Relevant bibliographies by topics / Iron overload

Contents

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

Academic literature on the topic 'Iron overload'

Author: Grafiati
Published: 4 June 2021
Last updated: 11 March 2023

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Journal articles on the topic "Iron overload"

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Marfil-Rivera, L. J. "Iron overload." Medicina Universitaria 17, no. 69 (October 2015): 240–42. http://dx.doi.org/10.1016/j.rmu.2015.08.001.

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Hulihan, Mary M., Cindy A. Sayers, Scott D. Grosse, Cheryl Garrison, and Althea M. Grant. "Iron Overload." American Journal of Preventive Medicine 41, no. 6 (December 2011): S422—S427. http://dx.doi.org/10.1016/j.amepre.2011.09.020.

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Siah, Chiang W., Debbie Trinder, and John K. Olynyk. "Iron overload." Clinica Chimica Acta 358, no. 1-2 (August 2005): 24–36. http://dx.doi.org/10.1016/j.cccn.2005.02.022.

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Zhabyeyev, Pavel, Subhash K. Das, Ratnadeep Basu, Mengcheng Shen, Vaibhav B. Patel, Zamaneh Kassiri, and Gavin Y. Oudit. "TIMP3 deficiency exacerbates iron overload-mediated cardiomyopathy and liver disease." American Journal of Physiology-Heart and Circulatory Physiology 314, no. 5 (May 1, 2018): H978—H990. http://dx.doi.org/10.1152/ajpheart.00597.2017.

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Chronic iron overload results in heart and liver diseases and is a common cause of morbidity and mortality in patients with genetic hemochromatosis and secondary iron overload. We investigated the role of tissue inhibitor of metalloproteinase 3 (TIMP3) in iron overload-mediated tissue injury by subjecting male mice lacking Timp3 ( Timp3−/−) and wild-type (WT) mice to 12 wk of chronic iron overload. Whereas WT mice with iron overload developed diastolic dysfunction, iron-overloaded Timp3−/− mice showed worsened cardiac dysfunction coupled with systolic dysfunction. In the heart, loss of Timp3 was associated with increased myocardial fibrosis, greater Timp1, matrix metalloproteinase ( Mmp) 2, and Mmp9 expression, increased active MMP-2 levels, and gelatinase activity. Iron overload in Timp3−/− mice showed twofold higher iron accumulation in the liver compared with WT mice because of constituently lower levels of ferroportin. Loss of Timp3 enhanced the hepatic inflammatory response to iron overload, leading to greater neutrophil and macrophage infiltration and increased hepatic fibrosis. Expression of inflammation-related MMPs (MMP-12 and MMP-13) and inflammatory cytokines (IL-1β and monocyte chemoattractant protein-1) was elevated to a greater extent in iron-overloaded Timp3−/− livers. Gelatin zymography demonstrated equivalent increases in MMP-2 and MMP-9 levels in WT and Timp3−/− iron-overloaded livers. Loss of Timp3 enhanced the susceptibility to iron overload-mediated heart and liver injury, suggesting that Timp3 is a key protective molecule against iron-mediated pathology. NEW & NOTEWORTHY In mice, loss of tissue inhibitor of metalloproteinase 3 ( Timp3) was associated with systolic and diastolic dysfunctions, twofold higher hepatic iron accumulation (attributable to constituently lower levels of ferroportin), and increased hepatic inflammation. Loss of Timp3 enhanced the susceptibility to iron overload-mediated injury, suggesting that Timp3 plays a key protective role against iron-mediated pathology.
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Jacobs, Allan, and A. V. Hoffbrand. "Iron deficiency and iron overload." Critical Reviews in Oncology/Hematology 3, no. 2 (January 1985): 143–86. http://dx.doi.org/10.1016/s1040-8428(85)80023-8.

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Díez-López, Carles, Josep Comín-Colet, and José González-Costello. "Iron overload cardiomyopathy." Current Opinion in Cardiology 33, no. 3 (May 2018): 334–40. http://dx.doi.org/10.1097/hco.0000000000000511.

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Camaschella, Clara. "Treating Iron Overload." New England Journal of Medicine 368, no. 24 (June 13, 2013): 2325–27. http://dx.doi.org/10.1056/nejmcibr1304338.

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Lombard, M., A. Bomford, and R. Williams. "Genetic Iron Overload." Journal of the Royal Society of Medicine 82, no. 12 (December 1989): 701–3. http://dx.doi.org/10.1177/014107688908201202.

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Kushner, James P., John P. Porter, and Nancy F. Olivieri. "Secondary Iron Overload." Hematology 2001, no. 1 (January 1, 2001): 47–61. http://dx.doi.org/10.1182/asheducation-2001.1.47.

