Relevant bibliographies by topics / H.R. 676

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Academic literature on the topic 'H.R. 676'

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Published: 4 June 2021
Last updated: 13 February 2022

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Journal articles on the topic "H.R. 676"

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Jones, E. Anthony, and Richard Morgan. "E. L. Krawitt, R. H. Wiesner and M. Nishioka. Elsevier, Amsterdam, 1998. ISBN 0 444 82803 6; hardback, 676 pages, illustrated; US 284.50." European Journal of Gastroenterology & Hepatology 11, no. 8 (August 1999): 942. http://dx.doi.org/10.1097/00042737-199908000-00029.

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Porksen, N., S. R. Munn, J. L. Steers, J. D. Veldhuis, and P. C. Butler. "Effects of somatostatin on pulsatile insulin secretion: elective inhibition of insulin burst mass." American Journal of Physiology-Endocrinology and Metabolism 270, no. 6 (June 1, 1996): E1043—E1049. http://dx.doi.org/10.1152/ajpendo.1996.270.6.e1043.

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Although it is well known that somatostatin inhibits net insulin secretion, it is unknown whether this is achieved by regulation of the basal or pulsatile components of insulin secretion and, if the latter, whether this is through modulation of pulse mass or frequency. We addressed these questions with a canine model. Portal vein blood was sampled at 1-min intervals in five dogs for 60 min before (basal) and 90 min after ingestion of 30 g glucose on two different occasions, during a saline (SAL) or a somatostatin (SMS, 175 ng/min) infusion. Plasma glucose concentrations were similar during SAL and SMS. SMS had no effect on pulse frequency before (8.4 +/- 0.7 vs. 9.2 +/- 1.0 pulses/h, SMS vs. SAL, P = 0.54) or after glucose (13.3 +/- 1.1 vs. 11.6 +/- 0.9 pulses/h, SMS vs. SAL, P = 0.22). In contrast, SMS decreased insulin pulse mass in the postabsorptive (84 +/- 28 vs. 214 +/- 73 pmol/pulse, SMS vs. SAL, P < 0.05) and fed states (676 +/- 143 vs. 913 +/- 183 pmol/pulse, SMS vs. SAL, P < 0.05). In the postabsorptive state, SMS decreased insulin clearance by approximately 50% (0.32 +/- 0.04 vs. 0.60 +/- 0.09 l/min, P < 0.05), but after glucose ingestion, insulin clearance was comparable during SMS or SAL (0.72 +/- 0.04 vs. 0.80 +/- 0.08 l/min, P = 0.4). SMS appeared to alter insulin clearance through modulation of insulin pulse amplitude, because in the postabsorptive state clearance was closely correlated to the pulse amplitude (r = + 0.87, P < 0.0001). In conclusion, somatostatin regulates the rate of insulin secretion by selective inhibition of pulsatile insulin secretion. Regulation of secretory burst mass (and amplitude) may secondarily influence transhepatic and thus total body clearance of endogenously secreted insulin and thereby serve as a novel mechanism to dictate the systemic insulin concentration.
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Do, S., J. H. Du, J. X. An, J. Wang, and A. Lin. "OP0133 THE PREVALENCE AND RISK FACTORS OF RETINAL TOXICITY ASSOCIATED WITH LONG-TERM HYDROXYCHLOROQUINE USE." Annals of the Rheumatic Diseases 80, Suppl 1 (May 19, 2021): 77–78. http://dx.doi.org/10.1136/annrheumdis-2021-eular.328.

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Background:Hydroxychloroquine (HCQ) is commonly used for the treatment of various autoimmune diseases. The medication is generally well-tolerated. However, long-term use after 5 years may increase the risk of retinopathy. One study in 2014 has demonstrated the risk can be as high as 7.5%. Optical Coherence Tomography (OCT) has become a major modality in screening retinopathy.Objectives:To evaluate the prevalence of retinal toxicity among patients using hydroxychloroquine and to determine various risk factors associated with hydroxychloroquine-associated retinal toxicity.Methods:We performed a retrospective chart review on a cohort of adult patients with long-term use (≥ 5 years cumulative) of HCQ between January 1st, 2011 to December 31st, 2018 from the Kaiser Permanente San Bernardino County and Riverside medical center areas in Southern California, USA. Patients were excluded if they had previously been diagnosed with retinopathy prior to hydroxychloroquine use, were deceased, or had incomplete OCT exam. Our primary endpoint was the prevalence of patients who developed retinal toxicity detected by OCT, and later confirmed by retinal specialist. Potential risk factors (age, duration of therapy, daily consumption per actual body weight, cumulative dose, confounding diseases and medication) for developing retinopathy were also evaluated. Univariable and multivariable logistic regression analyses were used to determine risk factors associated with retinal toxicity.Results:Among 676 patients exposed to more than 5 years of HCQ, the overall prevalence of retinal toxicity was 6.8%, and ranged from 2.5% to 22.2% depending on the age, weight-based dosing, duration of use and cumulative dose. Duration of therapy for 10 years or more increased risk of retinopathy by approximately 5 to 19 folds. Similarly, weight-based dose of 7 mg/kg/day or greater was assciated with increased risk of retinopathy by approximately 5 times. Patients with cumulative dose of 2000 grams or more had greater than 15 times higher risk of developing retinopathy. Duration of use for10 years or more (odd ratio 4.32, 95% CI 1.99 – 12.49), age (odd ratio 1.04; 95% CI 1.01 - 1.08), cumulative dose of more than 1500 g (odd ratio 7.4; 95% CI 1.40 – 39.04) and atherosclerosis of the aorta (odd ratio 2.59; 95% CI, 1.24 – 5.41) correlated with higher risk of retinal toxicity.Conclusion:The overall prevalence of retinopathy was 6.8%. Regular OCT screening, especially in patients with hydroxychloroquine use for more than 10 years, daily intake > 7 mg/kg, or cumulative dose > 1500 grams is important in detecting hydroxychloroquine-associated retinal toxicityReferences:[1]Hobbs HE. Sorsby A, & Freedman A. Retinopathy Following Chloroquine Therapy. The Lancet. 1959; 2(7101): 478-480.[2]Levy, G. D., Munz, S. J., Paschal, J., Cohen, H. B., Pince, K. J., & Peterson, T. Incidence of hydroxychloroquine retinopathy in 1,207 patients in a large multicenter outpatient practice. Arthritis & Rheumatism: 1997; 40(8): 1482-1486.[3]Ding, H. J., Denniston, A. K., Rao, V. K., & Gordon, C. Hydroxychloroquine-related retinal toxicity. Rheumatology. 2016; 55(6): 957-967.[4]Stelton, C. R., Connors, D. B., Walia, S. S., & Walia, H. S. Hydrochloroquine retinopathy: characteristic presentation with review of screening. Clinical rheumatology. 2013; 32(6): 895-898.[5]Marmor, M. F., Kellner, U., Lai, T. Y., Melles, R. B., & Mieler, W. F. Recommendations on screening for chloroquine and hydroxychloroquine retinopathy (2016 revision). Ophthalmology. 2016; 123(6): 1386-1394.[6]Melles, R. B., & Marmor, M. F. The risk of toxic retinopathy in patients on long-term hydroxychloroquine therapy. JAMA ophthalmology. 2014; 132(12): 1453-1460.Disclosure of Interests:None declared
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Hill, G. N., W. R. Henshall, and R. M. Beresford. "Manipulating rainfall to study symptom expression of Botrytis cinerea infection in wine grapes." New Zealand Plant Protection 70 (July 26, 2017): 301–9. http://dx.doi.org/10.30843/nzpp.2017.70.64.

