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Is Autism a Member of a Family of Diseases Resulting from Genetic/Cultural Mismatches? Implications for Treatment and Prevention

DOI: 10.1155/2012/910946

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Abstract:

Several lines of evidence support the view that autism is a typical member of a large family of immune-related, noninfectious, chronic diseases associated with postindustrial society. This family of diseases includes a wide range of inflammatory, allergic, and autoimmune diseases and results from consequences of genetic/culture mismatches which profoundly destabilize the immune system. Principle among these consequences is depletion of important components, particularly helminths, from the ecosystem of the human body, the human biome. Autism shares a wide range of features in common with this family of diseases, including the contribution of genetics/epigenetics, the identification of disease-inducing triggers, the apparent role of immunity in pathogenesis, high prevalence, complex etiologies and manifestations, and potentially some aspects of epidemiology. Fortunately, using available resources and technology, modern medicine has the potential to effectively reconstitute the human biome, thus treating or even avoiding altogether the consequences of genetic/cultural mismatches which underpin this entire family of disease. Thus, if indeed autism is an epidemic of postindustrial society associated with immune hypersensitivity, we can expect that the disease is readily preventable. 1. Introduction: Autism as a Member of a Large Family of Postindustrial Epidemics Involving a Hyperimmune Response In this paper, we outline a paradigm that points toward autism as one disease among many other well-known diseases which all share a common origin and, most likely, a common prevention strategy [1]. These emerging, noninfectious diseases are all epidemics of postindustrial culture, which are absent in antiquity in any culture, and absent in present day developing cultures. Members of this family of disease are invariably associated with a hyperimmune response and can have a very high prevalence in postindustrial populations, with prevalence often greater than 0.1% and sometimes greater than 1.0%. These hyperimmune-associated diseases include a wide range of allergic, autoimmune, and inflammatory diseases such as lupus, multiple sclerosis, hay fever, appendicitis, chronic fatigue syndrome, inflammatory bowel disease, asthma, celiac disease, type 1 diabetes, Graves’ disease, some types of eczema, and a wide range of food allergies. Here, based on a variety of evidence, we argue that autism is yet another member of this family of diseases, despite the slowness of the medical community to recognize it as such. Since the pathogenesis of at least one form of autism has

References

[1]  S. D. Bilbo, G. A. Wray, S. E. Perkins, and W. Parker, “Reconstitution of the human biome as the most reasonable solution for epidemics of allergic and autoimmune diseases,” Medical Hypotheses, vol. 77, no. 4, pp. 494–504, 2011.
[2]  V. T. Ramaekers, N. Blau, J. M. Sequeira, M. C. Nassogne, and E. V. Quadros, “Folate receptor autoimmunity and cerebral folate deficiency in low-functioning autism with neurological deficits,” Neuropediatrics, vol. 38, no. 6, pp. 276–281, 2007.
[3]  G. A. Mostafa and L. Y. Al-Ayadhi, “The relationship between the increased frequency of serum antineuronal antibodies and the severity of autism in children,” European Journal of Pediatric Neurology. In press.
[4]  P. Ashwood and A. J. Wakefield, “Immune activation of peripheral blood and mucosal CD3+ lymphocyte cytokine profiles in children with autism and gastrointestinal symptoms,” Journal of Neuroimmunology, vol. 173, no. 1-2, pp. 126–134, 2006.
[5]  P. Ashwood, S. Wills, and J. Van De Water, “The immune response in autism: a new frontier for autism research,” Journal of Leukocyte Biology, vol. 80, no. 1, pp. 1–15, 2006.
[6]  R. L. Blaylock, “A possible central mechanism in autism spectrum disorders, part 2: immunoexcitotoxicity,” Alternative Therapies in Health and Medicine, vol. 15, no. 1, pp. 60–67, 2009.
[7]  R. L. Blaylock and A. Strunecka, “Immune-glutamatergic dysfunction as a central mechanism of the autism spectrum disorders,” Current Medicinal Chemistry, vol. 16, no. 2, pp. 157–170, 2009.
[8]  N. C. Derecki, E. Privman, and J. Kipnis, “Rett syndrome and other autism spectrum disordersbrain diseases of immune malfunction,” Molecular Psychiatry, vol. 15, no. 4, pp. 355–363, 2010.