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Abstract Transfusion therapy for inherited anemias and acquired refractory anemias both improves the quality of life and prolongs survival. A consequence of chronic transfusion therapy is secondary iron overload, which adversely affects the function of the heart, the liver and other organs. This session will review the use of iron chelating agents in the management of transfusion-induced secondary iron overload. In Section I Dr. John Porter describes techniques for the administration of deferoxamine that exploit the pharmacokinetic properties of the drug and minimize potential toxic side effects. The experience with chelation therapy in patients with thalassemia and sickle cell disease will be reviewed and guidelines will be suggested for chelation therapy of chronically transfused adults with refractory anemias. In Section II Dr. Nancy Olivieri examines the clinical consequences of transfusion-induced secondary iron overload and suggests criteria useful in determining the optimal timing of the initiation of chelation therapy. Finally, Dr. Olivieri discusses the clinical trials evaluating orally administered iron chelators.
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Kasvosve, I., It Gangaidzo, Zar Gomo, and Vr Gordeuk. "African Iron Overload." Acta Clinica Belgica 55, no. 2 (January 2000): 88–93. http://dx.doi.org/10.1080/17843286.2000.11754276.

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Dissertations / Theses on the topic "Iron overload"

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Chua-anusorn, Wanida. "Iron oxide deposits in iron overload diseases." Thesis, Chua-anusorn, Wanida (1997) Iron oxide deposits in iron overload diseases. PhD thesis, Murdoch University, 1997. https://researchrepository.murdoch.edu.au/id/eprint/52151/.

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Iron overload diseases such as thalassaemia are a major public health problem in many parts of the world. Excess iron deposited in such tissues occurs in the form of ultrafine particles of iron oxyhydroxide. At low levels of iron loading, the iron(III) oxyhydroxide particles are mostly found in the iron storage protein, ferritin. At higher levels of loading, iron(III) oxyhydroxide particles are found in insoluble aggregates known as haemosiderin. Three different structures of these iron deposits are known: (i) ferrihydrite (5Fe203.9H20), (ii) poorly crystalline goethite (α-FeOOH), and (iii) non-crystalline hydrated iron(III) oxyhydroxide. In this thesis, Mössbauer spectroscopy has been used to study the form of iron oxyhydroxide present in the tissues of thalassaemic patients who had undergone regular blood transfusion and chelation therapy as well as those receiving little, if any, such treatment. The data show a higher fraction of non-haem iron occurs as the goethite-like form in patients undergoing regular transfusion and chelation treatment. The poorly crystalline goethite form was not found in normal human tissues. To define further some of the factors involved in the deposition of these different iron oxides, an iron-loaded rat system was established. Two routes of administration were chosen. The first involved regular administration of red blood cells injected intraperitoneally for up to one year. The second involved the oral administration of carbonyl-iron as a dietary supplement for nearly two years. Mössbauer spectra of livers and spleens at 78 K consisted of a relatively intense central doublet with spectral parameters indicative of paramagnetic or superparamagnetic high-spin iron(III). Many spectra obtained from parenterally iron-loaded spleens and dietary iron-loaded livers also showed a clear sextet at 78 K, which is indicative of the presence of the goethite-like form of iron oxyhydroxide. The relative intensity of this sextet spectral component in the livers from the dietary iron-loaded rats increased significantly with the age of rats. In order to distinguish iron present in the parenchymal versus non-parenchymal cells in the livers, an indirect quantitative assessment of the iron concentration was performed from liver histological sections using computer-assisted morphometric analysis. The goethite-like form increased significantly as the fraction of iron in non-parenchymal cells increased (r = 0.71, p < 0.005), suggesting that its formation may be associated with the nonparenchymal cells. The ultrastructure of the iron oxide deposits and associated organic components was studied using a combination of scanning probe microscopy and transmission electron microscopy. Liver samples with ferrihydrite or goethite-like haemosiderin were studied as well as aggregated ferritin in the form of ferritin crystals, ferrihydrite-like form of haemosiderin shows topographies of iron aggregation similar to In contrast, liver with goethite-like form of Liver tissue with the that found in the ferritin crystals, haemosiderin showed a different topography. Haemosiderin was isolated from a selection of tissues. Crude haemosiderin from patients who had undergone regular blood transfusion and chelation therapy showed a high fraction of goethite-like form of iron oxyhydroxide with a wide range of particle size. Infrared spectroscopy indicated that the iron oxyhydroxide in haemosiderins is associated with organic components. The availability of the different forms of iron oxyhydroxide present in different haemosiderins was assessed using the iron chelator desferrioxamine. The percentage of iron released showed a negative correlation (r = 0.82, p < 0.001) with the percentage of goethite-like iron oxyhydroxide present in these haemosiderins. In summary, these studies indicate that the chemical forms of iron oxyhydroxide deposits are related to their deposition, toxicity and relative ease of removal. The study has implications for the clinical management of different groups of thalassaemic patients.
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Baptista-Hon, Daniel Tomas. "Cellular substrates of iron overload cardiomyopathies." Thesis, University of Edinburgh, 2011. http://hdl.handle.net/1842/15878.