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Botrytis cinerea infection of wine grapes can result in a variety of symptoms. The most common symptom is botrytis bunch rot (BBR), where infected berries rot and shrivel, and eventually produce fungal sporulation. Another symptom is slip skin, where the skins of infected ripe berries slide easily from the pulp. It is hypothesised that a reduction in osmotic potential in grape berries due to late-season rainfall leads to slip skin symptom development. Hyphal growth of B. cinerea on osmotically adjusted agar was inhibited at osmotic potentials associated with near-ripe berries. Vine sheltering was used in a research vineyard to manipulate rainfall artificially and to alter berry sugar content in Vitis vinifera Sauvignon blanc vines, with the aim of increasing osmotic potential and altering symptom expression. Both BBR and slip skin symptoms were affected by the various sheltering conditions, with sheltered vines having lower BBR and higher slip skin at harvest. REFERENCES Becker T, Grimm E, Knoche M 2012. Substantial water uptake into detached grape berries occurs through the stem surface. Australian Journal of Grape and Wine Research 18: 109-114. https://doi.org/10.1111/j.1755-0238.2011.00177.x Beever RE, Laracy EP 1986. Osmotic adjustment in the filamentous fungus Aspergillus nidulans. Journal of Bacteriology 168: 1358-1365. https://doi.org/10.1128/jb.168.3.1358-1365.1986 Beresford RM, Hill GN 2008. Botrytis control without fungicide residues - is it just a load of rot? New Zealand Winegrower 12: 104-106. Beresford RM, Evans KJ, Wood PN, Mundy DC 2006. Disease assessment and epidemic monitoring methodology for bunch rot (Botrytis cinerea) in grapevines. New Zealand Plant Protection 59: 355-360. Bondada BR, Matthews MA, Shackel KA 2005. Functional xylem in the post-véraison grape berry. Journal of Experimental Botany 56: 2949-2957. https://doi.org/10.1093/jxb/eri291 Choat B, Gambetta GA, Shackel KA, Matthews MA 2009. Vascular function in grape berries across development and its relevance to apparent hydraulic isolation. Plant Physiology 151: 1677-1687. https://doi.org/10.1104/pp.109.143172 Clarke SJ, Hardie WJ, Rogiers SY 2010. Changes in susceptibility of grape berries to splitting are related to impaired osmotic water uptake associated with losses in cell vitality. Australian Journal of Grape and Wine Research 16: 469-476. https://doi.org/10.1111/j.1755-0238.2010.00108.x Diakou P, Moing A, Svanella L, Ollat N, Rolin DB, Gaudillere M, Gaudillere JP 1997. Biochemical comparison of two grape varieties differing in juice acidity. Australian Journal of Grape and Wine Research 3: 1-10. https://doi.org/10.1111/j.1755-0238.1997.tb00122.x Grolemund G, Wickham H 2011. Dates and times made easy with lubridate. 2011 40: 25. Harris RF 1981. Effect of water potential on microbial growth and activity. In: Parr JF, Gardner WR, Elliott LF eds. Water Potential Relations in Soil Microbiology. SSSA Special Publication. Soil Science Society of America. Pp. 23-95. Hill GN, Beresford RM, Evans KJ 2010. Tools for accurate assessment of botrytis bunch rot (Botrytis cinerea) on wine grapes. New Zealand Plant Protection 63: 174-181. Hill GN, Evans KJ, Beresford RM 2014a. Use of nitrate non-utilising (nit) mutants to determine phenological stages at which Botrytis cinerea infects wine grapes causing botrytis bunch rot. Plant Pathology 63: 1316-1325. https://doi.org/10.1111/ppa.12225 Hill GN, Evans KJ, Beresford RM, Dambergs RG 2014b. Comparison of methods for the quantification of botrytis bunch rot in white wine grapes. Australian Journal of Grape and Wine Research 20: 432—441. https://doi.org/10.1111/ajgw.12101 Keller M, Smith JP, Bondada BR 2006. Ripening grape berries remain hydraulically connected to the shoot. Journal of Experimental Botany 57: 2577-2587. https://doi.org/10.1093/jxb/erl020 Loschiavo A, Scholefield P, Morrison J, Ferris M 2010. The cost of pests and diseases to the Australian winegrape industry. Australian Viticulture 14: 15-19. McCarthy MG, Coombe BG 1999. Is weight loss in ripening grape berries cv. Shiraz caused by impeded phloem transport? Australian Journal of Grape and Wine Research 5: 17-21. https://doi.org/10.1111/j.1755-0238.1999.tb00146.x Mendiburu Fd 2016. agricolae: Statistical Procedures for Agricultural Research. https://CRAN.R-project.org/package=agricolae. Mundy DC, Beresford RM 2007. Susceptibility of grapes to Botrytis cinerea in relation to berry nitrogen and sugar concentration. New Zealand Plant Protection 60: 123-127. Nelson KE 1956. The effect of Botrytis infection on the tissue of Tokay grapes. Phytopathology 46: 223-229. NIWA 2017. Mean monthly rainfall (mm). https://www.niwa.co.nz/education-and-training/schools/resources/climate/meanrain (05-05-2017). Pezet R, Viret O, Perret C, Tabacchi R 2003. Latency of Botrytis cinerea Pers.: Fr. and biochemical studies during growth and ripening of two grape berry cultivars, respectively susceptible and resistant to grey mould. Journal of Phytopathology 151: 208-214. https://doi.org/10.1046/j.1439-0434.2003.00707.x R Core Team 2016. R: A language and environment for statistical computing. R Foundation for Statistical Computing, Vienna, Austria. https://www.R-project.org/. R Studio Team 2016. RStudio: Integrated Development for R. RStudio, Inc., Boston, MA. http://www.rstudio.com/. Rogiers SY, Smith JA, White R, Keller M, Holzapfel BP, Virgona JM 2001. Vascular function in berries of Vitis vinifera (L) cv. Shiraz. Australian Journal of Grape and Wine Research 7: 47-51. https://doi.org/10.1111/j.1755-0238.2001.tb00193.x Schindelin J, Arganda-Carreras I, Frise E, Kaynig V, Longair M, Pietzsch T, Preibisch S, Rueden C, Saalfeld S, Schmid B, Tinevez J-Y, White DJ, Hartenstein V, Eliceiri K, Tomancak P, Cardona A 2012. Fiji: an open-source platform for biological-image analysis. Nature Methods 9: 676-682. https://doi.org/10.1038/nmeth.2019 Smart R, Robinson M 1991. Sunlight into Wine. Winetitles, Adelaide, Australia. Taiz L, Zeiger E 1998. Plant Physiology. Sinauer Associates, Sunderland, MA, USA. Tyerman SD, Tilbrook J, Pardo C, Kotula L, Sullivan W, Steudle E 2004. Direct measurement of hydraulic properties in developing berries of Vitis vinifera L. cv Shiraz and Chardonnay. Australian Journal of Grape and Wine Research 10: 170-181. https://doi.org/10.1111/j.1755-0238.2004.tb00020.x Whiting EC, Rizzo DM 1999. Effect of water potential on radial colony growth of Armillaria mellea and A. gallica isolates in culture. Mycologia 91: 627-635. https://doi.org/10.2307/3761248 Wickham H 2009. ggplot2: Elegant Graphics for Data Analysis. Springer-Verlag New York. Wickham H 2016. tidyverse: Easily Install and Load 'Tidyverse' Packages. https://CRAN.R-project.org/package=tidyverse. Wickham H, Bryan J 2017. readxl: Read Excel Files. https://CRAN.R-project.org/package=readxl. Wilcox WF, Gubler WD, Uyemoto JK 2015. Compendium of Grape Diseases, Disorders, and Pests: Second Edition. APS Press, St Paul, MN, USA.
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El-Nahal, Fady. "Coherent 16 Quadrature Amplitude Modulation (16QAM) Optical Communication Systems." Photonics Letters of Poland 10, no. 2 (June 30, 2018): 57. http://dx.doi.org/10.4302/plp.v10i2.809.

