770 research outputs found
A little known source of Saljuq history: ?asan-ı Yazd?’s J?mi’at-Taw?r?kh-i ?asan?
No full textUrl: http://usad.selcuk.edu.tr/usad/article/view/76Bu çalışma, Timurlu dönemi müellifi Hasan-ı Yezdî’nin Câmi‘u’t-tevârîh-i Hasenî isimli Farsça eserinin Selçuklular kısmının; tanıtımı ve değerlendirmesini ihtiva etmektedir. Müellifin hayatı ve eserlerine değinildikten sonra, eserin muhtevası, önemi ve kaynaklarından bahsedilmiş, eserin Selçuklular kısmının kaynak değeri ortaya konulmuş, ayrıca eserin dil ve imlâ hususiyetleri, nüshaları incelenmiş ve eser üzerinde yapılan çalışmaların bir değerlendirmesi yapılmıştır. Tam adı Tâcu’d-dîn Hasan b. Şihâb b. Huseyn-i Yezdî olan müellif takriben 793/1390-91 yılında doğmuş, Timurlular’dan Mîrzâ İskender b. ‘Omer Şeyh ve Mîrzâ Sultan Ebu’l-Muzaffer Muhammed Bahadır b. Baysungur’un hizmetinde bulunmuştur. Müellif Câmi‘u’t-tevârîh-i Hasenî isimli eserini telife Timurlular’dan Mîrzâ Sultan Ebu’l-Muzaffer Muhammed b. Baysungur b. Şâhruh adına 855/1451 yılında başlamışsa da, onun 855 yılı Zî’l-hicce ayında (25 Aralık 1451-22 Ocak 1452) kardeşi Ebu’l-Muzaffer Babür b. Baysungur tarafından öldürülmesi üzerine eserini Ebu’l-Muzaffer Babür b. Baysungur’a ithaf etmiştir. Müellifin hayatının bundan sonraki bölümü ve ölüm tarihi hakkında kaynaklarda herhangi bir bilgi yoktur. Câmi‘u’t-tevârîh-i Hasenî, başlangıçtan müellifin kendi zamanına kadar gelen genel bir İslâm tarihidir. Câmi?u’t-tevârîh-i Hasenî, Selçuklular ve özellikle de Sultan Sencer devri için en tafsilatlı kaynaklardan birisidir. Eserin Selçuklu tarihi için asıl önemi, müellifin, başta Sencer-nâme (veya Rezm-nâme-yi Sencerî ya da Rûz-nâme-yi Sencerî) olmak üzere, günümüze ulaşmayan bazı kaynaklardan sık sık alıntılar yapmış olmasından gelmektedir. Câmi?u’t-tevârîh-i Hasenî’nin iki yazma nüshası günümüze ulaşmıştır: 1. İran Millî Kütüphanesi (Kit?bkh?na-yi Mill?-yi ?r?n, Tahran), nr. 1330. 2. Süleymaniye Kütüphanesi (İstanbul), Fatih 4307.The present work, consisting of an introduction and two main parts, is an analytical study of the chapter on the Saljuqs in the Persian chronicle titled J?mi? at-taw?r?kh-i ?asan? (?asan?’s Compendium of Chronicles) by a Timurid author, ?asan-i Yazd?. After addressing the life and works of the author, the contents of his chronicle, its importance, and its sources (as far as they are mentioned in the text), the introduction discusses the significance of this chapter as a source on the Saljuqs. In addition, this study details linguistic and stylistic features of the text and provides in-depth analysis of its extant copies and an evaluation of its previous studies. T?j ad-D?n ?asan b. Shih?b b. ?usayn-i Yazd? was born around 793/1390-91. He served two Timurid rulers, M?rz? Iskandar b. ?Umar Shaykh and M?rz? Sul??n Mu?ammad Bah?dir b. Baysungur. The author started writing this book in 855/1451 at the order of the Timurid M?rz? Sul??n Mu?ammad