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Relevant bibliographies by topics / VDA 6.3

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Journal articles

Academic literature on the topic 'VDA 6.3'

Author: Grafiati

Published: 28 June 2021

Last updated: 3 February 2022

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Journal articles on the topic "VDA 6.3"

1

Shin, Yong Sam, Byung Moon Kim, Se-Hyuk Kim, et al. "Endovascular Treatment of Bilateral Intracranial Vertebral Artery Dissecting Aneurysms Presenting With Subarachnoid Hemorrhage." Operative Neurosurgery 70, suppl_1 (2011): ons75—ons81. http://dx.doi.org/10.1227/neu.0b013e31822ed1f0.

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Abstract BACKGROUND: Optimal management of bilateral vertebral artery dissecting aneurysms (bi-VDAs) causing subarachnoid hemorrhage (SAH) remains unclear. OBJECTIVE: To investigate the treatment methods and outcomes of bi-VDA causing SAH. METHODS: Seven patients were treated endovascularly for bi-VDA causing SAH. Treatment methods and outcomes were evaluated retrospectively. RESULTS: Two patients were treated with 2 overlapping stents for both ruptured and unruptured VDAs, 2 with 2 overlapping stents and coiling for ruptured VDA and with conservative treatment for unruptured VDA, 1 with inter

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2

Prisk, G. K., A. R. Elliott, H. J. Guy, J. M. Kosonen, and J. B. West. "Pulmonary gas exchange and its determinants during sustained microgravity on Spacelabs SLS-1 and SLS-2." Journal of Applied Physiology 79, no. 4 (1995): 1290–98. http://dx.doi.org/10.1152/jappl.1995.79.4.1290.

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We measured resting pulmonary gas exchange in eight subjects exposed to 9 or 14 days of microgravity (microG) during two Spacelab flights. Compared with preflight standing measurements, microG resulted in a significant reduction in tidal volume (15%) but an increase in respiratory frequency (9%). The increased frequency was caused chiefly by a reduction in expiratory time (10%), with a smaller decrease in inspiratory time (4%). Anatomic dead space (VDa) in microG was between preflight standing and supine values, consistent with the known changes in functional residual capacity. Physiological d

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3

Sekhon, H. S., and W. M. Thurlbeck. "Lung cytokinetics after exposure to hypobaria and/or hypoxia and undernutrition in growing rats." Journal of Applied Physiology 79, no. 4 (1995): 1299–309. http://dx.doi.org/10.1152/jappl.1995.79.4.1299.

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We measured resting pulmonary gas exchange in eight subjects exposed to 9 or 14 days of microgravity (microG) during two Spacelab flights. Compared with preflight standing measurements, microG resulted in a significant reduction in tidal volume (15%) but an increase in respiratory frequency (9%). The increased frequency was caused chiefly by a reduction in expiratory time (10%), with a smaller decrease in inspiratory time (4%). Anatomic dead space (VDa) in microG was between preflight standing and supine values, consistent with the known changes in functional residual capacity. Physiological d

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4

Hutson, Thomas E., Long H. Dang, Richard C. Lauer, et al. "Phase I/II study of a BNC105P/everolimus regimen for progressive metastatic renal cell carcinoma (mRCC) following prior tyrosine kinase inhibitors (Hoosier Oncology Group)." Journal of Clinical Oncology 30, no. 5_suppl (2012): 373. http://dx.doi.org/10.1200/jco.2012.30.5_suppl.373.

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373 Background: BNC105P is a Vascular Disruption Agent (VDA) that destabilizes tubulin polymers leading to selective damage of tumor vasculature, hypoxia and associated tumor necrosis. BNC105P also has a direct anti-proliferative action on cancer cells. Up regulation of the mTOR pathway has been identified as a survival response by the tumor to hypoxic insult. Preclinical investigations demonstrated that BNC105P is effective at selectively damaging the vasculature in primary and metastatic lesions. Furthermore, BNC105P monotherapy compared well with sunitinib in mice bearing kidney tumors. It

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5

Chebil, M., J. Soria, L. Chami, et al. "Interest of DCE-US with quantification to demonstrate the VDA effect on vascularization in patients with advanced solid tumors treated with AVE8062." Journal of Clinical Oncology 27, no. 15_suppl (2009): e14522-e14522. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.e14522.

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e14522 Background: To determine the optimal time for the assessment of the perfusion in patients receiving AVE8062 (Vascular Disrupting Agent) at different doses combined with a fixed dose of cisplatin and then to correlate these results with the tumor response. Methods: Patients (pts) with advanced solid tumors, treated with AVE8062 (from 11.5 to 30 mg/m2) in combination with 75 mg/m2 cisplatin given every 3 weeks, were prospectively followed by DCE-US. DCE-US was performed before treatment, at 3 time points (0, 6 and 24 hours (h)) on Day 1 of the first (C1) and second cycle (C2), then every

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6

Desai, J., S. Wong, G. Chong, et al. "Phase I, pharmacokinetic, and pharmacodynamic evaluation of BNC105P, a novel anticancer agent that is both a vascular disrupting agent (VDA) and an inhibitor of cancer cell proliferation." Journal of Clinical Oncology 27, no. 15_suppl (2009): e14512-e14512. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.e14512.

