Relevant bibliographies by topics / Metabolic activation

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Metabolic activation'

Author: Grafiati
Published: 4 June 2021
Last updated: 25 April 2022

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Journal articles on the topic "Metabolic activation"

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Pence, Brandt D., and Jeffrey A. Woods. "Metabolic Activation." Medicine & Science in Sports & Exercise 47 (May 2015): 716. http://dx.doi.org/10.1249/01.mss.0000478681.15510.ae.

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Oyarzún, Diego, Brian Ingalls, Richard Middleton, and Dimitrios Kalamatianos. "Optimal Metabolic Pathway Activation." IFAC Proceedings Volumes 41, no. 2 (2008): 12587–92. http://dx.doi.org/10.3182/20080706-5-kr-1001.02130.

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Wang, Ching Y., and Charles M. King. "Metabolic activation of benzidine." International Journal of Cancer 121, no. 7 (2007): 1640–41. http://dx.doi.org/10.1002/ijc.22905.

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Peter Guengerich, F. "Metabolic activation of carcinogens." Pharmacology & Therapeutics 54, no. 1 (January 1992): 17–61. http://dx.doi.org/10.1016/0163-7258(92)90050-a.

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White, Ian N. H., Melanie L. Green, Eric Bailey, and Peter B. Farmer. "Metabolic activation of olefins." Biochemical Pharmacology 35, no. 9 (May 1986): 1569–75. http://dx.doi.org/10.1016/0006-2952(86)90126-7.

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Holthaus, Lisa, Virag Sharma, Daniel Brandt, Anette-Gabriele Ziegler, Martin Jastroch, and Ezio Bonifacio. "Functional and metabolic fitness of human CD4+ T lymphocytes during metabolic stress." Life Science Alliance 4, no. 12 (September 27, 2021): e202101013. http://dx.doi.org/10.26508/lsa.202101013.

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Human CD4+ T cells are essential mediators of immune responses. By altering the mitochondrial and metabolic states, we defined metabolic requirements of human CD4+ T cells for in vitro activation, expansion, and effector function. T-cell activation and proliferation were reduced by inhibiting oxidative phosphorylation, whereas early cytokine production was maintained by either OXPHOS or glycolytic activity. Glucose deprivation in the presence of mild mitochondrial stress markedly reduced all three T-cell functions, contrasting the exposure to resveratrol, an antioxidant and sirtuin-1 activator, which specifically inhibited cytokine production and T-cell proliferation, but not T-cell activation. Conditions that inhibited T-cell activation were associated with the down-regulation of 2′,5′-oligoadenylate synthetase genes via interferon response pathways. Our findings indicate that T-cell function is grossly impaired by stressors combined with nutrient deprivation, suggesting that correcting nutrient availability, metabolic stress, and/or the function of T cells in these conditions will improve the efficacy of T-cell–based therapies.
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Park, B. K., D. J. Naisbitt, S. F. Gordon, N. R. Kitteringham, and M. Pirmohamed. "Metabolic activation in drug allergies." Toxicology 158, no. 1-2 (February 2001): 11–23. http://dx.doi.org/10.1016/s0300-483x(00)00397-8.

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Mekenyan, O., S. Dimitrov, N. Dimitrova, G. Dimitrova, T. Pavlov, G. Chankov, S. Kotov, K. Vasilev, and R. Vasilev. "Metabolic activation of chemicals:in-silicosimulation†." SAR and QSAR in Environmental Research 17, no. 1 (February 2006): 107–20. http://dx.doi.org/10.1080/10659360600562087.

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Skonberg, Christian, Jrgen Olsen, Kim Grimstrup Madsen, Steen Honor Hansen, and Mark P. Grillo. "Metabolic activation of carboxylic acids." Expert Opinion on Drug Metabolism & Toxicology 4, no. 4 (April 2008): 425–38. http://dx.doi.org/10.1517/17425255.4.4.425.

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Vrijsen, Raf, Yvette Michotte, and Albert Boeyé. "Metabolic activation of quercetin mutagenicity." Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis 232, no. 2 (October 1990): 243–48. http://dx.doi.org/10.1016/0027-5107(90)90130-v.

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Dissertations / Theses on the topic "Metabolic activation"

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Lei, Hua. "Studies on the metabolic activation of glyceryl trinitrate." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape17/PQDD_0013/MQ31223.pdf.

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Ayrton, Andrew David. "Food mutagens : factors that modulate their metabolic activation." Thesis, University of Surrey, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.328576.

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Anari, Mohammad Reza. "Cytochrome P450 peroxidase/peroxygenase-dependent metabolic activation of xenobiotics." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp03/NQ28269.pdf.

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Preston, Kyle J. "Macronutrient Activation of Endothelium Dependent Leukocyte Trafficking: Metabolic Implications." Diss., Temple University Libraries, 2015. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/361365.