b. Baysungur. In Dhu’l-?ijja 855 (25 December 1451-22 January 1452) Mu?ammad b. Baysungur was killed by his brother B?bur. The author then dedicated this work to Babur b. Baysungur. No further information exists in the sources about the author’s life thereafter or the date of his death. J?mi? at-taw?r?kh-i ?asan? can be considered a general history of Islam from its very beginning until the time of its author. This work is one of the most extensive sources on the Saljuqs, particularly about the reign of Sultan Sanjar. For this reason it deserves to be taken into account on the Seljuq historiography. The author had access to Sanjar-n?ma (or Razm-n?ma-yi Sanjar? - R?z-n?ma-yi Sanjar?). He recurrently quotes from this and some other sources that are not extant. Two copies of J?mi? at-taw?r?kh-i ?asan? have survived to our time: 1.MS. Tehran, Iran Library (Kit?bkh?na-yi Mill?-yi ?r?n), 1330. 2. MS. Istanbul, Süleymaniye Library, Fatih 4307
Delta(3)-1,3,4-oxadiazolines: Photochemical precursors to diazoalkanes and sec-alkanediazonium ions in acidic solution
No full textPT: J; CR: ADAM W, 1990, TETRAHEDRON LETT, V31, P863 ALBERY WJ, 1972, J CHEM SOC P2, P2206 BELL RP, 1973, PROTON CHEM BROSCH D, 1991, J ORG CHEM, V56, P907 BROSCH D, 1993, J ORG CHEM, V58, P1118 BROWN HC, 1957, TETRAHEDRON, V1, P214 BROWN HC, 1957, TETRAHEDRON, V1, P221 BUNSE M, 1993, CHEM BER, V126, P1499 CHIANG Y, 1995, J AM CHEM SOC, V117, P9165 CHIANG Y, 1996, J AM CHEM SOC, V118, P4366 COLLINS CJ, 1971, ACCOUNTS CHEM RES, V4, P315 FINNEMAN JI, 1993, J AM CHEM SOC, V115, P3016 FINNEMAN JI, 1994, J ORG CHEM, V59, P6251 FINNEMAN JI, 1995, J AM CHEM SOC, V117, P4228 GOLD B, 1984, J AM CHEM SOC, V106, P2072 HO J, 1994, J AM CHEM SOC, V116, P6611 HOVINEN J, 1992, J AM CHEM SOC, V114, P10321 HUISGEN R, 1955, ANGEW CEHM, V67, P273 IZUTSU K, 1990, IUPAC CHEM DATA SERI, V35 KAZANIS S, 1991, J PHYS CHEM-US, V95, P4430 KIRMSE W, 1976, ANGEW CHEM INT EDIT, V15, P251 KRESGE AJ, 1973, CHEM SOC REV, V2, P475 KRESGE AJ, 1975, PROTON TRANSFER REAC, CH7 KRESGE AJ, 1986, J ORG CHEM, V51, P819 KRESGE AJ, 1986, J ORG CHEM, V51, P822 LAALI K, 1986, REV CHEM INTERMED, V6, P237 LARSON JW, 1987, J AM CHEM SOC, V109, P6230 LAWSON T, 1988, CARCINOGENESIS, V9, P1007 LEUNG KH, 1984, CHEM-BIOL INTERACT, V48, P169 LIBERATO DJ, 1989, CHEM RES TOXICOL, V2, P307 LIJINSKY W, 1992, CHEM BIOL N NITROSO MAJCHRZAK MW, 1989, J ORG CHEM, V54, P1842 MARCUS RA, 1968, J PHYS CHEM-US, V72, P891 MCGARRITY JF, 1980, J AM CHEM SOC, V102, P7303 MOSS RA, 1974, ACCOUNTS CHEM RES, V7, P421 MURRAY CJ, 1990, J AM CHEM SOC, V112, P1880 OFERRALL RAM, 1967, ADV PHYS ORG CHEM, V5, P331 WAGNER BD, UNPUB WASHABAUGH MW, 1988, BIOCHEMISTRY-US, V27, P5044 WASHABAUGH MW, 1989, J AM CHEM SOC, V111, P674 WHITTAKER D, 1978, CHEM DIAZONIUM DIAZO, P617 YOUNG JC, 1975, CAN J CHEM, V53, P2530 ZOLLINGER H, 1995, DIAZO CHEM, V1; NR: 43; TC: 11; J9: J AMER CHEM SOC; PG: 2; GA: WJ097Source type: Electronic(1
