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Journal of Neurochemistry

Cover image for Vol. 122 Issue 2

July 2012

Volume 122, Issue 2

Pages 231–483

  1. EDITORIAL HIGHLIGHT

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. SYSTEMATIC REVIEW
    4. SHORT COMMUNICATION
    5. ORIGINAL ARTICLES
    6. CORRIGENDUM
    7. RETRACTION
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      Power tools for Alzheimer’s disease – an electrochemical preamp for Aβ (pages 231–232)

      Henrik Zetterberg and Per Hammarström

      Version of Record online: 2 JUL 2012 | DOI: 10.1111/j.1471-4159.2012.07730.x

  2. SYSTEMATIC REVIEW

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. SYSTEMATIC REVIEW
    4. SHORT COMMUNICATION
    5. ORIGINAL ARTICLES
    6. CORRIGENDUM
    7. RETRACTION
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      Evidence for the efficacy of statins in animal stroke models: a meta-analysis (pages 233–243)

      Lidia García-Bonilla, Mireia Campos, Dolors Giralt, David Salat, Pilar Chacón, Mar Hernández-Guillamon, Anna Rosell and Joan Montaner

      Version of Record online: 21 MAY 2012 | DOI: 10.1111/j.1471-4159.2012.07773.x

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      Statins for acute stroke: Pooled data from the bench gives clues for clinical trials design. Although the protective effect of statins on experimental stroke is not novel, a peer evaluation is needed to provide faithful translation into the clinics. This systematic review and meta-analysis supports the evidence of statin benefit to reduce infarct growth and improve neurological outcome in experimental stroke. Moreover, the analysis establishes the main factors influencing statin neuroprotective effect, such as type of statin, routes and timing of administration that might be used in clinical trials.

  3. SHORT COMMUNICATION

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. SYSTEMATIC REVIEW
    4. SHORT COMMUNICATION
    5. ORIGINAL ARTICLES
    6. CORRIGENDUM
    7. RETRACTION
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      Lmx1a regulates dopamine transporter gene expression during ES cell differentiation and mouse embryonic development (pages 244–250)

      Sangmi Chung, Chun-Hyung Kim and Kwang-Soo Kim

      Version of Record online: 23 MAY 2012 | DOI: 10.1111/j.1471-4159.2012.07779.x

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      Lmx1a, an early regulator of midbrain dopamine neural progenitor, is also expressed in post-mitotic dopaminergic neurons, implicating a role for dopaminergic maturation/maintenance. Here, we show that Lmx1a critically regulates the expression of a marker of mature dopamine neurons, the dopamine transporter. Thus, this study emphasizes a novel role of Lmx1a as a regulator of mature midbrain dopaminergic neurotransmitter phenotypes.

  4. ORIGINAL ARTICLES

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. SYSTEMATIC REVIEW
    4. SHORT COMMUNICATION
    5. ORIGINAL ARTICLES
    6. CORRIGENDUM
    7. RETRACTION
    1. Gene Regulation & Genetics

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      Hypoxia regulation of ATP13A2 (PARK9) gene transcription (pages 251–259)

      Qian Xu, Hongling Guo, Xiaojie Zhang, Beisha Tang, Fang Cai, Weihui Zhou and Weihong Song

      Version of Record online: 17 FEB 2012 | DOI: 10.1111/j.1471-4159.2012.07676.x

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      This study aimed to define the molecular mechanism underlying transcriptional regulation of a Parkinson disease-associated ATP13A2 gene. We cloned and functionally characterized the human ATP13A2 gene promoter, and found that hypoxia up-regulated ATP13A2 transcription via HIF-1α in HEK293 and dopaminergic MN9D cells. Our study indicates that hypoxia signaling plays a very important role in the regulation of human ATP13A2 gene expression, and further study is needed to determine the role of hypoxia in the pathogenesis of PD and its interaction with other PD causative genes.

