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1
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46449113977
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Schizophrenia, "just the facts" what we know in 2008. 2. Epidemiology and etiology
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Tandon R., Keshavan M.S., and Nasrallah H.A. Schizophrenia, "just the facts" what we know in 2008. 2. Epidemiology and etiology. Schizophr Res 102 (2008) 1-18
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(2008)
Schizophr Res
, vol.102
, pp. 1-18
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Tandon, R.1
Keshavan, M.S.2
Nasrallah, H.A.3
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2
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54249166128
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Gene-environment interactions in schizophrenia: review of epidemiological findings and future directions
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This is an excellent review on the gene-environment interactions in the etiology of schizophrenia, with an emphasis on major environmental factors.
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Van O.J., Rutten B.P., and Poulton R. Gene-environment interactions in schizophrenia: review of epidemiological findings and future directions. Schizophr Bull 34 (2008) 1066-1082. This is an excellent review on the gene-environment interactions in the etiology of schizophrenia, with an emphasis on major environmental factors.
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(2008)
Schizophr Bull
, vol.34
, pp. 1066-1082
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Van, O.J.1
Rutten, B.P.2
Poulton, R.3
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3
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0036308284
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Schizophrenia as a disorder of neurodevelopment
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Lewis D.A., and Levitt P. Schizophrenia as a disorder of neurodevelopment. Annu Rev Neurosci 25 (2002) 409-432
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Annu Rev Neurosci
, vol.25
, pp. 409-432
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Lewis, D.A.1
Levitt, P.2
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5
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33749986298
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Free radicals and antioxidants in normal physiological functions and human disease
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This is an excellent review on reactive oxygen species (ROS) and reactive nitrogen species (RNS, e.g. nitric oxide, NO{radical dot}) and their dual role as both deleterious and beneficial species. ROS and RNS are normally generated by tightly regulated enzymes, such as NO synthase (NOS) and NAD(P)H oxidase isoforms, respectively. Overproduction of ROS results in oxidative stress, a deleterious process and important mediator of damage to cell structures, including lipids and membranes, proteins, and DNA. At low/moderate concentrations, beneficial effects of ROS/RNS involve physiological roles in cellular responses to noxia, as for example in defense against infectious agents, in the function of a number of cellular signaling pathways, and the induction of a mitogenic response. Various ROS-mediated actions in fact protect cells against ROS-induced oxidative stress and re-establish or maintain 'redox balance' termed also 'redox homeostasis'.
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Valko M., Leibfritz D., Moncol J., Cronin M.T., Mazur M., and Telser J. Free radicals and antioxidants in normal physiological functions and human disease. Int J Biochem Cell Biol 39 (2007) 44-84. This is an excellent review on reactive oxygen species (ROS) and reactive nitrogen species (RNS, e.g. nitric oxide, NO{radical dot}) and their dual role as both deleterious and beneficial species. ROS and RNS are normally generated by tightly regulated enzymes, such as NO synthase (NOS) and NAD(P)H oxidase isoforms, respectively. Overproduction of ROS results in oxidative stress, a deleterious process and important mediator of damage to cell structures, including lipids and membranes, proteins, and DNA. At low/moderate concentrations, beneficial effects of ROS/RNS involve physiological roles in cellular responses to noxia, as for example in defense against infectious agents, in the function of a number of cellular signaling pathways, and the induction of a mitogenic response. Various ROS-mediated actions in fact protect cells against ROS-induced oxidative stress and re-establish or maintain 'redox balance' termed also 'redox homeostasis'.
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(2007)
Int J Biochem Cell Biol
, vol.39
, pp. 44-84
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Valko, M.1
Leibfritz, D.2
Moncol, J.3
Cronin, M.T.4
Mazur, M.5
Telser, J.6
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6
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55149107716
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Radical-free biology of oxidative stress
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Besides free radical-induced macromolecular damage that has been studied extensively as a mechanism of oxidative stress, this timely review focuses on the involvement of redox dysregulation that can occur without free radical generation. Oxidative stress can also occur as a consequence of the disruption of thiol redox circuits, which normally function in cell signaling and physiological regulation. The redox states of thiol systems are sensitive to two electron oxidants and controlled by the thioredoxins (Trx), GSH, and cysteine. Trx and GSH systems are maintained under stable, but nonequilibrium conditions, because of the continuous oxidation of cell thiols at a rate of about 0.5% of the total thiol pool per minute.