Radiation-induced root surface caries restored with glass-ionomer cement placed in conventional and ART cavity preparations: Results at two years
Get PDFThe document attached has been archived with permission from the Australian Dental Association (8th Jan 2008). An external link to the publisher’s copy is included.Background: There are no published studies comparing the clinical performances of more-viscous glass-ionomer cement (GIC) restorations when placed using conventional and atraumatic restorative treatment (ART) cavity preparation methods to restore root surface caries. Methods: One dentist used encapsulated Fuji IX GP and Ketac-Molar to restore 72 conventional and 74 ART cavity preparations for 15 patients who had received cervicofacial radiation therapy. Two assessors evaluated the restorations at six, 12, and 24 months for retention, marginal defects and surface wear, and recurrent caries. Results: After two years, the cumulative restoration successes were 65.2 per cent for the conventional and 66.2 per cent for the ART cavity preparations, without statistical or clinical significance (P>0.50). Restoration dislodgement accounted for 82.8 per cent and marginal defects for 17.2 per cent of all failures. There were no instances of unsatisfactory restoration wear or recurrent caries observed. Teeth with three or more restored cervical surfaces accounted for 79.3 per cent of all failures (P<0.0001). Conclusions: For root surface caries restored with GIC, the use of hand instruments only with the ART method was an equally effective alternative to conventional rotary instrumentation for cavity preparation. Larger restorations had higher failures, usually from dislodgement.JY Hu, XC Chen, YQ Li, RJ Smales and KH Yi
Structure-based sequence alignment of seven KH domains of high structural similarity to αCP1-KH3
No full text<p><b>Copyright information:</b></p><p>Taken from "Structure and RNA binding of the third KH domain of poly(C)-binding protein 1"</p><p>Nucleic Acids Research 2005;33(4):1213-1221.</p><p>Published online 24 Feb 2005</p><p>PMCID:PMC549569.</p><p>© The Author 2005. Published by Oxford University Press. All rights reserved</p> Each KH domain was structurally aligned using LSQMAN () against αCP1-KH3. Amino acid residues with α-carbon positions within 3.5 Å of a corresponding αCP1-KH3 residue are shown in black. Highlighted in purple are the amino acid residues that do not align well with residues of αCP1-KH3. Secondary structural elements, as defined in Lewis ., () are shown above the corresponding sequence in cartoon form. Parenthesized numbers represent the amino acid numbers at the start and finish of the superimposed core region for each structure, and indicate the extent of the structure used to calculate sequence identity with αCP1-KH3 (final column). The GXXG motif and the variable loop regions are blocked with grey. Amino acid residues reported to make contact with the oligonucleotide [in the cases of structures determined in complex with either RNA or ssDNA (–)] are highlighted in red, and the αCP1-KH3 predicted to make contact with oligonucleotide in the current study are highlighted in tan. NMR structures were structurally aligned on the basis of the first chain in the deposited PDB coordinate file and all were deemed to be representative of the set of structures