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Physiology
Ph.D.
Obesity and insulin resistance are characterized by elevated pro-inflammatory proteins in the blood and immune cell accumulation in the visceral adipose tissue. Resident leukocytes release tumor necrosis factor α (TNFα) and other inflammatory cytokines which stimulate adipocyte lipolysis, recruit leukocytes to adipose tissue, promote pro-inflammatory immune cell polarization, facilitate oxidative stress, and activate intracellular kinases which dull insulin signaling cascades in metabolic tissues. Immune cell mediated dysregulation of stromal and parenchymal cells has raised suspicion that insulin resistance is an immune disorder initiated by activated white blood cells with over-nutrition. Efforts to improve pathological metabolism by reducing inflammation have yielded mixed results in humans and animal models. The role of inflammation and immune cell accumulation in the visceral fat (VF) in the progression of insulin resistance remains presently debated. There is, however, a consensus that identifying the triggers for obesity and impaired insulin signaling is of the utmost importance. The goal of this report is to identify dietary fat absorption as a key initiator of inflammatory action and insulin desensitization which may be dampened by reducing immune cell accumulation in adipose tissue. To explore how lean, healthy organisms become obese and insulin resistant, we examined the inflammatory consequences of isocaloric but variable macronutrient loads in the VF of lean mice. Mice were administered single liquid meals composed of low-fat (10% fat) or high-fat (60% fat) diet and observed by intravital microscopy to quantify leukocyte-endothelium interactions in mesenteric postcapillary venules (MPCV) 1, 2, 3, and 4 hours after oral gavage. Leukocyte rolling and leukocyte adhesion were transiently elevated within 1 hour after feeding and returned to baseline levels 4 hours later. Endothelial cell surface expression of P-selectin (Psel), a rapidly activated cell adhesion molecule (CAM), confirmed that high-fat feeding induced Psel dependent leukocyte rolling through the VF microcirculation. Furthermore, leukocyte accumulation in the VF was modestly increased by a single high-fat meal (HFM). Repetitive high-fat diet (HFD) consumption for 24 hours prolonged elevated leukocyte-endothelium interactions and promoted neutrophil accumulation in the VF. The neutrophilic enzyme myeloperoxidase (MPO), a producer of the chlorinating agent hypochlorous acid, increased in abundance and activity in the VF of HFM fed mice. Elevated leukocyte-endothelium interactions, leukocyte infiltration, and MPO activity in VF were not observed in Psel deficient (Psel-/-) mice following lipid overload. To ascertain if MPO is required for sustained endothelial activation, leukocyte-endothelium interactions and leukocyte infiltration were monitored in high-fat fed MPO deficient (MPO-/-) mice. Similar to the Psel-/- mice, MPO-/- mice were protected from the inflammatory effects of high-fat feeding. Our data supports postprandial hyperlipemia as an inducer of transient and Psel dependent inflammatory reactions that are sustained by prolonged HFD consumption. To study whether early phase inflammatory interventions granted late phase metabolic improvements, wild-type (WT), Psel deficient (Psel-/-), and MPO deficient (MPO-/-) C57BL/6 mice were given ad libitum access to LFD (10% fat) or HFD (60% fat) for 12-16 weeks. All mouse groups given HFD became obese. Prolonged HFD consumption sustained elevated leukocyte-endothelium interactions in MPCVs and was accompanied by increased local and systemic TNFα in WT mice. High-fat fed WT mice were hyperglycemic, hyperinsulinemic, glucose intolerant, and insulin resistant compared to LFD fed controls. Psel-/- mice were protected from leukocyte-endothelium interactions as well as local and systemic TNFα accumulation despite extended HFD consumption. Surprisingly, high-fat fed Psel-/- mice were equally hyperglycemic, hyperinsulinemic, glucose intolerant, and insulin resistant as the inflamed, high-fat fed WT mice. MPO-/- mice were also protected from elevated systemic TNFα and gained slightly less weight than the other high-fat fed groups. While MPO-/- mice were hyperglycemic and glucose intolerant, they did have improved insulin stimulated glucose clearance. The data presented in this report demonstrates the pro-inflammatory nature of postprandial hyperlipemia and the insulin desensitizing nature of prolonged HFD consumption. Ablation of VF immune cell accumulation by Psel deletion is not sufficient for improving insulin signaling or glycemic control, which is consistent with prior reports. Deletion of MPO, however, did result in slightly less obesity and marginally improved insulin signaling. We conclude that while immune cell accumulation in the VF contributes to the progression of insulin resistance, it is not a prerequisite for metabolic pathology development.
Temple University--Theses
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Engelhart, David Albert. "Part~I. Metabolic activation of cyclic tertiary amines Part~II Neurotoxic activation of beta,beta'-iminodipropionitrile (IDPN)." Case Western Reserve University School of Graduate Studies / OhioLINK, 1994. http://rave.ohiolink.edu/etdc/view?acc_num=case1057933667.

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Roberts, Lee D. "Defining the metabolic effect of peroxisome proliferator-activated receptor δ activation." Thesis, University of Cambridge, 2010. https://www.repository.cam.ac.uk/handle/1810/226743.