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Coherent optical fiber communications for data rates of 100Gbit/s and beyond have recently been studied extensively primarily because high sensitivity of coherent receivers could extend the transmission distance. Spectrally efficient modulation techniques such as M-ary quadrature amplitude modulation (M-QAM) can be employed for coherent optical links. The integration of multi-level modulation formats based on coherent technologies with wavelength-division multiplexed (WDM) systems is key to meet the aggregate bandwidth demand. This paper reviews coherent 16 quadrature amplitude modulation (16QAM) systems to scale the network capacity and maximum reach of current optical communication systems to accommodate traffic growth. Full Text: PDF ReferencesK. Kikuchi, "Fundamentals of Coherent Optical Fiber Communications", J. Lightwave Technol., vol. 34, no. 1, pp. 157-179, 2016. CrossRef S. Tsukamoto, D.-S. Ly-Gagnon, K. Katoh, and K. Kikuchi, "Coherent Demodulation of 40-Gbit/s Polarization-Multiplexed QPSK Signals with16-GHz Spacing after 200-km Transmission", Proc. OFc, Paper PDP29, (2005). DirectLink K. Kikuchi, "Coherent Optical Communication Technology", Proc. OFC, Paper Th4F.4, (2015). CrossRef J. M. Kahn and K.-P. Ho, "Spectral efficiency limits and modulation/detection techniques for DWDM systems", IEEE J. Sel. Topics Quantum Electron., vol. 10, no. 2, pp. 259–272, (2004). CrossRef S. Tsukamoto, K. Katoh, and K. Kikuchi, "Coherent demodulation of optical multilevel phase-shift-keying signals using homodyne detection and digital signal processing", IEEE Photon. Technol. Lett., vol. 18, no. 10, pp. 1131–1133, (2006). CrossRef Y. Mori, C. Zhang, K. Igarashi, K. Katoh, and K. Kikuchi, "Unrepeated 200-km transmission of 40-Gbit/s 16-QAM signals using digital coherent receiver", Opt. Exp., vol. 17, no. 32, pp. 1435–1441, (2009). CrossRef H. Nakashima, Et al., "Digital Nonlinear Compensation Technologies in Coherent Optical Communication Systems", Proc. OFC, Paper W1G.5, (2017). CrossRef S. J. Savory, "Digital filters for coherent optical receivers", Opt. Exp., vol. 16, no. 2, pp. 804–817, (2008). CrossRef D. S. Millar, T. Koike-Akino, S. Ö. Arık, K. Kojima, K. Parsons, T. Yoshida, and T. Sugihara, "High-dimensional modulation for coherent optical communications systems", Opt. Express, vol. 22, no. 7, pp 8798-8812, (2014). CrossRef R. Griffin and A. Carter, "Optical differential quadrature phase-shift key (oDQPSK) for high capacity optical transmission", Proc. OFC, Paper WX6, (2002). DirectLink K. Kikuchi, "Digital coherent optical communication systems: fundamentals and future prospects", IEICE Electron. Exp., vol. 8, no. 20, pp. 1642–1662, (2011). CrossRef F. Derr, "Optical QPSK transmission system with novel digital receiver concept", Electron Lett., vol. 27, no. 23, pp. 2177–2179, (1991). CrossRef R. No’e, "Phase noise tolerant synchronous QPSK receiver concept with digital I&Q baseband processing", Proc. OECC, Paper 16C2-5, (2004). DirectLink D.-S. Ly-Gagnon, S. Tsukamoto, K. Katoh, and K. Kikuchi, "Coherent detection of optical quadrature phase-shift keying signals with carrier phase estimation", J. Lightw. Technol., vol. 24, no. 1, pp. 12–21, (2006). CrossRef M. Taylor, "Coherent detection method using DSP for demodulation of signal and subsequent equalization of propagation impairments", IEEE Photon. Technol. Lett., vol. 16, no. 2, pp. 674–676, (2004). CrossRef S. Tsukamoto, K. Katoh, and K. Kikuchi, "Unrepeated transmission of 20-Gb/s optical quadrature phase-shift-keying signal over 200-km standard single-mode fiber based on digital processing of homodyne-detected signal for Group-velocity dispersion compensation", IEEE Photon. Technol. Lett., vol. 18, no. 9, pp. 1016–1018, (2006). CrossRef S. Tsukamoto, Y. Ishikawa, and K. Kikuchi, "Optical Homodyne Receiver Comprising Phase and Polarization Diversities with Digital Signal Processing", Proc. ECOC, Paper Mo4.2.1, (2006). CrossRef K. Kikuchi and S. Tsukamoto, "Evaluation of Sensitivity of the Digital Coherent Receiver", J. Lightw. Technol., vol. 20, no. 13, pp. 1817–1822, (2008). CrossRef S. Ishimura and K. Kikuchi, "Multi-dimensional Permutation Modulation Aiming at Both High Spectral Efficiency and High Power Efficiency", Proc. OFC/NFOEC, Paper M3A.2, (2014). CrossRef F. I. El-Nahal and A. H. M. Husein, "Radio over fiber access network architecture employing RSOA with downstream OQPSK and upstream re-modulated OOK data", (Optik) Int. J. Light Electron Opt., vol. 123, no. 14, pp: 1301-1303, (2012). CrossRef T. Koike-Akino, D. S. Millar, K. Kojima, and K. Parsons, "Eight-Dimensional Modulation for Coherent Optical Communications", Proc. ECOC, Paper Tu.3.C.3, (2013). DirectLink B. Sklar, Digital communications: Fundamentals and Applications, Prentice-Hall, (2001).
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Myung, I. S., J. K. Choi, J. Y. Lee, M. J. Yoon, E. Y. Hwang, and H. S. Shim. "First Report of Bacterial Leaf Spot of Witloof, Caused by Pseudomonas cichorii in Korea." Plant Disease 97, no. 10 (October 2013): 1376. http://dx.doi.org/10.1094/pdis-04-13-0436-pdn.