The effect of temperature on the fatty acids and isozymes of a psychrotrophic and two mesophilic species of Xenorhabdus, a bacterial symbiont of entomopathogenic nematodes
No full textIn the first part of this study, generation times relative to temperature, together with cardinal and conceptual temperatures, were determined for four strains of Xenorhabdus bacteria that represented three geographically distinct species. The data showed that the NF strain of Xenorhabdus bovienii, like the Umea strain of the same species, is psychrotrophic, while Xenorhabdus sp. TX strain resembles Xenorhabdus nematophila All strain in being mesophilic. In the second part, the capacity of these bacteria to adapt to changes in temperature, shown by changes in fatty acid composition, was investigated. As temperature declined, the proportions of the two major unsaturated fatty acids, palmitoleic (16:1omega7) acid and oleic (18:1 pi9) acid, increased significantly in all of the strains. The proportion of the prevalent saturated fatty acid, which was palmitic acid (16:0), decreased. In the All, NF, and Umea strains, myristic acid (14:0), margaric acid (17:0), cyclopropane (17:0c), and arachidic acid (20:0) decreased with decreasing temperature. In the third part of the study, the synthesis of isozymes in response to changing temperature was investigated. For the seven enzymes studied, the numbers for which isozyme synthesis was temperature related were as follows: five for Umea, four for All, three for NF, and two for TX. Where the study dealt with fatty acid composition and isozyme synthesis, the results show a broad capacity for physiological temperature adaptation among strains of different climatic origin.PT: J; CR: AKHURST RJ, 1980, J GEN MICROBIOL, V121, P303 AKHURST RJ, 1982, J GEN MICROBIOL, V128, P3061 AKHURST RJ, 1990, ENTOMOPATHOGENIC NEM, P75 BLIGH EG, 1959, CAN J BIOCH PHYSL, V37, P911 BOEMARE N, 1997, SYMBIOSIS, V22, P21 BOEMARE NE, 1988, J GEN MICROBIOL 3, V134, P751 DUNPHY GB, 1990, ENTOMOPATHOGENIC NEM, P301 FISCHERLESAUX M, 1999, FEMS MICROBIOL ECOL, V29, P149 FISCHERLESAUX M, 1999, INT J SYST BACTERI 4, V49, P1645 FODOR E, 1997, APPL ENVIRON MICROB, V63, P2826 FORST S, 1996, MICROBIOL REV, V60, P21 GERHARDT P, 1994, METHODS GEN MOL BACT GOW JA, 1984, APPL ENVIRON MICROB, V47, P213 GREWAL PS, 1994, J THERM BIOL, V19, P245 GWYNN RL, 1994, IOBC WPRS WORKING GR, V17, P120 HATAB MAA, 1997, J APPL MICROBIOL, V82, P351 HE HJ, 2000, CAN J MICROBIOL, V46, P618 HEBERT PDN, 1989, METHODOLOGIES ALLOZY JAGDALE GB, 