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Peroxisome proliferator-activated receptors (PPARs) are nuclear receptors that function as ligand activated transcription factors. There are three identified isotypes: PPAR alpha, PPAR gamma and PPAR delta, together controlling the expression of genes involved in inflammation, cell differentiation, proliferation, lipid and carbohydrate metabolism and energy homeostasis. The PPARs are potential targets for the treatment of dyslipidaemia, type II diabetes mellitus and the metabolic syndrome. This thesis uses a multi-platform metabolomics approach, 13C-isotope substrate flux analysis, respirometry and transcriptomics to determine the role PPAR delta and PPAR gamma play in metabolic control both in adipose tissue and systemically. To achieve this, the metabolic phenotype of the 3T3-L1 adipocyte cell line was defined to generate a metabolically phenotyped in vitro model of adipose tissue. The importance of fatty acid alpha-oxidation in the differentiation of adipocytes was emphasised The effects of PPAR delta and PPAR gamma activation in white adipose tissue from the ob/ob mouse model of insulin resistance, and in the phenotyped 3T3-L1 adipocyte model, were investigated. PPAR delta activation was distinguished by oxidative catabolism of fatty acids and citric acid cycle intermediates. Conversely, PPAR gamma activation was identified by the sequestration of lipids into adipose tissue. Moreover, to address the systemic influence of PPAR activation, with a focus on the Cori cycle and the interactions of the liver and skeletal muscle, the metabolic changes that occur in these tissues following PPAR delta and PPAR gamma activation in the ob/ob mouse were examined. PPAR delta activation was characterised by the mobilisation and release of triacylglycerols (TAGs) into circulation as an energy source for peripheral tissues whereas PPAR gamma activation was defined by a reduction and sequestration of circulating TAGs. This thesis has better characterised the role of the PPARs as master regulators of metabolism and emphasised their potential as therapeutic targets for metabolic diseases of global importance.
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Cammann, Clemens [Verfasser], and Jonathan [Akademischer Betreuer] Lindquist. "Metabolic reprogramming upon CD8 T cell activation / Clemens Cammann ; Betreuer: Jonathan Lindquist." Magdeburg : Universitätsbibliothek, 2016. http://d-nb.info/1113687231/34.

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Tsui, Lok Hang Carlson. "Cell intrinsic regulation of B cell activation : metabolic reprogramming and mitochondrial remodelling." Thesis, University College London (University of London), 2018. http://discovery.ucl.ac.uk/10051228/.

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B cells are fundamental components of the adaptive immune system. B-cell activation leads to the formation of effector (plasma cells) and memory (memory B cells) compartments in vivo, which together provide a potent line of defense against pathogenic infections through the production of highly specific antibodies. At the cellular level, B-cell activation triggers the rapid reorganization of the cytoskeleton. It is now recognized that the dynamic remodeling of actin and microtubules is extremely important for B cells in aspects such as receptor signalling, cell motility, as well as intracellular trafficking of membrane compartments. B-cell activation in the longer-term triggers metabolic reprogramming and remodeling of many other intracellular organelles that are required to support increased cell growth, proliferation and differentiation. However, despite previous studies have shed light into the many characteristics of B cell activation and differentiation, our understanding on how B-cell activation and fate decision is coordinated is still incomplete. To address these questions, I set out to investigate firstly the mechanism of cytoskeleton regulation and its role on B-cell activation. This involved the study on the RhoGTPase RhoF and vimentin that were largely uncharacterised in B cells. RhoF- and vimentin-deficient mouse models were used in these contexts combined with techniques including super-resolution light microscopy and electron microscopy. The results obtained suggest that while RhoF does not seem to play a major role in B-cell development and function, the dynamic reorganisation of vimentin is critical for B-cell activation. Loss of vimentin in B cells also affected intracellular trafficking, antigen presentation and in vivo antibody responses. Next, I went on to study the role of metabolic reprogramming on B-cell fate decision using the PKC-deficient model. Despite this topic has been a recent hotspot in the field of T cells, it has so far not been extensively studied in B cells. Combining advanced sequencing and detailed metabolomics analysis, I found that while PKC played multiple roles in B cell function, it is specifically required to initiate an mTORC1-dependent metabolic program to promote plasma cell differentiation. Accordingly, the loss of PKC rendered activated B cells unable to sustain this metabolic program, and as a result favouring differentiation to memory cells. All together, these results provide mechanistic insights into B-cell differentiation and highlight the central role of metabolic reprogramming on fate decision in B cells.
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Riley, Robert John. "An evaluation of the importance of metabolic activation and detoxication in drug toxicity." Thesis, University of Liverpool, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.316895.

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McGlashon, Jacob. "Serotonin neurons maintain central mechanisms regulating metabolic homeostasis and are vital to thermogenic activation." Diss., University of Iowa, 2016. https://ir.uiowa.edu/etd/2121.