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Cardiomyopathies and arrhythmias are major causes of death in untreated hereditary haemochromatosis, acute iron poisoning and during secondary iron overload resulting from repeated blood transfusions in β-thalassaemia. Iron overload cardiomyopathies are associated with systolic and diastolic dysfunction, suggesting that Ca2+ homeostasis is impaired. However, the cellular mechanisms of these dysfunctions are unknown. The data presented in this thesis establishes for the first time iron effects on cardiomyocyte Ca2+ handling, as well as the potential cellular substrates responsible for this impairment during iron overload. Exposure of isolated rat ventricular cardiomyocytes to 200μM iron led to biphasic changes in systolic Ca2+ release. Phase 1: an initial reduction of systolic Ca2+ release followed by; Phase 2: increased Ca2+ release with arrhythmogenic spontaneous Ca2+ release, cell contracture and cell death. There is evidence that Fe2+ enters cardiomyocytes via L-type Ca2+ channels (LTCC) and reduces the Ca2+ trigger. The close apposition of LTCCs to cardiac ryanodine receptors (RyR2) suggests RyR2 may be a first target. Indeed RyR2 activity was drastically reduced on exposure to nanomolar [Fe2+] in single channel studies. Together with evidence that Fe2+ may reduce the Ca2+ trigger from LTCC, this is consistent with iron reducing sarcoplasmic reticulum (SR) Ca2+ release during Phase 1. In Phase 2, the presence of spontaneous Ca2+ release events is consistent with SR Ca2+ overload. Indeed, in single rat ventricular cardiomyocytes SR Ca2+ content was found to be increased by 27% during Phase 2. The cellular substrates responsible for this increased SR Ca2+ content were 2-fold: 1) through reduced extrusion via both the Na+ Ca2+ Exchanger (NCX) and Plasmalemmal Ca2+ ATPase (PMCA) and 2) through increased resequestration via the SR Ca2+ ATPase. Iron catalyses the production of reactive oxygen species (ROS) during the Fenton reaction. To investigate whether iron effects might be due to ROS, I used the cell permeant ROS scavenger Tempol. Tempol attenuated Phase 2 effects but Phase 1 effects were not affected. This is consistent with the hypothesis that Phase 1 effects were due to direct effects of Fe2+ affecting LTCC trigger and RyR2 function. The attenuation of Phase 2 effects suggests that ROS damage to key Ca2+ handling mechanisms, such as NCX and PMCA might account for a reduced Ca2+ extrusion and subsequent SR Ca2+ overload.
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Sarmento, Carlos V. 1980. "Assessment of new iron chelating agents for treatment of iron-overload." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=116063.

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Patients with acquired iron overload require chelation therapy using either Desferal or Exjade. Iron in excess may promote free radical formation in the Fenton reaction resulting in severe injuries of heart, liver and endocrine organs. Che1ators that bind ferric iron (Fe+3) in a 1:1 complex (Desferal) sequester it more efficiently than those che1ators that form 2:1 (Exjade) complexes. We initiated synthesis of new chelators derived from the tridentate chelator pyridoxal isonicotinoyl hydrazone (PIH) and its analogs. The aim of the synthesis was to generate chelators that bind iron in a 1:1 complex, which was confirmed for 8LK02, 10LK02, 11LK02 and 15LK03 by spectrophotometry. All novel chelators mobilized iron more efficiently compared to Desferal and Exjade from murine reticulocytes and human myeloid leukemia cells (K562). Additionally, aforementioned four chelators were also more efficient than PIH and were found to be less or equally toxic as Desferal and Exjade.
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Ward, Roberta J. "Tissue damage in iron overload and alcohol toxicity." Thesis, King's College London (University of London), 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.304198.

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Mouralian, Cindy. "Evaluation of novel iron chelators for therapeutic use in secondary iron overload disorders." Thesis, McGill University, 2000. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=33071.

