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Статті в журналах з теми "Drugs Metabolism":

1

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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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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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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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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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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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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8

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

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3

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

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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." Thesis, 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." Doctoral thesis, 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." Thesis, 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." Thesis, 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." Thesis, University of Leeds, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.329825.

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Книги з теми "Drugs Metabolism":

1

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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2

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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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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4

Garth, Powis, ed. Anticancer drugs: Reactive metabolism and drug interactions. Oxford, England: Pergamon Press, 1994.

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5

1938-, Bieck Peter R., ed. Colonic drug absorption and metabolism. New York: M. Dekker, 1993.

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6

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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7

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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H, Jeffery Elizabeth, ed. Human drug metabolism: From molecular biology to man. Boca Raton: CRC Press, 1993.

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9

1955-, Woolf Thomas F., ed. Handbook of drug metabolism. New York: Dekker, 1999.

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10

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

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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

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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4

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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5

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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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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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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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":

1

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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Анотація:
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

Mrkalić, Emina, Marina Ćendić Serafinović, Ratomir Jelić, Stefan Stojanović, and Miroslav Sovrlić. "INFLUENCE OF QUERCETIN ON THE BINDING OF TIGECYCLINE TO HUMAN SERUM ALBUMIN." In 1st INTERNATIONAL Conference on Chemo and BioInformatics. Institute for Information Technologies, University of Kragujevac, 2021. http://dx.doi.org/10.46793/iccbi21.363m.

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Serum albumin is the major soluble protein in the circulatory system of humans. The metabolism of drugs, their distribution, free concentration, and efficacy depend on the drug-serum albumin interaction [1]. Accordingly, it is important to study the interactions of drugs with serum albumin, which determines the pharmacology and pharmacodynamics of drugs. Quercetin (QUE), a natural polyphenol widely distributed in many plant foods, such as fruits, vegetables, nuts, seeds, grains, and tea [2], bind to serum albumin [3]. Tigecycline (TGC), is a tetracycline antibiotic widely used in the treatment of bacterial infections [4]. This study aimed to investigate the binding properties of TGC to HSA in the presence of QUE, under physiological conditions, by fluorescence spectroscopy.
3

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.
4

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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6

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.
7

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.
8

Astaf'eva, E. A., T. A. Tolochko, and A. A. Timofeeva. "THE EFFECT OF POLYMORPHISM OF THE MTHFR C677T GENE ON THE MORPHOFUNCTIONAL STATE OF LYMPHOCYTES DURING DRUG INTOXICATION." In I International Congress “The Latest Achievements of Medicine, Healthcare, and Health-Saving Technologies”. Kemerovo State University, 2023. http://dx.doi.org/10.21603/-i-ic-8.

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The prevalence of opioid dependence among the able-bodied population is an important medical and social problem. Methylenetetrahydrofolate reductase (MTHFR) plays a key role in the metabolism of narcotic drugs. A decrease in the enzyme activity in polymorphic variants of the gene encoding it is associated with a decrease in the immunity of opioid addiction patients.
9

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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Jovanović-Šanta, Suzana S., Aleksandar M. Oklješa, Antos B. Sachanka, Yaraslau U. Dzichenka, and Sergei A. Usanov. "17-SUBSTITUTED STEROIDAL TETRAZOLES – NOVEL LIGANDS FOR HUMAN STEROID-CONVERTING CYP ENZYMES." In 1st INTERNATIONAL Conference on Chemo and BioInformatics. Institute for Information Technologies, University of Kragujevac, 2021. http://dx.doi.org/10.46793/iccbi21.336js.

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In animal and human organisms, there are many enzymes, members of the family of heme- containing proteins, cytochromes P450 (CYPs), included in the biosynthesis and metabolism of many biomolecules, as cholesterol, bile acids, sex, and corticosteroid hormones, as well as in metabolism of drugs and xenobiotics. It is also well-known that different imidazole and triazole derivatives are efficient inhibitors of CYPs activity. In this study, we present in vitro screening of binding of novel androstane derivatives with tetrazole- containing substituents in position 17 to human recombinant steroid-converting CYP enzymes: CYP7A1, CYP7B1, CYP17A1, CYP19, and CYP21. Initial screening was performed using a high throughput screening approach, while the affinity of the ligands was analyzed using spectrophotometric titration. For some among tested compounds type I spectral response (substrate-like binding) for CYP7A1 selectively, while for one compound type II spectral response (inhibitor-like binding) for CYP21 were detected, with micromolar values of Kds. Interestingly, one compound with mixed spectral response was found to bind for CYP7B1, which means that there are two optimal positions of the ligand inside the protein active site. Such results could be useful in CYP-inhibiting drug development, during a fast, high-throughput screening of pharmacological potential of novel compounds, as well as in side- effects recognizing.

