49,198 research outputs found
Ascorbic acid induces apoptosis in adult T-cell leukemia
No full textBackground: Adult T-cell leukemia (ATL) is an acute malignancy of activated T-cells caused by the human T-cell lymphotrophic virus type-1 (HTLV-1). Materials and Methods: The effects of non-cytotoxic concentrations of ascorbic acid (AA) were evaluated against HTLV-1 positive and negative cells. The effect of AA on apoptosis and proliferation was evaluated by cell cycle analysis. The role of p53, p21 Bax and Bcl-2α on cell cycle modulation and apoptosis was also assessed. The anti-proliferative effects were tested by determining the changes in the expression of transforming growth factors (TGF-α, TGF-β1 and TGF-β2). Results: Ascorbic acid was found to reduce the proliferation of cells and induce apoptosis by the modulation of p53, p21, Bcl-2 and Bax. Conclusion: The results of this study show the anti-proliferative effects of AA against leukemic cells.ALEXANDROW MG, 1995, CANCER RES, V55, P1452; Bazarbachi A, 1996, J ACQ IMMUN DEF SYND, V13, pS186, DOI 10.1097-00042560-199600001-00028; BISSELL MJ, 1980, P NATL ACAD SCI-BIOL, V77, P2711, DOI 10.1073-pnas.77.5.2711; BLAKESLEE JR, 1985, CANCER RES, V45, P3471; Cameron E., 1979, CANC VITAMIN C, P132; CAMERON E, 1973, ONCOLOGY-BASEL, V27, P181; Carlisle DL, 2000, TOXICOL SCI, V55, P60, DOI 10.1093-toxsci-55.1.60; Carr A, 1999, FASEB J, V13, P1007; Casciari JJ, 2001, BRIT J CANCER, V84, P1544, DOI 10.1054-bjoc.2001.1814; Douglas RM, 1998, COCHRANE DB SYST REV, DOI [10.1002-14651858.CD000980, DOI 10.1002-14651858.CD000980]; Dunker N, 2002, GASTROENTEROLOGY, V122, P1364, DOI 10.1053-gast.2002.32991; El-Sabban ME, 2000, BLOOD, V96, P2849; FOLEY GE, 1965, CANCER, V18, P522, DOI 10.1002-1097-0142(196504)18:4522::AID-CNCR28201804183.0.CO;2-J; Gackowski D, 2002, INT J CANCER, V101, P395, DOI 10.1002-ijc.10610; Groninger E, 2002, INT J ONCOL, V21, P1339; Harakeh S, 2004, CHEM-BIOL INTERACT, V148, P101, DOI 10.1016-j.cbi.2004.05.002; Harakeh S, 1995, NUTRITION, V11, P684; HARAKEH S, 1990, P NATL ACAD SCI USA, V87, P7245, DOI 10.1073-pnas.87.18.7245; Harakeh S, 1997, AIDS RES HUM RETROV, V13, P235, DOI 10.1089-aid.1997.13.235; HARAKEH S, 1994, CHEM-BIOL INTERACT, V91, P207, DOI 10.1016-0009-2797(94)90041-8; HARAKEH S, 1991, AM J CLIN NUTR, V54, pS1231; Harakeh Steve, 1994, Journal of Nutritional Medicine, V4, P393, DOI 10.3109-13590849409003588; Jamison JM, 2004, BIOCHEM PHARMACOL, V67, P337, DOI 10.1016-j.bcp.2003.08.040; Kanai M, 2001, GASTROENTEROLOGY, V121, P56, DOI 10.1053-gast.2001.25544; KAZAKOV SA, 1988, NATURE, V335, P186, DOI 10.1038-335186a0; LIEHR JG, 1991, AM J CLIN NUTR, V54, pS1256; Martin A, 1997, ARTERIOSCL THROM VAS, V17, P1583; MEDINA MA, 1994, BIOCHEM MOL BIOL INT, V34, P871; MORTENSEON MM, 1986, J SURG RES, V114, P302; MURATA A, 1976, J NUTR SCI VITAMINOL, V22, P347; MURATA A, 1973, AGR BIOL CHEM TOKYO, V37, P1145; NAIDU A.K., 2003, NUTR J, V2, P7; PAGANELLI GM, 1992, J NATL CANCER I, V84, P47, DOI 10.1093-jnci-84.1.47; PAVELIC K, 1985, BRAIN RES, V342, P369, DOI 10.1016-0006-8993(85)91139-4; Reddy VG, 2001, BIOCHEM BIOPH RES CO, V282, P409, DOI 10.1006-bbrc.2001.4593; SCHWARZ RI, 1991, AM J CLIN NUTR, V54, pS1247; Van Orden K, 1999, J BIOL CHEM, V274, P26321, DOI 10.1074-jbc.274.37.26321; WAHL SM, 1992, J CLIN IMMUNOL, V12, P61, DOI 10.1007-BF00918135; Wang DG, 2002, ONCOGENE, V21, P2785, DOI 10.1038-sj-onc-120537515141