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Pyridoxal isonicotinoyl hydrazone (PIH) has been described as an orally effective Fe chelator. It is both membrane permeable and plasma soluble, and has a high affinity for Fe, making it an ideal model on which to base future chelators. Ten novel ligands have been synthesized based on these attributes. Characterization experiments were performed to determine the ligands' selectivity and binding affinity for iron, their lipophilicity as both free and Fe-ligand complexes, and their stoichiometric relationship with iron. Efficacy of the chelators has been determined through their ability to effectively mobilize non-heme 59Fe from pre-labeled cells. Intracellular levels of chelator bound 59Fe were also determined. Concentration-dependence and time-dependence mobilization experiments were performed to determine the minimal concentrations of ligands required to elicit maximal 59Fe release. Toxicity experiments with various ligand concentrations were performed in order to determine the concentration which inhibits at least half of cellular growth as compared with control. (Abstract shortened by UMI.)
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Baffour, Richard. "The development of iron exchange system for the treatment of chronic iron overload /." Thesis, McGill University, 1985. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=63195.

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Kilbarger, Amy K. "The effect of iron overload on osteoblast function in cell culture." Greensboro, N.C. : University of North Carolina at Greensboro, 2007. http://libres.uncg.edu/ir/listing.aspx?styp=ti&id=146.

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Thesis (M.S.)--University of North Carolina at Greensboro, 2007.
Title from PDF t.p. (viewed Feb. 29, 2008). Directed by Deborah Kipp; submitted to the School of Human Environmental Sciences. Embargoed until Dec. 20, 2008. Includes bibliographical references (p. 47-56).
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Hamilton, Jasmine La Juanie. "Innovative polymeric iron chelators with iron binding affinity and biocompatibility for the treatment of transfusional iron overload." Thesis, University of British Columbia, 2015. http://hdl.handle.net/2429/52624.

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Desferrioxamine (Desferal®, DFO), deferiprone (Ferriprox®, L1) and desferasirox (Exjade®, ICL-670) are clinically approved iron chelators used to treat transfusion associated iron overload, a common condition in patients with severe hemoglobin disorders like β-thalassemia, sickle-cell disease and the myelodysplastic syndromes. The poor pharmacokinetics and inefficacy of iron chelators necessitate administration of almost maximum tolerated doses to achieve adequate iron removal. This causes toxicity ranging from neurological dysfunction in DFO users, agranulocytosis and neutropenia in L1 users, and severe kidney toxicity in ICL-670 treated patients. This also hinders the use of iron chelators during gestation. Thus, developing iron chelators with improved long-term efficacy and reduced toxicity is essential. All currently approved iron chelators are of low molecular weight (MW) (< 600 Da) and the objectives reported for the “ideal” chelator of low MW is yet to be realized in practice. However, the limited attempts towards developing higher MW, long circulating iron chelators has shown tremendous promise. This thesis assesses the role of a new polymer, hyperbranched polyglycerol (HPG) in improving the properties of iron chelators. High MW iron chelators were developed by conjugating DFO to HPG of various MWs, forming a library of HPG-DFO conjugates. Iron binding affinity of HPG-DFO was investigated using isothermal titration calorimetry, UV-visible spectroscopy and studying iron removal from ferritin. Biocompatibility and toxicity were investigated using coagulation assays in human blood and cell culture. Since iron chelator toxicity during development remains an under-explored area, the second goal of this thesis was to expand knowledge of chelator toxicity during development. The toxicity of FDA-approved and HPG-DFO in developing embryos was investigated using zebrafish. Studies indicate that HPG-DFOs are biocompatible, efficient chelators, capable of binding ferritin iron and preventing harmful redox reactions. Moreover, combining a low MW iron chelator with HPG-DFO enhances chelation. In vivo chemical screening indicated that while low MW chelators L1 and ICL-670 may interact with zebrafish embryos and cause toxicity, DFO and HPG-DFO did not have this effect. Results indicate that HPG-DFO is a new class of efficient, biocompatible iron chelator, potentially useful for development into clinical agents for the prevention of transfusion associated iron overload.
Medicine, Faculty of
Pathology and Laboratory Medicine, Department of
Graduate
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Stuart, Katherine Anne. "Iron overload in end-stage liver disease : mechanisms and pathophysiological significance /." [St. Lucia, Qld.], 2005. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe18503.pdf.

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Liu, Zu Dong. "Design of orally active iron(II) chelators." Thesis, King's College London (University of London), 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.266259.

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Books on the topic "Iron overload"

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Yehuda, Shlomo, and David I. Mostofsky, eds. Iron Deficiency and Overload. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-59745-462-9.