1996, J NEMATOL, V28, P301 JAGDALE GB, 1997, CAN J ZOOL, V75, P2137 JAGDALE GB, 1997, COMP BIOCHEM PHYS A, V118, P1151 JAGDALE GB, 1997, J THERM BIOL, V22, P245 JAGDALE GB, 1998, FUND APPL NEMATOL, V21, P177 JAGDALE GB, 1998, FUNDAM APPL NEMATOL, V20, P147 KAYA HK, 1990, ENTOMOPATHOGENIC NEM, P93 LAWRENCE JV, 1977, APPL ENVIRON MICROB, V33, P482 LEHNINGER AI, 1979, BIOCHEMISTRY LIN JJ, 1995, PHYSIOL ZOOL, V68, P114 MARCUS NH, 1977, COMP BIOCH PHYSL, V58, P109 NEALSON KH, 1990, ENTOMOPATHOGENIC NEM, P271 RATKOWSKY DA, 1982, J BACTERIOL, V149, P1 SMART GC, 1995, J NEMATOL S, V27, P529 SOKAL RR, 1995, BIOMETRY PRINCIPLES, P242 SUMNER JL, 1969, J GEN MICROBIOL, V59, P215 SUUTARI M, 1994, CRIT REV MICROBIOL, V20, P285 YAMAWAKI H, 1979, COMP BIOCH PHYSL B, V62, P89; NR: 36; TC: 0; J9: CAN J MICROBIOL; PG: 10; GA: 430QZSource type: Electronic(1
Differences in population density and energy use between birds and mammals: A microecological perspective
No full text1. Data from 364 mammal and 564 bird species were used to compare these two taxa in the patterns of variation in population density and energy use as a function of body mass. 2. This study demonstrates previously unappreciated quantitative differences between mammals and birds. Over a wide range of sizes, population densities and rates of energy use are at least one order of magnitude higher in mammals than in birds of similar size, The highest population densities are found in species that weigh about 100 g in mammals and 30 g in birds. 3. Comparisons between mammals and birds from the same dietary category indicate that mammals maintain higher densities and use more energy than birds. Insectivorous mammals and birds maintain the lowest densities. 4. Flying mammals and birds reach lower densities and use more energy than non-flying forms. 5. These findings reveal relationships between the morphology, physiology and behaviour of individual organisms and the ecological performance of these endothermic vertebrates in populations, communities and ecosystems: relationships that have not previously been appreciated.PT: J; CR: ALLEN GT, 1987, J WILDLIFE MANAGE, V51, P739 ANDERSON S, 1977, AM MUS NOVIT, V2629, P1 ANDERSON S, 1984, AM MUS NOVIT, V2785, P1 ASHMOLE NP, 1968, SYST ZOOL, V17, P292 BARCLAY RMR, 1991, AM NAT, V137, P693 BLACKBURN TM, 1990, J ANIM ECOL, V59, P335 BLACKBURN TM, 1993, J ANIM ECOL, V62, P519 BLACKBURN TM, 1993, J ANIM ECOL, V62, P694 BLACKBURN TM, 1994, PHILOS T ROY SOC B, V343, P33 BLACKBURN TM, 1994, TRENDS ECOL EVOL, V9, P471 BLUEWEISS L, 1978, OECOLOGIA, V37, P257 BONNER JT, 1988, EVOLUTION COMPLEXITY BRADBURY JW, 1976, BEHAV ECOL SOCIOBIOL, V1, P337 BROWN JH, 1977, ECOLOGY, V54, P775 BROWN JH, 1986, NATURE, V324, P248 BROWN JH, 1987, AM NAT, V130, P1 BROWN JH, 1989, SCIENCE, V243, P1145 BROWN JH, 1993, AM NAT, V142, P573 CALDER WA, 1984, SIZE FUNCTION LIFE H CAMBEFORT Y, 1994, ACTA OECOL, V15, P165 CAMPBELL B, 1985, DICT BIRDS