Resistance of Brucella abortus isolated from Lebanese dairy-based food products against commonly used antimicrobials
No full textConsidering the marked importance of Brucella organisms as food-borne pathogens and the lack of published literature on the evaluation of the microbiological quality of dairy-based food products in the Middle East, this study was performed to address this gap. The main aim of the present study was to assess the antimicrobial resistance patterns of Brucella isolates recovered from a total of 164 cultured samples of Lebanese dairy-based food products (Baladi cheese, Shankleesh and Kishk). Standard polymerase chain reaction (PCR) was used to stereotype colonies previously confirmed by biochemical tests to be Brucella strains and to distinguish between the RB51 vaccine and field Brucella strains. Real-time PCR was applied to differentiate among the various Brucella species. Confirmed PCR field Brucella abortus isolates were evaluated for their susceptibility to eight commonly used antimicrobials. The highest number of resistant B. abortus isolates (n = 4 out of 6) was shown against Streptomycin and Ciprofloxacin, whereas 3 out of 6 isolates tested were resistant to Gentamicin. A lower number of resistant isolates were noted against Rifampicin, Tetracycline and Trimethoprim-sulfamethoxazole (n = 2 out of 6) and the lowest number for Doxycycline and Ceftriaxone (n = 1 out of 6). Such results are alarming and reflect the significance and importance of implementing more strict hygiene standards and regulations to reduce food-borne illnesses and control the excessive use of antimicrobials in this region. © INRA, EDP Sciences, 2010.Al Dahouk Sascha, 2003, Clin Lab, V49, P487; ANON JB, 1995, COMMUN DIS REP CDR W, V5, P151; Bricker BJ, 2002, VET MICROBIOL, V90, P435, DOI 10.1016-S0378-1135(02)00228-6; BRICKER BJ, 1994, J CLIN MICROBIOL, V32, P2660; Centers for Disease Control and Prevention, 2001, BAS LAB PROT PRES ID; DEBUYSER M, 2004, INT J FOOD MICROBIOL, V67, P1; DIANA MP, 2007, INFECT IMMUN, V75, P379; Downes F. P., 2001, COMPENDIUM METHODS M; FERNANDO AM, 2009, J BACTERIOL, V191, P2530; Gilbert R J, 2000, Commun Dis Public Health, V3, P163; HARAKEH S, 2009, SCI TOTAL ENVIRON, V408, P4022; Harakeh S, 2006, ENVIRON POLLUT, V143, P269, DOI 10.1016-j.envpol.2005.11.027; Hayes MC, 2001, J DAIRY SCI, V84, P292; Horwitz W, 2000, OFFICIAL METHODS ANA; LEALKLEVEZAS DS, 1995, J CLIN MICROBIOL, V33, P3087; *NAT COMM CLIN LAB, 2004, M2A6 NCCLS; OuahraniBettache S, 1996, J APPL BACTERIOL, V81, P154, DOI 10.1111-j.1365-2672.1996.tb04493.x; Redkar R, 2001, MOL CELL PROBE, V15, P43, DOI 10.1006-mcpr.2000.0338; Saleh I, 2009, ANN TROP MED PARASIT, V103, P39, DOI 10.1179-136485909X384965; Schelling E, 2003, PREV VET MED, V61, P279, DOI 10.1016-j.prevetmed.2003.08.004; Tantillo G, 2001, J FOOD PROTECT, V64, P164; Thakur S. D., 2002, Journal of Communicable Diseases, V34, P287; Vemulapalli R, 1999, CLIN DIAGN LAB IMMUN, V6, P760; WALLACH JC, 1998, FEMS IMMUNOL MED MIC, V19, P31511
Antimicrobial resistance of Listeria monocytogenes isolated from dairy-based food products
