Journal articles: 'Lyly'

1

King, Rosalind, David Bevington, Michael Pincombe, and John Lyly. "Endymion: John Lyly." Yearbook of English Studies 29 (1999): 294. http://dx.doi.org/10.2307/3508970.

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Handayani, Sutri. "PENERAPAN COST PLUS PRICING DENGAN PENDEKATAN FULL COSTING DALAM MENENTUKAN HARGA JUAL PADA UD. LYLY BAKERY LAMONGAN." Akuisisi: Jurnal Akuntansi 15, no. 1 (May 11, 2020): 42–47. http://dx.doi.org/10.24127/akuisisi.v15i1.386.

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Setiap usaha yang didirikan mempunyai tujuan penting yaitu pencapaian laba yang optimum dan dapat bersaing dalam pasar. Harga jual merupakan faktor penting dalam bisnis perusahaan, karena harga jual yang terlalu tinggi akan menjadikan produk kurang bersaing dalam pasar, sedangkan harga jual terlalu rendah tidak akan memberikan keuntungan perusahaan. Penelitian ini bertujuan untuk untuk mengetahui cara penetapan harga jual yang tepat dengan metode Cost Plus Pricing pada UD. Lyly Bakery Lamongan dan anaka cabangnya. Metode yang digunakan dalam penelitian ini adalah metode analisis deskriptif kuantitatif. Hasil penelitian menunjukkan strategi penetapan harga jual dari UD. Lyly Bakery Lamongan adalah strategi penetapan harga produk gabungan dan strategi penyesuaian harga. Kesimpulan dalam penelitian ini menunjukkan penetapan harga jual dengan metode Cost Plus Pricing dengan pendekatan full costing tahun 2013 – 2015 harga jualnya lebih rendah dibandingkan dengan harga jual yang ditetapkan oleh UD. Lyly Bakery Lamongan, namun pada tahun 2015 ada dua jenis produk bakery dan donat yang harga jualnya mendekati harga jual yang ditetapkan oleh UD. Lyly Bakery Lamongan.Kata kunci: Cost Plus Pricing, full costing, harga jual

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Matikainen, Olli. "Jäkkäniska. Julius Anselm Lyly (1856–1903) viipurilaisena lehtimiehenä ja paikallispoliitikkona." Viipurin Suomalaisen Kirjallisuusseuran toimitteita, no. 21 (March 31, 2018): 41–68. http://dx.doi.org/10.47564/vskst.94649.

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4

Daniel (book editor), Carter A., and J. Michael Richardson (review author). "The Plays of John Lyly." Renaissance and Reformation 27, no. 1 (January 30, 2009): 84–86. http://dx.doi.org/10.33137/rr.v27i1.11733.

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5

Sell, Jonathan P. A. ""Warts and all": John Lyly’s atheist aesthetics." Sederi, no. 24 (2014): 95–118. http://dx.doi.org/10.34136/sederi.2014.5.

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This paper finds some evidence of an atomist aesthetic in certain passages of John Lyly’s Euphues. The Anatomy of Wit. It then addresses the issue of how Lyly might have become acquainted with atomist philosophy and, in particular, the thought of Empedocles, whether through his reading or his membership of the Oxford circle. Finally, by showing how Lyly’s early play Campaspe combines his aesthetic views and atomist controversy, the paper confirms the reasonableness of its initial proposition and opens the way not only for a reassessment of Lyly and his works but also for a reappraisal of the baroque in early modern English literature and for a revision of standard accounts of the origins of English atomism.

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Scragg, Leah. "John Lyly and the Politics of Language." Essays in Criticism 55, no. 1 (January 1, 2005): 17–38. http://dx.doi.org/10.1093/escrit/cgi02.

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7

DONOVAN, KEVIN J. "Recent Studies in John Lyly (1969–1990)." English Literary Renaissance 22, no. 3 (September 1992): 435–50. http://dx.doi.org/10.1111/j.1475-6757.1992.tb01048.x.

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8

LUNNEY, RUTH. "Recent Studies in John Lyly (1990–2010)." English Literary Renaissance 41, no. 3 (September 2011): 529–54. http://dx.doi.org/10.1111/j.1475-6757.2011.01095.x.

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9

Potter, Lois. "Performance Review: Gallathea by John Lyly." Cahiers Élisabéthains: A Journal of English Renaissance Studies 106, no. 1 (November 2021): 94–98. http://dx.doi.org/10.1177/01847678211044445c.

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10

Sung-Kyun Yim. "Sir Topas Chronicle: Chaucer, Spenser, Lyly, and Shakespeare." Journal of Classic and English Renaissance Literature 25, no. 2 (December 2016): 5–27. http://dx.doi.org/10.17259/jcerl.2016.25.2.5.

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11

Yaskun, Mohammad, and Diah Ayu Novitasari. "PENGARUH RELATIONHIP MARKETINGTERHADAP LOYALITAS PELANGGAN LYLY BAKERY LAMONGAN." JURNAL MANAJEMEN 2, no. 3 (October 1, 2017): 8. http://dx.doi.org/10.30736/jpim.v2i3.55.

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12

HADFIELD, ANDREW. "THE NAME ‘PHILAUTUS’: BARNABY RICH AND JOHN LYLY." Notes and Queries 48, no. 3 (September 1, 2001): 313–14. http://dx.doi.org/10.1093/nq/48-3-313.

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HADFIELD, ANDREW. "THE NAME ‘PHILAUTUS’: BARNABY RICH AND JOHN LYLY." Notes and Queries 48, no. 3 (2001): 313–14. http://dx.doi.org/10.1093/nq/48.3.313.

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14

Pincombe, M. "'Philautus' in Rich and Lyly: A Suspicion Confirmed." Notes and Queries 49, no. 2 (June 1, 2002): 253–54. http://dx.doi.org/10.1093/nq/49.2.253.