CARRASCAL LM, 1991, AM NAT, V138, P777 CEBALLOS G, 1995, CONSERV BIOL, V9, P559 COTGREAVE P, 1991, NATURE, V290, P699 COTGREAVE P, 1992, FUNCT ECOL, V6, P248 COTGREAVE P, 1993, TRENDS ECOL EVOL, V8, P244 COTGREAVE P, 1994, FUNCT ECOL, V8, P219 COTGREAVE P, 1994, OIKOS, V71, P89 COTGREAVE P, 1994, P ROY SOC LOND B BIO, V256, P147 COTGREAVE P, 1995, FUNCT ECOL, V9, P285 CRAIGHEAD JJ, 1973, WILDLIFE MONOGR, V33, P1 CURRIE DJ, 1993, OIKOS, V66, P353 CURRIE DJ, 1993, OIKOS, V67, P56 DAMUTH J, 1981, BIOL J LINN SOC, V15, P185 DAMUTH J, 1981, NATURE, V290, P699 DAMUTH J, 1987, BIOL J LINN SOC, V31, P193 DAMUTH J, 1991, NATURE, V351, P268 DAMUTH J, 1993, NATURE, V365, P748 DELGIUDICE GD, 1991, J WILDLIFE MANAGE, V55, P653 DUNNING JB, 1984, W BIRD BAND ASS MONO, V1 DUNNING JB, 1992, CRC HDB AVIAN BODY M EBENMAN B, 1995, OIKOS, V73, P225 GAISLER J, 1975, ACTA SCI NAT BRNO, V9, P1 GAISLER J, 1979, ECOLOGY BATS GASTON KJ, 1990, BIOL REV, V65, P105 GASTON KJ, 1991, OIKOS, V61, P434 GASTON KJ, 1993, ECOL ENTOMOL, V18, P310 GASTON KJ, 1995, PHILOS T ROY SOC B, V347, P205 GREENWOOD JJD, 1996, PHILOS T ROY SOC B, V351, P265 GREGORY RD, 1995, OIKOS, V72, P151 GRIFFITHS D, 1992, J ANIM ECOL, V61, P307 GUJARATI D, 1978, BASIC ECONOMETRICS HANCOCK JA, 1992, STORKS IBISES SPOONB HARESTAD AS, 1979, ECOLOGY, V60, P389 HARVEY PH, 1991, COMP METHOD EVOLUTIO HEMKER TP, 1984, J WILDLIFE MANAGE, V48, P1275 HOLLING CS, 1992, ECOL MONOGR, V62, P447 JUANES F, 1986, AM NAT, V128, P921 KURZEJESKI EW, 1987, J WILDLIFE MANAGE, V51, P188 LAWTON JH, 1989, OIKOS, V55, P429 LAWTON JH, 1990, PHILOS T ROY SOC B, V330, P283 MACE GM, 1983, AM NAT, V121, P120 MARQUET PA, 1990, SCIENCE, V250, P1125 MARQUET PA, 1993, THESIS U NEW MEXICO MARQUET PA, 1995, J ANIM ECOL, V64, P325 MAURER BA, 1988, ECOLOGY, V69, P1923 MCNAB BK, 1980, AM NAT, V116, P106 MCNAB BK, 1986, ECOL MONOGR, V56, P1 MCNAB BK, 1994, AM NAT, V144, P628 MEDEL RG, 1995, AM NAT, V145, P155 MILLAR JS, 1991, FUNCT ECOL, V5, P588 NAGY KA, 1987, ECOL MONOGR, V57, P111 NEE S, 1991, NATURE, V351, P312 NORBERG UM, 1986, ORNIS SCAND, V17, P253 NORBERG UM, 1987, PHIL T R SOC B, V316, P335 NOVICK A, 1971, J MAMMAL, V52, P817 NOWAK RM, 1991, WALKERS MAMMALS WORL, V1 PAGEL MD, 1988, Q REV BIOL, V63, P413 PAGEL MD, 1991, AM NAT, V138, P836 PENNYCUICK CJ, 1978, OIKOS, V30, P165 PETERS RH, 1983, ECOLOGICAL IMPLICATI PETERS RH, 1983, OECOLOGIA, V60, P89 PETERS RH, 1984, AM NAT, V128, P665 PIMM SL, 1991, BALANCE NATURE ECOLO PULLIAM HR, 1975, ECOLOGY, V56, P1158 RAYNER JMV, 1981, S ZOOL SOC LONDON, V48, P137 REDFORD KH, 1991, LATIN AM MAMMALOGY H, P227 ROBINSON JG, 1986, AM NAT, V128, P665 ROSENZWEIG ML, 1968, AM MIDL NAT, V80, P299 SCHMIDTNIELSEN K, 1983, ANIMAL PHYSL ADAPTAT SCHMIDTNIELSEN K, 1984, SCALING WHY ANIMAL S SEIDENSTICKER JC, 1973, WILDLIFE MONOGR, V35, P1 SILVA M, 1994, CONSERV BIOL, V8, P732 SILVA M, 1995, AM NAT, V145, P704 SOULE ME, 1986, BIOL CONSERV, V35, P19 STEARNS SC, 