Relevant bibliographies by topics / Vessel normalization

Academic literature on the topic 'Vessel normalization'

Author: Grafiati
Published: 11 March 2023

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Journal articles on the topic "Vessel normalization"

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Augustin, Hellmut G., and Gou Young Koh. "Antiangiogenesis: Vessel Regression, Vessel Normalization, or Both?" Cancer Research 82, no. 1 (January 1, 2022): 15–17. http://dx.doi.org/10.1158/0008-5472.can-21-3515.

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Coulon, Cathy, Maria Georgiadou, Carmen Roncal, Katrien De Bock, Tobias Langenberg, and Peter Carmeliet. "From Vessel Sprouting to Normalization." Arteriosclerosis, Thrombosis, and Vascular Biology 30, no. 12 (December 2010): 2331–36. http://dx.doi.org/10.1161/atvbaha.110.214106.

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Li, Sai, Qi Zhang, and Yupeng Hong. "Tumor Vessel Normalization: A Window to Enhancing Cancer Immunotherapy." Technology in Cancer Research & Treatment 19 (January 1, 2020): 153303382098011. http://dx.doi.org/10.1177/1533033820980116.

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Hostile microenvironment produced by abnormal blood vessels, which is characterized by hypoxia, low pH value and increasing interstitial fluid pressure, would facilitate tumor progression, metastasis, immunosuppression and anticancer treatments resistance. These abnormalities are the result of the imbalance of pro-angiogenic and anti-angiogenic factors (such as VEGF and angiopoietin 2, ANG2). Prudent use of anti-angiogenesis drugs would normalize these aberrant tumor vessels, resulting in a transient window of vessel normalization. In addition, use of cancer immunotherapy including immune checkpoint blockers when vessel normalization is achieved brings better outcomes. In this review, we sum up the advances in the field of understanding and application of the concept of tumor vessels normalization window to treat cancer. Moreover, we also outline some challenges and opportunities ahead to optimize the combination of anti-angiogenic agents and immunotherapy, leading to improve patients’ outcomes.
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Cully, Megan. "Tumour vessel normalization takes centre stage." Nature Reviews Drug Discovery 16, no. 2 (February 2017): 87. http://dx.doi.org/10.1038/nrd.2017.4.

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Jones, Bryony. "Early vessel normalization improves glioblastoma outcomes." Nature Reviews Clinical Oncology 11, no. 1 (November 26, 2013): 4. http://dx.doi.org/10.1038/nrclinonc.2013.228.

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Urits, Ivan, Purna Mukherjee, Joshua Meidenbauer, and Thomas N. Seyfried. "Dietary Restriction Promotes Vessel Maturation in a Mouse Astrocytoma." Journal of Oncology 2012 (2012): 1–10. http://dx.doi.org/10.1155/2012/264039.

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Mature vasculature contains an endothelial cell lining with a surrounding sheath of pericytes/vascular smooth muscle cells (VSMCs). Tumor vessels are immature and lack a pericyte sheath. Colocalization of vascular endothelial growth factor receptor 2 (VEGFR-2) and platelet-derived growth factor receptor beta (PDGF-Rβ) reduces pericyte ensheathment of tumor vessels. We found that a 30% dietary restriction (DR) enhanced vessel maturation in the mouse CT-2A astrocytoma. DR reduced microvessel density and VEGF expression in the astrocytoma, while increasing recruitment of pericytes, positive for alpha-smooth muscle actin (α-SMA). Moreover, DR reduced colocalization of VEGF-R2 and PDGF-Rβ, but did not reduce total PDGF-Rβexpression. These findings suggest that DR promoted vessel normalization by preventing VEGF-induced inhibition of the PDGF signaling axis in pericytes. DR appears to shift the tumor vasculature from a leaky immature state to a more mature state. We suggest that vessel normalization could improve delivery of therapeutic drugs to brain tumors.
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Martin, John, Ryan Lanning, Dai Fukumura, Timothy Padera, and Rakesh Jain. "Abstract LB557: Multiphoton phosphorescence quenching microscopy reveals kinetics of tumor oxygenation during anti-angiogenesis and angiotensin signaling inhibition." Cancer Research 82, no. 12_Supplement (June 15, 2022): LB557. http://dx.doi.org/10.1158/1538-7445.am2022-lb557.