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Thermogenic brown and beige adipocytes convert chemical energy to heat by metabolizing glucose and lipids via uncoupling protein 1 (Ucp1), a process known as non-shivering thermogenesis. Serotonin (5-HT) neurons in the ventral medulla are known to regulate sympathetic efferent neurons in the intermediolateral nucleus (IML) necessary to maintain brown adipose tissue (BAT) activity. Previous studies show that mice lacking central 5-HT neurons are incapable of maintaining body temperature in cold, ambient conditions. Due to this direct linkage between 5-HT and thermoregulation, we hypothesized that central 5-HT neurons may be vital to the regulation of brown and beige adipocyte activity. Given that BAT consumes large amounts of substrate when active, we also hypothesized that inactivation of BAT due to deletion of the regulatory neural circuitry (5-HT neurons) would cause metabolic dysregulation. To test this, we generated mice in which the human diphtheria toxin (DT) receptor was selectively expressed in central 5-HT neurons under control of a Pet-1 promoter. Pet-1 is a transcription factor selectively located in mature, central 5-HT neurons. Coincidentally, some cells within pancreatic islets also express Pet-1, and contain adequate machinery to produce, release, and uptake 5-HT. Systemic treatment with DT eliminated 5-HT neurons and caused loss of thermoregulation, BAT steatosis, and a >50% decrease in Ucp1 expression in BAT and beige fat, indicative of reduced thermal production. In parallel, blood glucose increased 3.5-fold, free fatty acids 13.4-fold and triglycerides 6.5-fold. Intracerebroventricular (ICV) treatment with 1/30th the systemic dose of DT induced an even greater thermoregulatory impairment. The metabolic deficits following systemic DT treatment indicate that central 5-HT neurons are essential for proper metabolic regulation. However, such high levels of glucose and lipids also indicate failure of the pancreatic endocrine program following systemic treatment, likely due to moderate destruction of β-cells expressing Pet-1 and the DT receptor. Because ICV treatment caused even greater thermoregulatory and metabolic deficits, where little, if any, of the toxin would spread systemically, central 5-HT neurons are clearly essential for normal central regulation of metabolism. Interestingly, similar BAT and beige fat defects occurred in Lmx1bf/f/p mice, in which 5-HT neurons fail to develop in utero. Assessment of systemically treated animals using a euglycemic/hyperinsulinemic clamp showed extensive fasting hyperglycemia and systemic insulin resistance, coinciding with reduced glucose uptake in skeletal muscle and BAT. The hyperinsulinemic clamp failed to suppress hepatic glucose and fatty acid production, leading to the conclusion that loss of central 5-HT neurons disrupts central hepatic regulation. In attempts to induce BAT thermogenesis and metabolism, we optogenetically stimulated 5-HT neurons in the rostral raphe pallidus and measured BAT and body temperature along with blood glucose. Unfortunately, these stimulations were incapable of increasing BAT temperature and lowering blood glucose, perhaps limiting therapeutic potential of these 5-HT neurons. We conclude that 5-HT neurons are major players in central regulation of metabolic homeostasis, in part through recruitment and activation of brown and beige adipocytes and hepatic substrate production. Data also suggest that 5-HT neurons regulate glucose homeostasis via undefined neural mechanisms independently of BAT activity and pancreatic insulin secretion. Cumulative data on central 5-HT neurons indicate they are master regulators of whole-body metabolism.
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Books on the topic "Metabolic activation"

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Lau, Grace S. N. Metabolic activation of drugs and other xenobiotics in hepatocellular carcinoma. Hong Kong: Chinese University Press, 1997.

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Roland, Per E. Brain activation. New York: Wiley-Liss, 1993.

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Sideman, S., and R. Beyar, eds. Activation, Metabolism and Perfusion of the Heart. Dordrecht: Springer Netherlands, 1987. http://dx.doi.org/10.1007/978-94-009-3313-2.

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Regulation of enzyme activity. Oxford: IRL Press, 1988.

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E, Adams Gerald, and North Atlantic Treaty Organization. Scientific Affairs Division., eds. Selective activation of drugs by redox processes. New York: Plenum Press, 1990.

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Sideman, S. Activation, Metabolism and Perfusion of the Heart: Simulation and experimental models. Dordrecht: Springer Netherlands, 1987.

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Hedgehog signaling activation in human cancer and its clinical implications. New York: Springer, 2011.

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International Symposium "Brain Activation and CBF Control" ( 2001 Tokyo, Japan). Brain activation and CBF control: Proceedings of the Satellite meeting on Brain Activation and Cerebral Blood Flow Control, held in Tokyo, Japan 5-8 June 2001. Edited by Tomita M, Kanno I, and Hamel E. Amsterdam: Elsevier, 2002.

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Convegno nazionale Meccanismi di attivazione e tossicità degli xenobiotici (1st 1987 Istituto superiore di sanità). 1st Italian Symposium Mechanisms of Activation and Toxicity of Xenobiotics: Istituto superiore di Sanità, Rome, 26-27 March 1987 : abstract book. Roma: Il Istituto, 1987.

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Nederkoorn, Paul H. J. Signal transduction by G protein-coupled receptors: Bioenergetics and G protein activation : proton transfer and GTP synthesis to explain the experimental findings. New York: Springer, 1997.

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Book chapters on the topic "Metabolic activation"

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Bekki, Kanae. "Metabolic Activation." In Polycyclic Aromatic Hydrocarbons, 227–34. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-10-6775-4_17.

