Relevant bibliographies by topics / 3-fold flips

Academic literature on the topic '3-fold flips'

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Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "3-fold flips"

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Shokurov, V. V. "3-FOLD LOG FLIPS." Russian Academy of Sciences. Izvestiya Mathematics 40, no. 1 (February 28, 1993): 95–202. http://dx.doi.org/10.1070/im1993v040n01abeh001862.

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Shokurov, V. V. "SEMISTABLE 3-FOLD FLIPS." Russian Academy of Sciences. Izvestiya Mathematics 42, no. 2 (April 30, 1994): 371–425. http://dx.doi.org/10.1070/im1994v042n02abeh001541.

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Seal, Sudeshna, Daniella B. Kerbauy, Vladimir Lesnikov, Nissa Abbasi-Shafer, and H. Joachim Deeg. "FLIPLong(L) and FLIPShort(S) Overexpression in the Human Myeloid Leukemia Cell Line ML-1 and Its Role in TRAIL [Tumor Necrosis Factor(TNF)-Related Apoptosis-Inducing Ligand] and TNFa Induced Apoptosis." Blood 106, no. 11 (November 16, 2005): 4378. http://dx.doi.org/10.1182/blood.v106.11.4378.4378.

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Abstract TRAIL initiates activation of Caspase-8, which is blocked by the FLICE inhibitory protein (FLIP), resulting in resistance to apoptosis. Here we show that overexpression of FLIPL and FLIPS in ML1 cells, with low constitutive levels of FLIP, protects these cells against apoptosis induced by TRAIL, not only via Caspase-8 inhibition, but also via upregulation of anti-apoptotic molecules. Methods: 1) Apoptosis was determined by Annexin V/ 7-AAD following treatment with TRAIL (100–500ng/ml), or TNFa (20–100ng/ml) in ML1 cells transduced with FLIPL.GFP (green fluorescent protein), FLIPS.GFP or Neo.GFP (control). 2) Caspase-8, Caspase-3, Bid, Bcl-xL, XIAP, phosphorylated (P)-IKBa and P-Akt were determined by western blots. 3) Active Caspase-3 was determined using EnzChek Caspase-3 assay kit. Results: Both FLIPL and FLIPS transduction protected ML1 cells against apoptosis induced by TRAIL (300ng/ml), while no protection was observed in Neo.GFP cells. FLIPL had a more profound protective effect than FLIPS (Fig.1A). Both FLIPL and FLIPS, but not Neo.GFP, blocked Caspase-8 and Caspase-3 activation (Fig.1B); FLIPS cells showed two-fold higher levels of active Caspase-3 than FLIPL cells, consistent with higher apoptosis in FLIPS cells. Caspase-3 can be activated through Caspase-8 (extrinsic pathway) or via Caspase-8/Bid (intrinsic pathway). The latter was responsible for high active Caspase-3 levels in FLIPS cells as shown by the presence of cleaved Bid (t-Bid) (Fig.1B); cleavage of Bid was inhibited by combination of TRAIL and Z-IETD-FMK (Caspase-8 inhibitor). Anti-apoptotic molecules, including Bcl-xL, XIAP and FLIP are regulated by NF-kB and FLIP participates in an NF-kB auto-amplification loop. While Neo.GFP cells showed little Bcl-xL after 4h of TRAIL exposure and there was a twofold reduction in FLIPS cells, only a slight reduction of Bcl-xL was noted in FLIPL cells. FLIPL cells showed the lowest rates of apoptosis when exposed to TNFa and BMS543541, a specific inhibitor of IkB kinase (Fig. 1C). In the presence of BMS543541, phosphorylation of IkBa and levels of Bcl-xL and XIAP decreased in Neo.GFP and FLIPS but not in FLIPL cells. Additional data suggest that the PI3-kinase/Akt pathway is involved in constitutive NF-kB activation and differentially affected by FLIPL and FLIPS (Fig. 1D). Preliminary results in immunodeficient mice transplanted with transduced ML1 cells indicated the in vivo relevance of the differences between FLIPL and FLIPS with FLIPL cells engrafting earlier and showing earlier signs of sickness. Conclusions: FLIPL and FLIPS conferred resistance to TRAIL induced apoptosis but showed differential effects: Caspase-8/Bid was involved in the apoptosis pathway in FLIPS, but not in FLIPL cells. FLIPL cells’ resistance was due not only to caspase inhibition but to the recruitment of downstream anti-apoptotic pathways such as NF-kB and PI3K/Akt. In vivo data further substantiated the antiapoptotic/pro-survival behavior of FLIPL cells. Figure Figure
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Shokurov, V. V. "AN ADDENDUM TO THE PAPER “3-FOLD LOG FLIPS”." Russian Academy of Sciences. Izvestiya Mathematics 43, no. 3 (June 30, 1994): 527–58. http://dx.doi.org/10.1070/im1994v043n03abeh001579.