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      The human testis-determining factor SRY localizes in midbrain dopamine neurons and regulates multiple components of catecholamine synthesis and metabolism (pages 260–271)

      Daniel P. Czech, Joohyung Lee, Helena Sim, Clare L. Parish, Eric Vilain and Vincent R. Harley

      Version of Record online: 8 JUN 2012 | DOI: 10.1111/j.1471-4159.2012.07782.x

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      Y men are different - SRY, a male gene turned on in the male brain.On the basis of our rat studies, it was important to determine if SRY, a gene only found in men, regulates dopamine in the human brain. SRY is localized in the human substantia nigra. In vitro, SRY regulates the transcription of genes encoding multiple components of the dopamine synthesis. This article provides a genetic basis for sex differences in normal and diseased catecholamine transmission.

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      Molecular mechanism of Jmjd3-mediated interleukin-6 gene regulation in endothelial cells underlying spinal cord injury (pages 272–282)

      Kwanghyun Lee, Wonho Na, Jee Youn Lee, Jungtae Na, Heejung Cho, Hongjin Wu, Tae Young Yune, Won-Sun Kim and Bong-Gun Ju

      Version of Record online: 6 JUN 2012 | DOI: 10.1111/j.1471-4159.2012.07786.x

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      Inflammatory responses contribute to secondary injury cascades following spinal cord injury. We demonstrate that histone H3K27me3 demethylase Jmjd3 is crucial for IL-6 gene activation in microvessel endothelial cells upon ischemic/reperfusion injury. This study implies that regulation of Jmjd3 expression offers a new therapeutic strategy to modulate IL-6 expression in the blood-brain barrier following spinal cord injury.

    4. Signal Transduction & Synaptic Transmission

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      Domain-dependent effects of DAT inhibition in the rat dorsal striatum (pages 283–294)

      I. Mitch Taylor, Andrea Jaquins-Gerstl, Susan R. Sesack and Adrian C. Michael

      Version of Record online: 28 MAY 2012 | DOI: 10.1111/j.1471-4159.2012.07774.x

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      DAT Inhibition by Nomifensine is Domain DependentRecent evidence demonstrates the existence of kinetic domains in the striatal DA terminal. We find that nomifensine has distinct effects on DA in the fast and slow domains. We conclude that the actions of drugs on DA are domain-dependent.

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      Bi-directional regulation of CaMKIIα phosphorylation at Thr286 by NMDA receptors in cultured cortical neurons (pages 295–307)

      Xianju Zhou, Fei Zheng, Changjong Moon, Oliver M. Schlüter and Hongbing Wang

      Version of Record online: 6 JUN 2012 | DOI: 10.1111/j.1471-4159.2012.07787.x

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      NMDAR-mediated phosphorylation of CaMKII α is involved in many aspects of neuroplasticity. By using pharmacological and molecular manipulations, we demonstrate that NR2A or NR2B bi-directionally regulates CaMKII α phosphorylation under different strength of activation. This study further supports the notion that activation of NMDAR may cause different and even opposing effects on intracellular signaling.

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      Hyperdopaminergic modulation of inhibitory transmission is dependent on GSK-3β signaling-mediated trafficking of GABAA receptors (pages 308–320)

      Yan-Chun Li, Min-Juan Wang and Wen-Jun Gao

      Version of Record online: 7 JUN 2012 | DOI: 10.1111/j.1471-4159.2012.07790.x

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      Emerging evidence has shown that D2 receptors also exert their effects through the glycogen synthase kinase 3 (GSK-3) signaling cascade, a cAMP-independent mechanism. We explored the role of GSK-3β in dopaminergic modulation of GABAA receptor-mediated inhibitory transmission in the cortical neurons. Our data suggest that GSK-3β signaling pathway is critically involved in the hyperdopamine- and D2-induced suppression of GABAA receptors in the prefrontal neurons.

    7. Neuroinflammation & Neuroimmunology

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      Intravenous immunoglobulin protects neurons against amyloid beta-peptide toxicity and ischemic stroke by attenuating multiple cell death pathways (pages 321–332)

      Alexander Widiapradja, Viktor Vegh, Ker Zhing Lok, Silvia Manzanero, John Thundyil, Mathias Gelderblom, Yi-Lin Cheng, Dale Pavlovski, Sung-Chun Tang, Dong-Gyu Jo, Tim Magnus, Sic L. Chan, Christopher G. Sobey, David Reutens, Milan Basta, Mark P. Mattson and Thiruma V. Arumugam