1983, OIKOS, V41, P173 STORK NE, 1987, ECOL ENTOMOL, V12, P69 STORK NE, 1993, OIKOS, V67, P483 TERBORGH J, 1990, ECOL MONOGR, V60, P213 THOMAS CD, 1990, CONSERV BIOL, V4, P324 TURNER DC, 1975, VAMPIRE BAT FIELD ST WATSON J, 1992, J ANIM ECOL, V61, P543 WELSH AH, 1988, AM NAT, V132, P277 WICKSTROM ML, 1984, J WILDLIFE MANAGE, V48, P1285 WIENS JA, 1977, GRANIVOROUS BIRDS EC, P205; NR: 105; TC: 18; J9: J ANIM ECOL; PG: 14; GA: WY474Source type: Electronic(1
Chemisorption on contaminated metals
No full textPT: J; CR: ANDERSON PW, 1961, PHYS REV, V124, P41 DAVISON SG, 1968, INT J QUANTUM CHEM S, V2, P313 DAVISON SG, 1972, INT J QUANTUM CHEM, V6, P549 EINSTEIN TL, 1973, PHYS REV B, V7, P3629 EINSTEIN TL, 1978, SURF SCI, V75, L161 EINSTEIN TL, 1980, THEORY CEHMISORPTION, CH7 FAIRBAIRN WM, 1971, SURFACE SCI, V25, P587 GERLACH E, 1969, SURFACE SCI, V13, P446 GODWIN VE, 1973, SURF SCI, V34, P108 LAU KH, 1978, SURF SCI, V75, P69 MASUDA K, 1979, PHYS STATUS SOLIDI B, V92, K103 MUSCAT JP, 1978, PROG SURF SCI, V9, P1 MUSCAT JP, 1983, J PHYS C SOLID STATE, V16, P3641 NEWNS DM, 1969, PHYS REV, V178, P1123 UEBA H, 1980, PHYS STATUS SOLIDI B, V99, P763; NR: 15; TC: 18; J9: SURFACE SCI; PG: 10; GA: AAH42Source type: Electronic(1
Regulation and drug resistance mechanisms of mammalian ribonucleotide reductase, and the significance to DNA synthesis
No full textPT: J; CR: ALBERT DA, 1987, J CELL PHYSIOL, V130, P262 ASHIHARA T, 1979, METHOD ENZYMOL, V58, P248 BOLIN RW, 1982, CANCER, V50, P1683 CARLSON J, 1984, P NATL ACAD SCI USA, V81, P4294 CARTER GL, 1989, CANCER COMMUN, V1, P13 CHOY BK, 1988, CANCER RES, V48, P2029 CHOY BK, 1989, BIOCHEM BIOPH RES CO, V162, P1417 COCKING JM, 1987, SOMAT CELL MOLEC GEN, V13, P221 COWAN KH, 1986, MOL PHARMACOL, V30, P69 DICK JE, 1984, MECH AGEING DEV, V26, P37 DONOVAN PB, 1984, AM J HEMATOL, V17, P329 DRYSDALE JW, 1988, PROG NUCLEIC ACID RE, V35, P127 ENGSTROM Y, 1984, EMBO J, V3, P863 ERIKSSON S, 1981, J BIOL CHEM, V256, P9436 FOX RM, 1989, INT ENCY PHARM THER, V128, P113 HANKE PD, 1983, J BACTERIOL, V156, P1192 HARDS RG, 1984, ARCH BIOCHEM BIOPHYS, V231, P9 HOPPER S, 1972, J BIOL CHEM, V247, P3336 HURTA RAR, 1990, BIOCHEM BIOPH RES CO, V167, P258 HURTA RAR, 1990, IN PRESS BIOCH BIOPH LEWIS WH, 1974, BIOCHEM BIOPH RES CO, V60, P926 LEWIS WH, 1978, J CELL PHYSL, V97, P73 LEWIS WH, 1978, J CELL PHYSL, V97, P87 LEWIS WH, 1979, SOMATIC CELL GENET, V5, P83 LYNCH JB, 1989, J BIOL CHEM, V264, P8091 MCCLARTY GA, 1986, CANCER RES, V46, P4516 MCCLARTY GA, 1986, SOMAT CELL MOLEC GEN, V12, P121 MCCLARTY GA, 1987, BIOCHEM BIOPH RES CO, V145, P1276 MCCLARTY GA, 1987, BIOCHEMISTRY-US, V26, P8004 MCCLARTY GA, 1988, BIOCHEM BIOPH RES CO, V154, P975 MCCLARTY GA, 1988, BIOCHEMISTRY-US, V27, P7524 MCCLARTY GA, 1990, J BIOL CHEM, V265, P7539 MCCONLOGUE L, 1986, MOL CELL BIOL, V6, P2865 MCDONALD CJ, 1981, PHARMACOL THERAPEUT, V14, P1 PIVER MS, 1983, AM J OBSTET GYNECOL, V147, P803 RICHARD P, 1988, ANNU REV