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Magistretti, Pierre J., and Luc Pellerin. "Metabolic Coupling during Activation." In Advances in Experimental Medicine and Biology, 161–66. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4899-0056-2_18.

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Perucca, Emilio, and Luigi Manzo. "Metabolic Activation of Neurotoxicants." In Recent Advances in Nervous System Toxicology, 67–86. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4613-0887-4_4.

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Chen, Chang-Hwei. "Metabolic Conversion of Lipophilic Compounds." In Activation and Detoxification Enzymes, 17–24. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4614-1049-2_3.

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Longo, Frank J. "Metabolic alterations at egg activation." In Fertilization, 101–16. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4899-3264-8_9.

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Guan, Xiangming. "Metabolic Activation and Drug Targeting." In Drug Delivery, 201–44. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2005. http://dx.doi.org/10.1002/0471475734.ch11.

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Penning, Trevor M. "Metabolic Activation of Chemical Carcinogens." In Chemical Carcinogenesis, 135–58. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-61737-995-6_7.

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Guan, Xiangming. "Metabolic Activation and Drug Targeting." In Drug Delivery, 383–434. Hoboken, NJ: John Wiley & Sons, Inc, 2016. http://dx.doi.org/10.1002/9781118833322.ch17.

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Püschel, Franziska, and Cristina Muñoz-Pinedo. "Measuring the Activation of Cell Death Pathways upon Inhibition of Metabolism." In Metabolic Signaling, 163–72. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8769-6_12.

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Chen, Chang-Hwei. "Bioactivation Metabolism: Activation Enzymes." In Xenobiotic Metabolic Enzymes: Bioactivation and Antioxidant Defense, 45–58. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-41679-9_5.

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Conference papers on the topic "Metabolic activation"

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Verhaeghe, Jeroen, and Andrew J. Reader. "Simultaneous water activation and glucose metabolic rate imaging with PET." In 2011 IEEE Nuclear Science Symposium and Medical Imaging Conference (2011 NSS/MIC). IEEE, 2011. http://dx.doi.org/10.1109/nssmic.2011.6153660.

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Gohlke, S., C. Mancini, J. Gerdes, and T. Schulz. "Ciliary dysfunction impairs metabolic activation of brown and white adipose tissue." In Abstracts des Adipositas-Kongresses 2020 zur 36. Jahrestagung der Deutschen Adipositas Gesellschaft e.V. (DAG). © Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1714481.

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Kam, Yoonseok, Pamela M. Swain, and Brian P. Dranka. "Abstract A67: Bi-phasic metabolic responses to in situ macrophage activation." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; October 1-4, 2017; Boston, MA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/2326-6074.tumimm17-a67.

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Jackson, Klarissa D., Gracia M. Amaya, Rebecca Durandis, Kahari J. Wines, Arsany A. Abouda, Samuel A. Starks, and R. Nathan Daniels. "Abstract 4911: Metabolic activation of sunitinib: Implications for sunitinib-induced toxicities." 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.am2018-4911.

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Dunn, Andrew K., Anna Devor, Anders M. Dale, and David A. Boas. "High Resolution Imaging of the Hemodynamic and Metabolic Response to Functional Activation." In Biomedical Topical Meeting. Washington, D.C.: OSA, 2004. http://dx.doi.org/10.1364/bio.2004.fe2.

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Franklin, Derek A., Joe T. Sharick, Paula I. Ericsson-Gonzalez, Violeta Sanchez, Phillip T. Dean, Susan R. Opalenik, Stefano Cairo, et al. "Abstract 1511: MEK activation modulates immunosuppressive MDSCs and metabolic phenotypes in TNBC." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-1511.

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Franklin, Derek A., Joe T. Sharick, Paula I. Ericsson-Gonzalez, Violeta Sanchez, Phillip T. Dean, Susan R. Opalenik, Stefano Cairo, et al. "Abstract 1511: MEK activation modulates immunosuppressive MDSCs and metabolic phenotypes in TNBC." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-1511.

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Wen, Yang-an, Xiaopeng Xiong, Jennifer Harris, Yekaterina Zaytseva, and Tianyan Gao. "Abstract 4088: Adipocytes-mediated autophagy activation and metabolic reprogramming promotes colon cancer survival." 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.am2016-4088.

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Jentgen, Vanessa, Katharina Dinger, Christina Vohlen, Swati Dabral, Johannes Will, Silke V. Koningsbruggen-Rietschel, Margarete Odenthal, Soni Pullamsetti, Jörg Dötsch, and Miguel A. Alejandre Alcazar. "FoxO1 activation protects against IL-6-mediated perinatal metabolic programming of lung micro-vessels." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.oa3608.

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Murray, Jessica R., Meng Huang, Tianzhu Zang, Volker M. Arlt, Heinz H. Schmeiser, and Trevor M. Penning. "Abstract 4580A: Metabolic activation of 3-nitrobenzanthrone by human aldo-keto reductases (AKR1C1-AKR1C4)." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-4580a.