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e14512 Background: BNC105P is a novel anticancer agent that inhibits tubulin polymerization and acts as a VDA. BNC105P is a phosphorylated parent compound which rapidly becomes the active agent BNC105. BNC105 exhibits 100-fold specificity for activated endothelial cells compared to quiescent endothelial cells. Methods: BNC105P (2.1 to 18.9 mg/m2) was given IV over 10 min on day 1 and 8 every 21 days to patients (pts) with advanced solid tumors (ECOG 0–2) and adequate organ function. The objectives were to determine safety, tolerability, MTD and pharmacokinetics (PK). A pharmacodynamic response

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7

Ricart, A. D., M. Cooney, J. Sarantopoulos, et al. "A phase I pharmacokinetic (PK) and pharmacodynamic (PD) study of MN-029, a novel vascular disrupting agent (VDA), in patients (pts) with advanced solid tumors." Journal of Clinical Oncology 24, no. 18_suppl (2006): 3096. http://dx.doi.org/10.1200/jco.2006.24.18_suppl.3096.

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3096 Background: MN-029 is a novel VDA that binds reversibly to the colchicine-binding site on tubulin and inhibits microtubule assembly, resulting in disruption of the cytoskeleton of tumor endothelial cells (EC). Disruption of the tumor EC cytoskeleton ultimately leads to a temporary reduction in tumor blood flow. Methods: MN-029 is administered IV as a 10–20 min infusion, at 3-wk intervals in pts with advanced cancer. The study has followed an accelerated titration design, with intrapatient dose escalation. PD effects on tumor blood flow are evaluated using dynamic contrast-enhanced magneti

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8

Lam, T. C., N. G. Shrive, and C. B. Frank. "Variations in Rupture Site and Surface Strains at Failure in the Maturing Rabbit Medial Collateral Ligament." Journal of Biomechanical Engineering 117, no. 4 (1995): 455–61. http://dx.doi.org/10.1115/1.2794207.

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The relationship between the pattern of surface strain and the site of failure in maturing rabbit ligaments was studied in vitro. Bone-medial collateral ligament (MCL)-bone complexes of 24 female New Zealand White rabbits at 3, 6, 9 and 12 months of age (n = 6 rabbits, 12 MCLs per group) were tested in tension to failure. A video dimension analysis (VDA) system was used to map the surface strain at failure across the width and along the length of the medial side of each MCL during testing. Results showed that the highest strains were consistently located at the femoral insertion decreasing tow

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9

Rischin, Danny, Daniela Matei, Jeffrey C. Goh, et al. "A phase I/II study of the vascular disrupting agent BNC105P in combination with gemcitabine-carboplatin in partially platinum-sensitive ovarian cancer patients in first or second relapse: An international collaborative group trial of ANZGOG and HOG." Journal of Clinical Oncology 31, no. 15_suppl (2013): TPS5612. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.tps5612.

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TPS5612 Background: BNC105P is a tubulin polymerization inhibitor and a vascular disrupting agent (VDA). In vivo exposure to BNC105P leads to selective damage of tumor vasculature in both primary and metastatic lesions, causing disruption of blood flow to tumors, hypoxia, and associated tumor necrosis. BNC105P also has a direct anti-proliferative action on cancer cells, including ovarian cancer cell lines. Pre-clinical data has demonstrated synergistic activity of BNC105P when combined with platinum or with gemcitabine, supporting the proposed study design. This study will determine the safety

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10

Libutti, Steven K., Lowell Brian Anthony, David J. Chaplin, and Julie Ann Sosa. "A phase II study of combretastatin A4-phosphate (CA4P) in the treatment of well-differentiated, low- to intermediate-grade, unresectable, recurrent, or metastatic pancreatic, or GI neuroendocrine tumors/carcinoid (GI-NETs/PNETs) with elevated biomarkers." Journal of Clinical Oncology 35, no. 4_suppl (2017): 432. http://dx.doi.org/10.1200/jco.2017.35.4_suppl.432.

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432 Background: GI-NETs/PNETs are highly vascular tumors. CA4P, a vascular disrupting agent (VDA), occludes tumor vasculature resulting in ischemic necrosis. Pre-clinical studies of CA4P have shown activity in GI-NETs/PNETs. Methods: OX4218s is a phase II, single-arm, open-label study (NCT02132468) of CA4P in patients (pts) with GI-NETs/PNETs with elevated biomarkers who relapsed during or after standard-of-care treatment. Pts received CA4P 60 mg/m2 IV on days 1, 8, and 15 of a 21-day cycle for 3 cycles. Primary endpoint was change in biomarkers from baseline. Secondary endpoints were safety,

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