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15

Pincombe, Mike. "‘Philautus’ in Rich and Lyly: A Suspicion Confirmed." Notes and Queries 49, no. 2 (June 1, 2002): 253–54. http://dx.doi.org/10.1093/nq/490253.

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16

Scragg, Leah. "Angling for Answers: Looking for Lyly in the 1590s." Review of English Studies 67, no. 279 (November 18, 2015): 237–49. http://dx.doi.org/10.1093/res/hgv094.

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17

Cartwright, Kent. "The Confusions of Gallathea: John Lyly as Popular Dramatist." Comparative Drama 32, no. 2 (1998): 207–39. http://dx.doi.org/10.1353/cdr.1998.0000.

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18

Pincombe, M. "JOHN LYLY, The Woman in the Moon, ed. LEAH SCRAGG." Notes and Queries 54, no. 4 (December 1, 2007): 509–11. http://dx.doi.org/10.1093/notesj/gjm213.

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19

Scragg, L. "Note. Old versus new spelling: John Lyly - a special case?" Review of English Studies 50, no. 197 (February 1, 1999): 53–59. http://dx.doi.org/10.1093/res/50.197.53.

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20

Mentz, Steve. "Escaping Italy: From Novella to Romance in Gascoigne and Lyly." Studies in Philology 101, no. 2 (2004): 153–71. http://dx.doi.org/10.1353/sip.2004.0008.

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21

Pincombe, M. "Lyly and Golding: A New Source for Euphues and His England." Notes and Queries 51, no. 3 (September 1, 2004): 243–44. http://dx.doi.org/10.1093/nq/51.3.243.

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22

Pincombe, Mike. "Lyly and Golding: A New Source for Euphues and His England." Notes and Queries 51, no. 3 (September 1, 2004): 243–44. http://dx.doi.org/10.1093/nq/510243.

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23

Kawanami, Ayako. "John Lyly,Euphues: The Anatomy of Wit and Euphues and His England." Reformation 11, no. 1 (June 2006): 204–6. http://dx.doi.org/10.1558/refm.v11.204.

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24

Porter, Chloe. "Idolatry, Iconoclasm and Agency: Visual Experience in Works by Lyly and Shakespeare." Literature & History 18, no. 1 (May 2009): 1–15. http://dx.doi.org/10.7227/lh.18.1.1.

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25

STRÓBL, Erzsébet. "A TUDOR UDVARI KULTÚRA ÉS AZ ERZSÉBET-KULTUSZ." Hungarológiai Közlemények 17, no. 2 (September 19, 2016): 28. http://dx.doi.org/10.19090/hk.2016.2.28-41.

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A tanulmány a XVI. századi angol udvar kiemelkedő kulturális hatását vizsgálja. A korszak meghatározó alakja VIII. Henrik, aki mind humanista művészetpártolása, mind a politikai célok érdekében bevezetett vallási reformjai által megteremtette az alapját a század második felében kibontakozó pezsgő irodalmi életnek. A korszak másik nagy uralkodója, I. Erzsébet udvarának tagjai között található például Philip Sidney és Walter Ralegh, kik politikai befolyásuk mellett ezen időszak kiemelkedő költői is. Az Erzsébet királynőt körülvevő reprezentáció részeként írta legjelentősebb műveit John Lyly, George Gascoigne és Edmund Spenser, sőt a királynő dicsőítésére létrejött külön nyelvezet áthatja a kor alkotásait. Míg a Tudor-uralkodók udvara mind irodalmi, mind művészeti téren iránymutató, addig a XVII. században a királyi udvar e szerepköre elhalványul.

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26

Chiu, Sung Kai, Cedric Tremblay, Jesslyn Saw, and David J. Curtis. "Scl and Lyl1 Are Redundant in Erythropoiesis." Blood 126, no. 23 (December 3, 2015): 1182. http://dx.doi.org/10.1182/blood.v126.23.1182.1182.

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Abstract Stem cell leukaemia (Scl) and Lymphoblastic lymphoma derived sequence 1 (Lyl1) are the only hematopoiesis-specific basic Helix-loop-helix (bHLH) transcription factors. During development, Lyl1 is unable to compensate for Scl; with death of Scl-null embryos at e9.5 due complete absence of primitive hematopoiesis and defective vascular development. In contrast, Lyl1 can compensate for Scl in adult hematopoietic stem cells. To further explore the role of these two bHLH factors during hematopoietic development, we deleted Scl with Cre recombinase under the control of the Epo receptor, which is active in late erythroid progenitors. Surprisingly, embryos lacking Scl in erythroid progenitors (EpoR-Cre SclD/D) were born at the expected Mendelian frequency with only a mild anemia in adult mice. In contrast EpoR-Cre SclD/D mice lacking Lyl1 died at e11.5-12.5 due to erythropoietic collapse (see figure 1). These experiments provide the first evidence for an important role of Lyl1 in erythroid development and suggest that death of Scl-null embryos is due to defects in endothelial development rather than lack of primitive erythropoiesis. Figure 1. (A) Wildtype and (B) Scl/Lyl dko yolk sacs & embryos at e11.5. Benzidine stains of (C) wildtype & (D) Scl/Lyl dko yolk sacs at e11.5. Figure 1. (A) Wildtype and (B) Scl/Lyl dko yolk sacs & embryos at e11.5. / Benzidine stains of (C) wildtype & (D) Scl/Lyl dko yolk sacs at e11.5. Disclosures No relevant conflicts of interest to declare.

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27

BATES, CATHERINE. "‘A LARGE OCCASION OF DISCOURSE’ JOHN LYLY AND THE ART OF CIVIL CONVERSATION." Review of English Studies XLII, no. 168 (1991): 469–86. http://dx.doi.org/10.1093/res/xlii.168.469.

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28

Scragg, L. "Re-Editing Lyly for the Modern Reader, or the Case of Mother Bombie's Stool." Review of English Studies 63, no. 258 (February 23, 2011): 20–33. http://dx.doi.org/10.1093/res/hgr007.