[9]  A. M. Enstrom, C. E. Onore, J. A. Van de Water, and P. Ashwood, “Differential monocyte responses to TLR ligands in children with autism spectrum disorders,” Brain, Behavior, and Immunity, vol. 24, no. 1, pp. 64–71, 2010.
[10]  I. Maezawa and L. W. Jin, “Rett syndrome microglia damage dendrites and synapses by the elevated release of glutamate,” Journal of Neuroscience, vol. 30, no. 15, pp. 5346–5356, 2010.
[11]  C. A. Pardo, D. L. Vargas, and A. W. Zimmerman, “Immunity, neuroglia and neuroinflammation in autism,” International Review of Psychiatry, vol. 17, no. 6, pp. 485–495, 2005.
[12]  W. J. Streit, “Microglia as neuroprotective, immunocompetent cells of the CNS,” GLIA, vol. 40, no. 2, pp. 133–139, 2002.
[13]  D. L. Vargas, C. Nascimbene, C. Krishnan, A. W. Zimmerman, and C. A. Pardo, “Neuroglial activation and neuroinflammation in the brain of patients with autism,” Annals of Neurology, vol. 57, no. 1, pp. 67–81, 2005.
[14]  W. J. Streit, “Microglia and neuroprotection: implications for Alzheimer's disease,” Brain Research Reviews, vol. 48, no. 2, pp. 234–239, 2005.
[15]  A. J. Husband, “The immune system and integrated homeostasis,” Immunology and Cell Biology, vol. 73, no. 4, pp. 377–382, 1995.
[16]  L. Vitkovic, J. Bockaert, and C. Jacque, “'Inflammatory' cytokines' neuromodulators in normal brain?” Journal of Neurochemistry, vol. 74, no. 2, pp. 457–471, 2000.
[17]  R. Dantzer and K. W. Kelley, “Twenty years of research on cytokine-induced sickness behavior,” Brain, Behavior, and Immunity, vol. 21, no. 2, pp. 153–160, 2007.
[18]  S. F. Maier and L. R. Watkins, “Cytokines for psychologists: implications of bidirectional immune-to-brain communication for understanding behavior, mood, and cognition,” Psychological Review, vol. 105, no. 1, pp. 83–107, 1998.
[19]  F. Mignini, V. Streccioni, and F. Amenta, “Autonomic innervation of immune organs and neuroimmune modulation,” Autonomic and Autacoid Pharmacology, vol. 23, no. 1, pp. 1–25, 2003.
[20]  D. Wrona, “Neural-immune interactions: an integrative view of the bidirectional relationship between the brain and immune systems,” Journal of Neuroimmunology, vol. 172, no. 1-2, pp. 38–58, 2006.
[21]  F. Ginhoux, M. Greter, M. Leboeuf et al., “Fate mapping analysis reveals that adult microglia derive from primitive macrophages,” Science, vol. 330, no. 6005, pp. 841–845, 2010.
[22]  P. Rezaie and D. Male, “Mesoglia and microglia—a historical review of the concept of mononuclear phagocytes within the central nervous system,” Journal of the History of the Neurosciences, vol. 11, no. 4, pp. 325–374, 2002.
[23]  D. Giulian, D. G. Young, J. Woodward, D. C. Brown, and L. B. Lachman, “Interleukin-1 is an astroglial growth factor in the developing brain,” Journal of Neuroscience, vol. 8, no. 2, pp. 709–714, 1988.
[24]  S. Rakic and N. Zecevic, “Programmed cell death in the developing human telencephalon,” European Journal of Neuroscience, vol. 12, no. 8, pp. 2721–2734, 2000.
[25]  W. J. Streit, “Microglia and macrophages in the developing CNS,” NeuroToxicology, vol. 22, no. 5, pp. 619–624, 2001.
[26]  G. A. Garden and T. M?ller, “Microglia biology in health and disease,” Journal of Neuroimmune Pharmacology, vol. 1, no. 2, pp. 127–137, 2006.
[27]  M. J. Bell and J. M. Hallenbeck, “Effects of intrauterine inflammation on developing rat brain,” Journal of Neuroscience Research, vol. 70, no. 4, pp. 570–579, 2002.