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Abstract Purpose: The abnormal function of tumor blood vessels causes hypoxia fueling disease progression and conferring treatment resistance. The local level of oxygen experienced by a cell will determine its response, making it critical to understand tissue oxygen levels with a spatial resolution on the order of the size of a cell. While microenvironment normalization strategies alleviate global hypoxia, how local oxygen levels change are not known because there are no in vivo techniques to longitudinally assess tumor vessels and interstitial oxygen in tumors with sufficient resolution. Understanding the heterogeneity of oxygen levels after microenvironmental normalization will help improve the efficacy of various normalization strategies. Experimental Design: We developed a multiphoton phosphorescence quenching microscopy system using a low-molecular weight palladium porphyrin probe to measure perfused vessels, oxygen tension and their spatial correlations in vivo in mouse skin, bone marrow, and tumors. Further, we measured the temporal and spatial changes in oxygen and vessel perfusion in tumors in response to microenvironmental normalization. Results: We found that vessel function was highly dependent on tumor type. Although some tumors had vessels with greater oxygen carrying ability than normal skin, most tumors had inefficient vessels. Further, inter-vessel heterogeneity in tumors coincided with heterogeneous response to microenvironmental normalizing agents. Using both vascular and stromal normalizing agents, we show that spatial heterogeneity in oxygen levels persist, even with global reductions in hypoxia. Conclusions: We present the first study to examine the high-resolution spatial and temporal response of tumor vessels to two agents known to improve vascular perfusion globally. Our measurements demonstrate that the heterogeneities in the local imbalance of pro- and anti-angiogenic signaling lead to spatially heterogeneous changes in vessel structure and function. Microscale dynamic vascular changes should be considered in optimizing the dose and schedule of microenvironment normalizing therapies to improve function. Citation Format: John Martin, Ryan Lanning, Dai Fukumura, Timothy Padera, Rakesh Jain. Multiphoton phosphorescence quenching microscopy reveals kinetics of tumor oxygenation during anti-angiogenesis and angiotensin signaling inhibition [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr LB557.
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Slavnoe, N. V., V. V. Markov, N. A. Kovpan, V. M. Rudichenko, and G. N. Terekhova. "Peripheral circulation regulation in patients with the hypothalamic syndrome neuroendocrine metabolic form." Problems of Endocrinology 39, no. 6 (December 15, 1993): 17–20. http://dx.doi.org/10.14341/probl11928.

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Peripheral circulation and regulating hormonal (renin- angiotensin-aldosterone system) and electrolytic (plasma sodium and potassium) factors were studied in 102 patients with the hypothalamic syndrome neuroendocrine metabolic form administered pathogenetic therapy with antiserotonin and dopaminergic drugs as well as routine therapy. Blood plasma sodium vasopressin and aldosterone levels were found increased, arterial vessel reactivity in the forearm reduced, and venous circulation disordered in these patients. Routine therapy failed to normalize electrolytes and hormonal parameters and was conducive to a still more marked reduction of arterial vessel reactivity. Peritol therapy resulted in a reduction of vasopressin concentration and normalization of blood plasma sodium and aldosterone, as well as in improvement of the myogenic mechanisms of vascular tone regulation and normalization of venous circulation parameters. A course of parlodel therapy lead to normalization of blood plasma levels of vasopressin, aldosterone, and sodium but no changes in the regional vessels were observed.
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Mpekris, Fotios, James W. Baish, Triantafyllos Stylianopoulos, and Rakesh K. Jain. "Role of vascular normalization in benefit from metronomic chemotherapy." Proceedings of the National Academy of Sciences 114, no. 8 (February 7, 2017): 1994–99. http://dx.doi.org/10.1073/pnas.1700340114.