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WALDRON, JOE. "THE LMMP FOR LOG CANONICAL 3-FOLDS IN CHARACTERISTIC." Nagoya Mathematical Journal 230 (February 20, 2017): 48–71. http://dx.doi.org/10.1017/nmj.2017.2.

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We prove that one can run the log minimal model program for log canonical 3-fold pairs in characteristic $p>5$. In particular, we prove the cone theorem, contraction theorem, the existence of flips and the existence of log minimal models for pairs with log divisor numerically equivalent to an effective divisor. These follow from our main results, which are that certain log minimal models are good.
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Troeger, Anja, Ingo Schmitz, Ludmila Glouchkova, Meinolf Siepermann, Gritta Janka-Schaub, Klaus Schulze-Osthoff, and Dagmar Dilloo. "Upregulation of FLIPs upon CD40 Stimulation - A Novel Inhibititory Mechanism of CD95-Induced Apoptosis in Precursor B-ALL Blasts in Children." Blood 106, no. 11 (November 16, 2005): 855. http://dx.doi.org/10.1182/blood.v106.11.855.855.

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Abstract The influence of the microenvironment on the activation status and behaviour of ALL blasts is critical for interactions with the immune system in vivo. The capacity of B cells to respond to CD40-ligand (CD40L) stimulation is critical for their sensitisation to immunological control mechanisms and susceptibility to apoptotic signals. Primary precursor B-ALL blasts (BCP-ALL; n=32) lack CD95-expression (mean±SE; 4.2±0.6% positive cells) and are resistant to apoptosis while significant up-regulation of CD95 is apparent upon CD40-stimulation in BCP-ALL blasts that reaches a plateau after 72 h. Yet, in spite of equivalent CD95-upregulation in ALL blasts (58.3±6.5%; n=17) and normal B cells (59.3±13.1%) specific apoptosis is markedly lower in ALL compared to mature B cells (19.1±3% vs 36.7±5.5%). Resistance to apoptosis in ALL blasts and its reversibility after cycloheximid treatment suggest that anti-apoptotic mechanisms prevent induction of cell death via CD95 ligation in CD40 activated blasts. In accordance, in CD40-activated ALL blasts caspase 8 and 3 activity is not enhanced upon CD95 ligation in contrast to an 1.8±0.3 and 1.7±0.3 fold increase in caspase activity in stimulated normal B cells (n=7), suggesting a block of the apoptotic cascade in BCP-ALLrelatively close to the receptor level. CD40L-activated ALL blasts and normal B cells were submitted to western blot analysis with respect to the molecules associated to the death-inducing signalling complex (DISC). FADD and the zymogen form of caspase-8 are constitutively expressed in both malignant and non malignant B cells with no modulation following CD40 ligation. In contrast, the anti-apoptotic short isoform of the c-FLICE inhibitory protein FLIPS is weakly expressed in naïve blasts and B cells, but strongly up-regulated upon 72h CD40-ligation in ALL with only barely detectable levels in CD40-activated normal B cells. We therefore propose, that prolonged induction of the FLIPS expression inhibits the onset of apoptosis despite high CD95 surface expression levels in BCP-ALL blasts. As an additional anti-apoptotic mechanism inhibiting the downstream effector caspases we demonstrated significant upregulation of the inhibitor of apoptosis protein (IAP) survivin in CD40-activated BCP-ALL (n=6) compared to the unstimulated control (632pg/ml±200pg/ml vs 180pg/ml±52pg/ml). Thus, we identified FLIPS as a CD40-regulated upstream anti-apoptotic element and concomitant downstream upregulation of survivin protein expression as critical mechanisms contributing to blast cell resistance to apoptosis.
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Qin, Haixia, Michael A. Frohman, and Wendy B. Bollag. "Phospholipase D2 Mediates Acute Aldosterone Secretion in Response to Angiotensin II in Adrenal Glomerulosa Cells." Endocrinology 151, no. 5 (March 10, 2010): 2162–70. http://dx.doi.org/10.1210/en.2009-1159.