[28]  E. M. Ullian, S. K. Sapperstein, K. S. Christopherson, and B. A. Barres, “Control of synapse number by glia,” Science, vol. 291, no. 5504, pp. 657–661, 2001.
[29]  K. S. Christopherson, E. M. Ullian, C. C. A. Stokes et al., “Thrombospondins are astrocyte-secreted proteins that promote CNS synaptogenesis,” Cell, vol. 120, no. 3, pp. 421–433, 2005.
[30]  ?. Eroglu, N. J. Allen, M. W. Susman et al., “Gabapentin receptor alpha2delta-1 is a neuronal thrombospondin receptor responsible for excitatory CNS synaptogenesis,” Cell, vol. 139, no. 2, pp. 380–392, 2009.
[31]  O. Garcia, M. Torres, P. Helguera, P. Coskun, and J. Busciglio, “A role for thrombospondin-1 deficits in astrocyte-mediated spine and synaptic pathology in down's syndrome,” PLoS ONE, vol. 5, no. 12, Article ID e14200, 2010.
[32]  C. M. Muller and J. Best, “Ocular dominance plasticity in adult cat visual cortex after transplantation of cultured astrocytes,” Nature, vol. 342, no. 6248, pp. 427–430, 1989.
[33]  L. Bennet and A. Gunn, “The fetal origins of adult mental illness,” in Early Life Origins of Health and Disease (Advances in Experimental Medicine and Biology), M. Wintour-Coghlan and J. Owens, Eds., pp. 204–211, Springer, New York, NY, USA, 2006.
[34]  D. Rice and S. Barone Jr, “Critical periods of vulnerability for the developing nervous system: evidence from humans and animal models,” Environmental Health Perspectives, vol. 108, supplement 3, pp. 511–533, 2000.
[35]  M. Hornig, H. Weissenb?ck, N. Horscroft, and W. I. Lipkin, “An infection-based model of neurodevelopmental damage,” Proceedings of the National Academy of Sciences of the United States of America, vol. 96, no. 21, pp. 12102–12107, 1999.
[36]  K. B. Nelson and R. E. Willoughby, “Infection, inflammation and the risk of cerebral palsy,” Current Opinion in Neurology, vol. 13, no. 2, pp. 133–139, 2000.
[37]  P. Rantakallio, P. Jones, J. Moring, and L. Von Wendt, “Association between central nervous system infections during childhood and adult onset schizophrenia and other psychoses: a 28-year follow-up,” International Journal of Epidemiology, vol. 26, no. 4, pp. 837–843, 1997.
[38]  L. Shi, S. H. Fatemi, R. W. Sidwell, and P. H. Patterson, “Maternal influenza infection causes marked behavioral and pharmacological changes in the offspring,” Journal of Neuroscience, vol. 23, no. 1, pp. 297–302, 2003.
[39]  N. V. Malkova, C. Z. Yu, E. Y. Hsiao, M. J. Moore, and P. H. Patterson, “Maternal immune activation yields offspring displaying mouse versions of the three core symptoms of autism,” Brain, Behavior, and Immunity, vol. 26, no. 4, pp. 607–616, 2012.
[40]  S. D. Bilbo and J. M. Schwarz, “Early-life programming of later-life brain and behavior: a critical role for the immune system,” Frontiers in Behavioral Neuroscience, vol. 3, p. 14, 2009.
[41]  S. D. Bilbo, S. H. Smith, and J. M. Schwarz, “A lifespan approach to neuroinflammatory and cognitive disorders: a critical role for glia,” Journal of Neuroimmune Pharmacology, pp. 1–18, 2011.
[42]  R. B. Elliott, H. E. Wasmuth, N. J. Bibby, A. K. H. Macgibbon, and J. P. Hill, “The effect of beta-casein polymorphism on the stimulation of diabetes in the non-obese diabetic mouse and effect of beta-casomorphin-7 on immune cell activity,” International Dairy Journal, vol. 8, p. 580, 1998.
[43]  G. A. W. Rook, “Review series on helminths, immune modulation and the hygiene hypothesis: the broader implications of the hygiene hypothesis,” Immunology, vol. 126, no. 1, pp. 3–11, 2009.
[44]  G. Borkow, Q. Leng, Z. Weisman et al., “Chronic immune activation associated with intestinal helminth infections results in impaired signal transduction and anergy,” Journal of Clinical Investigation, vol. 106, no. 8, pp. 1053–1060, 2000.