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Reports on the topic "Metabolic activation"

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Hong, Jun-Yan. Inter-Individual Variation in the Metabolic Activation of Heterocyclic Amines and Susceptibility to Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2005. http://dx.doi.org/10.21236/ada470103.

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Song, Jian. Test for Chemical Induction of Chromosome Aberrations in Cultured Chinese Hamster Ovary (CHO) Cells with and without Metabolic Activation, Test Article: 3-Nitro-1,2,4-Triazol-5-one (NTO). Fort Belvoir, VA: Defense Technical Information Center, October 2008. http://dx.doi.org/10.21236/ada518834.

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Song, Jian. Test for Chemical Induction of Chromosome Aberration in Cultured Chinese Hamster Ovary (CHO) Cells With and Without Metabolic Activation. Test Article: N,N,N',N'-tetramethyl Ethanediamine (TMEDA). Fort Belvoir, VA: Defense Technical Information Center, June 2008. http://dx.doi.org/10.21236/ada519474.

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Jope, Richard S. Activation of Phosphoinositide Metabolism by Cholinergic Agents. Fort Belvoir, VA: Defense Technical Information Center, December 1990. http://dx.doi.org/10.21236/ada235299.

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Levin, Ilan, Avtar K. Handa, Avraham Lalazar, and Autar K. Mattoo. Modulating phytonutrient content in tomatoes combining engineered polyamine metabolism with photomorphogenic mutants. United States Department of Agriculture, December 2006. http://dx.doi.org/10.32747/2006.7587724.bard.

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Fruit constitutes a major component of our diet, providing fiber, vitamins, minerals, and many other phytonutrients that promote good health. Fleshy fruits, such as tomatoes, already contain high levels of several of these ingredients. Nevertheless, efforts have been invested in increasing and diversifying the content of phytonutrients, such as carotenoids and flavonoids, in tomato fruits. Increasing levels of phytonutrients, such as lycopene, is highly justified from the perspective of the lycopene extraction industry due to cost effectiveness reasons. Diversifying phytonutrients, in particular those that contribute to fruit color, could potentially provide an array of attractive colors to our diet. Our major goal was to devise a novel strategy for developing tomato fruits with enhanced levels of phytochemicals known to promote good health with special emphasis on lycopene content. A further important goal was to analyze global gene expression of selected genetic lines produced throughout this study in order is to dissect the molecular mechanisms regulating phytonutrients accumulation in the tomato fruit. To achieve these goals we proposed to: 1. combine, by classical breeding, engineered polyamine metabolism with photomorphogenic high pigment mutants in order generate tomato plant with exceptionally high levels of phytonutrients; 2. use gene transfer technology for genetic introduction of key genes that promote phytonutrient accumulation in the tomato fruit, 3. Analyze accumulation patterns of the phytonutrients in the tomato fruit during ripening; 4. Analyze global gene expression during fruit ripening in selected genotypes identified in objectives 1 and 2, and 5. Identify and analyze regulatory mechanisms of chloroplast disassembly and chromoplast formation. During the 3 years research period we have carried out most of the research activities laid out in the original proposal and our key conclusions are as follows: 1. the engineered polyamine metabolism strategy proposed by the US collaborators can not increase lycopene content either on its own or in combination with an hp mutant (hp-2ᵈᵍ); 2. The hp-2ᵈᵍ affects strongly the transcriptional profile of the tomato fruit showing a strong tendency for up- rather than down-regulation of genes, 3. Ontology assignment of these miss-regulated genes revealed a consistent up-regulation of genes related to chloroplast biogenesis and photosynthesis in hp-2ᵈᵍ mutants throughout fruit development; 4. A tendency for up-regulation was also usually observed in structural genes involved in phytonutrientbiosynthesis; however this up-regulation was not as consistent. 5. Microscopic observations revealed a significantly higher number of chloroplasts in pericarp cells of mature-green hp-2ᵈᵍ/hp-2ᵈᵍ fruits in comparison to their normal fully isogenic counterparts. 6. The relative abundance of chloroplasts could be observed from early stages of fruit development. Cumulatively these results suggest that: 1. the overproduction of secondary metabolites, characterizing hp-2ᵈᵍ/hp-2ᵈᵍ fruits, is more due to chloroplast number rather then to transcriptional activation of structural genes of the relevant metabolic pathways, and 2. The molecular trigger increasing metabolite levels in hp-2ᵈᵍ mutant fruits should be traced at early stage of fruit development.
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Naseem, Syed M., K. A. Mereish, Rikki Solow, and Harry Hines. Toxin-Induced Activation of Rat Hepatocyte Prostaglandin Synthesis and Phospholipid Metabolism. Fort Belvoir, VA: Defense Technical Information Center, April 1990. http://dx.doi.org/10.21236/ada221157.

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Research, Gratis. Brown Fat Activation: A Future Treatment for Obesity & Diabetes. Gratis Research, November 2020. http://dx.doi.org/10.47496/gr.blog.01.