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Jones D.P. Radical-free biology of oxidative stress. Am J Physiol Cell Physiol 295 (2008) C849-C868. Besides free radical-induced macromolecular damage that has been studied extensively as a mechanism of oxidative stress, this timely review focuses on the involvement of redox dysregulation that can occur without free radical generation. Oxidative stress can also occur as a consequence of the disruption of thiol redox circuits, which normally function in cell signaling and physiological regulation. The redox states of thiol systems are sensitive to two electron oxidants and controlled by the thioredoxins (Trx), GSH, and cysteine. Trx and GSH systems are maintained under stable, but nonequilibrium conditions, because of the continuous oxidation of cell thiols at a rate of about 0.5% of the total thiol pool per minute. Redox-sensitive thiols are critical for signal transduction (e.g. H-Ras and PTP-1B), transcription factor binding to DNA (e.g. Nrf-2, nuclear factor-κB), receptor activation (e.g. NMDA receptor), and other processes. Nonradical oxidants, including peroxides, quinones are generated enzymatically from both endogenous (e.g. dopamine) and exogenous precursors and do not require free radicals as intermediates to oxidize or modify these thiols and disrupt function.
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(2008)
Am J Physiol Cell Physiol
, vol.295
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Jones, D.P.1
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7
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12944305859
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Glutathione synthesis is essential for mouse development but not for cell growth in culture
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Shi Z.Z., Osei-Frimpong J., Kala G., Kala S.V., Barrios R.J., Habib G.M., Lukin D.J., Danney C.M., Matzuk M.M., and Lieberman M.W. Glutathione synthesis is essential for mouse development but not for cell growth in culture. Proc Natl Acad Sci U S A 97 (2000) 5101-5106
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Proc Natl Acad Sci U S A
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, pp. 5101-5106
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Shi, Z.Z.1
Osei-Frimpong, J.2
Kala, G.3
Kala, S.V.4
Barrios, R.J.5
Habib, G.M.6
Lukin, D.J.7
Danney, C.M.8
Matzuk, M.M.9
Lieberman, M.W.10
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8
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0036752945
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Cysteine regulation of protein function - as exemplified by NMDA-receptor modulation
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Lipton S.A., Choi Y.B., Takahashi H., Zhang D., Li W., Godzik A., and Bankston L.A. Cysteine regulation of protein function - as exemplified by NMDA-receptor modulation. Trends Neurosci 25 (2002) 474-480
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Trends Neurosci
, vol.25
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Lipton, S.A.1
Choi, Y.B.2
Takahashi, H.3
Zhang, D.4
Li, W.5
Godzik, A.6
Bankston, L.A.7
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9
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65049089113
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Regulation of glutathione synthesis
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This is an extensive review on the biological functions of GSH, its synthesis and metabolism and on transcription factors controlling its regulation. This is a brief survey of its perturbation in various pathologies.
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Lu S.C. Regulation of glutathione synthesis. Mol Aspects Med 30 (2009) 42-59. This is an extensive review on the biological functions of GSH, its synthesis and metabolism and on transcription factors controlling its regulation. This is a brief survey of its perturbation in various pathologies.