      Version of Record online: 27 APR 2012 | DOI: 10.1111/j.1471-4159.2012.07754.x

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      Intravenous immunoglobulin for Stroke Intravenous immunoglobulin(IVIg) is a therapeutic modality approved for the treatment of various condition. This study was performed in order to understand the mechanism ofhow IVIg elicits its neuroprotective effect in stroke and amyloid beta induced neuronal apoptosis. The findings from this study showed that IVIg elicits its neuroprotective effects by not only inhibiting the cell death pathways but also elevating the anti-apoptotic protein Bcl2. This study provides a better understanding of how IVIg plays a role in neuroprotection and therefore provides more evidence to encourage the use of IVIg as therapeutic modality in stroke and Alzheimer’s disease.

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      RGS10 exerts a neuroprotective role through the PKA/c-AMP response-element (CREB) pathway in dopaminergic neuron-like cells (pages 333–343)

      Jae-Kyung Lee, Jaegwon Chung, Kirk M. Druey and Malú G. Tansey

      Version of Record online: 30 MAY 2012 | DOI: 10.1111/j.1471-4159.2012.07780.x

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      Identifying important molecular regulators of dopaminergic (DA) neuron responses to insults is pre-requisite for development of neuroprotective strategies that could exert disease-modifying effects if advanced to the clinic. We demonstrate that over-expression of WT RGS10 in dopaminergic neuron-like cells from ventral mesencephalon renders them resistant to TNF-induced cytotoxicity through activation of protein kinase A (PKA) and the downstream phospho-cAMP response element-binding (CREB) signaling pathway. This is the first demonstration that RGS10 can exert pro-survival functions in neurons with a dopaminergic phenotype and could hence be a novel therapeutic target for the treatment of Parkinson’s disease

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      High molecular weight hyaluronan reduces lipopolysaccharide mediated microglial activation (pages 344–355)

      James W. Austin, Chris Gilchrist and Michael G. Fehlings

      Version of Record online: 1 JUN 2012 | DOI: 10.1111/j.1471-4159.2012.07789.x

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      Hyaluronan Keeps Microglia CalmToll-like receptor-4 (TLR4) mediated inflammation can damage cells following spinal cord injury (SCI). Hyaluronan (HA) was shown to reduce TLR4 mediated inflammation in cultured microglia – resident CNS immune cells, however, this was not associated with an increase in TLR4 negative regulation – previously demonstrated in macrophages. Therapeutic use of HA could possibly reduce inflammatory cell damage and improve recovery following SCI.

    10. Neuronal Plasticity & Behavior

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      Characterization of ovolin, an orally active tryptic peptide released from ovalbumin with anxiolytic-like activity (pages 356–362)

      Ayako Oda, Kentaro Kaneko, Takafumi Mizushige, Michael Lazarus, Yoshihiro Urade and Kousaku Ohinata

      Version of Record online: 30 MAY 2012 | DOI: 10.1111/j.1471-4159.2012.07777.x

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      Ovolin: discovery of anxiolytic peptide derived from eggEgg and its components are frequently used for a variety of foods, having high palatability; however, the effects on emotional behavior have been largely unknown. Here, we show that ovolin, a pentapeptide released from egg white ovalbumin by tryptic digestion, has anxiolytic activity. This is an intriguing example indicating potential interactions between the nervous system and molecules derived from foods.

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      Spermidine-induced improvement of memory involves a cross-talk between protein kinases C and A (pages 363–373)

      Gustavo P. Guerra, Carlos F. Mello, Guilherme V. Bochi, Andréia M. Pazini, Michelle M. Rosa, Juliano Ferreira and Maribel A. Rubin

      Version of Record online: 24 MAY 2012 | DOI: 10.1111/j.1471-4159.2012.07778.x

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      Spermidine improves memory by facilitating crosstalk between protein kinases C (PKC) and A (PKA)Spermidine (SPD) facilitates memory consolidation and NMDA receptor (NMDAr) functioning. This study shows that SPD sequentially activates PKC and PKA/CREB signaling in the hippocampus, probably by direct and indirect PKC-induced activation of adenylyl cyclases (AC). Indirect mechanisms may include neurogranin (Ng) phosphorylation and consequent increased calmodulin availability. Downstream mechanisms involved in memory facilitation by SPD, an endogenous polyamine, are proposed.

