Postmeiotic Segregration Increased 2, Clone EP51 // 0.2 ml, 1 mlM3649 // Monoclonal Mouse Anti-Human Octamer-Binding Transcription Factor 3 // 4, Clone N1NK // 0.2 ml, 1 mlM3651 // Monoclonal Rabbit Anti-Human Terminal Deoxynucleotidyl Transferase (TdT), Clone EP266 // 1 mlM3653// Monoclonal Mouse Anti-Human PD-L1 Clone 22C3//0.2 ml M3666// Monoclonal Mouse Anti-Human PD-L1, Clone 22C3/ 0.2 mLM7019 // Monoclonal Mouse Anti-Human Cytokeratin 20, Clone Ks20.8 // 0.2 ml, 1 mlM7020 // Monoclonal Mouse Anti-Vimentin, Clone Vim 3B4 // 1 mlM7191 // Monoclonal Mouse Anti-Human Placental Alkaline Phosphatase,Clone 8A9 // 0.2 ml, 1 mlM7235 // Monoclonal Mouse Anti-Human Grannzyme B, Clone GrB-7 // 1 ml M7237 // Monoclonal Mouse Anti-Human Cytokeratin 5 // 6, Clone D5 // 16 B4 // 0.2 ml, 1 mlM7240 // Monoclonal Mouse Anti-Human Ki-67 Antigen, Clone MIB-1 // 0.2 ml,1 mlM7271 // Monoclonal Mouse Anti-Human CD57, Clone TB01 // 0.2 mlM7310 // Monoclonal Mouse Anti-Human CD4, Clone 4B12 // 0.2 ml, 1 mlSK310 // Mouse anti-Human ER Antibody Cocktail // ER/PR pharmDx Kit (Link)// 12 mLSK310 // Mouse anti-Human PR Antibody // ER/PR pharmDx Kit (Link) // 12 mL SK310 // Negative Control Reagent // ER/PR pharmDx Kit (Link) // 12 mL 参考号码: SDS347本安全技术说明书责任人的e-mail地址:***************有关环境保护措施，请参阅第 12 节。

木犀草素对白血病K562

木犀草素对白血病K562/ADR细胞多药耐药的逆转作用及机制研究周欣宇1，李京敏2，张婷1，贾秀红1△摘要：目的探究木犀草素（Lut）对慢性髓系白血病K562/ADR细胞多药耐药性的逆转作用及其机制。

方法K562和K562/ADR细胞经不同浓度阿霉素（ADR）处理24h后，采用CCK-8实验检测K562/ADR细胞耐药倍数。

Lut 单独或联合ADR作用K562/ADR细胞24h后，采用CCK-8实验检测Lut的细胞毒性及对ADR的增敏作用。

取对数生长期K562/ADR细胞分为0μmol/L Lut组、2μmol/L Lut组、4μmol/L Lut组，采用流式细胞术检测细胞内ADR蓄积量的变化；RT-PCR法和Western blot法分别检测核因子E2相关因子2（Nrf2）、多药耐药相关蛋白1（MRP1）、P-糖蛋白（P-gp）、谷胱甘肽-S-转移酶pi（GST-pi）mRNA和蛋白的表达；谷胱甘肽（GSH）试剂盒检测细胞内GSH的含量。

结果与K562细胞相比，K562/ADR细胞株对ADR具有明显的耐药性，耐药倍数为53.69倍。

与0μmol/L Lut相比，不同浓度Lut作用于K562/ADR细胞后，细胞生长均受到不同程度的抑制（P＜0.05），其中2、4μmol/L Lut对K562/ ADR细胞的增殖抑制率＜10%，为无毒性的Lut浓度。

与0μmol/L Lut组相比，2、4μmol/L Lut组可明显增强ADR对K562/ADR的细胞增殖抑制率，增加细胞内ADR蓄积量，提高逆转耐药倍数，降低细胞内GSH含量，下调细胞中MRP1、P-gp、GST-pi、Nrf2mRNA及蛋白的表达（P＜0.05）；且4μmol/L Lut作用效果较2μmol/L Lut更显著。

结论Lut可抑制K562/ADR细胞增殖，逆转其对ADR的耐药性，其机制可能与Lut下调Nrf2、MRP1、P-gp、GST-pi表达，进而增加细胞内ADR蓄积量有关。