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Mol Aspects Med
, vol.30
, pp. 42-59
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Lu, S.C.1
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10
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0036842383
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Reduced erythrocyte membrane essential fatty acids and increased lipid peroxides in schizophrenia at the never-medicated first-episode of psychosis and after years of treatment with antipsychotics
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Khan M.M., Evans D.R., Gunna V., Scheffer R.E., Parikh V.V., and Mahadik S.P. Reduced erythrocyte membrane essential fatty acids and increased lipid peroxides in schizophrenia at the never-medicated first-episode of psychosis and after years of treatment with antipsychotics. Schizophr Res 58 (2002) 1-10
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Schizophr Res
, vol.58
, pp. 1-10
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Khan, M.M.1
Evans, D.R.2
Gunna, V.3
Scheffer, R.E.4
Parikh, V.V.5
Mahadik, S.P.6
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11
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29244464827
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Altered glutathione redox state in schizophrenia
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Yao J.K., Leonard S., and Reddy R. Altered glutathione redox state in schizophrenia. Dis Markers 22 (2006) 83-93
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Dis Markers
, vol.22
, pp. 83-93
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Yao, J.K.1
Leonard, S.2
Reddy, R.3
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12
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0035133525
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Evidence that the activities of erythrocyte free radical scavenging enzymes and the products of lipid peroxidation are increased in different forms of schizophrenia
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Herken H., Uz E., Ozyurt H., Sogut S., Virit O., and Akyol O. Evidence that the activities of erythrocyte free radical scavenging enzymes and the products of lipid peroxidation are increased in different forms of schizophrenia. Mol Psychiatry 6 (2001) 66-73
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Mol Psychiatry
, vol.6
, pp. 66-73
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Herken, H.1
Uz, E.2
Ozyurt, H.3
Sogut, S.4
Virit, O.5
Akyol, O.6
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13
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2942604863
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Mitochondrial dysfunction in schizophrenia: evidence for compromised brain metabolism and oxidative stress
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643
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Prabakaran S., Swatton J.E., Ryan M.M., Huffaker S.J., Huang J.T., Griffin J.L., Wayland M., Freeman T., Dudbridge F., Lilley K.S., et al. Mitochondrial dysfunction in schizophrenia: evidence for compromised brain metabolism and oxidative stress. Mol Psychiatry 9 (2004) 684-697 643
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Mol Psychiatry
, vol.9
, pp. 684-697
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Prabakaran, S.1
Swatton, J.E.2
Ryan, M.M.3
Huffaker, S.J.4
Huang, J.T.5
Griffin, J.L.6
Wayland, M.7
Freeman, T.8
Dudbridge, F.9
Lilley, K.S.10
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14
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67650911472
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Redox dysregulation in schizophrenia: genetic susceptibility and pathophysiological mechanisms
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Lajtha A. (Ed), Springer, New York. This is a review covering in detail some topics of the present paper.
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Do K.Q., Bovet P., Cabungcal J.H., Conus P., Gysin R., Lavoie S., Steullet P., and Cuenod M. Redox dysregulation in schizophrenia: genetic susceptibility and pathophysiological mechanisms. In: Lajtha A. (Ed). Handbook of Neurochemistry and Molecular Neurobiology vol 27 (2009), Springer, New York. This is a review covering in detail some topics of the present paper.
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Handbook of Neurochemistry and Molecular Neurobiology
, vol.27
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Do, K.Q.1
Bovet, P.2
Cabungcal, J.H.3
Conus, P.4
Gysin, R.5
Lavoie, S.6
Steullet, P.7
Cuenod, M.8
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15
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33748676111
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Schizophrenia and oxidative stress: glutamate cysteine ligase modifier as a susceptibility gene
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Tosic M., Ott J., Barral S., Bovet P., Deppen P., Gheorghita F., Matthey M.L., Parnas J., Preisig M., Saraga M., et al. Schizophrenia and oxidative stress: glutamate cysteine ligase modifier as a susceptibility gene. Am J Hum Genet 79 (2006) 586-592
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Am J Hum Genet
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, pp. 586-592
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Tosic, M.1
Ott, J.2
Barral, S.3
Bovet, P.4
Deppen, P.5
Gheorghita, F.6
Matthey, M.L.7
Parnas, J.8
Preisig, M.9
Saraga, M.10
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16
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36749104268
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Impaired glutathione synthesis in schizophrenia: convergent genetic and functional evidence
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This paper presents the trinucleotid polymorphism associated with schizophrenia in the gene of the GSH synthesizing enzyme and its functional consequences in fibroblasts challenged by an oxidative stress, revealing dysregulation of the redox homeostasis.
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Gysin R., Kraftsik R., Sandell J., Bovet P., Chappuis C., Conus P., Deppen P., Preisig M., Ruiz V., Steullet P., et al. Impaired glutathione synthesis in schizophrenia: convergent genetic and functional evidence. Proc Natl Acad Sci U S A 104 (2007) 16621-16626. This paper presents the trinucleotid polymorphism associated with schizophrenia in the gene of the GSH synthesizing enzyme and its functional consequences in fibroblasts challenged by an oxidative stress, revealing dysregulation of the redox homeostasis.