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Metronomic dosing of chemotherapy—defined as frequent administration at lower doses—has been shown to be more efficacious than maximum tolerated dose treatment in preclinical studies, and is currently being tested in the clinic. Although multiple mechanisms of benefit from metronomic chemotherapy have been proposed, how these mechanisms are related to one another and which one is dominant for a given tumor–drug combination is not known. To this end, we have developed a mathematical model that incorporates various proposed mechanisms, and report here that improved function of tumor vessels is a key determinant of benefit from metronomic chemotherapy. In our analysis, we used multiple dosage schedules and incorporated interactions among cancer cells, stem-like cancer cells, immune cells, and the tumor vasculature. We found that metronomic chemotherapy induces functional normalization of tumor blood vessels, resulting in improved tumor perfusion. Improved perfusion alleviates hypoxia, which reprograms the immunosuppressive tumor microenvironment toward immunostimulation and improves drug delivery and therapeutic outcomes. Indeed, in our model, improved vessel function enhanced the delivery of oxygen and drugs, increased the number of effector immune cells, and decreased the number of regulatory T cells, which in turn killed a larger number of cancer cells, including cancer stem-like cells. Vessel function was further improved owing to decompression of intratumoral vessels as a result of increased killing of cancer cells, setting up a positive feedback loop. Our model enables evaluation of the relative importance of these mechanisms, and suggests guidelines for the optimal use of metronomic therapy.
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Yu, Xianzhe, Shan He, Jian Shen, Qiushi Huang, Peng Yang, Lin Huang, Dan Pu, et al. "Tumor vessel normalization and immunotherapy in gastric cancer." Therapeutic Advances in Medical Oncology 14 (January 2022): 175883592211101. http://dx.doi.org/10.1177/17588359221110176.

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Gastric cancer (GC) is a common malignant tumor, and patients with GC have a low survival rate due to limited effective treatment methods. Angiogenesis and immune evasion are two key processes in GC progression, and they act synergistically to promote tumor progression. Tumor vascular normalization has been shown to improve the efficacy of cancer immunotherapy, which in turn may be improved through enhanced immune stimulation. Therefore, it may be interesting to identify synergies between immunomodulatory agents and anti-angiogenic therapies in GC. This strategy aims to normalize the tumor microenvironment through the action of the anti-vascular endothelial growth factor while stimulating the immune response through immunotherapy and prolonging the survival of GC patients.
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Dissertations / Theses on the topic "Vessel normalization"

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Carrer, Alessandro. "AVV-mediated delivery of Semaphorin 3A influences tumor miscroenvironment and inhibits tumorigenesis in vivo." Doctoral thesis, Università degli studi di Trieste, 2009. http://hdl.handle.net/10077/3131.