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In August 2011, bacterial leaf spot was observed on witloof (Cichorium intybus L. var. foliosum) grown in a commercial field with 15% incidence in Injae, Korea. Symptoms on leaves included irregular brown to reddish brown spots in the center. Bacterial streaming from the lesions was observed microscopically. Bacterial isolates (BC3286, BC3287, and BC3308-BC3310) were recovered on Trypticase soy agar from lesions surface-sterilized in 70% ethyl alcohol for 30 s. The isolates were gram negative, urease negative, fluorescent on King's B agar, and had aerobic rods with 2 to 6 polar flagella. Pathogenicity tests were separately performed in different greenhouses located in Suwon (National Academy of Agricultural Science) and Chuncheon (Gangwondo Agricultural Research and Extension Services) in Korea. Pathogenicity was confirmed by spray inoculation of healthy, 10-day-old leaves of witloof plants (two plants/isolate) with a suspension of original field isolate (106 CFU/ml). Sterile distilled water was used as negative control. The inoculated plants were incubated in a growth chamber (25°C and 95% relative humidity [RH]) overnight, then transferred to a greenhouse at 23 to 27°C and 60 to 70% RH. Characteristic leaf spot symptoms were observed on inoculated witloof plants 8 days after inoculation. No symptoms were observed on control plants. The bacterium reisolated from the inoculated leaves was confirmed by analyzing sequence of the gyrB gene with direct sequencing method of PCR products using primers gyr-F and gyr-R (2). The sequence of reisolated bacteria shared 100% similarity with inoculated ones. In LOPAT (1) tests, all isolates and the reference strain of Pseudomonas cichorii CFBP2101T (=BC2595) were levan negative, oxidase positive, potato rot negative, arginine dihydrolase negative, and tobacco hypersensitivity positive, indicative of group III (–, +, –, –, +) of fluorescent pseudomonads. The 16S rRNA (1,408 bp), and gyrB (676 bp) regions were sequenced to aid in identification of the original field isolates as well as P. cichorii CFBP 2101T (=BC2595) using reported sets of PCR primers, fD1/rP2 and gyr-F/gyr-R, respectively (2,4). Phylogenetic analyses based on partial sequences of the gyrB and the 16S rRNA of Psudomonas spp. available in GenBank, the reference strain of P. cichorii CFBP2101T (=BC2595), and the witloof field isolates were conducted using the neighbor-joining method with Juke-Cantor model of distance calculation in MEGA version 5.1 (3). The isolates and the reference strain of P. cichorii CFBP2101T (=BC2595) was clustered in one group with P. cichorii strains in both phylogenetic trees based on the two sequences. Sequences of the 16S rRNA region had a distance index value ranging from 0.000 to 0.001 between the reference strain of P. cichori CFBP2101T (GenBank JX913784) and the field isolates (JX913785 to JX913789), and ranged from 0.000 to 0.001 within the field isolates. Sequences of the gyrB region had a distance index value ranging 0.029 to 0.033 between the reference strain (JX913790) and the field isolates (JX913791 to JX913795), and ranged from 0.000 to 0.041 within the field isolates. To our knowledge, this is the first report of bacterial leaf spot of witloof caused by P. cihorii in Korea. P. cichorii has a wide host range, and an important economic impact on vegetables. The disease is expected to result in a significant economic impact on root production of witloof in Korea. References: (1) R. A. Lelliott et al. J. Appl. Bacteriol. 29:470, 1966. (2) H. Sawada et al. J. Mol. Evol. 49:627, 1999. (3) K. Tamura et al. Mol. Biol. Evol. 28:2731, 2011. (4) W. G. Weinsburg et al. J. Bacteriol. 173, 697, 1991.
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Wang, Hongxin, Yoshitaka Yoda, Hideaki Ogata, Yoshihito Tanaka, and Wolfgang Lubitz. "A strenuous experimental journey searching for spectroscopic evidence of a bridging nickel–iron–hydride in [NiFe] hydrogenase." Journal of Synchrotron Radiation 22, no. 6 (October 23, 2015): 1334–44. http://dx.doi.org/10.1107/s1600577515017816.