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29

Holderness, Graham, and Anne Kelley. "A review ofthe plays of John Lyly, Eros and Eliza,edited by Michael Pincombe." Contemporary Theatre Review 7, no. 4 (January 1998): 117–20. http://dx.doi.org/10.1080/10486809808568484.

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30

Frankland, Emma, and Andy Kesson. ""Perhaps John Lyly was a trans woman?": An Interview about performing Galatea's Queer, Transgender Stories." Journal for Early Modern Cultural Studies 19, no. 4 (2019): 284–98. http://dx.doi.org/10.1353/jem.2019.0048.

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31

van Es, Bart. "Captive children: John Lyly, A Midsummer Night's Dream , and child impressment on the early modern stage." Renaissance Studies 33, no. 2 (February 14, 2018): 166–84. http://dx.doi.org/10.1111/rest.12389.

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32

Kesson, Andy. "“It is a pity you are not a woman”: John Lyly and the Creation of Woman." Shakespeare Bulletin 33, no. 1 (2015): 33–47. http://dx.doi.org/10.1353/shb.2015.0001.

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33

Ristyanadi, Bhiaztika, and Yunni Rusmawati Dwi Jayanti. "PENGARUH CITRA MERK DAN KEPUASAN PELANGGAN TERHADAP LOYALITAS KONSUMEN (Studi Kasus Perilaku Konsumen Toko Roti Lyly Bakery)." JURNAL MANAJEMEN 3, no. 2 (June 25, 2018): 690. http://dx.doi.org/10.30736/jpim.v3i2.184.

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34

Schmidt, Gabriela. "Jürgen Meyer,Textvarianz und Schriftkritik: Dialogische Schreib- und Lesekultur bei Thomas More, George Gascoigne & John Lyly." Anglia - Zeitschrift für englische Philologie 129, no. 3-4 (December 2011): 516–19. http://dx.doi.org/10.1515/angl.2011.066.

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35

Gilbert, Sky. "Shakespearean Pedagogy and Copious Paradox: How Might we Queer Shakespeare’s Work?" Brock Education Journal 28, no. 1 (December 10, 2018): 63–73. http://dx.doi.org/10.26522/brocked.v28i1.782.

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Despite opposition to ‘queering the text’ by established Shakespeare critics, this essay sets out to ponder the possibility of teaching Shakespeare in a queer context. The essay begins by examining the social and sexual conditions of the early modern period, making the observation that there were a wide variety of sexualities, moral attitudes, and sexual practices at that time, and that often the early modern moral codes of conduct contradicted each other. It then traces the significance of the rhetorical device of paradox through Lyly and Castiglione, and examines the method of Elizabethan rhetoric, which involved ‘copia’ (the elaboration of one idea into a variety of ideas through language) and its associated variety of meanings. The essay then turns to the text of Shakespeare’s Venus and Adonis, observing that its subject matter—the love of an older woman for a younger man—may have reflected the early modern heterosexual fear of women’s sexuality—and continues to baffle male critics today. Finally, turning to the poem itself—analyzing it in terms of ‘copia’ and paradox—the conclusion suggests that perhaps there was a relationship between Shakespeare’s use of these rhetorical techniques and the sexuality of his time.

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36

Van-Brunt, Alexander, and Matt Visser. "Explicit Baker–Campbell–Hausdorff Expansions." Mathematics 6, no. 8 (August 8, 2018): 135. http://dx.doi.org/10.3390/math6080135.

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The Baker–Campbell–Hausdorff (BCH) expansion is a general purpose tool of use in many branches of mathematics and theoretical physics. Only in some special cases can the expansion be evaluated in closed form. In an earlier article we demonstrated that whenever [X,Y]=uX+vY+cI, BCH expansion reduces to the tractable closed-form expression Z(X,Y)=ln(eXeY)=X+Y+f(u,v)[X,Y], where f(u,v)=f(v,u) is explicitly given by the the function f(u,v)=(u−v)eu+v−(ueu−vev)uv(eu−ev)=(u−v)−(ue−v−ve−u)uv(e−v−e−u). This result is much more general than those usually presented for either the Heisenberg commutator, [P,Q]=−iℏI, or the creation-destruction commutator, [a,a†]=I. In the current article, we provide an explicit and pedagogical exposition and further generalize and extend this result, primarily by relaxing the input assumptions. Under suitable conditions, to be discussed more fully in the text, and taking LAB=[A,B] as usual, we obtain the explicit result ln(eXeY)=X+Y+Ie−LX−e+LYI−e−LXLX+I−e+LYLY[X,Y]. We then indicate some potential applications.

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37

Billington, Sandra. "The Plays of John Lyly. Edited by Carter A. Daniel. London and Toronto: Golden Cockerel Press, 1989. Pp. 384. £29.95." Theatre Research International 15, no. 2 (1990): 175–77. http://dx.doi.org/10.1017/s0307883300009263.

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38

Chess, Simone. "“Or whatever you be”: Crossdressing, Sex, and Gender Labour in John Lyly’s Gallathea." Renaissance and Reformation 38, no. 4 (February 9, 2016): 145–66. http://dx.doi.org/10.33137/rr.v38i4.26377.

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This article explores sociologist Jane Ward’s gender and sexuality theory: the notion of “gender labour,” in which a cisgender (not crossdressed or trans*) partner participates in co-creating his or her partner’s queer gender. While work on gender labour thus far has focused on contemporary subjects, this article demonstrates the ways in which the concept can be generatively applied to an early modern context. The concept is pushed to its extremes in John Lyly’s Gallathea, in which the two genderqueer crossdressers, Gallathea and Phillida, each thinking that the other is male, create and enact romantic love scenes that involve gender play and a co-created divestment from biological sex. Cet article examine la théorie du sexe et du genre de la sociologue Jane Ward, en particulier la notion de « négociation du genre » dans laquelle des partenaires cissexuel (ni travesti, ni trans) contribuent à créer l’identité homosexuelle de l’un et de l’autre. Alors que la recherche sur cette « négociation du genre » s’est surtout penchée sur des questions contemporaines, cet article montre comment cette notion peut être appliquée à des contextes relevant des débuts de la modernité. Cette notion est poussée à l’extrême limite dans le Gallathea de John Lyly, pièce dans laquelle deux personnages travestis et homosexuels, Gallathea et Phillida, qui pensent que leur vis-à-vis est un autre homme, créent et réalisent des scènes d’amour entraînant des jeux de genre et une révélation commune de leur sexe biologique.