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

Xiang, Kemeng, Huiming Hou, and Ming Zhou. The efficacy of Cerus and Cucumis Polypeptide injection combined with Bisphosphonates on postmenopausal women with osteoporosis:A protocol for systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2022. http://dx.doi.org/10.37766/inplasy2022.5.0067.

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Review question / Objective: The aim of this review is to evaluate the effectiveness of Cerus and Cucumis Polypeptide injection combined with Bisphosphonates for postmenopausal osteoporosis. Condition being studied: Postmenopausal osteoporosis (PMOP) is a disorder of bone metabolism caused by estrogen deficiency in women after menopause, which manifests clinically as pain, spinal deformities and even fragility fractures, affecting the quality of life of patients and possibly shortening their life span. Bisphosphonates are commonly used to control and delay the progression of the disease, improve the patient's symptoms and reduce the incidence of fragility fractures. However, single drugs are still lacking in controlling the progression of the disease, and the combination of drugs is the clinical priority.
3

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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4

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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5

Liu, Shuang, Zheng-Miao Wang, Dong-Mei Lv, and Yi-Xuan Zhao. Advances in highly active one-carbon metabolism in cancer diagnosis, treatment, and drug resistance: a systematic review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, November 2022. http://dx.doi.org/10.37766/inplasy2022.11.0099.

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6

Jin, Dachuan, Gao Peng, Shunqin Jin, Tao Zhou, Baoqiang Guo, and Guangming Li. Comparison of therapeutic effects of anti-diabetic drugs on non-alcoholic fatty liver disease patients without diabetes: A network meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, November 2022. http://dx.doi.org/10.37766/inplasy2022.11.0014.

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Review question / Objective: To evaluate the efficacy of different anti-diabetic drugs in the treatment of non-diabetic non-alcoholic disease by network meta-analysis, and find the best intervention. Condition being studied: Non-alcoholic fatty liver disease (NAFLD) refers to the disease in which the liver fat content exceeds 5%, and excludes the secondary causes of alcohol, infection, drugs or other specific metabolic diseases. As a spectrum of disorders, it includes hepatocyte steatosis and steatohepatitis at the initial stage, liver fibrosis at the later stage, cirrhosis at the final stage, and even liver cancer. Nowadays Non-alcoholic fatty liver disease (NAFLD) has become the most common chronic liver disease in the world with an incidence rate as high as 25% which has been rising steadily worldwide in the past 30 years. Currently there are still no approved specific therapeutic agents and global treatment guidelines for NAFLD. For non-diabetic NAFLD, there is far from a consensus, too.
7

Ghosal, Samit, and Binayak Sinha. The cardiovascular benefits of GLP1-RA are directly related to their positive effect on glycaemic control: A meta-regression analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, January 2022. http://dx.doi.org/10.37766/inplasy2022.1.0071.

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Review question / Objective: P (patient population) = Type 2 diabetes patients with high CV risk or established atherosclerotic cardiovascular disease; I (intervention) = Received drugs: GLP1-RA; C (control group) = Compared to a control group that received a placebo; O (outcome) = Outcomes of interest included primary CV outcomes (MACE, CV death, MI, and Stroke). Condition being studied: To explore whether the heterogeneity associated with the primary outcomes benefits can be attributed to the metabolic improvements associated with GLP1-RA. The plan is to use HBA1c, weight, and SBP reduction as moderators attempting to explain any variance between the true and observed effect size.
8

Hu, Yang Yang, Xing Zhang, Yue Luo, and Yadong Wang. Systematic review and Meta analysis of the efficacy and safety of rifaximin in the prevention and treatment of hepatic encephalopathy. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, February 2023. http://dx.doi.org/10.37766/inplasy2023.2.0061.