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Direct spectroscopic evidence for a hydride bridge in the Ni–R form of [NiFe] hydrogenase has been obtained using iron-specific nuclear resonance vibrational spectroscopy (NRVS). The Ni–H–Fe wag mode at 675 cm−1is the first spectroscopic evidence for a bridging hydride in Ni–R as well as the first iron-hydride-related NRVS feature observed for a biological system. Although density function theory (DFT) calculation assisted the determination of the Ni–R structure, it did not predict the Ni–H–Fe wag mode at ∼675 cm−1before NRVS. Instead, the observed Ni–H–Fe mode provided a critical reference for the DFT calculations. While the overall science about Ni–R is presented and discussed elsewhere, this article focuses on the long and strenuous experimental journey to search for and experimentally identify the Ni–H–Fe wag mode in a Ni–R sample. As a methodology, the results presented here will go beyond Ni–R and hydrogenase research and will also be of interest to other scientists who use synchrotron radiation for measuring dilute samples or weak spectroscopic features.
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Son, Myeongjoo, Seyeon Oh, Chang Hu Choi, Kook Yang Park, Kuk Hui Son, and Kyunghee Byun. "Pyrogallol-Phloroglucinol-6,6-Bieckol from Ecklonia cava Attenuates Tubular Epithelial Cell (TCMK-1) Death in Hypoxia/Reoxygenation Injury." Marine Drugs 17, no. 11 (October 24, 2019): 602. http://dx.doi.org/10.3390/md17110602.

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The hypoxia/reoxygenation (H/R) injury causes serious complications after the blood supply to the kidney is stopped during surgery. The main mechanism of I/R injury is the release of high-mobility group protein B1 (HMGB1) from injured tubular epithelial cells (TEC, TCMK-1 cell), which triggers TLR4 or RAGE signaling, leading to cell death. We evaluated whether the extracts of Ecklonia cava (E. cava) would attenuate TEC death induced by H/R injury. We also evaluated which phlorotannin—dieckol (DK), phlorofucofuroeckol A (PFFA), pyrogallol phloroglucinol-6,6-bieckol (PPB), or 2,7-phloroglucinol-6,6-bieckol (PHB)—would have the most potent effect in the context of H/R injury. We used for pre-hypoxia treatment, in which the phlorotannins from E. cava extracts were added before the onset of hypoxia, and a post- hypoxia treatment, in which the phlorotannins were added before the start of reperfusion. PPB most effectively reduced HMGB1 release and the expression of TLR4 and RAGE induced by H/R injury in both pre- and post-hypoxia treatment. PPB also most effectively inhibited the expression of NF-kB and release of the inflammatory cytokines TNF-α and IL-6 in both models. PPB most effectively inhibited cell death and expression of cell death signaling molecules such as Erk/pErk, JNK/pJNK, and p38/pp38. These results suggest that PPB blocks the HGMB1–TLR4/RAGE signaling pathway and decreases TEC death induced by H/R and that PPB can be a novel target for renal H/R injury therapy.
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Plešek, Jaromír, Bohumír Grüner, and Josef Holub. "Synthesis and Properties of Cobaltacarboranes with Substituted Monoatomic Bridges Between Ligands of the 6,6'-μ-RnE(1,7-C2B9H10)2-2-Co Type." Collection of Czechoslovak Chemical Communications 62, no. 6 (1997): 884–93. http://dx.doi.org/10.1135/cccc19970884.