BIOCHEM, V57, P349 RITTBERG DAH, 1989, BIOCHEM CELL BIOL, V67, P352 SRINIVASAN PR, 1987, J BIOL CHEM, V262, P12871 TAGGER AY, 1987, BIOCH CELL BIOL, V65, P925 TAGGER AY, 1988, INT J CANCER, V42, P760 THEIL EC, 1987, ANNU REV BIOCHEM, V56, P289 THELANDER L, 1980, J BIOL CHEM, V255, P7426 THELANDER L, 1986, MOL CELL BIOL, V6, P3433 THELANDER M, 1985, J BIOL CHEM, V260, P2737 THOMAS CE, 1986, J BIOL CHEM, V261, P13064 TILL JE, 1973, FED PROC, V32, P29 TONIN PN, 1987, CYTOGENET CELL GENET, V45, P102 TONIN PN, 1989, ONCOGENE, V4, P1117 ULLMAN B, 1979, P NATL ACAD SCI USA, V76, P1074 VEALE D, 1988, BRIT J CANCER, V58, P70 WEBER G, 1983, CANCER RES, V43, P3466 WECKBECKER G, 1988, J NATL CANCER I, V80, P491 WEINBERG G, 1981, P NATL ACAD SCI USA, V78, P2447 WILLIAMS SR, 1987, J BIOL CHEM, V262, P2332 WRIGHT JA, 1974, J CELL PHYSIOL, V83, P437 WRIGHT JA, 1980, CAN J GENET CYTOL, V22, P443 WRIGHT JA, 1981, ADV ENZYME REGUL, V19, P105 WRIGHT JA, 1987, SOMAT CELL MOLEC GEN, V13, P155 WRIGHT JA, 1989, DRUG RESISTANCE MAMM, V1, P15 WRIGHT JA, 1989, INT ENCY PHARM THERA, V128, P89 YANGFENG TL, 1987, GENOMICS, V1, P77; NR: 61; TC: 75; J9: BIOCHEM CELL BIOL; PG: 8; GA: EM994Source type: Electronic(1
Carboxylation of carbenes in low-temperature matrixes
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Angiotensin II induces soluble fms-Like tyrosine kinase-1 release via calcineurin signaling pathway in pregnancy
Get PDFMaternal endothelial dysfunction in preeclampsia is associated with increased soluble fms-like tyrosine kinase-1 (sFlt-1), a circulating antagonist of vascular endothelial growth factor and placental growth factor. Angiotensin II (Ang II) is a potent vasoconstrictor that increases concomitant with sFlt-1 during pregnancy. Therefore, we speculated that Ang II may promote the expression of sFlt-1 in pregnancy. Here we report that infusion of Ang II significantly increases circulating levels of sFlt-1 in pregnant mice, thereby demonstrating that Ang II is a regulator of sFlt-1 secretion in vivo. Furthermore, Ang II stimulated sFlt-1 production in a dose- and time-dependent manner from human villous explants and cultured trophoblasts but not from endothelial cells, suggesting that trophoblasts are the primary source of sFlt-1 during pregnancy. As expected, Ang II-induced sFlt-1 secretion resulted in the inhibition of endothelial cell migration and in vitro tube formation. In vitro and in vivo studies with losartan, small interfering RNA specific for calcineurin and FK506 demonstrated that Ang II-mediated sFlt-1 release was via Ang II type 1 receptor activation and calcineurin signaling, respectively. These findings reveal a previously unrecognized regulatory role for Ang II on sFlt-1 expression in murine and human pregnancy and suggest that elevated sFlt-1 levels in preeclampsia may be caused by a dysregulation of the local renin/angiotensin system
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