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2007/2008
Le semaforine di classe 3 costituiscono una piccola famiglia di proteine che sono state inizialmente studiate per la loro capacità di dirigere la crescita del cono assonico durante lo sviluppo. Tuttavia, tali molecole sono state recentemente coinvolte in ulteriori processi biologici, tra cui merita particolare attenzione il processo angiogenetico, in cui diverse semaforine sembrano partecipare attivamente anche se con ruoli e funzioni variegati. Tale eterogeneità funzionale ha spesso dato origine a risultati apparentemente contraddittori, dovuti per lo più alla scarsa conoscenza del reale coinvolgimento delle diverse semaforine nell’angiogenesi. Questo studio è stato incentrato sul ruolo della semaforina-3A (Sema3A), analizzando nel dettaglio i mutamenti apportati al microambiente locale da una sua overespressione in vivo. Questa proprietà non è stata finora riportata in letteratura e si esplica principalmente attraverso il reclutamento di cellule mononucleate di derivazione midollare. Ciò è stato inizialmente osservato nel muscolo scheletrico di topi wild-type a seguito di trasferimento genico della Sema3A mediate tecnologia AAV. Sia a 15 giorni che a un mese dopo l’iniezione del vettore virale è stato possibile osservare la presenza di un imponente numero di cellule mononucleate che infiltravano le fibre muscolari. Attraverso analoghi esperimenti mediante vettori AAV, il nostro laboratorio aveva precedentemente dimostrato un simile richiamo di cellule a seguito di espressione di VEGF165, un potente fattore pro-angiogenetico (Arsic et al, Mol. Ther., 2003). Viceversa, molte indicazioni suggerivano che Sema3A fosse in realtà un fattore anti-angiogenetico, come successivamente è stato appurato (Acevedo et al, Blood, 2008 & Zacchigna et al, J.Clin.Invest., 2008). Era perciò ragionevole pensare che i due fattori (VEGF165 e Sema3A) reclutassero in situ due popolazioni cellulari differenti, in grado di accompagnare attività biologiche contrapposte. Diversi approcci sperimentali, tuttavia, ci hanno condotto a sostenere l’ipotesi che entrambe le molecole in realtà richiamino la medesima sub-popolazione mieloide agendo attraverso l’attivazione di neuropilina-1 (Nrp-1), un recettore in grado di legare sia VEGF165 che Sema3A. Da notare che VEGF121, un’isoforma del gene VEGF carente dell’esone 7, quando overespressa nel muscolo scheletrico non causa il reclutamento di cellule infiltranti, coerentemente con la sua incapacità di legare Nrp-1. Oltre a ciò, l’espressione ectopica di VEGF121, contrariamente a quanto accade per VEGF165, non determina la formazione di arteriole (vasi di media grandezza, ricoperti da cellule della parete vascolare come periciti e cellule muscolari lisce), pur causando un eguale aumento del letto vascolare attraverso iper-proliferazione capillare. Ciò ci ha indotto a pensare che la presenza di cellule richiamate attraverso Nrp-1 (chiamate da noi NEM) sia in realtà indispensabile per la maturazione dei vasi neo-formati. In effetti, la co-iniezione di AAV-VEGF121 e NEM ci ha permesso di osservare a 15 giorni un fenotipo chiaramente arteriogenico (presenza di vasi α-SMA+), contrariamente al fenotipo esclusivamente capillogenico determinato dalla sola iniezione di AAV-VEGF121. Attraverso una caratterizzazione estensiva delle cellule richiamate da VEGF165 o Sema3A, abbiamo potuto riconoscere i NEM come una popolazione mieloide precedentemente mai descritta e differente da altre popolazioni midollari coinvolte nell’angiogenesi. In aggiunta, attraverso l’analisi della loro espressione genica abbiamo potuto riconoscere alcuni geni tipicamente espressi da macrofagi polarizzati in senso M1, noti per essere pro-infiammatori e anti-tumorigenici. I NEM sono stati inoltre visti esprimere alti livelli di PDGFβ e TGFβ, due molecole coinvolte nella maturazione vascolare. Il fenotipo M1-like e la capacità di indurre la maturazione della vascolatura sono entrambe caratteristiche potenzialmente in grado di influire negativamente sulla crescita tumorale. Abbiamo quindi deciso di investigare più nel dettaglio come il reclutamento di questo particolare tipo cellulare influisse su un modello tumorale ottenuto tramite xenotrapianto di cellule singeniche direttamente nel muscolo scheletrico. Muscolo precedentemente condizionato mediante trasferimento genico di VEGF165, VEGF121 o Sema3A. In linea con l’ipotesi da dimostrare, la precedente espressione di VEGF165 o Sema3A rende meno efficace l’attecchimento del tumore, rallentandone la crescita, mentre il trasferimento del gene codificante per VEGF121 addirittura accelera tale crescita, come d’altra parte prevedibile per un fattore angiogenetico. Una dettagliata analisi morfologica della rete vascolare tumorale ci ha permesso di constatare come il richiamo di NEM mediante pre-condizionamento da Sema3A causasse una più matura struttura vascolare (in termini di mural cell coverage, di dimensioni e di tortuosità dei vasi). Per avvalorare definitivamente il ruolo dei NEM nell’inibizione tumorale osservata dopo trasferimento genico, abbiamo purificato tali cellule direttamente da muscoli scheletrici di topi precedentemente iniettati con AAV-Sema3A. Tali cellule sono poi state amministrate direttamente in masse tumorali in crescita in topi singenici. Esse sono risultate effettive nel rallentare la crescita tumorale in fasi tardive, consistentemente con una loro capacità di sostenere la maturazione della vascolatura tumorale. Un’analisi più approfondita di ha permesso di rilevare diversi segni di una “normalizzazione” vascolare a seguito della somministrazione dei NEM, essendo i vasi più maturi, meno dilatati, meno tortuosi e, dato importante, meno permeabili.
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Book chapters on the topic "Vessel normalization"

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Park, Jin-Sung, Intae Park, and Gou Young Koh. "Benefits and Pitfalls of Tumor Vessel Normalization." In Tumor Angiogenesis, 51–71. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-33673-2_46.

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Park, Jin-Sung, Intae Park, and Gou Young Koh. "Benefits and Pitfalls of Tumor Vessel Normalization." In Tumor Angiogenesis, 1–21. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-31215-6_46-1.