    12. Molecular Basis of Disease

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      Microbiosensor for Alzheimer’s disease diagnostics: detection of amyloid beta biomarkers (pages 374–381)

      Shradha Prabhulkar, Rudolph Piatyszek, John R. Cirrito, Ze-Zhi Wu and Chen-Zhong Li

      Version of Record online: 23 APR 2012 | DOI: 10.1111/j.1471-4159.2012.07709.x

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      Amyloid-β (Aβ) peptide accumulates in Alzheimer’s disease patients and is believed to precipitate disease onset. We developed an electrical immuno microsensor for highly sensitive and specific detection of different isoforms of Aβ. The label-free detection is based on quantitatively measuring redox signals of Aβ using a carbon fiber microelectrode array. Real-time detection capabilities and miniature size of sensor may allow for clinical diagnostic and potential in vivo animal study.

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      Ketone bodies protection against HIV-1 Tat-induced neurotoxicity (pages 382–391)

      Liang Hui, Xuesong Chen, Dhaval Bhatt, Nicholas H. Geiger, Thad A. Rosenberger, Norman J. Haughey, Susan A. Masino and Jonathan D. Geiger

      Version of Record online: 17 MAY 2012 | DOI: 10.1111/j.1471-4159.2012.07764.x

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      The pathogenesis of HIV-1-associated neurocognitive disorder (HAND) is unclear and effective treatments are unavailable. We found that pre-treatment of neurons with ketone bodies attenuated HIV-1 Tat-induced neuronal injury, calcium overload, and alterations in mitochondrial function and ATP levels. Ketogenic strategies might be considered a potential therapeutic intervention against HAND.

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      Bacterial lipopolysaccharide protects the retina from light-induced damage (pages 392–403)

      Melina P. Bordone, María Florencia Lanzani, Juan José López-Costa, Mónica S. Chianelli, Pablo Franco, Daniel A. Sáenz and Ruth E. Rosenstein

      Version of Record online: 23 MAY 2012 | DOI: 10.1111/j.1471-4159.2012.07767.x

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      A moderate inflammation protects the retina from light damageIntense light induces retinal degeneration. We examined whether bacterial lipopolysaccharide (LPS) protects the retina against light-induced injury. LPS affords significant morphologic and functional protection in eyes exposed to intense light. The retinal protection against light damage induced by a moderate dose of LPS could constitute a future fertile avenue for promoting the survival of retinal cells.

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      Alpha-synuclein impairs normal dynamics of mitochondria in cell and animal models of Parkinson’s disease (pages 404–414)

      Weilin Xie and Kenny K. K. Chung

      Version of Record online: 23 MAY 2012 | DOI: 10.1111/j.1471-4159.2012.07769.x

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      This study was performed to determine how alpha-synuclein can impair normal dynamics of mitochondria. Alpha-synuclein impairs normal dynamics of mitochondria through Mfn1 and Mfn2. We provide a novel mechanism of how alpha-synuclein contributes to PD through impairment of mitochondrial dynamics.

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      The neuroprotective and neurogenic effects of neuropeptide Y administration in an animal model of hippocampal neurodegeneration and temporal lobe epilepsy induced by trimethyltin (pages 415–426)

      Valentina Corvino, Elisa Marchese, Stefano Giannetti, Wanda Lattanzi, Davide Bonvissuto, Filippo Biamonte, Adriana Maria Mongiovì, Fabrizio Michetti and Maria Concetta Geloso

      Version of Record online: 21 MAY 2012 | DOI: 10.1111/j.1471-4159.2012.07770.x

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      Neuropeptide Y: neuroprotection and pro-neurogenic effects in an animal model of hippocampal neurodegeneration and temporal lobe epilepsy. With regard to the intriguing issue of neuroprotection, the study was performed to investigate the possibility to counteract neuronal death during neurodegeneration and to modulate injury induced neurogenesis, possibly directing the process towards a reparative outcome, using NPY, which is a candidate for an adjuvant role in neurodegeneration and epilepsy.The most relevant novel finding is the direct demonstration that NPY administration induces the early activation of antiapoptotic pathways and neurogenic genes.This study adds useful information concerning the role of in vivo NPY administration on mechanisms that counteract neurodegenerative processes, such as cellular events leading to neuroprotection and the stimulation of endogenous neurogenesis.

