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Статті в журналах з теми "Drugs Metabolism":

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Desouza, Cyrus, Mary Keebler, Dennis B. McNamara, and Vivian Fonseca. "Drugs Affecting Homocysteine Metabolism." Drugs 62, no. 4 (2002): 605–16. http://dx.doi.org/10.2165/00003495-200262040-00005.

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Lambie, David G., and Ralph H. Johnson. "Drugs and Folate Metabolism." Drugs 30, no. 2 (August 1985): 145–55. http://dx.doi.org/10.2165/00003495-198530020-00003.

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Reiher, Jean. "Metabolism of Antiepileptic Drugs." Journal of Clinical Neurophysiology 2, no. 3 (July 1985): 309. http://dx.doi.org/10.1097/00004691-198507000-00007.

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Jann, Michael W., Y. W. Francis Lam, Eric C. Gray, and Wen-Ho Chang. "REVERSIBLE METABOLISM OF DRUGS." Drug Metabolism and Drug Interactions 11, no. 1 (January 1994): 1–24. http://dx.doi.org/10.1515/dmdi.1994.11.1.1.

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Franceschini, Guido, and Rodolfo Paoletti. "Drugs controlling triglyceride metabolism." Medicinal Research Reviews 13, no. 2 (March 1993): 125–38. http://dx.doi.org/10.1002/med.2610130202.

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Ghiselli, Giancarlo, and Marco Maccarana. "Drugs affecting glycosaminoglycan metabolism." Drug Discovery Today 21, no. 7 (July 2016): 1162–69. http://dx.doi.org/10.1016/j.drudis.2016.05.010.

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Kostner, G. M. "Drugs affecting lipid metabolism." Chemistry and Physics of Lipids 51, no. 1 (July 1989): 73–74. http://dx.doi.org/10.1016/0009-3084(89)90068-6.

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Durrington, P. "Drugs Affecting Lipid Metabolism." International Journal of Cardiology 45, no. 2 (June 1994): 153–54. http://dx.doi.org/10.1016/0167-5273(94)90276-3.

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Sitar, Daniel S. "Metabolism of Thioamide Antithyroid Drugs." Drug Metabolism Reviews 22, no. 5 (January 1990): 477–502. http://dx.doi.org/10.3109/03602539008991448.

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10

Kelly, Patrick, and Barry Kahan. "Review: Metabolism of Immunosuppressant Drugs." Current Drug Metabolism 3, no. 3 (June 2002): 275–87. http://dx.doi.org/10.2174/1389200023337630.

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Дисертації з теми "Drugs Metabolism":

1

Bai, Shuang. "Effect of immunosuppressive agents on drug metabolism in rats." Thesis, Full text (PDF) from UMI/Dissertation Abstracts International, 2001. http://wwwlib.umi.com/cr/utexas/fullcit?p3008270.

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王漪雯 and Belinda Wong. "Haloperidol metabolism in man and animals." PG_Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1993. http://hub.hku.hk/bib/B3121194X.

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Britt, Adrian John. "Cocaine metabolism in Pseudomonas maltophilia MB11L." Electronic Thesis or Diss., University of Cambridge, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.386328.

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Wong, Belinda. "Haloperidol metabolism in man and animals /." [Hong Kong] : University of Hong Kong, 1993. http://sunzi.lib.hku.hk/hkuto/record.jsp?B13671546.

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Daneshmend, T. K. "Observations on presystemic metabolism of drugs in man." Electronic Thesis or Diss., University of Bristol, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.482894.

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Pereira, Maria J. "Effects of immunosuppressive drugs on human adipose tissue metabolism." DoctoralThesis, University of Gothenburg, 2012. http://hdl.handle.net/10400.1/4916.