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Syntheses, properties and constitutions of eleven asymmetric cobaltacarboranes with various substituents on monoatomic bridges between both ligands of the type 6,6'-μ-RnE(1,7-C2B9H10)2-2-Co (E = O, R = methyl; E = S, R = ethyl, propyl, isopropyl, allyl, butyl, hexyl and CH3OCOCH2; E = N, R = H (H), methyl, (H), and dimethyl) are described. Constitution assignation of all compounds are based on 1H and 11B NMR spectroscopy experiments complemented by 11B-11B COSY NMR and mass spectrometry; UV-VIS, melting points and TLC parameters are also presented. Only the racemic forms were obtained, although in principle, the meso-forms might result as well.
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Segnana, L. Gonzalez, M. Ramirez de Lopez, A. P. O. A. Mello, J. A. M. Rezende, and E. W. Kitajima. "First Report of Cowpea aphid-borne mosaic virus on Sesame in Paraguay." Plant Disease 95, no. 5 (May 2011): 613. http://dx.doi.org/10.1094/pdis-07-10-0498.

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Sesame (Sesamum indicum L.) is cultivated mainly in the central region of the Departamento de San Pedro in Paraguay from October to February and the seed are exported to Asia. The crop is grown on 100,000 ha annually and Escoba blanca is the most common cultivar. The crop plays an important socioeconomical role since it is cultivated mostly by small growers. A disease characterized by yellowing and curling down leaves and shortening of the internodes has been observed in almost all sesame-growing areas. It is referred to locally as “ka'are” because the affected sesame plant resembles Chenopodium ambrosioides L. This disease occurred occasionally and was of marginal importance prior to 2005, but during the last five growing seasons the disease incidence has increased substantially, with some growers losing the entire crop. To determine the causal agent, symptomatic leaf samples were collected from five commercial fields near Colonia San Pedro and Choré, Departamento San Pedro in December 2009. Preliminary transmission electron microscopy (TEM; Zeiss EM900) of extracts from symptomatic leaves revealed the presence of elongated flexible particles resembling a potyvirus. Mechanical transmission assays resulted in chlorotic local lesions on C. quinoa and C. amaranticolor, mosaic on Vigna unguiculata and Nicotiana benthamiana, and symptoms on sesame that are similar to those observed in the field. The disease could also be reproduced in sesame by aphid (Myzus persicae) transmission in a nonpersistent manner. TEM examination of leaf sections of these naturally or experimentally infected plants showed the presence of the type I cylindrical inclusions and masses of filamentous particles. Leaf extracts of naturally or experimentally infected sesame and test plants were positive for Cowpea aphid-borne mosaic virus (CABMV) on the basis of plate-trapped antigen (PTA)-ELISA. CABMV as the causal agent of “ka'are” disease of sesame in Paraguay was further confirmed by analyzing part of the nucleotide sequence of CABMV coat protein and 3′ nontranslated region that were obtained directly from reverse transcription-PCR product amplified with PV1-antisense primer (5′-gatttaggtgacactatagt17-3′) and WCIEN-sense primer (5′-atggtttggtgyatygaraat-3′) (1,2). Comparisons of the 676-bp nucleotide sequence of two sesame virus isolates (GenBank Accession Nos. HQ336402 and HQ336403) revealed 92% identity with the corresponding nucleotide sequence of CABMV available in the GenBank (Accession No. AF348210). Thus, all the assays indicated that the “ka'are” disease of sesame in Paraguay is caused by an isolate of CABMV. Several cowpea fields, nearby sesame diseased crops, also contained plants exhibiting mosaic symptoms. Transmission assays, electron microscopy, PTA-ELISA, and nucleotide sequence analysis indicated that they were also infected by CABMV and may play an important role in the epidemiology of this disease on sesame. CABMV isolates from passion fruit and cowpea from Brazil were mechanically transmitted to sesame but induced milder symptoms. CABMV-infected sesame was described in the United States (3), but to our knowledge, this is the first report of a severe disease on sesame caused by this virus in Paraguay. References: (1) A. Gibbs and A. Mackenzie. J. Virol. Methods 63:9, 1997. (2) L. D. C. Mota et al. Plant Pathol. 53:368, 2004. (3) H. R. Pappu et al. Arch. Virol. 142:1919, 1997.
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Dissertations / Theses on the topic "H.R. 676"

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Gnana, Mani Joseph Wilfred [Verfasser], H. [Akademischer Betreuer] Altenbach, H. J. [Akademischer Betreuer] Radusch, and R. H. [Akademischer Betreuer] Schuster. "Continuous mixing of silica based rubber, filler-composites in twin screw extruder / Joseph Wilfred Gnana Mani. Betreuer: H. Altenbach ; H.-J. Radusch ; R. H. Schuster." Halle, Saale : Universitäts- und Landesbibliothek Sachsen-Anhalt, 2010. http://d-nb.info/1024976033/34.

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Books on the topic "H.R. 676"

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Various bills and resolutions: Markup before the Committee on Foreign Affairs, House of Representatives, One Hundred Tenth Congress, first session, on H.R. 885, H.R. 2446, S. 676, H. Con. Res. 21, H. Con. Res. 80, H. Con. Res. 151, H. Con. Res. 152, H. Res. 137, H. Res. 226, H.Res. 233, H. Res. 295, H. Res. 395, H. Res. 397, H. Res. 412, H. Res. 418, H. Res. 422, H. Res. 430, and H. R. 2420, May 23, 2007. Washington: U.S. G.P.O., 2007.