[45]  M. P. Muehlenbein, “Parasitological analyses of the male chimpanzees (Pan troglodytes schweinfurthii) at Ngogo, Kibale National Park, Uganda,” American Journal of Primatology, vol. 65, no. 2, pp. 167–179, 2005.
[46]  M. Scaglia, M. Tinelli, R. Revoltella, et al., “Relationship between serum IgE levels and intestinal parasite load in African populations,” International Archives of Allergy and Applied Immunology, vol. 59, no. 4, pp. 465–468, 1979.
[47]  J. P. Hewitson, J. R. Grainger, and R. M. Maizels, “Helminth immunoregulation: the role of parasite secreted proteins in modulating host immunity,” Molecular and Biochemical Parasitology, vol. 167, no. 1, pp. 1–11, 2009.
[48]  R. W. Summers, D. E. Elliott, K. Qadir, J. F. Urban Jr, R. Thompson, and J. V. Weinstock, “Trichuris suis seems to be safe and possibly effective in the treatment of inflammatory bowel disease,” American Journal of Gastroenterology, vol. 98, no. 9, pp. 2034–2041, 2003.
[49]  J. Correale and M. Farez, “Association between parasite infection and immune responses in multiple sclerosis,” Annals of Neurology, vol. 61, no. 2, pp. 97–108, 2007.
[50]  A. P. Devalapalli, A. Lesher, K. Shieh et al., “Increased levels of IgE and autoreactive, polyreactive IgG in wild rodents: implications for the hygiene hypothesis,” Scandinavian Journal of Immunology, vol. 64, no. 2, pp. 125–136, 2006.
[51]  A. Lesher, B. Li, P. Whitt et al., “Increased IL-4 production and attenuated proliferative and pro-inflammatory responses of splenocytes from wild-caught rats (Rattus norvegicus),” Immunology and Cell Biology, vol. 84, no. 4, pp. 374–382, 2006.
[52]  N. Q. Liu, A. T. Kaplan, V. Lagishetty et al., “Vitamin D and the regulation of placental inflammation,” Journal of Immunology, vol. 186, no. 10, pp. 5968–5974, 2011.
[53]  R. M. Lucas, A. L. Ponsonby, K. Dear et al., “Sun exposure and vitamin D are independent risk factors for CNS demyelination,” Neurology, vol. 76, no. 6, pp. 540–548, 2011.
[54]  S. Sharief, S. Jariwala, J. Kumar, P. Muntner, and M. L. Melamed, “Vitamin D levels and food and environmental allergies in the United States: results from the National Health and Nutrition Examination Survey 2005-2006,” Journal of Allergy and Clinical Immunology, vol. 127, no. 5, pp. 1195–1202, 2011.
[55]  M. F. Holick, “Vitamin D deficiency,” The New England Journal of Medicine, vol. 357, pp. 266–281, 2007.
[56]  M. J. Dealberto, “Prevalence of autism according to maternal immigrant status and ethnic origin,” Acta Psychiatrica Scandinavica, vol. 123, no. 5, pp. 339–348, 2011.
[57]  J. J. Cannell, “Autism and vitamin D,” Medical Hypotheses, vol. 70, no. 4, pp. 750–759, 2008.
[58]  M. Waldman, S. Nicholson, N. Adilov, and J. Williams, “Autism prevalence and precipitation rates in California, Oregon, and Washington counties,” Archives of Pediatrics and Adolescent Medicine, vol. 162, no. 11, pp. 1026–1034, 2008.
[59]  V. Gilsanz, A. Kremer, A. O. Mo, T. A. L. Wren, and R. Kremer, “Vitamin D status and its relation to muscle mass and muscle fat in young women,” Journal of Clinical Endocrinology and Metabolism, vol. 95, no. 4, pp. 1595–1601, 2010.
[60]  A. L. Kau, P. P. Ahern, N. W. Griffin, A. L. Goodman, and J. I. Gordon, “Human nutrition, the gut microbiome and the immune system,” Nature, vol. 474, no. 7351, pp. 327–336, 2011.