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(2007)
Proc Natl Acad Sci U S A
, vol.104
, pp. 16621-16626
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Gysin, R.1
Kraftsik, R.2
Sandell, J.3
Bovet, P.4
Chappuis, C.5
Conus, P.6
Deppen, P.7
Preisig, M.8
Ruiz, V.9
Steullet, P.10
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17
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0033787297
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Schizophrenia: glutathione deficit in cerebrospinal fluid and prefrontal cortex in vivo
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Do K.Q., Trabesinger A.H., Kirsten-Kruger M., Lauer C.J., Dydak U., Hell D., Holsboer F., Boesiger P., and Cuenod M. Schizophrenia: glutathione deficit in cerebrospinal fluid and prefrontal cortex in vivo. Eur J Neurosci 12 (2000) 3721-3728
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(2000)
Eur J Neurosci
, vol.12
, pp. 3721-3728
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Do, K.Q.1
Trabesinger, A.H.2
Kirsten-Kruger, M.3
Lauer, C.J.4
Dydak, U.5
Hell, D.6
Holsboer, F.7
Boesiger, P.8
Cuenod, M.9
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18
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44849102210
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Negative correlation between brain glutathione level and negative symptoms in schizophrenia: a 3T 1H-MRS study
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GSH levels measured by MRS in posterior medial frontal cortex of 20 schizophrenia patients were negatively correlated with negative symptoms. There was no significant changes in GSH levels when compared with normal controls, probably because of genotypes heterogeneity.
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Matsuzawa D., Obata T., Shirayama Y., Nonaka H., Kanazawa Y., Yoshitome E., Takanashi J., Matsuda T., Shimizu E., Ikehira H., et al. Negative correlation between brain glutathione level and negative symptoms in schizophrenia: a 3T 1H-MRS study. PLoS ONE 3 (2008) e1944. GSH levels measured by MRS in posterior medial frontal cortex of 20 schizophrenia patients were negatively correlated with negative symptoms. There was no significant changes in GSH levels when compared with normal controls, probably because of genotypes heterogeneity.
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(2008)
PLoS ONE
, vol.3
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Matsuzawa, D.1
Obata, T.2
Shirayama, Y.3
Nonaka, H.4
Kanazawa, Y.5
Yoshitome, E.6
Takanashi, J.7
Matsuda, T.8
Shimizu, E.9
Ikehira, H.10
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19
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57149120578
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Functional polymorphisms in PRODH are associated with risk and protection for schizophrenia and fronto-striatal structure and function
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Kempf L., Nicodemus K.K., Kolachana B., Vakkalanka R., Verchinski B.A., Egan M.F., Straub R.E., Mattay V.A., Callicott J.H., Weinberger D.R., and Meyer-Lindenberg A. Functional polymorphisms in PRODH are associated with risk and protection for schizophrenia and fronto-striatal structure and function. PLoS Genet 4 (2008) e1000252
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(2008)
PLoS Genet
, vol.4
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Kempf, L.1
Nicodemus, K.K.2
Kolachana, B.3
Vakkalanka, R.4
Verchinski, B.A.5
Egan, M.F.6
Straub, R.E.7
Mattay, V.A.8
Callicott, J.H.9
Weinberger, D.R.10
Meyer-Lindenberg, A.11
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20
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53849096017
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The metabolism of proline, a stress substrate, modulates carcinogenic pathways
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Phang J.M., Donald S.P., Pandhare J., and Liu Y. The metabolism of proline, a stress substrate, modulates carcinogenic pathways. Amino Acids 35 (2008) 681-690
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Amino Acids
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, pp. 681-690
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Phang, J.M.1
Donald, S.P.2
Pandhare, J.3
Liu, Y.4
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21
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58149316420
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Epigenetic regulation in human brain-focus on histone lysine methylation
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Akbarian S., and Huang H.S. Epigenetic regulation in human brain-focus on histone lysine methylation. Biol Psychiatry 65 (2009) 198-203
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(2009)
Biol Psychiatry
, vol.65
, pp. 198-203
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Akbarian, S.1
Huang, H.S.2
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22