No full textIn this study Listeria monocytogenes (L. monocytogenes) was isolated from three traditionally consumed Lebanese dairy-based food products. One hundred and sixty four samples (45 samples of Baladi cheese, 36 samples of Shankleesh and 83 of Kishk) were collected from the Bekaa Valley in the Northeast region of Lebanon. Suspected Listeria colonies were selected and initially identified by using standard biochemical tests. Initial identification of the positive L. monocytogenes colonies was confirmed at the molecular level by Polymerase Chain Reaction (n = 30) and the confirmed isolates were evaluated for their susceptibility to 10 commonly used antimicrobials. All of the 30 isolates were confirmed to be L. monocytogenes yielding a PCR product of ∼ 660 base pairs (bp). L. monocytogenes was detected in 26.67percent, 13.89percent and 7.23percent of the Baladi cheese, Shankleesh and Kishk samples, respectively. The highest resistance in L. monocytogenes isolates was noted against oxacillin (93.33percent) followed by penicillin (90percent). The results provide an indication of the contamination levels of dairy-based foods in Lebanon and highlight the emergence of multi-drug resistant Listeria in the environment. © 2009 Elsevier B.V. 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Informetrics on M. N. Srinivas
Get PDFM. N. Srinivas, the well known sociologist is widely recognised as architect of modern Indian sociology and social anthropology. His publications have been analysed by year, domain, authorship pattern, channels of communication used. Keywords, etc. The results indicate that the papers published by him are of a nature that qualify him to be a 'role model' for the younger generations to emulate.
By the end of 1995, Srinivas had to his credit 144 papers which, included 33 broad papers in sociology and anthropology; 18 papers in social change; 28 papers in village studies; 12 papers on religion; 17 papers on caste and 36 papers of general popular interest. The periods 1958-61 and 1974-77, when Srinivas was 38-41 and 58-61 years old. were his most productive periods with highest publication activity
Adsorption of atomic hydrogen at a nanostructured electrode of polyacrylate-capped Pt nanoparticles in polyelectrolyte
No full textAtomic hydrogen electrosorption is reported at crystallite sites of polyacrylate-capped Pt nanoparticles (〈d〉) = 2.5 ± 0.6 nm), by assembling nanostructured electrodes of polyacrylate-Pt nanocrystallites layer-by-layer in a cationic polyelectrolyte, poly(diallyldimethylammonium chloride). Cyclic voltammetry in 1 M H2 SO4 revealed a strongly adsorbed hydrogen state and a weakly adsorbed hydrogen state assigned to adsorption at (100) and (110) sites of the modified nanocrystallites, respectively. Resolving hydrogen adsorption states signifies that surface capping by the carboxylate groups is not irreversibly blocking hydrogen adsorption sites at the modified Pt nanoparticle surface. Adsorption peak currents increased with increasing the number of layers up to 16 bilayers, indicating the feasibility of nanoparticle charging via interparticle charge hopping and the accessibility of adsorption states within the thickness of the nanoparticle-polyelectrolyte multilayers. Despite similarity in hydrogen adsorption in the cyclic voltammorgrams in 1 M H2SO4, negative shifts in adsorption potentials were measured at the nanocrystallite Pt-polyelectrolyte multilayers relative to a polycrystalline bulk Pt surface. This potential shift is attributed to a kinetic limitation in the reductive hydrogen adsorption as a result of the Pt nanoparticle surface modification and the polyelectrolyte environment. © 2005 