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In primary bovine adrenal glomerulosa cells, the signaling enzyme phospholipase D (PLD) is suggested to mediate priming, the enhancement of aldosterone secretion after pretreatment with and removal of angiotensin II (AngII), via the formation of persistently elevated diacylglycerol (DAG). To further explore PLD’s role in priming, glomerulosa cells were pretreated with an exogenous bacterial PLD. Using this approach, phosphatidic acid (PA) is generated on the outer, rather than the inner, leaflet of the plasma membrane. Although PA is not readily internalized, the PA is nonetheless rapidly hydrolyzed by cell-surface PA phosphatases to DAG, which efficiently flips to the inner leaflet and accesses the cell interior. Pretreatment with bacterial PLD resulted in priming upon subsequent AngII exposure, supporting a role of DAG in this process, because the increase in DAG persisted after exogenous PLD removal. To determine the PLD isoform mediating aldosterone secretion, and presumably priming, primary glomerulosa cells were infected with adenoviruses expressing GFP, PLD1, PLD2, or lipase-inactive mutants. Overexpressed PLD2 increased aldosterone secretion by approximately 3-fold over the GFP-infected control under basal conditions, with a significant enhancement to about 16-fold over the basal value upon AngII stimulation. PLD activity was also increased basally and upon stimulation with AngII. In contrast, PLD1 overexpression had little effect on aldosterone secretion, despite the fact that PLD activity was enhanced. In both cases, the lipase-inactive PLD mutants showed essentially no effect on PLD activity or aldosterone secretion. Our results suggest that PLD2 is the isoform that mediates aldosterone secretion and likely priming.
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Miyazono, Kenichi, Yoshikazu Furuta, Miki Watanabe-Matsui, Takuya Miyakawa, Tomoko Ito, Ichizo Kobayashi, and Masaru Tanokura. "Sequence-specific DNA glycosylase found in a restriction-modification system." Acta Crystallographica Section A Foundations and Advances 70, a1 (August 5, 2014): C213. http://dx.doi.org/10.1107/s2053273314097861.

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Restriction-modification systems consist of genes that encode a restriction enzyme and a cognate modification methyltransferase. It was believed that restriction enzymes are sequence-specific endonucleases that introduce double-strand breaks at specific sites by catalyzing the cleavages of phosphodiester bonds. R.PabI is a type II restriction enzyme from a hyperthermophilic archaea Pyrococcus abyssi that recognizes 5'-GTAC-3' sequence and cleaves DNA duplexes without the addition of a divalent cation. The structural and mutational analyses of R.PabI in our previous work showed that R.PabI forms a homodimer and has a novel DNA-binding fold called a "half-pipe," which consists of a highly curved anti-parallel β-sheet. Because the structure of R.PabI shares no structural similarity to any other protein, the structural basis of the sequence-recognition and DNA-cleavage mechanisms remained unclear. In this study, we report the crystal structure of R.PabI in complex with a DNA duplex containing the R.PabI recognition sequence. The structure of the R.PabI-DNA complex shows that R.PabI unwinds a DNA duplex at a 5'-GTAC-3' site and flips the guanine and adenine bases out of the DNA helix to recognize the sequence. The electron-density map of the R.PabI-DNA complex shows that R.PabI releases adenine bases from the R.PabI recognition sequence. Biochemical assays using HPLC and MALDI-TOF MS spectrometry also support the observation that R.PabI releases adenine bases by hydrolysis. These results show that R.PabI is not an endonuclease but a sequence-specific adenine DNA glycosylase. R.PabI is the first example of a restriction enzyme that shows DNA glycosylase activity. Mutational analysis reveals the active site of the adenine DNA glycosylase activity of R.PabI. The two opposing apurinic/apyrimidinic (AP) sites generated by R.PabI are cleaved by heat promoted β elimination and/or by endogenous AP endonucleases of host cells to introduce a double-strand break.
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Tan, GMY, SMAR Hosseini, A. Poudel, and AD Mclellan. "O6 Expression of anti-apoptotic gene cFLIP to enhance persistence in CAR T cells." Journal for ImmunoTherapy of Cancer 8, Suppl 2 (October 2020): A6.1—A6. http://dx.doi.org/10.1136/jitc-2020-itoc7.11.