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39

Gilman, Todd. "Homosexualities in the English Theatre: From Lyly to Wilde. By John Franceschina. Westport, CT: Greenwood Press, 1997. Pp. xiv + 340. $59.95. Hb." Theatre Research International 24, no. 3 (1999): 295. http://dx.doi.org/10.1017/s0307883300019209.

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40

Weye, Nanna, Natalie Momen, Maria Christensen, Kim Iburg, John McGrath, and Oleguer Plana-Ripoll. "S130. ALTERNATIVE METRICS TO QUANTIFY PREMATURE MORTALITY IN MENTAL DISORDERS. A POPULATION-BASED COHORT STUDY." Schizophrenia Bulletin 46, Supplement_1 (April 2020): S84—S85. http://dx.doi.org/10.1093/schbul/sbaa031.196.

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Abstract Background The Global Burden of Disease (GBD) study uses Years of Life Lost (YLLs) to quantify premature mortality. This is a useful metric from many perspectives, however because GBD acknowledges only a small number of mental disorders as causes of death (CoDs), the true impact of mental disorders on premature mortality is underestimated. Recently, methods have been introduced that compare people with a disorder to the general population by estimating Life Years Lost (LYLs). The aim of this study was to present register-based estimates of both YLLs and LYLs related to mental disorders. Methods We used nationwide registers to examine a cohort of all 6,989,627 people aged 0–94 years living in Denmark in 2000–2015. Using the GBD approved set of mental health-related CoDs (eating disorders, drug use disorders, alcohol use disorder and suicide), YLLs were estimated. In addition, we calculated all-cause and cause-specific differences in life expectancy after a mental disorder diagnosis as excess LYLs between those with a specific mental disorder and the age- and sex-matched general Danish population. The disorders of interest were alcohol use disorder, drug use disorders, schizophrenia, bipolar disorders, depressive disorders, anxiety disorders, eating disorders, personality disorders, developmental intellectual disability, autism spectrum disorders, ADHD and conduct disorder. Excess LYLs related to counts of comorbid mental disorders were also examined (i.e. those diagnosed with at least two, three or four disorders). Results Alcohol use disorder and suicide were the leading causes of YLLs (alcohol use disorder: Men 568.7 YLLs, women 155.5 YLLs per 100,000 person-years; suicide: Men 590.1 YLLs, women 202.3 YLLs per 100,000 person-years). However, all mental disorders were associated with shorter life expectancies using LYLs. Men and women diagnosed with any mental disorder had 11.22 (95% CI 11.09; 11.35) and 7.89 (95% CI 7.76; 8.01) years shorter life expectancies respectively, and the difference increased in those with comorbid mental disorders. Drug use disorders were associated with the largest excess LYLs (17.99 (95% CI 17.49; 18.53) in men and 15.29 (95% CI 14.70; 15.88) in women), however common disorders such as depressive disorders and anxiety disorders were also associated with substantive premature mortality (e.g. in men, 8.27 and 7.52 LYLs, respectively). Schizophrenia was associated with 13.80 (95% CI 13.47; 14.14) excess LYLs in men and 11.77 (95% CI 11.38; 12.13) in women. Discussion Register-based studies allow the calculation of precise individual YLLs and LYLs. The novel LYL metric seems to better capture the true impact of mental disorders on premature mortality and also facilitates the exploration of comorbidity and specific CoDs in those with mental disorders.

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Zohren, Fabian, George Souroullas, Min Luo, Ulrike Gerdemann, Nicola K. Wilson, Berthold Göttgens, Georgi L. Lukov, and Margaret Goodell. "The Lymphoblastic Leukemia Gene 1 (Lyl1) Regulates Lymphoid Specification and Maintenance of Early T Lineage Progenitors." Blood 118, no. 21 (November 18, 2011): 548. http://dx.doi.org/10.1182/blood.v118.21.548.548.