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Maione, Federica, and Enrico Giraudo. "Tumor Angiogenesis: Methods to Analyze Tumor Vasculature and Vessel Normalization in Mouse Models of Cancer." In Methods in Molecular Biology, 349–65. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2297-0_17.

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Abu Elhasan, Hosni, Pablo Albiña Palmarola, Marta Aguilar Pérez, Birgit Herting, Hansjörg Bäzner, and Hans Henkes. "Cervical Internal Carotid Artery Aneurysm: Spontaneous Dissection of the Cervical Internal Carotid Artery Resulting in Elongation and Pseudoaneurysm Formation Causing Hypoglossal Nerve Palsy; Endovascular Vessel Reconstruction with Stenting, Followed by Telescoping Flow Diversion, Achieving Straightening of the Artery, Aneurysm Occlusion, Hypoglossal Nerve Recovery, and Normalization of the Tongue." In The Aneurysm Casebook, 3–16. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-319-77827-3_154.

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Abu Elhasan, Hosni, Pablo Albiña Palmarola, Marta Aguilar Pérez, Birgit Herting, Hansjörg Bäzner, and Hans Henkes. "Cervical Internal Carotid Artery Aneurysm: Spontaneous Dissection of the Cervical Internal Carotid Artery Resulting in Elongation and Pseudoaneurysm Formation Causing Hypoglossal Nerve Palsy; Endovascular Vessel Reconstruction with Stenting, Followed by Telescoping Flow Diversion, Achieving Straightening of the Artery, Aneurysm Occlusion, Hypoglossal Nerve Recovery, and Normalization of the Tongue." In The Aneurysm Casebook, 1–14. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-70267-4_154-1.

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Chen, Peiwen, and Paolo Bonaldo. "Role of Macrophage Polarization in Tumor Angiogenesis and Vessel Normalization." In International Review of Cell and Molecular Biology, 1–35. Elsevier, 2013. http://dx.doi.org/10.1016/b978-0-12-407704-1.00001-4.

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Ouarné, Marie, Claire Bouvard, Gabriela Boneva, Christine Mallet, Johnny Ribeiro, Agnès Desroches-Castan, Emmanuelle Soleilhac, Emmanuelle Tillet, Olivier Peyruchaud, and Sabine Bailly. "BMP9, but Not BMP10, Acts as a Quiescence Factor on Tumor Growth, Vessel Normalization and Metastasis in a Mouse Model of Breast Cancer." In Immunology and Cancer Biology. Vide Leaf, Hyderabad, 2021. http://dx.doi.org/10.37247/imcac.1.2021.20.

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Chauhan, Vikash P., Triantafyllos Stylianopoulos, John D. Martin, Zoran Popović, Ou Chen, Walid S. Kamoun, Moungi G. Bawendi, Dai Fukumura, and Rakesh K. Jain. "Normalization of Tumour Blood Vessels Improves the Delivery of Nanomedicines in a Size-Dependent Manner." In Nano-Enabled Medical Applications, 279–311. Jenny Stanford Publishing, 2020. http://dx.doi.org/10.1201/9780429399039-10.

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Conference papers on the topic "Vessel normalization"

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Serganova, Inna, Kiranmayi Vemuri, Ivan Cohen, Matthew Lubin, Sheryl Roberts, Masatomo Maeda, Mayuresh Mane, et al. "Abstract 1476: Vessel normalization following LDH-A knockdown in murine breast tumors." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-1476.

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Sarhan, Abdullah, Jon Rokne, Reda Alhajj, and Andrew Crichton. "Transfer Learning Through Weighted Loss Function and Group Normalization for Vessel Segmentation from Retinal Images." In 2020 25th International Conference on Pattern Recognition (ICPR). IEEE, 2021. http://dx.doi.org/10.1109/icpr48806.2021.9412378.

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Kaiguo Yan, P. Wachsberger, and Yan Yu. "Acoustic radiation force and optical spectroscopy for assessing tumor vessel normalization during anti-angiogenic therapy." In 2009 Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2009. http://dx.doi.org/10.1109/iembs.2009.5333814.

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Ackermann, Maximilian, Frank Hilberg, and Moritz Anton Konerding. "Abstract B09: Nintedanib inhibits tumor and vessel growth and leads to vascular normalization in A549-NSCLC-xenografts." In Abstracts: AACR Special Conference: Tumor Angiogenesis and Vascular Normalization: Bench to Bedside to Biomarkers; March 5-8, 2015; Orlando, FL. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-8514.tumang15-b09.