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(undifferentiated), David Smith. Iron overload and birth defects. Leicester: De Montfort University, 1993.

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Barton, James C., Corwin Q. Edwards, Pradyumna D. Phatak, Robert S. Britton, and Bruce R. Bacon, eds. Handbook of Iron Overload Disorders. Cambridge: Cambridge University Press, 2009. http://dx.doi.org/10.1017/cbo9780511777035.

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C, Barton James, ed. Handbook of iron overload disorders. Cambridge: Cambridge University Press, 2010.

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Christos, Kattamis, and International Conference on Thalassemia and the Hemoglobinopathies (2nd : 1987 : Herakleion, Crete), eds. Iron overload and chelation in thalassaemia. Toronto: H. Huber Publishers, 1989.

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Yehuda, Shlomo. Iron deficiency and overload: From basic biology to clinical medicine. New York, N.Y: Humana Press, 2010.

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Stobie, Shannon Blaire. The novel oral iron chelator, L1, in acute and chronic iron overload. Ottawa: National Library of Canada, 1993.

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1939-, Weinberg Hedy, ed. Living with hemochromatosis: Answers to questions about iron overload. New York: Healthy Living Books, 2003.

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The unexpected consequences of iron overload: A fund raiser for the Haemochromatosis Society. England]: James Minter, 2014.

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Christos, Kattamis, ed. Iron overload and chelation in thalassaemia: A symposium held during the 2nd International Conference on Thalass[a]emia and the Hemoglobinopathies, Herakleion, Crete, 1987. Toronto: H. Huber Publishers, 1989.

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Book chapters on the topic "Iron overload"

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Angelucci, Emanuele. "Iron Overload." In The EBMT Handbook, 353–56. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-030-02278-5_46.

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Wick, Manfred, Wulf Pinggera, and Paul Lehmann. "Iron Overload." In Clinical Aspects and Laboratory — Iron Metabolism, Anemias, 113–16. Vienna: Springer Vienna, 2011. http://dx.doi.org/10.1007/978-3-7091-0087-5_9.

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Camaschella, Clara, A. Victor Hoffbrand, and Maria Domenica Cappellini. "Iron Overload." In Postgraduate Haematology, 40–52. Oxford, UK: John Wiley & Sons, Ltd, 2015. http://dx.doi.org/10.1002/9781118853771.ch4.

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Beck, Norman. "Iron Overload." In Diagnostic Hematology, 426–31. London: Springer London, 2009. http://dx.doi.org/10.1007/978-1-84800-295-1_20.

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Wick, Manfred, Paul Lehmann, and Wulf Pinggera. "Iron Overload." In Clinical Aspects and Laboratory Iron Metabolism, Anemias, 120–23. Vienna: Springer Vienna, 2003. http://dx.doi.org/10.1007/978-3-7091-3719-2_9.

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Camaschella, Clara, and A. Victor Hoffbrand. "Iron Overload." In Postgraduate Haematology, 47–60. Oxford, UK: Wiley-Blackwell, 2010. http://dx.doi.org/10.1002/9781444323160.ch4.

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Godbold, Michael, and Patrick D. McFarland. "Iron Overload." In Essentials of Blood Product Management in Anesthesia Practice, 433–37. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-59295-0_45.

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Adams, Paul, and Heinz Zoller. "Iron Overload States." In Sherlock's Diseases of the Liver and Biliary System, 511–25. Chichester, UK: John Wiley & Sons, Ltd, 2018. http://dx.doi.org/10.1002/9781119237662.ch26.

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Adams, Paul. "Iron Overload States." In Sherlock's Diseases of the Liver and Biliary System, 521–33. Oxford, UK: Wiley-Blackwell, 2011. http://dx.doi.org/10.1002/9781444341294.ch26.

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Sheth, Sujit. "Transfusional iron overload." In Rossi's Principles of Transfusion Medicine, 685–94. Chichester, WestSussex: John Wiley & Sons, Ltd., 2016. http://dx.doi.org/10.1002/9781119013020.ch61.

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Conference papers on the topic "Iron overload"

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Baldassarre, Luca, Annalisa Barla, Barbara Gianesin, and Mauro Marinelli. "Vector valued regression for iron overload estimation." In 2008 19th International Conference on Pattern Recognition (ICPR). IEEE, 2008. http://dx.doi.org/10.1109/icpr.2008.4761759.

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Quanjel, Marian, Bart Luijk, Aryan Vink, H. Stigter, and Jos Rooijackers. "Pulmonary siderosis as a cause of systemic iron overload." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa1156.

