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153. JC virus conversion rates in natalizumab treated patients: the melbourne longitudinal cohort study

Author

Dwyer, Chris, primary, Jokubaitis, Vilija, additional, Baker, Josephine, additional, Haartsen, Jodi, additional, Rath, Louise, additional, Coleman, Jennifer, additional, Fryer, Kylie, additional, Macintyre, Jennifer, additional, Cartwright, Adriana, additional, Skibina, Olga, additional, Macdonell, Richard, additional, Butler, Ernest, additional, Shuey, Neil, additional, Butzkueven, Helmut, additional, Kilpatrick, Trevor, additional, and Walt, Anneke van der, additional

Published
2017
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154. A Brain-Derived Neurotrophic Factor-Based p75NTRPeptide Mimetic Ameliorates Experimental Autoimmune Neuritis Induced Axonal Pathology and Demyelination

Author

Gonsalvez, David G., primary, Tran, Giang, additional, Fletcher, Jessica L., additional, Hughes, Richard A., additional, Hodgkinson, Suzanne, additional, Wood, Rhiannon J., additional, Yoo, Sang Won, additional, De Silva, Mithraka, additional, Agnes, Wong W., additional, McLean, Catriona, additional, Kennedy, Paul, additional, Kilpatrick, Trevor J., additional, Murray, Simon S., additional, and Xiao, Junhua, additional

Published
2017
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158. Galanin is an autocrine myelin and oligodendrocyte trophic signal induced by leukemia inhibitory factor

Author

Gresle, Melissa M, Butzkueven, Helmut, Perreau, Victoria M, Jonas, Anna, Xiao, Junhua, Thiem, Stefan, Holmes, Fiona E, Doherty, William, Soo, Pik-Ying, Binder, Michele D, Akkermann, Rainer, Jokubaitis, Vilija G, Cate, Holly S, Marriott, Mark P, Gundlach, Andrew L, Wynick, David, and Kilpatrick, Trevor J

Subjects
endocrine system, galanin, nervous system, digestive, oral, and skin physiology, oligodendrocytes, hormones, hormone substitutes, and hormone antagonists, leukemia inhibitory factor
Abstract

In order to further investigate the molecular mechanisms that regulate oligodendrocyte (OC) survival, we utilized microarrays to characterize changes in OC gene expression after exposure to the cytokines neurotrophin3, insulin, or leukemia inhibitory factor (LIF) in vitro. We identified and validated the induction and secretion of the neuropeptide galanin in OCs, specifically in response to LIF. We next established that galanin is an OC survival factor and showed that autocrine or paracrine galanin secretion mediates LIF-induced OC survival in vitro. We also revealed that galanin is up-regulated in OCs in the cuprizone model of central demyelination, and that oligodendroglial galanin expression is significantly regulated by endogenous LIF in this context. We also showed that knock-out of galanin reduces OC survival and exacerbates callosal demyelination in the cuprizone model. These findings suggest a potential role for the use of galanin agonists in the treatment of human demyelinating diseases.

Published
2015

159. Higher Non-processed Red Meat Consumption Is Associated With a Reduced Risk of Central Nervous System Demyelination.

Author

Black, Lucinda J., Bowe, Gabrielle S., Pereira, Gavin, Lucas, Robyn M., Dear, Keith, van der Mei, Ingrid, Sherriff, Jill L., Chapman, Caron, Coulthard, Alan, Dwyer, Terry, Kilpatrick, Trevor, Lucas, Robyn, McMichael (dec), Tony, Pender, Michael P, Ponsonby, Anne-Louise, Taylor, Bruce, Valery, Patricia, and Williams, David

Subjects
MEAT industry, DEMYELINATION, MULTIPLE sclerosis, MULTIPLE sclerosis diagnosis, LOGISTIC regression analysis, EICOSAPENTAENOIC acid
Abstract

The evidence associating red meat consumption and risk of multiple sclerosis is inconclusive. We tested associations between red meat consumption and risk of a first clinical diagnosis of central nervous system demyelination (FCD), often presaging a diagnosis of multiple sclerosis. We used food frequency questionnaire data from the 2003–2006 Ausimmune Study, an incident, matched, case-control study examining environmental risk factors for FCD. We calculated non-processed and processed red meat density (g/1,000 kcal/day). Conditional logistic regression models (with participants matched on age, sex, and study region) were used to estimate odds ratios (ORs), 95% confidence intervals (95% CI) and p- values for associations between non-processed (n = 689, 250 cases, 439 controls) and processed (n = 683, 248 cases, 435 controls) red meat density and risk of FCD. Models were adjusted for history of infectious mononucleosis, serum 25-hydroxyvitamin D concentrations, smoking, race, education, body mass index and dietary misreporting. A one standard deviation increase in non-processed red meat density (22 g/1,000 kcal/day) was associated with a 19% reduced risk of FCD (AOR = 0.81; 95%CI 0.68, 0.97; p = 0.02). When stratified by sex, higher non-processed red meat density (per 22 g/1,000 kcal/day) was associated with a 26% reduced risk of FCD in females (n = 519; AOR = 0.74; 95%CI 0.60, 0.92; p = 0.01). There was no statistically significant association between non-processed red meat density and risk of FCD in males (n = 170). We found no statistically significant association between processed red meat density and risk of FCD. Further investigation is warranted to understand the important components of a diet that includes non-processed red meat for lower FCD risk. [ABSTRACT FROM AUTHOR]