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AERA Symposium 65.065A Stakeholder Process for District-WideSystemic TransformationCharles M. Reigeluth, Indiana UniversityRoberto Joseph, Purdue UniversityKurt Richter, Indiana UniversityYun-Jo An, Indiana UniversityAn Overview of the Systemic Transformation ProjectCharles M. Reigeluth Instructional Systems Technology Department Indiana University School of EducationThe ProjectResearch on theSystemic Transformation Process MSD Decatur Township in Indianapolis Guidance System for Transforming EducationThe GSTEThe Big PictureCore Ideas (values about the change process) Process(phases, continuous events, principles)Core IdeasImportance of ….☐process vs. product☐mindset change☐stakeholder ownership☐leadership/political support☐participatory/developmental leadership☐a culture for change-collaboration, consensus, systems thinking, trust, disclosure, no blame ☐idealized design☐focusing on redesigning the learning experiences firstThe Revised GSTE ProcessI. Initiate an EffortII. Develop Starter TeamIII. Develop a District-Wide FrameworkIV. Create Ideal DesignsV. Implement and Evolve the New SystemThe Revised GSTE ProcessI. Initiate an Effort1.Facilitators assessed and enhanced their own readiness for theprocess and formed a Support Team at IU. (No change)2.Facilitators explored working with four school districts andestablished a relationship with one. (No change)3.Facilitators assessed and enhanced Decatur’s readiness. (Nochange from 3.1)4.Facilitators did not develop a contract for Phase II. (Old 3.2)The Revised GSTE ProcessII. Develop Starter Team5.Facilitators & superintendent formed the Starter Team (Nochange)6.ST designed and held a retreat to develop Starter Teamdynamic. (No change)7.Developed Starter Team understanding of the systemicchange process, systems design, dialogue, and small-group facilitation. (No change)(Continued)The Revised GSTE ProcessII. Develop Starter Team (Cont.)ed community forums to assess and enhance district andcommunity capacity and culture for change. (Old 4, 10, 11) 9.Did not develop a contract with the Starter Team and SchoolBoard for a systemic change process and funding, scope out resource needs, and plan a proposal for external funding.(New) –Not needed10.Starter Team partially developed a compact with allstakeholders to engage in a systemic change process; did not have a large public signing ceremony. (New)The Revised GSTE ProcessIII. Develop a District-Wide Framework11.Starter Team expanded into Leadership Team. (Old 13)12.Did not hold a retreat to develop the Leadership Team dynamic.(Old 13)13.Facilitators are developing Leadership Team understanding ofsystems, design, mental models, systemic change process,dialogue, and small-group facilitation. (Address throughoutEvents 14-15.) (Old 13)14.Leadership Team began to develop a district-wide frame-workwith broad stakeholder participation (community forums). This entailed identifying changes in the community’s educationalneeds. (Old 11, 17, 18)(Continued)The Revised GSTE ProcessIII. Develop a District-Wide Framework (Cont.)15.Leadership Team is finishing the district-wide framework withbroad stakeholder participation (community forums). Thisentails developing core values or beliefs for an ideal schoolsystem. (Old 11, 17, 18)16.Leadership Team identifies current and recent change effortsand decides what relation those should have with this effort.(Old 9)17.Leadership Team develops a change process strategy, includingdistrict office capacity building, leadership development, and budget, and gets funding for Phase IV. (New)The Revised GSTE ProcessIV. Create Ideal Designs18.Leadership Team forms and capacitates school-based DesignTeams and conducts workshops on the framework. (Old 19) 19.Design Teams create ideal designs for their schools andevaluation criteria with broad stakeholder input. (Old 20). 20.Leadership Team forms and capacitates a district-level DesignTeam. (New)21.District Design Team creates a design for ideal districtadministrative and governance systems, and criteria forevaluating that design, with broad stakeholder involvement.(Old 24).The Revised GSTE ProcessV. Implement and Evolve the New System22.Design Teams create building-level processes for evolving asclose as possible to their ideal designs. This includesidentifying existing programs and resources, and identifying gaps where they must design their own. (Old 25)23.Design Teams prepare for implementation with remodeling,equipment installation, resource procurement, teacher training, etc. (Old 26)24.Everyone carries out implementation plans, formativeevaluations, and revisions of the evolving designs and theimplementation processes. (Old 26)25.Periodically evolve the ideal designs (Old 26).Research Studies☐Events 1-3:Joseph, R., & Reigeluth, C.M. (submitted). Formative Research on the Initial Stage of the Systemic Change Process in a Small Urban School System. Journal of Educational Change.☐Events 5-7:Joseph, R., & Reigeluth, C.M. (in final preparation).Formative Research on Building a Starter Team for SystemicChange in a School District.☐Event 8:Rokopou, C., Hwang, J., & Reigeluth, C.M. (in progress).Community Forums: Their Value and Alternative Ways forEffective Planning and Conducting.☐Event 9:Richter, K., & Reigeluth, C.M. (in preparation).Formative Research on Identifying Competing Change Efforts for Systemic Change in a School District.Research Studies☐Event 11:Essex, C., & Reigeluth, C.M. (in progress). Formative Research on Expanding a Starter Team into a Leadership Team for Systemic Change in a School District.☐Events 13-15:Richter, K, & Reigeluth, C.M. (in progress).Formative Research on Integrating the Decision-Making Process and Learning Process in a Newly Formed Leadership Team forSystemic Change in a School District.☐Events 7 & 13:Pascoe, S.M., Sari, D., & Reigeluth, C.M. (in progress). Aspects and components of Mindset Change in theSystemic Transformation of a School District.Research Studies☐Joseph, R. (in progress). Formative Research on Student involvement in a Systemic Change Process in a SchoolDistrict.☐An, Y.J., & Reigeluth, C.M. (in progress). An Electronic Performance Support System (EPSS) for Systemic Change Efforts.☐Pascoe, S.M., & Reigeluth, C.M. (in progress). Formative Research on a Support Team for a facilitator of Systemic Transformation of a School District.Information about the Decatur Project: /~syschang/decatur/index.htmlCharles M. Reigeluthreigelut@Presenters☐Roberto Joseph, Purdue UniversityFormative Research on Student involvement in a Systemic Change Process in a School District.☐Kurt Richter, Indiana UniversityFormative Research on Integrating the Decision-MakingProcess and Learning Process in a Newly Formed Leadership Team for Systemic Change in a School District.☐Yun-Jo An, Indiana UniversityAn Electronic Performance Support System (EPSS) forSystemic Change Efforts.。