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Анотація:
Tese de doutoramento, Philosophy (Medicine), Institute of Medicine, Department of Molecular and Clinical Medicine, University of Gothenburg, Sahlgrenska Academy, 2012
The immunosuppressive agents (IAs) rapamycin, cyclosporin A and tacrolimus, as well as glucocorticoids are used to prevent rejection of transplanted organs and to treat autoimmune disorders. Despite their desired action on the immune system, these agents have serious longterm metabolic side-effects, including dyslipidemia and new onset diabetes mellitus after transplantation. The overall aim is to study the effects of IAs on human adipose tissue glucose and lipid metabolism, and to increase our understanding of the molecular mechanisms underlying the development of insulin resistance during immunosuppressive therapy. In Paper I and II, it was shown that rapamycin and the calcineurin inhibitors, cyclosporin A and tacrolimus, at therapeutic concentrations, had a concentration-dependent inhibitory effect on basal and insulin-stimulated glucose uptake in human subcutaneous and omental adipocytes. Rapamycin inhibited mammalian target of rapamycin complex (mTORC) 1 and 2 assembly and phosphorylation of protein kinase B (PKB) at Ser473 and of the PKB substrate AS160, and this leads to impaired insulin signalling (Paper I). On the other hand, cyclosporin A and tacrolimus had no effects on expression or phosphorylation of insulin signalling proteins (insulin receptor substrate 1 and 2, PKB, AS160), as well as the glucose transport proteins, GLUT4 and GLUT1 (Paper II). Instead, removal of GLUT4 from the cell surfasse was observed, probably mediated through increased endocytosis, as shown in L6 musclederived cells. These studies suggest a different mechanism for cyclosporin A and tacrolimus, in comparison to rapamycin, with respect to impairment of glucose uptake in adipocytes. In Paper III, all three IAs increased isoproterenol-stimulated lipolysis and enhanced phosphorylation of one of the main lipases involved in lipolysis, hormone-sensitive lipase. The agents also inhibited lipid storage, and tacrolimus and rapamycin down-regulated gene expression of lipogenic genes in adipose tissue. All three IAs increased interleukin-6 (IL-6), but not tumor necrosis factor α (TNF-α ) or adiponectin, gene expression and secretion. In Paper IV, we proposed that FKBP5 is a novel gene regulated by dexamethasone, a synthetic glucocorticoid, in both subcutaneous and omental adipose tissue. FKBP5 expression in subcutaneous adipose tissue is correlated with clinical and biochemical markers of insulin resistance and adiposity. In addition, the FKBP5 gene product was more abundant in omental than in subcutaneous adipose tissue. In conclusion, adverse effects of immunosuppressive drugs on human adipose tissue glucose and lipid metabolism can contribute to the development of insulin resistance, type 2 diabetes and dyslipidemia in patients on immunosuppressive therapy. The cellular mechanisms that are described in this thesis should be further explored in order to mitigate the metabolic perturbations caused by current immunosuppressive therapies. The findings in this thesis could potentially also provide novel pharmacological mechanisms for type 2 diabetes as well as other forms of diabetes.
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Priston, Melanie Jane. "Studies on the pharmacokinetics and metabolism of mitozantrone." Electronic Thesis or Diss., University of Exeter, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.303766.

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Godwin, Bryan. "Discrete sliding mode control of drug infusions." Thesis, Georgia Institute of Technology, 1991. http://hdl.handle.net/1853/16806.

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Benchaoui, Hafid Abdelaali. "Factors affecting the pharmacokinetics, metabolism and efficacy of anthelmintic drugs." Electronic Thesis or Diss., University of Glasgow, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.284569.

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Ngulube, Thabale Jack. "The interaction of anti-malarial drugs and steroid hormone metabolism." Electronic Thesis or Diss., University of Leeds, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.329825.

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Книги з теми "Drugs Metabolism":

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Gotto, A. M., R. Paoletti, L. C. Smith, A. L. Catapano, and A. S. Jackson, eds. Drugs Affecting Lipid Metabolism. Dordrecht: Springer Netherlands, 1996. http://dx.doi.org/10.1007/978-94-009-0311-1.