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      Dietary intake of unsaturated fatty acids modulates physiological properties of entorhinal cortex neurons in mice (pages 427–443)

      Dany Arsenault, Carl Julien, Chuck T. Chen, Richard P. Bazinet and Frédéric Calon

      Version of Record online: 23 MAY 2012 | DOI: 10.1111/j.1471-4159.2012.07772.x

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      High-MUFA intake increased oleic acid (OLA) and decreased arachidonic acid (ARA) in phospholipids of myelinated axons in the brain white matter. Such diet-induced changes were associated with narrower action potentials and shorter postsynaptic responses in pyramidal neurons from the entorhinal cortex, which could have profound impact on brain function.

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      Distinct molecular mechanisms of acquired resistance to temozolomide in glioblastoma cells (pages 444–455)

      Caroline Happold, Patrick Roth, Wolfgang Wick, Natalie Schmidt, Ana-Maria Florea, Manuela Silginer, Guido Reifenberger and Michael Weller

      Version of Record online: 28 MAY 2012 | DOI: 10.1111/j.1471-4159.2012.07781.x

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      Identification of molecular mechanisms leading to temozolomide resistanceAcquired resistance to temozolomide is an important challenge in the setting of therapy failure in glioblastoma patients. Here, we identify distinct mechanisms by which glioma cells become resistant to the anti-tumor effects of temozolomide. These findings highlight the importance of different therapy-induced molecular changes, which might be exploited for novel therapeutic approaches in the future.

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      Abcg2 deficiency augments oxidative stress and cognitive deficits in Tg-SwDI transgenic mice (pages 456–469)

      Yu Zeng, Debbie Callaghan, Huaqi Xiong, Ze Yang, Peilin Huang and Wandong Zhang

      Version of Record online: 6 JUN 2012 | DOI: 10.1111/j.1471-4159.2012.07783.x

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      ABCG2 is a transmembrane protein and up-regulated in Alzheimer’s brain with cerebral amyloid angiopathy. In vitro studies show that ABCG2 is involved in transport of intracellular reduced GSH to extracellular space and in response to oxidative stress. This study shows that Abcg2 deficiency increases oxidative stress, alters inflammatory response and exacerbates cognitive/memory deficit in Tg-SwDI mice at different developmental stages.

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      Preconditioning induces tolerance by suppressing glutamate release in neuron culture ischemia models (pages 470–481)

      Joseph S. Tauskela, Amy Aylsworth, Melissa Hewitt, Eric Brunette and Geoffrey A. R. Mealing

      Version of Record online: 1 JUN 2012 | DOI: 10.1111/j.1471-4159.2012.07791.x

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      A pre-synaptic based mechanism of neuroprotection by preconditioningThe purpose of this study was to determine how preconditioned neurons respond to oxygen-glucose deprivation (OGD) to result in neuroprotection instead of neurotoxicity. Tolerance to OGD, as well as to OGD-mimics (pharmacological insults intended to mimic key neurotoxic stages of OGD) converged to a single mechanistic locus: suppression of cellular glutamate release which, in turn, resulted in delayed up-regulated activity of glutamate transporters during OGD. This novel pre-synaptic based mechanism of neuroprotection by preconditioning may have clinical implications if the exact nature of this target can be identified.

  5. CORRIGENDUM

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. SYSTEMATIC REVIEW
    4. SHORT COMMUNICATION
    5. ORIGINAL ARTICLES
    6. CORRIGENDUM
    7. RETRACTION
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      Corrigendum (page 482)

      Version of Record online: 1 JUN 2012 | DOI: 10.1111/j.1471-4159.2012.07802.x

      This article corrects:
  6. RETRACTION

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. SYSTEMATIC REVIEW
    4. SHORT COMMUNICATION
    5. ORIGINAL ARTICLES
    6. CORRIGENDUM
    7. RETRACTION
    1. You have free access to this content
      Retraction (page 483)

      Version of Record online: 6 JUN 2012 | DOI: 10.1111/j.1471-4159.2012.07803.x

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