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BackgroundCAR T cell therapy has been successful for targeting blood cancers, but treatment of solid cancers has been limited due to the heterogenous nature of tumour-associated antigen expression on solid cancers, and the suppressive tumour microenvironment.1 Another major obstacle to CAR T cell therapy is activation-induced cell death (AICD) of the CAR T cells.2 In this study, we expressed the anti-apoptotic cellular FLICE-like inhibitory protein (c-FLIP short; c-FLIPs) together with the CAR construct to enhance CAR T cell persistence.3Materials and MethodsThe anti-Her2 FRP5 CAR T construct with P2A-linked cFLIPs or cFLIPp43 was cloned into the Sleeping Beauty (SB) transposon vector (pSBtet-GP) or lentiviral vector, under the control of either a tet-on or a constitutive promoter. Construct expression was validated by qPCR and immunoblot analysis. CAR T cells were generated by SB transposition or lentiviral transduction of CD3/CD28 stimulated primary human T cells that were subsequently maintained with IL-2. Mitochondrial function and apoptosis were determined by resazurin assay and by flow cytometry using tetramethyl rhodamine (TMRE).ResultsOverexpression of cFLIP (cFLIPp43 and cFLIPs) in pSBtet-GP demonstrated protection in both Jurkat T cell line and primary human T cells. pSBtet-GP was modified to overexpress cFLIPs and cFLIPp43 under tet-on promoter, with the anti-her2 CAR, GFP and rtTA under constitutive promoter. Transfer of the inducible cassette from the SB transposon to a lentiviral system resulted in a significant loss of tightness. Doxycycline treated CAR T cells showed only ~13-fold overexpression of cFLIPs or cFLIPp43 compared to untreated cells, and doxycycline significantly inhibited (approximately 30%) primary CAR T cell expansion. In contrast, constitutive expression of CAR-cFLIPs or cFLIPp43 construct gave a >3 × 105-fold cFLIP overexpression, as compared to CAR-only control. While the transduction efficiency of CAR-only was around 70–80% control in primary T cells, this dropped to 20–25% when using the more genetically complex tet-on system.ConclusionscFLIP protects T cells from Fas-induced apoptosis. The tet-on system demonstrates several drawbacks in the lentiviral system, including toxicity of the inducer drug (and/or squelching effects resulting in lowered viability), loss of responsiveness and lowered transduction frequencies. Therefore, a constitutive promoter system is preferred in lentiviral systems for the control of genes of interest within CAR T cells, while the SB transposon system may be preferred for tet-on control within CAR T cells.ReferencesPitt JM, Marabelle A, Eggermont A, Soria JC, Kroemer G, and Zitvogel L. Targeting the tumor microenvironment: removing obstruction to anticancer immune responses and immunotherapy. Ann Oncol 2016;27:1482–1492.Yeku O, Li X, Brentjens RJ. Adoptive T-Cell Therapy for Solid Tumors. Am Soc Clin Oncol Educ Book 2017;37:193–204.Dohrman A, Kataoka T, Cuenin S, Russell JQ, Tschopp J, and Budd RC. Cellular FLIP (long form) regulates CD8+ T cell activation through caspase-8-dependent NF-kappa B activation. J Immunol 2005; 174:5270–5278.Disclosure InformationG.M.Y. Tan: None. S.M.A.R. Hosseini: None. A. Poudel: None. A.D. Mclellan: None.
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Donovan, Will, and Michael Wemyss. "Twists and braids for general 3-fold flops." Journal of the European Mathematical Society 21, no. 6 (February 1, 2019): 1641–701. http://dx.doi.org/10.4171/jems/868.

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Dissertations / Theses on the topic "3-fold flips"

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Zhang, Zhao-Zhi, and 張詔智. "A Discussion of Existence of 3-fold Flips." Thesis, 2007. http://ndltd.ncl.edu.tw/handle/dtj95n.