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Paoletti, Rodolfo, David Kritchevsky, and William L. Holmes, eds. Drugs Affecting Lipid Metabolism. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71702-4.

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Catapano, A. L., A. M. Gotto, Louis C. Smith, and Rodolfo Paoletti, eds. Drugs Affecting Lipid Metabolism. Dordrecht: Springer Netherlands, 1993. http://dx.doi.org/10.1007/978-94-011-1703-6.

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4

International, Symposium on Drugs Affecting Lipid Metabolism (8th 1983 Philadelphia Pa ). Drugs affecting lipid metabolism VIII. New York: Plenum Press, 1985.

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5

Kritchevsky, David, William L. Holmes, and Rodolfo Paoletti, eds. Drugs Affecting Lipid Metabolism VIII. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2459-1.

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Coleman, Michael. Human Drug Metabolism. New York: John Wiley & Sons, Ltd., 2006.

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7

Gibson, G. Gordon. Introduction to drug metabolism. 2nd ed. London: Blackie Academic & Professional, 1994.

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Anzenbacher, Pavel, and Ulrich M. Zanger, eds. Metabolism of Drugs and Other Xenobiotics. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2012. http://dx.doi.org/10.1002/9783527630905.

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9

Gibson, G. Gordon. Introduction to drug metabolism. London: Chapman and Hall, 1986.

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10

Gibson, G. Gordon. Introduction to drug metabolism. 2nd ed. Cheltenham: Stanley Thornes, 1999.

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Частини книг з теми "Drugs Metabolism":

1

Dwyer, B. E., and C. G. Wasterlain. "Intermediary Metabolism." In Antiepileptic Drugs, 79–100. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-69518-6_4.

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2

Stene, Danny O., and Robert C. Murphy. "Metabolism of Sulfidopeptide Leukotrienes." In Prostanoids and Drugs, 37–46. New York, NY: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-7938-6_6.

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3

Meyer, Markus R., and Hans H. Maurer. "Drugs of Abuse (Including Designer Drugs)." In Metabolism of Drugs and Other Xenobiotics, 429–63. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2012. http://dx.doi.org/10.1002/9783527630905.ch16.

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4

Vuilhorgne, M., C. Gaillard, G. J. Sanderink, I. Royer, B. Monsarrat, J. Dubois, and M. Wright. "Metabolism of Taxoid Drugs." In ACS Symposium Series, 98–110. Washington, DC: American Chemical Society, 1994. http://dx.doi.org/10.1021/bk-1995-0583.ch007.

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Tatum, William O. "Metabolism and Antiseizure Drugs." In Epilepsy Case Studies, 87–93. Cham: Springer International Publishing, 2013. http://dx.doi.org/10.1007/978-3-319-01366-4_20.

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Khojasteh, Siamak Cyrus, Harvey Wong, and Cornelis E. C. A. Hop. "Approved Drugs." In Drug Metabolism and Pharmacokinetics Quick Guide, 193–200. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-5629-3_11.

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Riedmaier, Stephan, and Ulrich M. Zanger. "Cardiovascular Drugs." In Metabolism of Drugs and Other Xenobiotics, 331–63. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2012. http://dx.doi.org/10.1002/9783527630905.ch12.

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Schwab, Matthias, Elke Schaeffeler, and Hiltrud Brauch. "Anticancer Drugs." In Metabolism of Drugs and Other Xenobiotics, 365–78. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2012. http://dx.doi.org/10.1002/9783527630905.ch13.

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Moore, Michael R., Kenneth E. L. McColl, Claude Rimington, and Abraham Goldberg. "Drugs, Chemicals, and Porphyria." In Disorders of Porphyrin Metabolism, 139–65. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-1277-2_5.

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Chung, Y. L., and J. R. Griffiths. "Using Metabolomics to Monitor Anticancer Drugs." In Oncogenes Meet Metabolism, 55–78. Berlin, Heidelberg: Springer Berlin Heidelberg, 2008. http://dx.doi.org/10.1007/2789_2008_089.