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37849037738
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How environmental and genetic factors combine to cause autism: a redox/methylation hypothesis
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Deth R., Muratore C., Benzecry J., Power-Charnitsky V.A., and Waly M. How environmental and genetic factors combine to cause autism: a redox/methylation hypothesis. Neurotoxicology 29 (2008) 190-201
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(2008)
Neurotoxicology
, vol.29
, pp. 190-201
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Deth, R.1
Muratore, C.2
Benzecry, J.3
Power-Charnitsky, V.A.4
Waly, M.5
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23
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33845993973
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Elevated prenatal homocysteine levels as a risk factor for schizophrenia
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Brown A.S., Bottiglieri T., Schaefer C.A., Quesenberry Jr. C.P., Liu L., Bresnahan M., and Susser E.S. Elevated prenatal homocysteine levels as a risk factor for schizophrenia. Arch Gen Psychiatry 64 (2007) 31-39
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(2007)
Arch Gen Psychiatry
, vol.64
, pp. 31-39
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Brown, A.S.1
Bottiglieri, T.2
Schaefer, C.A.3
Quesenberry Jr., C.P.4
Liu, L.5
Bresnahan, M.6
Susser, E.S.7
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24
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54249162304
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Gene-environment interaction and covariation in schizophrenia: the role of obstetric complications
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Mittal V.A., Ellman L.M., and Cannon T.D. Gene-environment interaction and covariation in schizophrenia: the role of obstetric complications. Schizophr Bull 34 (2008) 1083-1094
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(2008)
Schizophr Bull
, vol.34
, pp. 1083-1094
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Mittal, V.A.1
Ellman, L.M.2
Cannon, T.D.3
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25
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45549083182
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Prenatal nutritional deficiency and risk of adult schizophrenia
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Brown A.S., and Susser E.S. Prenatal nutritional deficiency and risk of adult schizophrenia. Schizophr Bull 34 (2008) 1054-1063
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(2008)
Schizophr Bull
, vol.34
, pp. 1054-1063
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Brown, A.S.1
Susser, E.S.2
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26
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16844374020
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Peroxisome proliferator-activated receptor gamma activation decreases neuroinflammation in brain after stress in rats
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Garcia-Bueno B., Madrigal J.L., Lizasoain I., Moro M.A., Lorenzo P., and Leza J.C. Peroxisome proliferator-activated receptor gamma activation decreases neuroinflammation in brain after stress in rats. Biol Psychiatry 57 (2005) 885-894
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(2005)
Biol Psychiatry
, vol.57
, pp. 885-894
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Garcia-Bueno, B.1
Madrigal, J.L.2
Lizasoain, I.3
Moro, M.A.4
Lorenzo, P.5
Leza, J.C.6
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27
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42449118547
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Modulation of peroxisome proliferator-activated receptor-alpha activity by N-acetyl cysteine attenuates inhibition of oligodendrocyte development in lipopolysaccharide stimulated mixed glial cultures
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Prenatal inflammation (via LPS) induces selective depletion of developing oligodendrocytes and hypomyelination via a decrease in GSH, increase in ROS, and dysfunction of peroxisomes. N-Acetylcysteine prevents LPS-induced redox dysregulation and attenuates hypomyelination via a PPAR-α-dependent mechanism.
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Paintlia M.K., Paintlia A.S., Khan M., Singh I., and Singh A.K. Modulation of peroxisome proliferator-activated receptor-alpha activity by N-acetyl cysteine attenuates inhibition of oligodendrocyte development in lipopolysaccharide stimulated mixed glial cultures. J Neurochem 105 (2008) 956-970. Prenatal inflammation (via LPS) induces selective depletion of developing oligodendrocytes and hypomyelination via a decrease in GSH, increase in ROS, and dysfunction of peroxisomes. N-Acetylcysteine prevents LPS-induced redox dysregulation and attenuates hypomyelination via a PPAR-α-dependent mechanism.