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Mazzone, Massimiliano. "Abstract IA17: Influence on vessel shape of macrophage metabolism in the tumor hypoxic niche." In Abstracts: AACR Special Conference: Tumor Angiogenesis and Vascular Normalization: Bench to Bedside to Biomarkers; March 5-8, 2015; Orlando, FL. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-8514.tumang15-ia17.

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Scarabeli Barbosa, Vitor, Felipe Ezsias Fiumarelli, and Claudio Ruggieri. "Fracture Toughness Testing of a Pressure Vessel Steel Using Clamped SE(T) Specimens and the Normalization Method." In 26th International Congress of Mechanical Engineering. ABCM, 2021. http://dx.doi.org/10.26678/abcm.cobem2021.cob2021-0606.

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Nanstad, Randy K., Xiang Chen, Mikhail A. Sokolov, Barry H. Rabin, and Ying Yang. "Master Curve and J-R Fracture Toughness of SA508/SA533-B-1 Weld and HAZ." In ASME 2013 Pressure Vessels and Piping Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/pvp2013-97033.

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A large heat of low-alloy steel that met both specifications for SA508 Grade 3 Class1 forging steel and SA533 Type B Class 1 plate steel (A508/A533) was procured and used to fabricate a submerged-arc weldment for potential application in high temperature gas-cooled reactors. Compact specimens, 1TC(T), were machined from the weld metal and from the heat-affected-zone (HAZ) of the weldment. Tests of both materials were performed to obtain the fracture toughness reference temperature, To, using the Master Curve procedure of ASTM E-1921, and J-R curves to evaluate material behavior at various threshold temperatures in Code Case N-499-2 (2001) of the ASME Boiler and Pressure Vessel Code. Tests were performed at various temperatures up to 593°C. Unloading compliance was the primary technique used, although dc-potential drop was also monitored during the tests, and the normalization procedure of E1820 was used to compare the results from each procedure. Moreover, many tests at the highest temperatures were performed with no unloading and the normalization procedure provided in E1820 was used to analyze the load-displacement measurements. The fracture toughness for the HAZ is superior to that of the weld metal both in terms of transition temperature and ductile fracture toughness.
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Gilles, Maud-Emmanuelle, Federica Maione, Mélissande Cossutta, Gilles Carpentier, Laure Caruana, Silvia Di Maria, Damien Destouches, et al. "Abstract 3366: NCL targeting impairs the progression of pancreatic ductal adenocarcinoma and promotes tumor vessel normalization through Ang-2 inhibition." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-3366.

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Shuen, Wai Ho, Richard Ong, Chloe Yeo, Rebecca Banu, Lip Seng Koh, Chit Lai Chee, Qihui Seet, et al. "Abstract 3992: Varlitinib demonstrates tumor regression and vessel normalization in ErbB-dependent and mutated beta-catenin hepatocellular carcinoma patient-derived xenograft model." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-3992.

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Sokolov, Mikhail A. "Estimation of Crack-Arrest Toughness Transition and NDT Temperatures From Charpy Force-Displacement Impact Traces." In ASME 2009 Pressure Vessels and Piping Conference. ASMEDC, 2009. http://dx.doi.org/10.1115/pvp2009-77894.

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A force-displacement trace of a Charpy impact test of a reactor pressure vessel (RPV) steel in the transition range has a characteristic point, the so-called “force at the end of unstable crack propagation”, Fa. A two-parameter Weibull probability function is used to model the distribution of the Fa in Charpy tests performed at ORNL on different RPV steels in the unirradiated and irradiated conditions. These data have a good replication at a given test temperature, thus, the statistical analysis was applicable. It is shown that when temperature is normalized to TNDT (T-TNDT) or to T100a (T-T100a), the median Fa values of different RPV steels have a tendency to form the same shape of temperature dependence. Depending on normalization temperature, TNDT or T100a, it suggests a universal shape of the temperature dependence of Fa for different RPV steels. The best fits for these temperature dependencies are presented. These dependencies are suggested for use in estimation of NDT or T100a from randomly generated Charpy impact tests. The maximum likelihood method is used to derive equations to estimate TNDT and T100a from randomly generated Charpy impact tests.
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