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Safitri, Ratu, Ani Melani Maskoen, Mas Rizky Anggun Adipurna Syamsunarno, Mohammad Ghozali, and Ramdan Panigoro. "Iron chelating activity of Caesalpinia sappan L. extract on iron status in iron overload rats (Rattus norvegicus L.)." In INVENTING PROSPEROUS FUTURE THROUGH BIOLOGICAL RESEARCH AND TROPICAL BIODIVERSITY MANAGEMENT: Proceedings of the 5th International Conference on Biological Science. Author(s), 2018. http://dx.doi.org/10.1063/1.5050146.

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Kapadia, Anuj J., Amy C. Sharma, Brian P. Harrawood, and Georgia D. Tourassi. "GEANT4 simulation of an NSECT system for iron overload detection." In 2007 IEEE Nuclear Science Symposium Conference Record. IEEE, 2007. http://dx.doi.org/10.1109/nssmic.2007.4437134.

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Wang, S., T. Peccerella, V. Rausch, and S. Mueller. "Hepatic iron overload in alcoholic liver disease: The role of sinusoidal endothelial cells in iron sensing." In 36. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0039-3402118.

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Wang, Shijin, Cheng Chen, Johannes Mueller, and Sebastian Mueller. "Liver iron overload in alcoholic liver disease: Crosstalk between endothelial cells and hepatocytes in iron regulation." In 38. Jahrestagung der Deutsche Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag, 2022. http://dx.doi.org/10.1055/s-0041-1740744.

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Wheeler, M., Y. Scindia, and B. Mehrad. "Iron Overload Worsens the Fibrotic Response in Bleomycin-Induced Pulmonary Fibrosis." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a4212.

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Kapadia, Anuj J., Brian P. Harrawood, and Georgia D. Tourassi. "GEANT4 simulation of NSECT for detection of iron overload in the liver." In Medical Imaging, edited by Jiang Hsieh and Ehsan Samei. SPIE, 2008. http://dx.doi.org/10.1117/12.773245.

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Loos, Nathalie, and Ba Vuong LE. "Effects Of Chronic Iron Overload upon Airway Responsiveness In Normal And Allergic Rats." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a2174.

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Rausch, V., I. Silva, T. Peccerella, and S. Mueller. "Hemolysis-mediated suppression of hepcidin causes hepatic iron overload in alcoholic liver disease." In Viszeralmedizin 2017. Georg Thieme Verlag KG, 2017. http://dx.doi.org/10.1055/s-0037-1605104.

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Reports on the topic "Iron overload"

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Yang, Ming, Youwei Wu, Tao Wang, and Wentao Wang. Iron overload, Infectious Complications and Survival In Liver Transplant Recipients: A Systematic Review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, November 2022. http://dx.doi.org/10.37766/inplasy2022.11.0022.

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Review question / Objective: Iron overload conditions is a well-established risk factor for infection of pathogens. The possible association of iron overload with infectious complications and prognosis of patients receiving transplants are not well understood. Condition being studied: Liver transplantation often represents a life-saving treatment for an increasing number of patients with end-stage liver disease. With the improvements in surgical techniques, immunosuppression strategies, and post-LT management of complications, the recipient mortality has steadily declined after LT. The survival rates were 83% at 1 year, 71% at 5 years in western countries. However, the use of immunosuppressants increased risk of infections as an adverse effect resulting in severe morbidity. Globally, infection caused by including bacteria, fungus, viruses remain one of the leading causes of morbidity and mortality among transplant recipients. Knowledge of modifiable risk factors and potentially reversible causes is essential to develop targeted preventive strategies.
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2

Templin, F., ed. The Internet Routing Overlay Network (IRON). RFC Editor, March 2011. http://dx.doi.org/10.17487/rfc6179.

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3

Tortorelli, P. F., G. M. Goodwin, M. Howell, and J. H. DeVan. Weld-overlay iron-aluminide coatings for use in high-temperature oxidizing/sulfidizing environments. Office of Scientific and Technical Information (OSTI), September 1995. http://dx.doi.org/10.2172/102150.

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4

Horwitz, Benjamin A., and Barbara Gillian Turgeon. Fungal Iron Acquisition, Oxidative Stress and Virulence in the Cochliobolus-maize Interaction. United States Department of Agriculture, March 2012. http://dx.doi.org/10.32747/2012.7709885.bard.