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Green, Carl R. Psychology: A Way To Grow (R 616 H). Amsco School Pubns, 1995.

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Book chapters on the topic "H.R. 676"

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MacFarland, Thomas W., and Jan M. Yates. "Kruskal–Wallis H-Test for Oneway Analysis of Variance (ANOVA) by Ranks." In Introduction to Nonparametric Statistics for the Biological Sciences Using R, 177–211. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-30634-6_6.

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Wordsworth, William, and Dorothy Wordsworth. "656. D. W. to H. C. R." In The Letters of William and Dorothy Wordsworth, Vol. 5: The Later Years: Part II: 1829–1834 (Second Revised Edition), 459–62. Oxford University Press, 2000. http://dx.doi.org/10.1093/oseo/instance.00083822.

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"• V Pr M ea r c . h ed at 1. i 678.By !; Fafting and Humilia tiitonb . e in ; g, a day of." In Life Writings, II, 171–72. Routledge, 2017. http://dx.doi.org/10.4324/9781315250489-6.

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"Paper 6.6: N. Bloembergen, H. Kurz, J.M. Liu and R. Yen, “Fundamentals of energy transfer during picosecond irradiation of silicon,” in Proceedings of Materials Research Society Symposium on Laser and Electric Beam Interactions with Solids, edited by B.R. Appleton and G.K. Celler, Elsevier, New York, 1982, pp. 3–11." In Encounters in Nonlinear Optics, 571–80. WORLD SCIENTIFIC, 1996. http://dx.doi.org/10.1142/9789812795793_0064.

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"Brownsword, R and Howells, G, ‘The implementation of the EC Directive on Unfair Terms in Consumer Contracts – some unresolved questions’ [1995] JBL 243. Brownsword, R, Howells, G and Wilhelmsson, T (eds), Welfarism in Contract, 1994, Aldershot: Dartmouth. Burrows, A, (ed), Essays on the Law of Restitution, 1991, Oxford: Clarendon. Burrows, A, The Law of Restitution, 1993, London: Butterworths. Burrows, A, Understanding the Law of Obligations, 1998, Oxford: Hart. Burrows, A, ‘Free acceptance and the law of restitution’ (1988) 104 LQR 576. Carr, C, ‘Lloyd’s Bank Ltd v Bundy’ (1975) 38 MLR 463. Cheshire, G, Fifoot, C and Furmston, M, Law of Contract, 13th edn, 1996, London: Butterworths/Tolley. Chitty (Guest, AG (ed)), Contracts: General Principles, 27th edn, 1994, London: Sweet & Maxwell. Coase, R, ‘The problem of social cost’ (1960) 3 Journal of Law and Economics 1. Collins, H, Law of Contract, 3rd edn, 1997, London: Butterworths. Collins, H, ‘Good faith in European contract law’ (1994) OJLS 229. Cooke, PJ and Oughton, DW, The Common Law of Obligations, 3rd edn, 2000, London: Butterworths. Coote, B, Exception Clauses, 1964, London: Sweet & Maxwell. Coote, B, ‘The Unfair Contract Terms Act 1977’ (1978) 41 MLR 312. De Lacey, J, ‘Selling in the course of a business under the Sale of Goods Act 1979’ (1999) 62 MLR 776. Dean, M, ‘Unfair contract terms – the European approach’ (1993) 56 MLR 581. Duffy, P, ‘Unfair terms and the draft EC Directive’ (1993) JBL 67. Evans, A, ‘The Anglo-American mailing rule’ (1966) 15 ICLQ 553. Fehlberg, B, ‘The husband, the bank, the wife and her signature – the sequel’ (1996) 59 MLR 675." In Sourcebook on Contract Law, 808. Routledge-Cavendish, 1995. http://dx.doi.org/10.4324/9781843141518-322.

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"BEDBOROUGH, D.R. & TROTT, P.E. 1979 The sensory measurement of odours by dynamic dilution. Report No LR 299 (AP). Warren Springs Laboratories, Stevenage. 13 BARTH, C.L., HILL, D.T. & POLKOWSKI, L.B. 1974 Correlating odour intensity index and odorous components in stored dairy manure. Transactions of the American Society of Agricultural Engineers 17(4), 742-4, 747. 14 SCHAEFER, J. 1977 Sampling, characterisation and analysis of malodours. Agriculture and Environment, 3(2,3), 121-128. 15 SCHAEFER, J. 1980 Development of instrumental methods for measuring odour levels in intensive livestock buildings. In: Effluents from Livestock (Gasser, J.K.R. (Ed.)). Applied Science Publishers, London pp 513-535. 16 KOWALEWSKY, H.H., SCHEV, R. & VETTER, H. 1980 Measurement of odour emissions and immissions. In: Effluents from Livestock (Gasser, J.K.R. (Ed)), Applied Science Publishers, London pp 609-626. 17 HARPER, R., BATESMITH, E.C. & LAND, D.G. 1968 Odour description and odour classification. J & A Churchill Ltd., London. 18 BELL, R.G. 1970 Fatty acid content as a measure of the odour potential of stored liquid poultry manure. Poultry Science, 49, 1126-9. 19 SOBEL, A.T. 1972 Olfactory measurement of animal manure odours. Transactions of the American Society of Agricultural Engineers. 15(4), 696-699 and 703. 20 AMOORE, J.E., VENSTROM, D. & DAVIS, A.R. 1968 Measurement of specific anosmia perceptual and motor skills 26, 143-164. 21 SPOELSTRA, S.F. (1980) Origin of objectionable odorous components in piggery wastes and the possibility of applying indicator components for studying odour development. Agriculture and Environments(3), 241-260. 22 OWENS, J.D., EVANS, M.R., THACKER, F.E., HISSETT, R. & BAINES S. 1973 Aerobic treatment of piggery waste. Water Research 7 1745-66. 23 EVANS, M.R., HISSETT, R., SMITH, M.P.W., THACKER, F.E. & WILLIAMS, A.G. (1980) Aerobic treatment of beef cattle and poultry waste compared with piggery waste. Agric. Wastes 2, 93-101." In Odour Prevention and Control of Organic Sludge and Livestock Farming, 329. CRC Press, 1986. http://dx.doi.org/10.1201/9781482286311-126.