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Brown fat holds a promising therapeutic approach to prevent obesity and type 2 diabetes by its profound effects on body weight reduction, heat generation, increased insulin sensitivity and glucose metabolism regulation
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Sionov, Edward, Nancy Keller, and Shiri Barad-Kotler. Mechanisms governing the global regulation of mycotoxin production and pathogenicity by Penicillium expansum in postharvest fruits. United States Department of Agriculture, January 2017. http://dx.doi.org/10.32747/2017.7604292.bard.

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The original objectives of the study, as defined in the approved proposal, are: To characterize the relationship of CreA and LaeA in regulation of P T production To understand how PacC modulates P. expansumpathogenicity on apples To examine if other secondary metabolites are involved in virulence or P. expansumfitness To identify the signaling pathways leading to PAT synthesis Penicilliumexpansum, the causal agent of blue mould rot, is a critical health concern because of the production of the mycotoxinpatulin (PAT) in colonized apple fruit tissue. Although PAT is produced by many Penicilliumspecies, the factors activating its biosynthesis were not clear. This research focused on host and fungal mechanisms of activation of LaeA (the global regulator of secondary metabolism), PacC (the global pH modulator) and CreA (the global carbon catabolite regulator) on PAT synthesis with intention to establish P. expansumas the model system for understanding mycotoxin synthesis in fruits. The overall goal of this proposal is to identify critical host and pathogen factors that mechanistically modulate P. expansumgenes and pathways to control activation of PAT production and virulence in host. Several fungal factors have been correlated with disease development in apples, including the production of PAT, acidification of apple tissue by the fungus, sugar content and the global regulator of secondary metabolism and development, LaeA. An increase in sucrose molarity in the culture medium from 15 to 175 mM negatively regulated laeAexpression and PAT accumulation, but, conversely, increased creAexpression, leading to the hypothesis that CreA could be involved in P. expansumPAT biosynthesis and virulence, possibly through the negative regulation of LaeA. We found evidence for CreAtranscriptional regulation of laeA, but this was not correlated with PAT production either in vitro or in vivo, thus suggesting that CreA regulation of PAT is independent of LaeA. Our finding that sucrose, a key ingredient of apple fruit, regulates PAT synthesis, probably through suppression of laeAexpression, suggests a potential interaction between CreA and LaeA, which may offer control therapies for future study. We have also identified that in addition to PAT gene cluster, CreA regulates other secondary metabolite clusters, including citrinin, andrastin, roquefortine and communesins, during pathogenesis or during normal fungal growth. Following creation of P. expansumpacCknockout strain, we investigated the involvement of the global pH regulator PacC in fungal pathogenicity. We demonstrated that disruption of the pH signaling transcription factor PacC significantly decreased the virulence of P. expansumon deciduous fruits. This phenotype is associated with an impairment in fungal growth, decreased accumulation of gluconic acid and reduced synthesis of pectolytic enzymes. We showed that glucose oxidase- encoding gene, which is essential for gluconic acid production and acidification during fruit colonization, was significantly down regulated in the ΔPepacCmutant, suggesting that gox is PacC- responsive gene. We have provided evidence that deletion of goxgene in P. expansumled to a reduction in virulence toward apple fruits, further indicating that GOX is a virulence factor of P. expansum, and its expression is regulated by PacC. It is also clear from the present data that PacC in P. expansumis a key factor for the biosynthesis of secondary metabolites, such as PAT. On the basis of RNA-sequencing (RNA-seq) analysis and physiological experimentation, the P. expansumΔlaeA, ΔcreAand ΔpacCmutants were unable to successfully colonize apples for a multitude of potential mechanisms including, on the pathogen side, a decreased ability to produce proteolytic enzymes and to acidify the environment and impaired carbon/nitrogen metabolism and, on the host side, an increase in the oxidative defence pathways. Our study defines these global regulatory factors and their downstream signalling pathways as promising targets for the development of strategies to fight against this post-harvest pathogen.
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Grafi, Gideon, and Brian Larkins. Endoreduplication in Maize Endosperm: An Approach for Increasing Crop Productivity. United States Department of Agriculture, September 2000. http://dx.doi.org/10.32747/2000.7575285.bard.