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Тези доповідей конференцій з теми "Drugs Metabolism":

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Tourlomousis, Filippos, and Robert C. Chang. "2D and 3D Multiscale Computational Modeling of Dynamic Microorgan Devices as Drug Screening Platforms." In ASME 2015 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2015. http://dx.doi.org/10.1115/imece2015-52734.

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The ability to incorporate three-dimensional (3D) hepatocyte-laden hydrogel constructs using layered fabrication approaches into devices that can be perfused with drugs enables the creation of dynamic microorgan devices (DMDs) that offer an optimal analog of the in vivo liver metabolism scenario. The dynamic nature of such in vitro metabolism models demands reliable numerical tools to determine the optimum process, material, and geometric parameters for the most effective metabolic conversion of the perfused drug into the liver microenvironment. However, there is a current lack of literature that integrates computational approaches to guide the optimum design of such devices. The groundwork of the present numerical study has been laid by our previous study [1], where the authors modeled in 2D an in vitro DMD of arbitrary dimensions and identified the modeling challenges towards meaningful results. These constructs are hosted in the chamber of the microfluidic device serving as walls of the microfluidic array of channels through which a fluorescent drug substrate is perfused into the microfluidic printed channel walls at a specified volumetric flow rate assuring Stokes flow conditions (Re<<1). Due to the porous nature of the hydrogel walls, a metabolized drug product is collected at the outlet port. A rigorous FEM based modeling approach is presented for a single channel parallel model geometry (1 free flow channel with 2 porous walls), where the hydrodynamics, mass transfer and pharmacokinetics equations are solved numerically in order to yield the drug metabolite concentration profile at the DMD outlet. The fluid induces shear stresses are assessed both in 3D, with only 27 cells modeled as single compartment voids, where all of the enzymatic reactions are assumed to take place. In this way, the mechanotransduction effect that alters the hepatocyte metabolic activity is assessed for a small scale model. This approach overcomes the numerical limitations imposed by the cell density (∼1012 cells/m3) of the large scale DMD device. In addition, a compartmentalization technique is proposed in order to assess the metabolism process at the subcellular level. The numerical results are validated with experiments to reveal the robustness of the proposed modeling approach and the necessity of scaling the numerical results by preserving dynamic and biochemical similarity between the small and large scale model.
2

Rautiola, Davin, and Ronald A. Siegel. "Nasal Spray Device for Administration of Two-Part Drug Formulations." In 2019 Design of Medical Devices Conference. American Society of Mechanical Engineers, 2019. http://dx.doi.org/10.1115/dmd2019-3216.

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Intranasal drug delivery is an attractive route to noninvasively achieve a rapid therapeutic effect, avoid first pass metabolism, and bypass the blood brain barrier. However, the types of drugs that can be administered by this route has been limited, in part, by device technology. Herein, we describe a pneumatic nasal spray device that is capable of mixing liquid and solid components of a drug formulation as part of the actuation process during dose administration. The ability to store a nasal spray drug formulation as two separate components can be leveraged to solve a variety of stability issues that would otherwise preclude intranasal administration. Examples of drugs that could be delivered intranasally by utilizing this two-part formulation strategy include biomolecules that are unstable in solution and low solubility drugs that can be rendered into metastable supersaturated solutions. A proof of concept nasal spray device prototype was constructed to demonstrate that a liquid and solid can be rapidly mixed and atomized into a spray in a single action. The primary breakup distance and angle of the spray cone were measured as a function of the function of the propellant gas pressure.
3

Lei, Xiang-He, Shawn Noble, and Barry R. Bochner. "Abstract B42: Metabolic pathway changes induced by a PIK3 mutation and reverted by drugs." In Abstracts: AACR Special Conference: Metabolism and Cancer; June 7-10, 2015; Bellevue, WA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1557-3125.metca15-b42.