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"M 18 a3c ( L 3) e : a2n07L -D 21 , 7 M , e1a9k7i5n . s TL, Taguchi K, Duignan TP, Dhillon KS, Gordon J. Ann Surg 4. Nielsen HJ, Hammer JH, Moesgaard F, Kehlet H. Surgery 105(6):711-719, 1989. 5. B 67 ro 6 w , n19R8 , 2 . Bancewicz J, Hamid J, Tillotson G, Ward C, Irving M. Ann Surg 196(6):672-6. Fernandez LA, MacSween JM, You CK, Gorelick M. Am J Surg 1613:263-270, 1992. 7. H 57 a , m 1 id 98J4 , . Bancewicz J, Brown R, Ward C, Irving MH, Ford WL. Clin Exp Immunol 56:49-8. Tartter PI, Steinberg B, Barron DM, Martinelli G. Arch Surg 122:1264-1268. 1987. 9. J M en o s ll eenr -N LS ie , ls A en ndCe , rsH en anAbJe , rg C -S hr oirse ti nasnesnenF , PHMo , klH an odk la M n . dBP, r J Ju Shul rg CO7 , 9 M :51 ad 3 s -5 en 16G , , 19M 92 o . rtensen J, 10. Fisher E, Lennard V, Siefert P Kluge A, Johannsen R. Human Immunol 3:187-194, 1980. 11. L 10 e1n5n , ar1d9V 83 , . Maassen G, Grosse-Wilde H, Wernet P, Opelz G. Transplant Proc 15(1): 1011-12. F1o9r8d7 . CD, Warnick CT, Sheets S, Quist R, Stevens LE. Transplant Proc 19( 1): 1:456-457, 13. Cox DR. Analysis of binary data, Methuen: London, 1970. 14. Murphy PJ, Connery C, Hicks GL Jr, Blumberg N. J Thoracic Cardiovasc Surgery (in press). 15. A Pa rc tc hheSnu rg Deerlyl in 1g2e3r ( E 1 , 1 ) M : 1i3 ll 2e0r -1 S3D2 , 7 , W1e9r8 tz 8 . MJ, Grypma M, Droppert B and Anderson PA. 16. D 12 e 3 ll : i1n3g2e0r -1 E3P2 , 5 M , 1 il 9 le 8r8 , SD, Wertz MJ, Grypha M, Droppert B, Anderson PA. Arch Surg 17. Dawes LG, Aprahamian C, Condon RE and Malongi MA. Surgery 100:796-803, 1986. 18. Tartter PI. Br J Surg 75:789-792,1988. 19. A Lo gsarAwnagleN le , s , MAuprrpihly1J9G 92 , . Cayten CG, Stahl WM. Presented to the Surgical Infection Society, 20. Truilzi DJ, Vanek K, Ryan DH and Blumberg N. Transfusion (accepted for publication). 21. Murphy P, Heal JM and Blumberg N. Transfusion 31:212-217,1991. 22. Mezrow CK, Berstein I and Tartter PI. Transfusion 32:27-30, 1992. 23. BMuesdch3R2C8 , : 1 H 37 o2p , W 19 C9J3 , . Hoynck van Zpapendrecht MAW, Marquet RL, Jeekel J. N Engl J 24. W 19 a8y7m . ackJP, Warden GD, Miskell P, Gonce S, Alexander JW. World J Surg 11:387-391, 25. WaymackJP, Robb E, Alexander JW. Arch Surg 122:935-939, 1987." In Transfusion Immunology and Medicine, 301. CRC Press, 1995. http://dx.doi.org/10.1201/9781482273441-30.

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Conference papers on the topic "H.R. 676"

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Sandset, P. M., P. A. Sirnes, U. Abildgaard, and M. Petterson. "PREACTIVATION AND INHIBITION OF EXTRINSIC COAGULATION PATHWAY IN ACUTE CORONARY DISEASE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643024.

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It has recently been shown that plasma from individuals with a high risk score for developing AMI shows an abnormal depression of factor VII (EVII) coagulant activity after treatment with phospholipase C (PLC), (Dalaker, K.& Prydz, H., Br . J . Haematol. 61,315, 1985) revealing the presence of “preactivated” FVII in complex with lipid. We have studied this phenomenon in patients in a coronary unit, by serial determinations of Normotest (NT) + PLC pretreatment (which correlates with FVII clotting) assay ± PLC) and EVII amidolytic assay (EVIIram) (OswaldsBn et al., Tromb.Haemostas. 54,26,1985). The newly described inhibitor of FVII-Tissue thromboplastin (EPI) was also measured. Mean patient values day 2 are listed:More than 20% depression of NT by PLC treatment was found in 2/14 controls, 9/19 AMI patients, 3/17 angina patients and 2/15 patients with other heart disease. The EVII:am values correlated better with NT (r = 0.81) than with PLC+NT (r=0.62). It has been suggested that FVII:am correlates with the molar concentration of FVII. If correct, our data precludes two chain FVII as contributing much to preactivation. EPI values were in the high normal range for all three groups of heart patients. The individual variation in EPI values was great, particularly in AMI patients. Apparently, EPI did not correlate to any of the FVII assays. Three patients with more then 50% reduced NT after PLC had EPI values 67, 149, and 130%. In conclusion, lipid activation was frequent in AMI patients, and was not related to EPI activity.
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