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碩士
國立中央大學
數學研究所
96
In this note, I attempt to offer a good-ordered and detailed explanation of Shokurov’s proof for the existence of 3-fold flips. For the most part, it is based on Corti’s paper. I hope that by reading this note, a beginner will catch the key idea of this proof easily and thus be interested in the latest development of Minimal Model Program.
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Books on the topic "3-fold flips"

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Flips for 3-folds and 4-folds. Oxford University Press, USA, 2007.

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Corti, Alessio. Flips for 3-Folds And 4-folds. Oxford University Press, Incorporated, 2007.

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Corti, Alessio, ed. Flips for 3-folds and 4-folds. Oxford University Press, 2007. http://dx.doi.org/10.1093/acprof:oso/9780198570615.001.0001.

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Corti, Alessio. Flips for 3-Folds and 4-Folds. Oxford Lecture Series in Mathematics and Its Applications, Volume 35. Oxford University Press, 2007.

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Smith, Amir. Samsung Galaxy Z Fold 3 / Z Flip 3 5G User's Guide: A Complete and Adequate User's Guide Including, Tips and Tricks on How to Get the Most Out of Your Galaxy Z Fold 3 / Z Flip 3 and Its Accessories. Independently Published, 2022.

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Book chapters on the topic "3-fold flips"

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Ilankovan, Velupillai, and Tian Ee Seah. "Surgical Facelift." In Oral and Maxillofacial Surgery for the Clinician, 759–73. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-15-1346-6_37.

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AbstractWith aging, a combination of gravitational forces, laxity of the skin due to loss of elasticity, decreased dermal thickness and loss of dermal appendages results in ptotic, hanging skin. Face lift or rhytidectomy as its name suggest is a procedure to partially eliminate folds, creases and wrinkles (rhytids) caused by gravity and degeneration. The creation of two large cervicofacial flaps which after suspension and trimming, produces an overall tightening the skin and the fascial envelope of the face and neck results in restored anatomical structure. Treatment of the SMAS layer is important and can be broadly categorized into 3 methods. They are plication, elevation and imbrication and SMASectomy. Platysma elevation and plication can be carried out simultaneously for the neck. Face lift can help to negate some of these gravitational problems and produce some intrinsic improvement. Complications include haematoma, skin ischaemia and necrosis, obvious scarring, sensory disturbances, motor nerve disturbances and ear lobe irregularities.
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Corti, Alessio. "3-fold flips after Shokurov." In Flips for 3-folds and 4-folds, 18–48. Oxford University Press, 2007. http://dx.doi.org/10.1093/acprof:oso/9780198570615.003.0002.

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Fujino, Osamu. "Special termination and reduction to pl flips." In Flips for 3-folds and 4-folds, 63–75. Oxford University Press, 2007. http://dx.doi.org/10.1093/acprof:oso/9780198570615.003.0004.

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Hacon, Christopher D., and James McKernan. "Extension theorems and the existence of flips." In Flips for 3-folds and 4-folds, 76–110. Oxford University Press, 2007. http://dx.doi.org/10.1093/acprof:oso/9780198570615.003.0005.

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Corti, Alessio. "Introduction." In Flips for 3-folds and 4-folds, 1–17. Oxford University Press, 2007. http://dx.doi.org/10.1093/acprof:oso/9780198570615.003.0001.

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Fujino, Osamu. "What is log terminal?" In Flips for 3-folds and 4-folds, 49–62. Oxford University Press, 2007. http://dx.doi.org/10.1093/acprof:oso/9780198570615.003.0003.

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Corti, Alessio, James McKernan, and Hiromichi Takagi. "Saturated mobile b-divisors on weak del Pezzo klt surfaces." In Flips for 3-folds and 4-folds, 111–20. Oxford University Press, 2007. http://dx.doi.org/10.1093/acprof:oso/9780198570615.003.0006.

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McKernan, James. "Confined divisors." In Flips for 3-folds and 4-folds, 121–33. Oxford University Press, 2007. http://dx.doi.org/10.1093/acprof:oso/9780198570615.003.0007.

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Kollár, János. "Kodaira's canonical bundle formula and adjunction." In Flips for 3-folds and 4-folds, 134–62. Oxford University Press, 2007. http://dx.doi.org/10.1093/acprof:oso/9780198570615.003.0008.

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Ambro, Florin. "Non-klt techniques." In Flips for 3-folds and 4-folds, 163–70. Oxford University Press, 2007. http://dx.doi.org/10.1093/acprof:oso/9780198570615.003.0009.

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