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The focus of this research project is to investigate the role of endoreduplication in maize endosperm development and the extent to which this process contributes to high levels of starch and storage protein synthesis. Although endoreduplication has been widely observed in many cells and tissues, especially those with high levels of metabolic activity, the molecular mechanisms through which the cell cycle is altered to produce consecutive cycles of S-phase without an intervening M-phase are unknown. Our previous research has shown that changes in the expression of several cell cycle regulatory genes coincide with the onset of endoreduplication. During this process, there is a sharp reduction in the activity of the mitotic cyclin-dependent kinase (CDK) and activation of the S-phase CDK. It appears the M-phase CDK is stable, but its activity is blocked by a proteinaceous inhibitor. Coincidentally, the S-phase checkpoint protein, retinoblastoma (ZmRb), becomes phosphorylated, presumably releasing an E2F-type transcriptional regulator which promotes the expression of genes responsible for DNA synthesis. To investigate the role of these cell cycle proteins in endoreduplication, we have created transgenic maize plants that express various genes in an endosperm-specific manner using a storage protein (g-zein) promoter. During the first year of the grant, we constructed point mutations of the maize M-phase kinase, p34cdc2. One alteration replaced aspartic acid at position 146 with asparagine (p3630-CdcD146N), while another changed threonine 161 to alanine (p3630-CdcT161A). These mutations abolish the activity of the CDK. We hypothesized that expression of the mutant forms of p34cdc2 in endoreduplicating endosperm, compared to a control p34cdc2, would lead to extra cycles of DNA synthesis. We also fused the gene encoding the regulatory subunit of the M- phase kinase, cyclin B, under the g-zein promoter. Normally, cyclin B is expected to be destroyed prior to the onset of endoreduplication. By producing high levels of this protein in developing endosperm, we hypothesized that the M-phase would be extended, potentially reducing the number of cycles of endoreduplication. Finally, we genetically engineered the wheat dwarf virus RepA protein for endosperm-specific expression. RepA binds to the maize retinoblastoma protein and presumably releases E2F-like transcription factors that activate DNA synthesis. We anticipated that inactivation of ZmRb by RepA would lead to additional cycles of DNA synthesis.
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10

Miller, Gad, and Jeffrey F. Harper. Pollen fertility and the role of ROS and Ca signaling in heat stress tolerance. United States Department of Agriculture, January 2013. http://dx.doi.org/10.32747/2013.7598150.bard.

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The long-term goal of this research is to understand how pollen cope with stress, and identify genes that can be manipulated in crop plants to improve reproductive success during heat stress. The specific aims were to: 1) Compare heat stress dependent changes in gene expression between wild type pollen, and mutants in which pollen are heat sensitive (cngc16) or heat tolerant (apx2-1). 2) Compare cngc16 and apx2 mutants for differences in heat-stress triggered changes in ROS, cNMP, and Ca²⁺ transients. 3) Expand a mutant screen for pollen with increased or decreased thermo-tolerance. These aims were designed to provide novel and fundamental advances to our understanding of stress tolerance in pollen reproductive development, and enable research aimed at improving crop plants to be more productive under conditions of heat stress. Background: Each year crop yields are severely impacted by a variety of stress conditions, including heat, cold, drought, hypoxia, and salt. Reproductive development in flowering plants is highly sensitive to hot or cold temperatures, with even a single hot day or cold night sometimes being fatal to reproductive success. In many plants, pollen tube development and fertilization is often the weakest link. Current speculation about global climate change is that most agricultural regions will experience more extreme environmental fluctuations. With the human food supply largely dependent on seeds, it is critical that we consider ways to improve stress tolerance during fertilization. The heat stress response (HSR) has been intensively studied in vegetative tissues, but is poorly understood during reproductive development. A general paradigm is that HS is accompanied by increased production of reactive oxygen species (ROS) and induction of ROS-scavenging enzymes to protect cells from excess oxidative damage. The activation of the HSR has been linked to cytosolic Ca²⁺ signals, and transcriptional and translational responses, including the increased expression of heat shock proteins (HSPs) and antioxidative pathways. The focus of the proposed research was on two mutations, which have been discovered in a collaboration between the Harper and Miller labs, that either increase or decrease reproductive stress tolerance in a model plant, Arabidopsis thaliana (i.e., cngc16--cyclic nucleotide gated channel 16, apx2-1--ascorbate peroxidase 2,). Major conclusions, solutions, achievements. Using RNA-seq technology, the expression profiles of cngc16 and apx2 pollen grains were independently compared to wild type under favourable conditions and following HS. In comparison to a wild type HSR, there were 2,776 differences in the transcriptome response in cngc16 pollen, consistent with a model in which this heat-sensitive mutant fails to enact or maintain a normal wild-type HSR. In a comparison with apx2 pollen, there were 900 differences in the HSR. Some portion of these 900 differences might contribute to an improved HSR in apx2 pollen. Twenty-seven and 42 transcription factor changes, in cngc16 and apx2-1, respectively, were identified that could provide unique contributions to a pollen HSR. While we found that the functional HS-dependent reprogramming of the pollen transcriptome requires specific activity of CNGC16, we identified in apx2 specific activation of flavonol-biosynthesis pathway and auxin signalling that support a role in pollen thermotolerance. Results from this study have identified metabolic pathways and candidate genes of potential use in improving HS tolerance in pollen. Additionally, we developed new FACS-based methodology that can quantify the stress response for individual pollen in a high-throughput fashion. This technology is being adapted for biological screening of crop plant’s pollen to identify novel thermotolerance traits. Implications, both scientific and agricultural. This study has provided a reference data on the pollen HSR from a model plant, and supports a model that the HSR in pollen has many differences compared to vegetative cells. This provides an important foundation for understanding and improving the pollen HSR, and therefor contributes to the long-term goal of improving productivity in crop plants subjected to temperature stress conditions. A specific hypothesis that has emerged from this study is that pollen thermotolerance can be improved by increasing flavonol accumulation before or during a stress response. Efforts to test this hypothesis have been initiated, and if successful have the potential for application with major seed crops such as maize and rice.
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