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Bing, Cheng, Guo Ke, Alex Wong, and Karen Crasta. "Abstract B59: Autophagy mediates senescence and supports survival upon treatment with anti-mitotic drugs." In Abstracts: AACR Special Conference: Metabolism and Cancer; June 7-10, 2015; Bellevue, WA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1557-3125.metca15-b59.

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5

Al-Qeraiwi, Maha, Manar Al-Rashid, Nasser Rizk, Abdelrahman El Gamal, and Amena Fadl. "Hepatic Gene Expression Profile of Lipid Metabolism of Obese Mice after treatment with Anti-obesity Drug." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0214.

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Obesity is a global disorder with multifactorial causes. The liver plays a vital role in fat metabolism. Disorder of hepatic fat metabolism is associated with obesity and causes fatty liver. High fat diet intake (HFD) to mice causes the development of dietinduced obesity (DIO). The study aimed to detect the effects of anti-obesity drugs (sulforaphane; SFN and leptin) on hepatic gene expression of fat metabolism in mice that were fed HFD during an early time of DIO. Twenty wild types (WT) CD1 male mice aged ten weeks were fed a high fat diet. The mice were treated with vehicle; Veh (control group), and SFN, then each group is treated with leptin or saline. Four groups of treatment were: control group (vehicle + saline), Group 2 (vehicle + leptin), group 3 (SFN + saline), and group 4 (SFN + leptin). Body weight and food intake were monitored during the treatment period. Following the treatments of leptin 24 hour, fasting blood samples and liver tissue was collected, and Total RNA was extracted then used to assess the gene expression of 84 genes involved in hepatic fat metabolism using RT-PCR profiler array technique. Leptin treatment upregulated fatty acid betaoxidation (Acsbg2, Acsm4) and fatty acyl-CoA biosynthesis (Acot6, Acsl6), and downregulated is fatty acid transport (Slc27a2). SFN upregulated acylCoA hydrolase (Acot3) and long chain fatty acid activation for lipids synthesis and beta oxidation (Acsl1). Leptin + SFN upregulated fatty acid beta oxidation (Acad11, Acam) and acyl-CoA hydrolase (Acot3, Acot7), and downregulated fatty acid elongation (Acot2). As a result, treatment of both SFN and leptin has more profound effects on ameliorating pathways involved in hepatic lipogenesis and TG accumulation and lipid profile of TG and TC than other types of intervention. We conclude that early intervention of obesity pa could ameliorate the metabolic changes of fat metabolism in liver as observed in WT mice on HFD in response to anti-obesity treatment.
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Ma, Liang, Jeremy Barker, Changchun Zhou, Biaoyang Lin, and Wei Li. "A Perfused Two-Chamber System for Anticancer Drug Screening." In ASME 2010 International Manufacturing Science and Engineering Conference. ASMEDC, 2010. http://dx.doi.org/10.1115/msec2010-34326.

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A cell culture microfluidic device has been developed to test the cytotoxicity of anticancer drugs while reproducing multi-organ interactions in vitro. Cells were cultured in separate chambers representing the liver and tumor. The two chambers were connected through a channel to mimick the blood flow. Glioblastoma (GBM) cancer cells (M059K) and hepatoma cells (HepG2) were cultured in the tumor and the liver chambers, respectively. The cytotoxic effect of cancer treatment drug Temolozomide (TMZ) was tested using this two chamber system. The experimental results showed that with the liver cells, the cancer cells showed much higher viability than those without the liver cells. This indicates that the liver metabolism has strong effect on the toxicity of the anticancer drug. The results demonstrated that the perfused two chamber cell culture system has the potential to be used as a platform for drug screening in a more physiologically realistic environment.
7

Chakrabarti, Gaurab, and David A. Boothman. "Abstract 1679: Inhibiting KRAS-reprogrammed glutamine metabolism sensitizes pancreatic cancer to NQO1-bioactivatable drugs." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-1679.

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8

Tourlomousis, Filippos, and Robert C. Chang. "Computational Modeling of 3D Printed Tissue-on-a-Chip Microfluidic Devices as Drug Screening Platforms." In ASME 2014 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2014. http://dx.doi.org/10.1115/imece2014-38454.