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Abstract Abstract 548 Long-term thymopoiesis crucially depends on the recruitment and expansion of bone marrow derived progenitor cells. Therefore, a tight regulation of the thymus-settling progenitor cells is required to maintain T cell lineage homeostasis. Lyl1, a transcription factor involved in homeostatic control of immature hematopoietic cells, remains expressed in early T-lineage progenitors (ETPs) until T cell lineage commitment. Here we demonstrate a critical requirement for Lyl1 in lymphoid priming of bone marrow (BM) progenitors and in the maintenance of ETPs. Lyl1 deficient hematopoiesis was unable to generate sufficient numbers of lymphoid-primed progenitor populations such as LMPPs, CLPs and in particular ETPs. We found a significant (p>0.001) 4-fold reduction of LMPPs in the BM and a 20-fold reduction (p<0.001) of ETPs in the thymus of Lyl1 KO mice compared to wildtype controls. Transplantation assays revealed a selective defect of Lyl1−/− LMPPs for thymic engraftment and T lineage development. Intra-thymic injections of Lyl1−/− LMPPs demonstrated, in absence of homing requirements, a cell autonomous defect of Lyl1−/− progenitors in their ability to undergo the ETP to DN2 transition and to expand in response to Notch. Injection of Lyl1+/+ LMPPs resulted in a 5-fold higher recovery of total donor cells compared to injections of Lyl1−/− LMPPs (p<0.001). 40% of the donor cells derived after intra-thymic injection of Lyl1+/+ LMPPs were committed to the T cell lineage (DN3, DP, SP), whereas T lineage commitment after injection of Lyl1−/− cells was only seen in 20% of the recovered cells (p<0.01). By absolute numbers, wildtype LMPPs had generated more DN3 (8-fold), more DP (21-fold) and more SP (9-fold) T cell lineage committed thymocytes, and fewer Lyl1+/+ cells remained in the c-kit positive “ETP/LMPP-like” stage (-0.5-fold). In contrast, reintroduction of Lyl1 cDNA into Lyl1−/− BM progenitors using retroviral vectors restored the thymic progenitor pool and enhanced T cell lineage output. At 12 weeks after transplantation of MIG-Lyl1 transduced cells we observed a significant expansion of transfected (GFPpos) cells in the peripheral blood solely attributable to expansion of normal, mature and poly-clonal T cells (p<0.001). The thymuses of MIG-Lyl1 transplanted recipients showed significantly greater overall cellularity (p<0.01) attributable to a significantly higher proportion of GFPpos thymocytes (p<0.01) compared to the MIG-GFP transplanted control group. To gain a more detailed understanding of the underlying molecular mechanisms of Lyl1-mediated T-lymphoid specification, we performed global gene expression profiling of wildtype and Lyl1−/− LMPPs as well as whole genome ChIP-seqencing in HPC-7 cells after pull-down with anti-Lyl1 antibodies. Here, we identified the lymphoid-promoting factor Gfi1 as a critical transcriptional target of Lyl1-mediated T lymphopoiesis. We found that Gfi1 expression was decreased in Lyl1−/− LMPPs and ETPs by 2- and 7.5- fold respectively. ChIP assays using ckitpos BM cells from Lyl1+/+ and Lyl1−/− mice revealed a strong enrichment of Lyl1 at a known enhancer region of the Gfi1 locus located 35kb upstream of Gfi1 (p<0.001). Binding of Lyl1 activated the Gfi1 35kb enhancer element in transactivation assays (p<0.001). Finally, intra-thymic injection of Lyl1−/− progenitors after retroviral transduction with Gfi1 cDNA allowed lymphoid development and enhanced the T cell lineage output compared to GFP-transduced controls (p=0.08). Collectively, our data provide evidence that pro-T cell expansion in the thymus is regulated through intrinsic control of thymus progenitor cells that employ a transcriptional program already established in hematopoietic stem and progenitor cells. We identify Lyl1 as a critical component of this regulatory network, which is vital for the maintenance of T cell lineage homeostasis. Finally, identification of important downstream mediators of Lyl1 function not only illuminates the molecular mechanisms underlying early T-cell development, but also suggests previously unrecognized pathways likely to play a role in Lyl1-mediated development of leukemia and lymphoma. Disclosures: No relevant conflicts of interest to declare.

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Miyamoto, A., X. Cui, L. Naumovski, and M. L. Cleary. "Helix-loop-helix proteins LYL1 and E2a form heterodimeric complexes with distinctive DNA-binding properties in hematolymphoid cells." Molecular and Cellular Biology 16, no. 5 (May 1996): 2394–401. http://dx.doi.org/10.1128/mcb.16.5.2394.

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LYL1 is a basic helix-loop-helix (HLH) protein that was originally discovered because of its translocation into the beta T-cell receptor locus in an acute lymphoblastic leukemia. LYL1 is expressed in many hematolymphoid cells, with the notable exceptions of thymocytes and T cells. Using the yeast two-hybrid system to screen a cDNA library constructed from B cells, we identified the E-box-binding proteins E12 and E47 as potential lymphoid dimerization partners for LYL1. The interaction of LYL1 with E2a proteins was further characterized in vitro and shown to require the HLH motifs of both proteins. Immunoprecipitation analyses showed that in T-ALL and other cell lines, endogenous LYL1 exists in a complex with E2a proteins. A preferred DNA-binding sequence, 5'-AACAGATG(T/g)T-3', for the LYL1-E2a heterodimer was determined by PCR-assisted site selection. Endogenous protein complexes containing both LYL1 and E2a bound this sequence in various LYL1-expressing cell lines and could distinguish between the LYL1 consensus and muE2 sites. These data demonstrate that E2a proteins serve as dimerization partners for the basic HLH protein LYL1 to form complexes with distinctive DNA-binding properties and support the hypothesis that the leukemic properties of the LYL1 and TAL subfamily of HLH proteins could be mediated by recognition of a common set of target genes as heterodimeric complexes with class I HLH proteins.

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Pirot, Nelly, Virginie Deleuze, Rawan El-Hajj, Christiane Dohet, Fred Sablitzky, Philippe Couttet, Danièle Mathieu, and Valérie Pinet. "LYL1 activity is required for the maturation of newly formed blood vessels in adulthood." Blood 115, no. 25 (June 24, 2010): 5270–79. http://dx.doi.org/10.1182/blood-2010-03-275651.

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Abstract The 2 related basic helix loop helix genes, LYL1 and TAL-1 are active in hematopoietic and endothelial lineages. While Tal-1 is essential for both hematopoietic and vascular development, the role of Lyl1 appears to be distinct as deficient mice are viable and display modest hematopoietic defects. Here, we reveal a role for Lyl1 as a major regulator of adult neovascularization. Tumors implanted into Lyl1-deficient mice showed higher proliferation and angiogenesis, as evidenced by enlarged lumens, reduced pericyte coverage and increased permeability, compared with wild type littermates. Of note, Lyl1-deficient tumor vessels exhibited an up-regulation of Tal-1, the VE-Cadherin target gene, as well as Angiopoietin-2, 3 major actors in angiogenesis. Hematopoietic reconstitution experiments demonstrated that this sustained tumor angiogenesis was of endothelial origin. Moreover, the angiogenic phenotype observed in the absence of Lyl1 function was not tumor-restricted as microvessels forming in Matrigel or originating from aortic explants were also more numerous and larger than their wild-type counterparts. Finally, LYL1 depletion in human endothelial cells revealed that LYL1 controls the expression of molecules involved in the stabilization of vascular structures. Together, our data show a role for LYL1 in the postnatal maturation of newly formed blood vessels.