American Chemical Society.Ahmadi TS, 1996, SCIENCE, V272, P1924, DOI 10.1126-science.272.5270.1924; Ahmadi TS, 1996, CHEM MATER, V8, P1161, DOI 10.1021-cm9601190; Barreira SVP, 2004, J PHYS CHEM B, V108, P17973, DOI 10.1021-jp0466845; Antipov AA, 2003, LANGMUIR, V19, P2444, DOI 10.1021-la026101n; BARD AJ, 2001, ELECTROCHEMICAL METH, pCH13; CLAVILIER J, 1988, ACS SYM SER, V378, P202; COCCO G, 1994, J MOL CATAL, V94, P299, DOI 10.1016-1381-1169(94)00130-8; DUARTE MY, 1980, ELECTROCHIM ACTA, V25, P1613, DOI 10.1016-0013-4686(80)80014-4; Eppler AS, 1997, J PHYS CHEM B, V101, P9973, DOI 10.1021-jp972818l; Farhat TR, 2003, J AM CHEM SOC, V125, P4627, DOI 10.1021-ja021448y; Farhat TR, 2001, LANGMUIR, V17, P1184, DOI 10.1021-la001298+; Ghannoum S, 2003, LANGMUIR, V19, P4804, DOI 10.1021-la0209839; Gomez R, 2004, J PHYS CHEM B, V108, P228, DOI 10.1021-jp034982g; Han S, 1999, ELECTROCHIM ACTA, V45, P845, DOI 10.1016-S0013-4686(99)00295-9; Harris JJ, 2000, LANGMUIR, V16, P2006, DOI 10.1021-la990620h; KINOSHITA K, 1978, ELECTROCHIM ACTA, V23, P45, DOI 10.1016-0013-4686(78)87032-7; KITA H, 1990, J ELECTROANAL CHEM, V295, P317, DOI 10.1016-0022-0728(90)85025-Z; Krasemann L, 2000, LANGMUIR, V16, P287, DOI 10.1021-1a991240z; Lebedev K, 2000, LANGMUIR, V16, P9941, DOI 10.1021-la0006420; Li Y, 2002, LANGMUIR, V18, P4921, DOI 10.1021-la011469q; Li Y, 2000, ORG LETT, V2, P2385, DOI 10.1021-ol0061687; Liu ZL, 2004, J PHYS CHEM B, V108, P8234, DOI 10.1021-jp049422b; MARKARIAN MZ, 2004, MATER RES SOC S P, V882, DOI UNSP S8.8-S8-S8.13; Markovic N. M., 2003, CATALYSIS ELECTROCAT; MARKOVIC NM, 1995, J PHYS CHEM-US, V99, P3411, DOI 10.1021-j100011a001; OTEROSCHIPPER PH, 1977, J CATAL, V50, P494, DOI 10.1016-0021-9517(77)90061-6; Pardo-Yissar V, 2001, LANGMUIR, V17, P1110, DOI 10.1021-la000729l; PETROVSKI JM, 1998, J PHYS CHEM B, V102, P331; Rmaile HH, 2003, J PHYS CHEM B, V107, P14401, DOI 10.1021-jp035921l; Thomas JM, 2003, ACCOUNTS CHEM RES, V36, P20, DOI 10.1021-ar990017q; TOSHIMA N, 1993, J CHEM SOC FARADAY T, V89, P2537, DOI 10.1039-ft9938902537; WILL FG, 1965, J ELECTROCHEM SOC, V112, P451, DOI 10.1149-1.2423567; YE S, 1992, J ELECTROANAL CHEM, V333, P299, DOI 10.1016-0022-0728(92)80398-N; Yoo JW, 2002, J PHYS CHEM A, V106, P2049, DOI 10.1021-jp012131829262
Enhanced conversion of light at TiO2 photonic crystals to the blue of a stop band and at TiO2 random films sensitized with Q-CdS: Order and disorder
No full textSignificant enhancements in the conversion of light to current were observed at the blue edge of TiO2 inverse opals (i-TiO2-o) and at highly disordered TiO2 films (i-TiO2-d) sensitized with Q-CdS in sulfide electrolyte. i-TiO2-o with stop bands centered at 390 and 450 nm were modified with mercaptopropionic acid-Q-CdS with absorption edges tuned to the red or to the blue of the stop-band edges. A 4.7 average enhancement factor was measured at the blue edge of the stop band when it coincided with low Q-CdS absorption, while a 1.4-1.8 average gain was measured at the red edge. The blue-edge gain can be ascribed to localized or slowed light in the low refractive index medium and was found to extend 30-70 nm to the blue of the stop-band center. Light localization effects were suppressed when the stop-band edges overlapped with appreciable absorption. A highly disordered TiO2 film fabricated by replicating a template from 150, 190, and 243 nm diameter polystyrene spheres exhibited a similar gain per adsorbed Q-CdS in the same spectral window as the blue edge of the photonic crystal when quantum dot absorption was low. This gain is ascribed to slowed light resulting from the interference of multiple internal scattering events in the disordered medium. © 2010 American Chemical Society.Albada M. P. 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Epigallocatechin-3-gallate induces apoptosis and cell cycle arrest in HTLV-1-positive and -negative leukemia cells