Published
2019
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160. Common and Low Frequency Variants in MERTK Are Independently Associated with Multiple Sclerosis Susceptibility with Discordant Association Dependent upon HLA-DRB1*15:01 Status

Author

Binder, Michele D., Fox, Andrew D., Merlo, Daniel, Johnson, Laura J., Giuffrida, Lauren, Calvert, Sarah E., Akkermann, Rainer, Ma, Gerry Z.M., Perera, Ashwyn A., Gresle, Melissa M., Laverick, Louise, Foo, Grace, Fabis-Pedrini, Marzena J., Spelman, Timothy, Jordan, Margaret A., Baxter, Alan G., Foote, Simon, Butzkueven, Helmut, Kilpatrick, Trevor J., Field, Judith, Kermode, Allan G., Taylor, Bruce, Booth, David R., Mason, Deborah, Stewart, Graeme J., Charlesworth, Jac, Wiley, James, Lechner-Scott, Jeannette, Tajouri, Lotti, Griffiths, Lyn, Slee, Mark, Brown, Matthew A., Moscato, Pablo, Scott, Rodney J., Broadley, Simon, Vucic, Steve, MCarroll, William, other, and, Binder, Michele D., Fox, Andrew D., Merlo, Daniel, Johnson, Laura J., Giuffrida, Lauren, Calvert, Sarah E., Akkermann, Rainer, Ma, Gerry Z.M., Perera, Ashwyn A., Gresle, Melissa M., Laverick, Louise, Foo, Grace, Fabis-Pedrini, Marzena J., Spelman, Timothy, Jordan, Margaret A., Baxter, Alan G., Foote, Simon, Butzkueven, Helmut, Kilpatrick, Trevor J., Field, Judith, Kermode, Allan G., Taylor, Bruce, Booth, David R., Mason, Deborah, Stewart, Graeme J., Charlesworth, Jac, Wiley, James, Lechner-Scott, Jeannette, Tajouri, Lotti, Griffiths, Lyn, Slee, Mark, Brown, Matthew A., Moscato, Pablo, Scott, Rodney J., Broadley, Simon, Vucic, Steve, MCarroll, William, and other, and

Abstract

Multiple Sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system. The risk of developing MS is strongly influenced by genetic predisposition, and over 100 loci have been established as associated with susceptibility. However, the biologically relevant variants underlying disease risk have not been defined for the vast majority of these loci, limiting the power of these genetic studies to define new avenues of research for the development of MS therapeutics. It is therefore crucial that candidate MS susceptibility loci are carefully investigated to identify the biological mechanism linking genetic polymorphism at a given gene to the increased chance of developing MS. MERTK has been established as an MS susceptibility gene and is part of a family of receptor tyrosine kinases known to be involved in the pathogenesis of demyelinating disease. In this study we have refined the association of MERTK with MS risk to independent signals from both common and low frequency variants. One of the associated variants was also found to be linked with increased expression of MERTK in monocytes and higher expression of MERTK was associated with either increased or decreased risk of developing MS, dependent upon HLA-DRB1*15:01 status. This discordant association potentially extended beyond MS susceptibility to alterations in disease course in established MS. This study provides clear evidence that distinct polymorphisms within MERTK are associated with MS susceptibility, one of which has the potential to alter MERTK transcription, which in turn can alter both susceptibility and disease course in MS patients.