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Souroullas, George, and Margaret Goodell. "Lyl1 and Scl Regulate Bcl2 Expression and Control Apoptosis at Different Stages of Hematopoietic Development." Blood 114, no. 22 (November 20, 2009): 569. http://dx.doi.org/10.1182/blood.v114.22.569.569.

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Abstract Abstract 569 The Lymphoblastic Leukemia gene 1 (Lyl1) encodes a basic-helix-loop-helix (bHLH) transcription factor that is involved in T cell acute lymphoblastic leukemia via chromosomal translocations. Lyl1 has an almost identical bHLH motif to Scl, a known master regulator of hematopoiesis. In our previous work, we used a double knock-out mouse model to demonstrate functional redundancy between Lyl1 and Scl in adult hematopoietic stem cells (HSCs), where in the absence of both genes in adult mice, HSCs and progenitors undergo rapid apoptosis. Despite their common and overlapping functions, the two genes appear to also function at different aspects of hematopoietic development. Lyl1 knock-out mice exhibit a unique defect in B-cell development. This phenotype is recapitulated in vitro, where Lyl1 progenitors grown on a layer of OP9 cells and allowed to differentiate with the addition of cytokines fail to differentiate to B cells as well as wild type progenitors. Rescue assays, where Lyl1 was transduced using a retrovirus into Lyl1 knock-out progenitors and transplanted into lethally irradiated recipients, showed complete rescue of the B cell lineage. Forced expression of Scl into Lyl1 knock-out progenitors failed to rescue, giving rise to only about 5% of peripheral blood B cells. This demonstrates the distinct functions of the two genes in differentiated cells types, despite their functional redundancy in the HSCs. We further sought to dissect the functions and differences between Lyl1 and Scl based on their target genes. Using bioinformatics analysis and a literature search, we identified a number of genes that were candidates for Lyl1 transcriptional regulation; these interactions with Lyl1 and Scl were confirmed by chromatin immunoprecipitation. We found that Bcl2, and genes belonging to this family, are direct target genes of both Lyl1 and Scl in progenitor cells, and that they are downregulated in Lyl1 and Scl single knock-out mouse models. Since Bcl2 is critical for B cell survival, we hypothesized that the B cell deficiency in Lyl1 knock-out mice could be partly due to a loss of Bcl2. We performed rescue assays where Bcl2 was transduced using a retrovirus into Lyl1 knock-out progenitors which were transplanted into lethally irradiated recipient mice. Bcl2 overexpression rescued the B-cell defect in Lyl1 knock-out bone marrow. Since Bcl2 was identified as a target gene for Scl as well, we tested whether Bcl2 could also rescue the rapid apoptosis phenotype of the Lyl1/Scl double knock-out progenitors. Forced expression of Bcl2 in these cells, followed by deletion of the floxed Scl allele, resulted in a delayed onset of apoptosis, but incomplete rescue of the progenitor cell death. These findings distinguish the activities of Lyl1 and Scl in B cells and demonstrate a possible mechanism for their functions, through in part by their activation of the antiapoptotic gene Bcl2. Disclosures: No relevant conflicts of interest to declare.

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Meng, Yuesheng, Wei Liu, Xiaoxia Ma, Xiuqin Meng, Gongwen Ai, and Yanxiang Zhang. "Decreased Proliferation of Myeloid Leukemia Cells through Down-Regulating LYL1 Expression with Small Interference RNA." Blood 110, no. 11 (November 16, 2007): 4158. http://dx.doi.org/10.1182/blood.v110.11.4158.4158.

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Abstract Ectopic expression of the basic helix-loop-helix transcription factor LYL1 has been implicated in T-cell acute lymphoblastic leukemia (T-ALL). It has also been found to be over-expressed in cells of acute myeloid leukemia (AML). Myeloid leukemia cells over-expressing LYL1 cDNA had accelerated growth rates, increased plating efficiency and a blockade of differentiation. To further investigate its role in the pathogenesis of leukemia, we used small interference RNA (siRNA) to silence the expression of LYL1 in human leukemia cell line K562, which expresses a moderate level of endogenous LYL1 protein. Three LYL1-specific RNA oligos, the Stealth Select RNAi HSS142834, HSS142835, and HSS142836, purchased from Invitrogen, were introduced into K562 cells by using Invitrogen transfection reagent Lipofectamine RNAiMAX. Two successive transfections at day 1 and day 2 were made according to manufacturer’s manual. Expression levels of LYL1 in LYL1 siRNA transfected cells and control cells (transfected with the Stealth RNAi Negative Controls) were determined with fluorescence real-time quantitative polymerase chain reaction assay. Our result showed that the application of any single RNAi oligo achieved observable inhibition of LYL1 expression levels (30–40%) while a combination of the three RNAi oligos remarkable inhibition (70.4%). The growth rates of K562 cells were not affected by any single RNAi oligo. However, a combination of three RNAi oligos did induce noticeable growth inhibition of cells. Plating efficiency assay showed that the clonogenic recovery rate of K562 cells treated with a combination of thee RNAi oligos was inhibited by 32.5% (P<0.05). The reduced growth rate and clonogenicity of cells was supposed to be secondary to the repressed expression of LYL1 because all other factors were controlled in our experiments. Further experiments are underway to define the changes of other genes in the LYL1-suppressed cells. We also tested the effect of specific siRNA on the expression of LYL1 and clonogenecity of leukemia cells in patient samples. Mononuclear cells separated from nine newly-diagnosed AML patients whose cells expressed comparatively higher levels of LYL1 were transfected with a combination of three LYL1 specific siRNA oligos for twice. We found that the siRNA oligos suppressed the expression of LYL1 in leukemia cells in most of the patients (7/9, decreased by 2 times or more) when compared with controls. Remarkably, the clonogenicity of AML cells in 3 patients was also inhibited by siRNA (P<0.05). In conclusion, the specific siRNA was effective to downregulate the expression of LYL1 in myeloid leukemia cells. It was also effective to affect cell proliferation in some cases. The data demonstrates that LYL1 plays a role for the malignant genotypes of leukemia cells and suggests that the RNA interference therapy targeting specific oncogenes might be clinically useful in the management of hematological malignancies.