No full textThe objective of this study is to evaluate the efficacy of epigallocatechin gallate against ATL cells. The anti-proliferative and pro-apoptotic effects of EGCG were evaluated in HTLV-1-positive and -negative cells. EGCG exhibited a marked decrease in proliferation of ATL cells at 96 h of treatment. The results indicated that TGF-α was down-regulated whereas levels of TGF-β2 increased. Cell cycle distribution analysis revealed an increase in cells in the pre-G1 phase which was confirmed by ELISA. The results on proteins showed an up-regulation of p53, Bax and p21 protein levels while the levels of Bcl-2α were down-regulated. © 2007 Humana Press Inc.Ahmad N, 2000, ARCH BIOCHEM BIOPHYS, V376, P338, DOI 10.1006-abbi.2000.1742; Arnulf B, 2002, BLOOD, V100, P4129, DOI 10.1182-blood-2001-12-0372; BAZARBACHI A, 1996, J ACQ IMMUN DEF R S1, V13, P5186; Cerwenka A, 1996, J IMMUNOL, V156, P459; Chen WJ, 1998, J EXP MED, V188, P1849, DOI 10.1084-jem.188.10.1849; Dotto G P, 2000, BIOCHIM BIOPHYS ACTA, V1471, pM43; Dupont S, 2004, CANCER LETT, V213, P129, DOI 10.1016-j.canlet.2004.06.008; Erba D, 1999, J NUTR, V129, P2130; Fujiki H, 1998, MUTAT RES-FUND MOL M, V402, P307, DOI 10.1016-S0027-5107(97)00310-2; GESSAIN A, 1996, HUMAN T CELL LYMPHOT, P33; Gupta S, 2000, TOXICOL APPL PHARM, V164, P82, DOI 10.1006-taap.1999.8885; Gupta S, 2003, ARCH BIOCHEM BIOPHYS, V410, P177, DOI 10.1016-S0003-9861(02)00668-9; Hare Y, 2001, GREEN TEA HLTH BENEF; Haupt S, 2004, SEMIN CANCER BIOL, V14, P244, DOI 10.1016-j.semcancer.2004.04.003; Hayakawa S, 2001, BIOCHEM BIOPH RES CO, V285, P1102, DOI 10.1006-bbrc.2001.5293; Heiser D, 2004, EXP GERONTOL, V39, P1125, DOI 10.1016-j.exger.2004.04.011; HERMINE O, 1995, NEW ENGL J MED, V332, P1749, DOI 10.1056-NEJM199506293322604; HINUMA Y, 1985, PNAS, V66, P1371; Hsu TC, 2001, CANCER GENET CYTOGEN, V124, P169, DOI 10.1016-S0165-4608(00)00337-X; Inman GJ, 2000, J IMMUNOL, V165, P2500; Javelaud D, 2004, INT J BIOCHEM CELL B, V36, P1161, DOI 10.1016-S1357-2725(03)00255-3; Kanai M, 2001, GASTROENTEROLOGY, V121, P56, DOI 10.1053-gast.2001.25544; KAPLAN JE, 1993, REV MED VIROL, V3, P137, DOI 10.1002-rmv.1980030304; Kawai K, 2003, J ALLERGY CLIN IMMUN, V112, P951, DOI [10.1067-mai.2003.1756, 10.1016-S0091-6749(03)02007-4]; Kuo PL, 2003, J BIOMED SCI, V10, P219, DOI 10.1159-000068711; Lee DK, 2002, J BIOL CHEM, V277, P38557, DOI 10.1074-jbc.M206786200; Letterio JJ, 1998, ANNU REV IMMUNOL, V16, P137, DOI 10.1146-annurev.immunol.16.1.137; Li HC, 2000, JPN J CANCER RES, V91, P34; Lozano G, 2005, J PATHOL, V205, P206, DOI 10.1002-path.1704; Lu X, 2005, CURR OPIN GENET DEV, V15, P27, DOI 10.1016-j.gde.2004.12.008; Macchi B, 1997, J GEN VIROL, V78, P1007; May P, 1999, ONCOGENE, V18, P7621, DOI 10.1038-sj.onc.1203285; Meek DW, 2004, DNA REPAIR, V3, P1049, DOI 10.1016-j.dnarep.2004.03.027; Mitscher LA, 1997, MED RES REV, V17, P327, DOI 