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Our project focused on genes for high affinity iron acquisition in Cochliobolus heterostrophus, a necrotrophic pathogen of maize, and their intertwined relationship to oxidative stress status and virulence of the fungus on the host. An intriguing question was why mutants lacking the nonribosomal peptide synthetase (NRPS) gene (NPS6) responsible for synthesis of the extracellular siderophore, coprogen, are sensitive to oxidative stress. Our overall objective was to understand the mechanistic connection between iron stress and oxidative stress as related to virulence of a plant pathogen to its host. The first objective was to examine the interface where small molecule peptide and reactive oxygen species (ROS) mechanisms overlap. The second objective was to determine if the molecular explanation for common function is common signal transduction pathways. These pathways, built around sensor kinases, response regulators, and transcription factors may link sequestering of iron, production of antioxidants, resistance to oxidative stress, and virulence. We tested these hypotheses by genetic manipulation of the pathogen, virulence assays on the host plant, and by following the expression of key fungal genes. An addition to the original program, made in the first year, was to develop, for fungi, a genetically encoded indicator of redox state based on the commercially available Gfp-based probe pHyper, designed for animal cell biology. We implemented several tools including a genetically encoded indicator of redox state, a procedure to grow iron-depleted plants, and constructed a number of new mutants in regulatory genes. Lack of the major Fe acquisition pathways results in an almost completely avirulent phenotype, showing how critical Fe acquisition is for the pathogen to cause disease. Mutants in conserved signaling pathways have normal ability to regulate NPS6 in response to Fe levels, as do mutants in Lae1 and Vel1, two master regulators of gene expression. Vel1 mutants are sensitive to oxidative stress, and the reason may be underexpression of a catalase gene. In nps6 mutants, CAT3 is also underexpressed, perhaps explaining the sensitivity to oxidative stress. We constructed a deletion mutant for the Fe sensor-regulator SreA and found that it is required for down regulation of NPS6 under Fe-replete conditions. Lack of SreA, though, did not make the fungus over-sensitive to ROS, though the mutant had a slow growth rate. This suggests that overproduction of siderophore under Fe-replete conditions is not very damaging. On the other hand, increasing Fe levels protected nps6 mutants from inhibition by ROS, implying that Fe-catalyzed Fenton reactions are not the main factor in its sensitivity to ROS. We have made some progress in understanding why siderophore mutants are sensitive to oxidative stress, and in doing so, defined some novel regulatory relationships. Catalase genes, which are not directly related to siderophore biosynthesis, are underexpressed in nps6 mutants, suggesting that the siderophore product (with or without bound Fe) may act as a signal. Siderophores, therefore, could be a target for intervention in the field, either by supplying an incorrect signal or blocking a signal normally provided during infection. We already know that nps6 mutants cause smaller lesions and have difficulty establishing invasive growth in the host. Lae1 and Vel1 are the first factors shown to regulate both super virulence conferred by T-toxin, and basic pathogenicity, due to unknown factors. The mutants are also altered in oxidative stress responses, key to success in the infection court, asexual and sexual development, essential for fungal dissemination in the field, aerial hyphal growth, and pigment biosynthesis, essential for survival in the field. Mutants in genes encoding NADPH oxidase (Nox) are compromised in development and virulence. Indeed the triple mutant, which should lack all Nox activity, was nearly avirulent. Again, gene expression experiments provided us with initial evidence that superoxide produced by the fungus may be most important as a signal. Blocking oxidant production by the pathogen may be a way to protect the plant host, in interactions with necrotrophs such as C. heterostrophus which seem to thrive in an oxidant environment.
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5

Brenan, J. M., K. Woods, J. E. Mungall, and R. Weston. Origin of chromitites in the Esker Intrusive Complex, Ring of Fire Intrusive Suite, as revealed by chromite trace element chemistry and simple crystallization models. Natural Resources Canada/CMSS/Information Management, 2021. http://dx.doi.org/10.4095/328981.