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Hussain, Abid, Virginie Deleuze, Leila El Kebriti, Hulya Turali, Nelly Pirot, Yaël Glasson, Danièle Mathieu, and Valérie Pinet. "In Lyl1 −/− mice, adipose stem cell vascular niche impairment leads to premature development of fat tissues." Stem Cells 39, no. 1 (October 13, 2020): 78–91. http://dx.doi.org/10.1002/stem.3286.

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Abstract Lyl1 encodes a hematopoietic- and endothelial-specific bHLH transcription factor. Lyl1-deficient mice are viable, but they display mild hematopoietic and vascular defects. Specifically, LYL1 is required for the maturation and stabilization of blood vessel endothelial adherens junctions. Here, we report that young adult Lyl1−/− mice exhibit transient overweight associated with general expansion of adipose tissue, without signs of metabolic disorder and unrelated to food intake. The increased fat tissue development in Lyl1−/− mice resulted from earlier differentiation of adipose stem cells (ASCs) into adipocytes through noncell autonomous mechanisms. Specifically, we found that in Lyl1−/− mice, the adipose tissue vascular structures are immature, as indicated by their high permeability, reduced coverage by pericytes, lower recruitment of VE-cadherin and ZO1 at cell junctions, and more prone to angiogenesis. Together, our data show that in Lyl1−/− mice, the impaired vascular compartment of the adipose niche promotes ASC differentiation, leading to early adipocyte expansion and premature ASC depletion. Our study highlights the major structural role of the adipose tissue vascular niche in coordinating stem cell self-renewal and differentiation into adipocytes.

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Souroullas, George, Jessica Salmon, David J. Curtis, and Margaret Goodell. "Lyl1 and Scl Dosage Is Critical for Adult Hematopoietic Stem Cell Function and Survival." Blood 112, no. 11 (November 16, 2008): 281. http://dx.doi.org/10.1182/blood.v112.11.281.281.

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Abstract The Stem Cell Leukemia gene (Scl) and the Lymphoblastic Leukemia gene 1 (Lyl1) genes encode two related basic-helix-loop-helix transcription factors that are involved in T-cell acute lymphoblastic leukemia via chromosomal translocations or aberrant expression due to other genetic or epigenetic abnormalities. Previous studies have shown that Scl is necessary for embryonic hematopoiesis and erythropoiesis, but dispensable for adult hematopoietic stem cell (HSC) function. Lyl1 on the other hand is important for adult HSC function and B-cell development. In order to elucidate in more detail the functions of Lyl1 and Scl in adult HSCs, we generated double knock-out mice and studied the function of their HSCs. Double knock-out mice demonstrate a striking genetic interaction between the two genes, with a clear dose-dependence for the presence of Scl or Lyl1 alleles for HSC function. Specifically, we carried out competitive fetal liver transplantation assays using mice with different combinations of Lyl1 and Scl alleles and analyzed their potential to repopulate the bone marrow of recipient mice. Peripheral blood chimerism of recipient mice shows that HSC function is lost with progressive loss of Lyl1 or Scl dosage, suggesting an overlap of function of the two genes in the HSCs (Figure) We have further investigated the function of Lyl1 and Scl in adult hematopoiesis by generating Lyl1/Scl-conditional double knock-out mice and studied adult HSC function measured by bone marrow repopulation assays. Donor engraftment dramatically decreased after deletion of the floxed Scl allele, demonstrating rapid loss of adult HSC function. Furthermore, Scl deletion in a Lyl1−/− background causes hematopoietic progenitors to rapidly undergo apoptosis in a cell-intrinsic fashion. These results demonstrate that at least one allele of either Lyl1 or Scl must be present for adult HSC survival, and show that their functions partly overlap in HSCs, suggesting that Lyl1 and Scl are crucial regulators of adult, as well as embryonic, hematopoiesis. Figure Figure

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Chan, Wan Y. I., George A. Follows, Georges Lacaud, John E. Pimanda, Josette-Renee Landry, Sarah Kinston, Kathy Knezevic, et al. "The paralogous hematopoietic regulators Lyl1 and Scl are coregulated by Ets and GATA factors, but Lyl1 cannot rescue the early Scl–/– phenotype." Blood 109, no. 5 (October 19, 2006): 1908–16. http://dx.doi.org/10.1182/blood-2006-05-023226.

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Abstract Transcription factors are key regulators of hematopoietic stem cells (HSCs), yet the molecular mechanisms that control their expression are largely unknown. Previously, we demonstrated that expression of Scl/Tal1, a transcription factor required for the specification of HSCs, is controlled by Ets and GATA factors. Here we characterize the molecular mechanisms controlling expression of Lyl1, a paralog of Scl also required for HSC function. Two closely spaced promoters directed expression to hematopoietic progenitor, megakaryocytic, and endothelial cells in transgenic mice. Conserved binding sites required for promoter activity were bound in vivo by GATA-2 and the Ets factors Fli1, Elf1, Erg, and PU.1. However, despite coregulation of Scl and Lyl1 by the same Ets and GATA factors, Scl expression was initiated prior to Lyl1 in embryonic stem (ES) cell differentiation assays. Moreover, ectopic expression of Scl but not Lyl1 rescued hematopoietic differentiation in Scl−/− ES cells, thus providing a molecular explanation for the vastly different phenotypes of Scl−/− and Lyl1−/− mouse embryos. Furthermore, coregulation of Scl and Lyl1 later during development may explain the mild phenotype of Scl−/− adult HSCs.