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(2008)
J Neurochem
, vol.105
, pp. 956-970
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Paintlia, M.K.1
Paintlia, A.S.2
Khan, M.3
Singh, I.4
Singh, A.K.5
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28
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41349105699
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Adult brain and behavioral pathological markers of prenatal immune challenge during early/middle and late fetal development in mice
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Meyer U., Nyffeler M., Yee B.K., Knuesel I., and Feldon J. Adult brain and behavioral pathological markers of prenatal immune challenge during early/middle and late fetal development in mice. Brain Behav Immun 22 (2008) 469-486
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(2008)
Brain Behav Immun
, vol.22
, pp. 469-486
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Meyer, U.1
Nyffeler, M.2
Yee, B.K.3
Knuesel, I.4
Feldon, J.5
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29
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33646926705
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The time of prenatal immune challenge determines the specificity of inflammation-mediated brain and behavioral pathology
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Meyer U., Nyffeler M., Engler A., Urwyler A., Schedlowski M., Knuesel I., Yee B.K., and Feldon J. The time of prenatal immune challenge determines the specificity of inflammation-mediated brain and behavioral pathology. J Neurosci 26 (2006) 4752-4762
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(2006)
J Neurosci
, vol.26
, pp. 4752-4762
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Meyer, U.1
Nyffeler, M.2
Engler, A.3
Urwyler, A.4
Schedlowski, M.5
Knuesel, I.6
Yee, B.K.7
Feldon, J.8
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30
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33947303215
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Neurodevelopmental damage after prenatal infection: role of oxidative stress in the fetal brain
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Lante F., Meunier J., Guiramand J., Maurice T., Cavalier M., de Jesus Ferreira M.C., Aimar R., Cohen-Solal C., Vignes M., and Barbanel G. Neurodevelopmental damage after prenatal infection: role of oxidative stress in the fetal brain. Free Radic Biol Med 42 (2007) 1231-1245
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Free Radic Biol Med
, vol.42
, pp. 1231-1245
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Lante, F.1
Meunier, J.2
Guiramand, J.3
Maurice, T.4
Cavalier, M.5
de Jesus Ferreira, M.C.6
Aimar, R.7
Cohen-Solal, C.8
Vignes, M.9
Barbanel, G.10
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31
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33846971625
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Chemically diverse toxicants converge on Fyn and c-Cbl to disrupt precursor cell function
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In previous study [64], the authors showed that the redox status induced by various growth factors determine the fate of oligodendrocyte precursors, with oxidizing factors favoring differentiation while reducing status promote precursor proliferation. Here they show that exposure of mercury and other pro-oxidant toxins lead to more oxidized conditions in oligodendrocyte precursors and suppress their division via the downregulation of PDGFR-α. This downregulation is due to enhanced degradation of PDGFR-α through activation of Fyn and c-CBl. The antioxidant N-acetylcysteine prevents this deleterious effect of the pro-oxidant toxins.
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Li Z., Dong T., Proschel C., and Noble M. Chemically diverse toxicants converge on Fyn and c-Cbl to disrupt precursor cell function. PLoS Biol 5 (2007) e35. In previous study [64], the authors showed that the redox status induced by various growth factors determine the fate of oligodendrocyte precursors, with oxidizing factors favoring differentiation while reducing status promote precursor proliferation. Here they show that exposure of mercury and other pro-oxidant toxins lead to more oxidized conditions in oligodendrocyte precursors and suppress their division via the downregulation of PDGFR-α. This downregulation is due to enhanced degradation of PDGFR-α through activation of Fyn and c-CBl. The antioxidant N-acetylcysteine prevents this deleterious effect of the pro-oxidant toxins.
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(2007)
PLoS Biol
, vol.5
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Li, Z.1
Dong, T.2
Proschel, C.3
Noble, M.4
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32
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33947612606
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Possible involvement of free radicals in the differential neurobehavioral responses to stress in male and female rats
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Chakraborti A., Gulati K., Banerjee B.D., and Ray A. Possible involvement of free radicals in the differential neurobehavioral responses to stress in male and female rats. Behav Brain Res 179 (2007) 321-325
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(2007)
Behav Brain Res
, vol.179
, pp. 321-325
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Chakraborti, A.1
Gulati, K.2
Banerjee, B.D.3
Ray, A.4
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33
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0033638576
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Catching up on schizophrenia: natural history and neurobiology
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Lewis D.A., and Lieberman J.A. Catching up on schizophrenia: natural history and neurobiology. Neuron 28 (2000) 325-334
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(2000)
Neuron
, vol.28
, pp. 325-334
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Lewis, D.A.1
Lieberman, J.A.2
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34
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39949083018
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A glutathione deficit alters dopamine modulation of L-type calcium channels via D2 and ryanodine receptors in neurons
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This paper describes a mechanism by which dopamine signaling can be affected in conditions of impaired GSH synthesis. In cultured cortical neurons, a GSH deficit changes the dopamine modulation of NMDA-mediated calcium responses, from enhanced responses in control neurons to decreased responses in low GSH neurons. This is due to a change in dopamine modulation of L-type calcium channels which is dependent on redox-sensitive ryanodine receptors (RyRs), whose function is enhanced in low GSH neurons. Blocking D2R receptors prevents the alteration of dopamine modulation induced by a GSH deficit. Data suggest that enhanced RyRs in low GSH neurons strengthens intracellular calcium-dependent pathways following activation of D2-type receptors and causes a decrease in function of L-type channels.
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