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To better constrain the origin of the chromitites associated with the Esker Intrusive Complex (EIC) of the Ring of Fire Intrusive Suite (RoFIS), a total of 50 chromite-bearing samples from the Black Thor, Big Daddy, Blackbird, and Black Label chromite deposits have been analysed for major and trace elements. The samples represent three textural groups, as defined by the relative abundance of cumulate silicate phases and chromite. To provide deposit-specific partition coefficients for modeling, we also report on the results of laboratory experiments to measure olivine- and chromite-melt partitioning of V and Ga, which are two elements readily detectable in the chromites analysed. Comparison of the Cr/Cr+Al and Fe/Fe+Mg of the EIC chromites and compositions from previous experimental studies indicates overlap in Cr/Cr+Al between the natural samples and experiments done at &amp;gt;1400oC, but significant offset of the natural samples to higher Fe/Fe+Mg. This is interpreted to be the result of subsolidus Fe-Mg exchange between chromite and the silicate matrix. However, little change in Cr/Cr+Al from magmatic values, owing to the lack of an exchangeable reservoir for these elements. A comparison of the composition of the EIC chromites and a subset of samples from other tectonic settings reveals a strong similarity to chromites from the similarly-aged Munro Township komatiites. Partition coefficients for V and Ga are consistent with past results in that both elements are compatible in chromite (DV = 2-4; DGa ~ 3), and incompatible in olivine (DV = 0.01-0.14; DGa ~ 0.02), with values for V increasing with decreasing fO2. Simple fractional crystallization models that use these partition coefficients are developed that monitor the change in element behaviour based on the relative proportions of olivine to chromite in the crystallizing assemblage; from 'normal' cotectic proportions involving predominantly olivine, to chromite-only crystallization. Comparison of models to the natural chromite V-Ga array suggests that the overall positive correlation between these two elements is consistent with chromite formed from a Munro Township-like komatiitic magma crystallizing olivine and chromite in 'normal' cotectic proportions, with no evidence of the strong depletion in these elements expected for chromite-only crystallization. The V-Ga array can be explained if the initial magma responsible for chromite formation is slightly reduced with respect to the FMQ oxygen buffer (~FMQ- 0.5), and has assimilated up to ~20% of wall-rock banded iron formation or granodiorite. Despite the evidence for contamination, results indicate that the EIC chromitites crystallized from 'normal' cotectic proportions of olivine to chromite, and therefore no specific causative link is made between contamination and chromitite formation. Instead, the development of near- monomineralic chromite layers likely involves the preferential removal of olivine relative to chromite by physical segregation during magma flow. As suggested for some other chromitite-forming systems, the specific fluid dynamic regime during magma emplacement may therefore be responsible for crystal sorting and chromite accumulation.
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6

Horwitz, Benjamin, and Barbara Gillian Turgeon. Secondary Metabolites, Stress, and Signaling: Roles and Regulation of Peptides Produced by Non-ribosomal Peptide Synthetases. United States Department of Agriculture, 2005. http://dx.doi.org/10.32747/2005.7696522.bard.

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Fungal pathogens of plants produce a diverse array of small molecules. Often referred to as secondary metabolites because they were thought to be dispensable for basic functions, they may indeed have central roles as signals for the fungal cell, and in interactions with the host. We have identified more than a dozen genes encoding nonribosomal peptide synthetases (NPS) in Cochliobolusheterostrophus, the agent of southern corn leaf blight. The aim of this project was to identify roles of these genes in stress responses and signaling. The first objective was to test a complete collection of C. heterostrophus nonribosomal peptide synthetase (NRPS)-encoding gene deletion mutant and wildtype (WT) strains for sensitivity to various agents of oxidative (ROS) and nitrosative (RNOS) stress, in vitro. The second objective and next step in this part of the project was to study the relevance of sensitivity to ROS and RNOS in the host pathogen interaction, by measuring the production of ROS and RNOS in planta, when plants are inoculated with wild type and mutant strains. A third objective was to study expression of any genes shown to be involved in sensitivity to ROS or RNOS, in vitro and in planta. Another objective was to determine if any of the genes involved in oxidative or nitrosative stress responses are regulated by components of signal transduction pathways (STP) that we have identified and to determine where mechanisms overlap. Study of the collection of nps mutants identified phenotypes relevant for virulence, development and oxidative stress resistance for two of the genes, NPS2 and NPS6. Mutants in genes related to RNOS stress have no virulence phenotypes, while some of those related to ROS stress have reduced virulence as well as developmental phenotypes, so we focused primarily on ROS stress pathways. Furthermore, the identification of NPS2 and NPS6 as encoding for NRPS responsible for siderophore biosynthesis lent a new focus to the project, regulation by Fe. We have not yet developed good methods to image ROS in planta and work in this direction is continuing. We found that NPS6 expression is repressed by Fe, responding over the physiological Fe concentration range. Studying our collection of mutants, we found that conserved MAPK and G protein signal transduction pathways are dispensable for Fe regulation of NPS6, and initiated work to identify other pathways. The transcription factor SreA is one candidate, and is responsible for part, but not all, of the control of NPS6 expression. The results of this project show that the pathogen contends with oxidative stress through several signaling pathways. Loss of the siderophore produced by Nps6 makes the fungus sensitive to oxidative stress, and decreases virulence, suggesting a central role of the ability to sequester and take up extracellular iron in the host-pathogen interaction. Siderophores, and manipulation of Fe levels, could be targets for new strategies to deal with fungal pathogens of maize and other plants.
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