[61]  M. H. de Borst, R. A. de Boer, R. P. Stolk, J. P. J. Slaets, B. H. R. Wolffenbuttel, and G. Navis, “Vitamin D deficiency: universal risk factor for multifactorial diseases?” Current Drug Targets, vol. 12, no. 1, pp. 97–106, 2011.
[62]  S. V. Ramagopalan, A. Heger, A. J. Berlanga et al., “A ChIP-seq defined genome-wide map of vitamin D receptor binding: associations with disease and evolution,” Genome Research, vol. 20, no. 10, pp. 1352–1360, 2010.
[63]  J. P. Gouin, L. V. Hantsoo, and J. K. Kiecolt-Glaser, “Stress, negative emotions, and inflammation,” in Handbook of Social Neurosciences, J. T. C. J. Decety, Ed., pp. 814–829, John Wiley and Sons, New York, NY, USA, 2011.
[64]  J. K. Kiecolt-Glaser, K. L. Heffner, R. Glaser et al., “How stress and anxiety can alter immediate and late phase skin test responses in allergic rhinitis,” Psychoneuroendocrinology, vol. 34, no. 5, pp. 670–680, 2009.
[65]  R. Glaser and J. K. Kiecolt-Glaser, “Stress damages immune ssytem and health,” Discovery Medicine, vol. 5, pp. 165–169, 2005.
[66]  P. M?ller, H. Wallin, and L. E. Knudsen, “Oxidative stress associated with exercise, psychological stress and life-style factors,” Chemico-Biological Interactions, vol. 102, no. 1, pp. 17–36, 1996.
[67]  E. Puterman, J. Lin, E. Blackburn, A. O'Donovan, N. Adler, and E. Epel, “The power of exercise: buffering the effect of chronic stress on telomere length,” PLoS ONE, vol. 5, no. 5, Article ID e10837, 2010.
[68]  P. Salmon, “Effects of physical exercise on anxiety, depression, and sensitivity to stress: a unifying theory,” Clinical Psychology Review, vol. 21, no. 1, pp. 33–61, 2001.
[69]  U. Rimmele, R. Seiler, B. Marti, P. H. Wirtz, U. Ehlert, and M. Heinrichs, “The level of physical activity affects adrenal and cardiovascular reactivity to psychosocial stress,” Psychoneuroendocrinology, vol. 34, no. 2, pp. 190–198, 2009.
[70]  T. G. Merrett, M. L. Burr, B. K. Butland, J. Merrett, F. G. Miskelly, and E. Vaughan-Williams, “Infant feeding and allergy: 12-month prospective study of 500 babies born into allergic families,” Annals of Allergy, vol. 61, no. 6, pp. 13–20, 1988.
[71]  R. K. Chandra, S. Puri, and A. Hamed, “Influence of maternal diet during lactation and use of formula feeds on development of atopic eczema in high risk infants,” British Medical Journal, vol. 298, no. 6693, pp. 228–230, 1989.
[72]  S. Koletzko, P. Sherman, M. Corey, A. Griffiths, and C. Smith, “Role of infant feeding practices in development of Crohn's disease in childhood,” British Medical Journal, vol. 298, no. 6688, pp. 1617–1618, 1989.
[73]  G. Dick, “President's address. The etiology of multiple sclerosis,” Proceedings of the Royal Society of Medicine, vol. 69, no. 8, pp. 611–615, 1976.
[74]  D. Fava, R. D. G. Leslie, and P. Pozzilli, “Relationship between dairy product consumption and incidence of IDDM in childhood in Italy,” Diabetes Care, vol. 17, no. 12, pp. 1488–1490, 1994.
[75]  L. B. Ray, “Linking inflammation and metabolism,” Science's STKE, vol. 386, Article ID tw165, 2007.
[76]  M. Assem, E. G. Schuetz, M. Leggas et al., “Interactions between hepatic Mrp4 and Sult2a as revealed by the constitutive androstane receptor and Mrp4 knockout mice,” Journal of Biological Chemistry, vol. 279, no. 21, pp. 22250–22257, 2004.
[77]  O. Burk, K. A. Arnold, A. K. Nussler et al., “Antimalarial artemisinin drugs induce cytochrome P450 and MDR1 expression by activation of xenosensors pregnane X receptor and constitutive androstane receptor,” Molecular Pharmacology, vol. 67, no. 6, pp. 1954–1965, 2005.