10.1002-(SICI)1098-1128(199707)17:4327::AID-MED23.0.CO;2-Y; Nihal M, 2005, INT J CANCER, V114, P513, DOI 10.1002-ijc.20785; Otsuka T, 1998, LIFE SCI, V63, P1397, DOI 10.1016-S0024-3205(98)00406-8; Patil S, 2000, J BIOL CHEM, V275, P38363, DOI 10.1074-jbc.M004861200; Pavletich NP, 1999, J MOL BIOL, V287, P821, DOI 10.1006-jmbi.1999.2640; Roomi MW, 2005, IN VIVO, V19, P179; Roomi MW, 2005, MED ONCOL, V22, P129, DOI 10.1385-MO:22:2:129; Roomi MW, 2005, ONCOL REP, V13, P253; Roy M, 2003, MUTAT RES-FUND MOL M, V523, P33, DOI 10.1016-S0027-5107(02)00319-6; SAEKI K, 2000, J BIOL CHEM, V272, P3; Sanchez-Capelo A, 2005, CYTOKINE GROWTH F R, V16, P15, DOI 10.1016-j.cytogtf.2004.11.002; Szeto YT, 2002, FREE RADICAL RES, V36, P113, DOI 10.1080-10715760290001227; Wang YC, 2002, AMINO ACIDS, V22, P131, DOI 10.1007-s007260200002; Wolfraim LA, 2004, J IMMUNOL, V173, P3093; Yang CS, 2004, J NUTR, V134, p3181S; Yang CS, 1998, EXP LUNG RES, V24, P629; Zhang J, 2001, VIRUS RES, V78, P67, DOI 10.1016-S0168-1702(01)00285-422242
Inhibition of proliferation and induction of apoptosis by 2-benzoyl-3-phenyl-6,7-dichloroquinoxaline 1,4-dioxide in adult T-cell leukemia cells
No full textHuman T-cell lymphotrophic virus type-1 (HTLV-1) is a retrovirus which causes adult T-cell leukemia (ATL), an aggressive malignancy of activated T-cells. So far, there is no proven therapy for this disease. The compound 2-benzoyl-3-phenyl-6,7-dichloro quinoxaline 1,4-dioxide (DCQ) has been shown to exhibit a wide range of antibacterial activities and to induce antiproliferation and apoptosis of human colon cancer cell lines. In the present study, we investigated the in vitro effects of DCQ in HTLV-1 positive (C91-PL and HuT-102) and negative (CEM and Jurkat) malignant T-cells. The results indicate that DCQ induced growth inhibition in all four cell lines examined in a dose-dependent manner. The inhibitory effect was mainly due to the induction of apoptosis which was verified by flow cytometry analyses and ELISA-based apoptosis assays. The role of transforming growth factor (TGF) in mediating the antiproliferative and apoptotic effects of DCQ in ATL cells was investigated. Interestingly, in three of the four cell lines used, DCQ increased the TGF-β1 transcript levels and decreased TGF-α mRNA, but did not induce changes in TGF-β2 expression. DCQ treatment also induced an upregulation of p53 and p21 protein levels, key mediators of cell cycle arrest and apoptosis. The anti-apoptotic Bcl-2α protein level was found to be reduced. These findings indicate that DCQ inhibits the growth of ATL cell lines, at least in part, by inducing apoptosis mediated by the modulation of TGF expression, the upregulation in p53 and p21 proteins and downregulation in Bcl-2α expression. The present findings suggest that DCQ merits further investigation as a potential therapeutic agent for this incurable disease. © 2004 Elsevier Ireland Ltd. All rights reserved.ALEXANDROW MG, 1995, CANCER RES, V55, P1452; Ashcroft M, 1999, MOL CELL BIOL, V19, P1751; Bazarbachi A, 1999, BLOOD, V93, P278; Bazarbachi A, 1996, J ACQ IMMUN DEF SYND, V13, pS186, DOI 10.1097-00042560-199600001-00028; BRADY J, 1987, J VIROL, V61, P2175; Bunz F, 1999, J CLIN INVEST, V104, P263, DOI 10.1172-JCI6863; Carta A, 2002, EUR J MED CHEM, V37, P355, DOI 10.1016-S0223-5234(02)01346-6; Colgin MA, 1998, J VIROL, V72, P9396; CROSS SL, 1987, CELL, V49, P47, DOI 10.1016-0092-8674(87)90754-9; DEMARTIN