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Pirot, Nelly, Hélène Delpech, Virginie Deleuze, Christiane Dohet, Monique Courtade-Saïdi, Céline Basset-Léobon, Elias Chalhoub, Danièle Mathieu, and Valérie Pinet. "Lung endothelial barrier disruption in Lyl1-deficient mice." American Journal of Physiology-Lung Cellular and Molecular Physiology 306, no. 8 (April 15, 2014): L775—L785. http://dx.doi.org/10.1152/ajplung.00200.2013.

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Maturation of newly formed vessels is a multistep phenomenon during which functional endothelial barriers are established. Disruption of vessel integrity is an important feature in many physiological and pathological processes. We previously reported that lymphoblastic leukemia-derived sequence 1 (LYL1) is required for the late stages of postnatal angiogenesis to limit the formation of new blood vessels, notably by regulating the activity of the small GTPase Rap1. In this study, we show that LYL1 is also required during the formation of the mature endothelial barrier in the lungs of adult mice. Specifically, LYL1 knockdown in human endothelial cells downregulated the expression of ARHGAP21 and ARHGAP24, which encode two Rho GTPase-activating proteins, and this was correlated with increased RhoA activity and reorganization of the actin cytoskeleton into stress fibers. Importantly, in lungs of Lyl1-deficient mice, both vascular endothelial (VE)-cadherin and p120-catenin were poorly recruited to endothelial adherens junctions, indicative of defective cell-cell junctions. Consistent with this, higher Evans blue dye extravasation, edema, and leukocyte infiltration in the lung parenchyma of Lyl1−/− mice than in wild-type littermates confirmed that lung vascular permeability is constitutively elevated in Lyl1−/− adult mice. Our data show that LYL1 acts as a stabilizing signal for adherens junction formation by operating upstream of VE-cadherin and of the two GTPases Rap1 and RhoA. As increased vascular permeability is a key feature and a major mechanism of acute respiratory distress syndrome, molecules that regulate LYL1 activity could represent additional tools to modify the endothelial barrier permeability.

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Sah, Naresh, Swetha Peddibhotla, Bayley Richardson, Pamela Luna, Neel A. Bansal, Chinnadurai Mani, Mark Reedy, and Komaraiah Palle. "Abstract A084: Oncogenic role for upregulated lymphoblastic leukemia derived sequence-1 in the progression of ovarian cancer and its metastasis." Cancer Epidemiology, Biomarkers & Prevention 32, no. 1_Supplement (January 1, 2023): A084. http://dx.doi.org/10.1158/1538-7755.disp22-a084.

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Abstract In 2022, about 19,880 women will be newly diagnosed with ovarian cancer (OC), out of which around 12,180 will die. Epithelial Ovarian Cancer (EOC) represents approximately 95% of all OC and is the fifth leading cause of cancer-related deaths in women (deadliest among all gynecological malignancies). Standard treatment for EOC includes surgery, platinum-based chemotherapy, and radiation therapy. Despite these advancements (more than 90% of patients relapse), not all racial and ethnic groups have benefited equally. For instance, the five-year survival rate for OC grew from 33% to 48% among non-Hispanic White women but declined from 44% to 41% among African American (AA) women. The higher tendency to develop chemoresistance in AA women further contributes to their worst survival. No precise mechanisms that contribute to OC racial health disparity have been explained. We aim to delineate the genetic and molecular mechanisms responsible for driving aggressive tumor growth in AA women that disproportionately affect outcomes. This would aid in developing precision therapeutics and eliminate racial disparity in OC outcomes. Analysis of the TCGA data for OC revealed that the Lymphoblastic Leukemia-Derived Sequence 1 (LYL1) gene is one of the frequently amplified genes in OC. About 12% of all the OC shows LYL1 gene amplification. Interestingly, analysis based on ethnicity revealed a remarkable 36% of LYL1 amplification in AA EOC patients, which is one of the top genes after MYC. Importantly, EOC patients with high levels of LYL1 expression (n=202) had a lower survival rate (p=0.003) than those with low levels of LYL1 expression (n=1640). To further confirm the oncogenic functions of LYL1, we analyzed LYL1 expression in EOC cell lines compared to normal fallopian tube epithelial cells (FTECs) and its contribution to OC cell growth and metastatic potential. As expected, LYL1 is upregulated in most of the EOC cell lines compared to normal FTECs, and siRNA-mediated downregulation of LYL1 in EOC cell lines decreased their clonogenic, migration and invasion potential. Conversely, ectopic expression of LYL1 in an EOC cell line expressing low or undetectable levels of LYL1 exhibited increased potential for migration, invasion, and ability to form tumor spheroids. To validate these in vitro studies, we implanted the OVCAR8 cell xenografts transuded with lentivirus-mediated non-targeting shRNAs or shLYL1 into immunocompromised mice. Consistent with the in vitro data, LYL1 expressing OVCAR8 cell xenograft tumors grew aggressively with widespread metastasis in the peritoneum and distant organs. In contrast, LYL1 knockdown tumor xenografts grew slow and showed decreased metastasis. Together, our results show that upregulated or amplified LYL1 in EOC promotes aggressive tumor growth and may contribute to racial disparity in EOC, as this gene is amplified in over 36% of AA OC patients compared to 12% of White patients. Additionally, our studies suggest that LYL1 could be a poor prognostic marker for OC and racial disparities in OC outcomes. Citation Format: Naresh Sah, Swetha Peddibhotla, Bayley Richardson, Pamela Luna, Neel A. Bansal, Chinnadurai Mani, Mark Reedy, Komaraiah Palle. Oncogenic role for upregulated lymphoblastic leukemia derived sequence-1 in the progression of ovarian cancer and its metastasis [abstract]. In: Proceedings of the 15th AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2022 Sep 16-19; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2022;31(1 Suppl):Abstract nr A084.

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Journal articles on the topic 'Lyly'

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