[78]  A. Geick, M. Eichelbaum, and O. Burk, “Nuclear receptor response elements mediate induction of Intestinal MDR1 by Rifampin,” Journal of Biological Chemistry, vol. 276, no. 18, pp. 14581–14587, 2001.
[79]  H. R. Kast, B. Goodwin, P. T. Tarr et al., “Regulation of multidrug resistance-associated protein 2 (ABCC2) by the nuclear receptors pregnane X receptor, farnesoid X-activated receptor, and constitutive androstane receptor,” Journal of Biological Chemistry, vol. 277, no. 4, pp. 2908–2915, 2002.
[80]  E. G. Schuetz, A. H. Schinkel, M. V. Relling, and J. D. Schuetz, “P-glycoprotein: a major determinant of rifampicin-inducible expression of cytochrome P4503A in mice and humans,” Proceedings of the National Academy of Sciences of the United States of America, vol. 93, no. 9, pp. 4001–4005, 1996.
[81]  K. W. Renton, “Alteration of drug biotransformation and elimination during infection and inflammation,” Pharmacology and Therapeutics, vol. 92, no. 2-3, pp. 147–163, 2001.
[82]  A. P. Beigneux, A. H. Moser, J. K. Shigenaga, C. Grunfeld, and K. R. Feingold, “Reduction in cytochrome P-450 enzyme expression is associated with repression of CAR (constitutive androstane receptor) and PXR (pregnane X receptor) in mouse liver during the acute phase response,” Biochemical and Biophysical Research Communications, vol. 293, no. 1, pp. 145–149, 2002.
[83]  G. Hartmann, A. K. Y. Cheung, and M. Piquette-Miller, “Inflammatory cytokines, but not bile acids, regulate expression of murine hepatic anion transporters in endotoxemia,” Journal of Pharmacology and Experimental Therapeutics, vol. 303, no. 1, pp. 273–281, 2002.
[84]  E. Siewert, C. G. Dietrich, F. Lammert et al., “Interleukin-6 regulates hepatic transporters during acute-phase response,” Biochemical and Biophysical Research Communications, vol. 322, no. 1, pp. 232–238, 2004.
[85]  C. S. Song, I. Echchgadda, Y. K. Seo et al., “An essential role of the CAAT/enhancer binding protein-α in the vitamin D-induced expression of the human steroid/bile acid-sulfotransferase (SULT2A1),” Molecular Endocrinology, vol. 20, no. 4, pp. 795–808, 2006.
[86]  L. A. Schieve, S. Boulet, S. J. Blumberg, et al., “Association between parental nativity and autism spectrum disorder among US-born non-Hispanic white and Hispanic children, 2007 National Survey of Children's Health,” Disability and Health Journal, vol. 5, no. 1, pp. 18–25, 2012.
[87]  J. Correale, M. Farez, and G. Razzitte, “Helminth infections associated with multiple sclerosis induce regulatory B cells,” Annals of Neurology, vol. 64, no. 2, pp. 187–199, 2008.
[88]  J. M. Burton, S. Kimball, R. Vieth et al., “A phase I/II dose-escalation trial of vitamin D3 and calcium in multiple sclerosis,” Neurology, vol. 74, no. 23, pp. 1852–1859, 2010.
[89]  Y. Shen, K. A. Dies, I. A. Holm et al., “Clinical genetic testing for patients with autism spectrum disorders,” Pediatrics, vol. 125, no. 4, pp. e727–e735, 2010.
[90]  H. ó. Atladóttir, P. Thorsen, L. ?stergaard et al., “Maternal infection requiring hospitalization during pregnancy and autism spectrum disorders,” Journal of Autism and Developmental Disorders, vol. 40, no. 12, pp. 1423–1430, 2010.
[91]  L. S. Mills, M. F. Soule, and D. F. Doak, “The keystone-species concept in ecology and conservation,” Bioscience, vol. 43, no. 4, pp. 219–224, 1993.
[92]  C. D. Bethell, M. D. Kogan, B. B. Strickland, E. L. Schor, J. Robertson, and P. W. Newacheck, “A national and state profile of leading health problems and health care quality for US children: key insurance disparities and across-state variations,” Academic Pediatrics, vol. 11, no. 3, pp. S22–S33, 2011.

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