R, 1987, EMBO J, V6, P3673; Diab-Assef M, 2002, MOL CARCINOGEN, V33, P198, DOI 10.1002-mc.10036; DIRLAM JP, 1979, J MED CHEM, V22, P1118, DOI 10.1021-jm00195a022; Dunker N, 2002, GASTROENTEROLOGY, V122, P1364, DOI 10.1053-gast.2002.32991; El-Sabban ME, 2000, BLOOD, V96, P2849; FOLEY GE, 1965, CANCER, V18, P522, DOI 10.1002-1097-0142(196504)18:4522::AID-CNCR28201804183.0.CO;2-J; FUJII M, 1988, P NATL ACAD SCI USA, V85, P8526, DOI 10.1073-pnas.85.22.8526; Gali-Muhtasib H, 2004, INT J ONCOL, V24, P1121; Gali-Muhtasib HU, 2001, ONCOL REP, V8, P679; Gessain A., 1996, HUMAN T CELL LYMPHOT, P33; GREEN PL, 1994, RETROVIRIDAE, V3, P227; HADDADIN MJ, 1993, HETEROCYCLES, V35, P1503; HINUMA Y, 1982, INT J CANCER, V29, P631, DOI 10.1002-ijc.2910290606; Hollsberg P, 1999, MICROBIOL MOL BIOL R, V63, P308; HOSKIN BD, 1972, VET REC, V90, P396; INOUE J, 1986, EMBO J, V5, P2883; Jin DY, 1999, J BIOL CHEM, V274, P17402, DOI 10.1074-jbc.274.25.17402; Kanai M, 2001, GASTROENTEROLOGY, V121, P56, DOI 10.1053-gast.2001.25544; Kaplan JE, 1996, J ACQ IMMUN DEF SYND, V12, P193; KEHRL JH, 1986, J EXP MED, V163, P1037, DOI 10.1084-jem.163.5.1037; Low KG, 1997, J VIROL, V71, P1956; MARUYAMA M, 1987, CELL, V48, P343, DOI 10.1016-0092-8674(87)90437-5; MIYATAKE S, 1988, MOL CELL BIOL, V8, P5581; MIYOSHI I, 1980, GANN, V71, P155; Mortenson M.M., 2003, J SURG RES, V114, P302, DOI 10.1016-j.jss.2003.08.103; NAGATA K, 1989, J VIROL, V63, P3220; OHTANI K, 1989, NUCLEIC ACIDS RES, V17, P1589, DOI 10.1093-nar-17.4.1589; SCHONFELDER D, 1988, PHARMAZIE, V43, P837; SEIKI M, 1986, EMBO J, V5, P561; SHIMOYAMA M, 1992, GANN MONOGRAPH CANCE, V39, P43; SIEKEVITZ M, 1987, P NATL ACAD SCI USA, V84, P5389, DOI 10.1073-pnas.84.15.5389; SUTTER W, 1978, ANTIMICROB AGENTS CH, V13, P770; Takabatake T, 1996, YAKUGAKU ZASSHI, V116, P491; Tsukasaki K, 1997, BLOOD, V89, P948; Van Orden K, 1999, J BIOL CHEM, V274, P26321, DOI 10.1074-jbc.274.37.26321; WAHL SM, 1992, J CLIN IMMUNOL, V12, P61, DOI 10.1007-BF00918135; Wang DG, 2002, ONCOGENE, V21, P2785, DOI 10.1038-sj-onc-1205375; WANO Y, 1988, P NATL ACAD SCI USA, V85, P9733, DOI 10.1073-pnas.85.24.973314151
Experimental investigation into the effect of substrate clamping on the piezoelectric behaviour of thick-film PZT elements
No full textThis paper details an experimental investigation of the clamping effect associated with thick-film piezoelectric elements printed on a substrate. The clamping effect reduces the measured piezoelectric coefficient, d33, of the film. This reduction is due to the influence of the d31 component in the film when a deformation of the structure occurs, by either the direct or indirect piezoelectric effect. Theoretical analysis shows a reduction in the measured d33 of 62%, i.e. a standard bulk lead zirconate titanate (PZT)-5H sample with a manufacturer specified d33 of 593pC/N would fall to 227.8pC/N. To confirm this effect, the d33 coefficients of five thin bulk PZT-5H samples of 220µm thickness were measured before and after their attachment to a metallized 96% alumina substrate. The experimental results show a reduction in d33 of 74% from 529pC/N to 139pC/N. The theoretical analysis was then applied to existing University of Southampton thick-film devices. It is estimated that the measured d33 value of 131pC/N of the thick-film devices is the equivalent of an unconstrained d33 of 345pC/N
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