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Review question / Objective: P:Liver cirrhosis patients with risk factors associated with HE attack;HE patients caused by chronic liver diseases represented by cirrhosis. I: Rifaximin treatment. C: Other drugs or placebo. O:HE incidence; HE improvement; All-cause mortality; Blood ammonia level; PSE index; mental state; NCT-A; NCT-B; Adverse events. Condition being studied: Hepatic encephalopathy(HE) is a neuropsychiatric disorder syndrome based on metabolic disorders, which is caused by severe acute and chronic liver dysfunction or various abnormalities of portosystemic shunt (hereinafter referred to as portosystemic shunt). The research data shows that the prevalence of OHE in patients with cirrhosis is 10-14%, and the prevalence of HE in patients with decompensated cirrhosis is 16-21%. HE can lead to 60-80% of patients with liver cirrhosis with mild cognitive impairment, affecting their ability of daily life and quality of life. When OHE occurs, the one-year mortality rate of patients with liver cirrhosis is 64%, which brings a heavy economic burden to patients and public health resources. Therefore, the prevention and early management of HE is very important.
9

Cytryn, Eddie, Mark R. Liles, and Omer Frenkel. Mining multidrug-resistant desert soil bacteria for biocontrol activity and biologically-active compounds. United States Department of Agriculture, January 2014. http://dx.doi.org/10.32747/2014.7598174.bard.

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Control of agro-associated pathogens is becoming increasingly difficult due to increased resistance and mounting restrictions on chemical pesticides and antibiotics. Likewise, in veterinary and human environments, there is increasing resistance of pathogens to currently available antibiotics requiring discovery of novel antibiotic compounds. These drawbacks necessitate discovery and application of microorganisms that can be used as biocontrol agents (BCAs) and the isolation of novel biologically-active compounds. This highly-synergistic one year project implemented an innovative pipeline aimed at detecting BCAs and associated biologically-active compounds, which included: (A) isolation of multidrug-resistant desert soil bacteria and root-associated bacteria from medicinal plants; (B) invitro screening of bacterial isolates against known plant, animal and human pathogens; (C) nextgeneration sequencing of isolates that displayed antagonistic activity against at least one of the model pathogens and (D) in-planta screening of promising BCAs in a model bean-Sclerotiumrolfsii system. The BCA genome data were examined for presence of: i) secondary metabolite encoding genes potentially linked to the anti-pathogenic activity of the isolates; and ii) rhizosphere competence-associated genes, associated with the capacity of microorganisms to successfully inhabit plant roots, and a prerequisite for the success of a soil amended BCA. Altogether, 56 phylogenetically-diverse isolates with bioactivity against bacterial, oomycete and fungal plant pathogens were identified. These strains were sent to Auburn University where bioassays against a panel of animal and human pathogens (including multi-drug resistant pathogenic strains such as A. baumannii 3806) were conducted. Nineteen isolates that showed substantial antagonistic activity against at least one of the screened pathogens were sequenced, assembled and subjected to bioinformatics analyses aimed at identifying secondary metabolite-encoding and rhizosphere competence-associated genes. The genome size of the bacteria ranged from 3.77 to 9.85 Mbp. All of the genomes were characterized by a plethora of secondary metabolite encoding genes including non-ribosomal peptide synthase, polyketidesynthases, lantipeptides, bacteriocins, terpenes and siderophores. While some of these genes were highly similar to documented genes, many were unique and therefore may encode for novel antagonistic compounds. Comparative genomic analysis of root-associated isolates with similar strains not isolated from root environments revealed genes encoding for several rhizospherecompetence- associated traits including urea utilization, chitin degradation, plant cell polymerdegradation, biofilm formation, mechanisms for iron, phosphorus and sulfur acquisition and antibiotic resistance. Our labs are currently writing a continuation of this feasibility study that proposes a unique pipeline for the detection of BCAs and biopesticides that can be used against phytopathogens. It will combine i) metabolomic screening of strains from our collection that contain unique secondary metabolite-encoding genes, in order to isolate novel antimicrobial compounds; ii) model plant-based experiments to assess the antagonistic capacities of selected BCAs toward selected phytopathogens; and iii) an innovative next-generation-sequencing based method to monitor the relative abundance and distribution of selected BCAs in field experiments in order to assess their persistence in natural agro-environments. We believe that this integrated approach will enable development of novel strains and compounds that can be used in large-scale operations.

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