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Анотація:
Physiological tissue-on-a-chip technology is enabled by adapting microfluidics to create micro scale drug screening platforms that replicate the complex drug transport and reaction processes in the human liver. The ability to incorporate three-dimensional (3d) tissue models using layered fabrication approaches into devices that can be perfused with drugs offer an optimal analog of the in vivo scenario. The dynamic nature of such in vitro metabolism models demands reliable numerical tools to determine the optimum tissue fabrication process, flow, material, and geometric parameters for the most effective metabolic conversion of the perfused drug into the liver microenvironment. Thus, in this modeling-based study, the authors focus on modeling of in vitro 3d microfluidic microanalytical microorgan devices (3MD), where the human liver analog is replicated by 3d cell encapsulated alginate hydrogel based tissue-engineered constructs. These biopolymer constructs are hosted in the chamber of the 3MD device serving as walls of the microfluidic array of channels through which a fluorescent drug substrate is perfused into the microfluidic printed channel walls at a specified volumetric flow rate assuring Stokes flow conditions (Re<<1). Due to the porous nature of the hydrogel walls, a metabolized drug product is collected as an effluent stream at the outlet port. A rigorous modeling approached aimed to capture both the macro and micro scale transport phenomena is presented. Initially, the Stokes Flow Equations (free flow regime) are solved in combination with the Brinkman Equations (porous flow regime) for the laminar velocity profile and wall shear stresses in the whole shear mediated flow regime. These equations are then coupled with the Convection-Diffusion Equation to yield the drug concentration profile by incorporating a reaction term described by the Michael-Menten Kinetics model. This effectively yields a convection-diffusion–cell kinetics model (steady state and transient), where for the prescribed process and material parameters, the drug concentration profile throughout the flow channels can be predicted. A key consideration that is addressed in this paper is the effect of cell mechanotransduction, where shear stresses imposed on the encapsulated cells alter the functional ability of the liver cell enzymes to metabolize the drug. Different cases are presented, where cells are incorporated into the geometric model either as voids that experience wall shear stress (WSS) around their membrane boundaries or as solid materials, with linear elastic properties. As a last step, transient simulations are implemented showing that there exists a tradeoff with respect the drug metabolized effluent product between the shear stresses required and the residence time needed for drug diffusion.
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Ros, S., P. D’Santos, D. Hu, AJ Wright, RL Hesketh, AS Batra, E. Mannion, A. Bruna, C. Caldas, and KM Brindle. "6 Imaging tumour metabolism to guide treatment of breast cancer with drugs targeted at PI3K alpha." In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.6.

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Zamora Auñón, P., L. Trilla-Fuertes, M. Díaz-Almirón, A. Gamez-Pozo, G. Prado-Vázquez, A. Zapater-Moros, S. Llorente-Armijo, F. Gaya Romero, E. Espinosa Arranz, and JA Fresno-Vara. "Abstract P1-02-06: Computational modeling predicts drugs response to targeting metabolism in breast cancer cells." In Abstracts: 2017 San Antonio Breast Cancer Symposium; December 5-9, 2017; San Antonio, Texas. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.sabcs17-p1-02-06.

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Звіти організацій з теми "Drugs Metabolism":

1

Chipiso, Kudzanai. Biomimetic Tools in Oxidative Metabolism: Characterization of Reactive Metabolites from Antithyroid Drugs. Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.3078.

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2

Hawkins, David R. Determination of Drug Pharmacokinetics and Metabolic Profile. Volume 2. Fort Belvoir, VA: Defense Technical Information Center, March 1988. http://dx.doi.org/10.21236/ada192428.

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3

Halim, Nader. Regulation of Brain Glucose Metabolic Patterns by Protein Phosphorlyation and Drug Therapy. Fort Belvoir, VA: Defense Technical Information Center, March 2007. http://dx.doi.org/10.21236/ad1013984.

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