Published
2016

163. Blocking LINGO-1 in vivo reduces degeneration and enhances regeneration of the optic nerve

Author

Gresle, Melissa M, primary, Liu, Yaou, additional, Kilpatrick, Trevor J, additional, Kemper, Dennis, additional, Wu, Qi-Zhu, additional, Hu, Bing, additional, Fu, Qing-Ling, additional, So, Kwok-Fai, additional, Sheng, Guoqing, additional, Huang, Guanrong, additional, Pepinsky, Blake, additional, Butzkueven, Helmut, additional, and Mi, Sha, additional

Published
2016
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164. A rare P2X7 variant Arg307Gln with absent pore formation function protects against neuroinflammation in multiple sclerosis

Author

Gu, Ben, Field, Judith, Dutertre, Sebastien, Ou, Amber, Kilpatrick, Trevor, Lechner-Scott, Jeannette, Scott, Rodney, Lea, Rodney, Taylor, Bruce, Stankovich, Jim, other, and, Gu, Ben, Field, Judith, Dutertre, Sebastien, Ou, Amber, Kilpatrick, Trevor, Lechner-Scott, Jeannette, Scott, Rodney, Lea, Rodney, Taylor, Bruce, Stankovich, Jim, and other, and

Abstract

Multiple sclerosis (MS) is a chronic relapsing-remitting inflammatory disease of the central nervous system characterized by oligodendrocyte damage, demyelination and neuronal death. Genetic association studies have shown a 2-fold or greater prevalence of the HLA-DRB1*1501 allele in the MS population compared with normal Caucasians. In discovery cohorts of Australasian patients with MS (total 2941 patients and 3008 controls), we examined the associations of 12 functional polymorphisms of P2X7, a microglial/macrophage receptor with proinflammatory effects when activated by extracellular adenosine triphosphate (ATP). In discovery cohorts, rs28360457, coding for Arg307Gln was associated with MS and combined analysis showed a 2-fold lower minor allele frequency compared with controls (1.11% for MS and 2.15% for controls, P = 0.0000071). Replication analysis of four independent European MS case–control cohorts (total 2140 cases and 2634 controls) confirmed this association [odds ratio (OR) = 0.69, P = 0.026]. A meta-analysis of all Australasian and European cohorts indicated that Arg307Gln confers a 1.8-fold protective effect on MS risk (OR = 0.57, P = 0.0000024). Fresh human monocytes heterozygous for Arg307Gln have >85% loss of ‘pore’ function of the P2X7 receptor measured by ATP-induced ethidium uptake. Analysis shows Arg307Gln always occurred with 270His suggesting a single 307Gln–270His haplotype that confers dominant negative effects on P2X7 function and protection against MS. Modeling based on the homologous zP2X4 receptor showed Arg307 is located in a region rich in basic residues located only 12 Å from the ligand binding site. Our data show the protective effect against MS of a rare genetic variant of P2RX7 with heterozygotes showing near absent proinflammatory ‘pore’ function.

Published
2015

165. A new era in the treatment of multiple sclerosis

Author

Broadley, Simon A., Barnett, Michael H., Boggild, Mike, Brew, Bruce J., Butzkueven, Helmut, Heard, Robert, Hodgkinson, Suzanne, Kermode, Allan G., Lechner-Scott, Jeanette, Macdonell, Richard A., Marriott, Mark, Mason, Deborah F., Parratt, John, Reddel, Stephen W., Shaw, Cameron P., Slee, Mark, Spies, Judith M., Taylor, Bruce V., Carroll, William M., Kilpatrick, Trevor J., King, John, McCombe, Pamela A., Pollard, John D., Willoughby, Ernest, Broadley, Simon A., Barnett, Michael H., Boggild, Mike, Brew, Bruce J., Butzkueven, Helmut, Heard, Robert, Hodgkinson, Suzanne, Kermode, Allan G., Lechner-Scott, Jeanette, Macdonell, Richard A., Marriott, Mark, Mason, Deborah F., Parratt, John, Reddel, Stephen W., Shaw, Cameron P., Slee, Mark, Spies, Judith M., Taylor, Bruce V., Carroll, William M., Kilpatrick, Trevor J., King, John, McCombe, Pamela A., Pollard, John D., and Willoughby, Ernest

Abstract

Multiple sclerosis (MS) is an autoimmune disease of the central nervous system with a multifactorial aetiology and highly variable natural history. A growing understanding of the immunopathogenesis of the condition has led to an expanding array of therapies for this previously untreatable disease. While a cure for MS remains elusive, the potential to reduce inflammatory disease activity by preventing relapses and minimising disease progression is achievable. The importance of early treatment in minimising long-term disability is increasingly recognised. Most of the newer, more effective therapies are associated with risks and practical problems that necessitate an active management strategy and continuous vigilance. While the initiation of these therapies is likely to remain the responsibility of neurologists, other specialist physicians and general practitioners will be involved in the identification and management of adverse effects.

Published
2015

166. The MS risk allele of CD40 is associated with reduced cell-membrane bound expression in antigen presenting cells: Implications for gene function

Author

Field, Judith, Shahijanian, Fernando, Schibeci, Stephen, Johnson, Laura, Gresle, Melissa, Laverick, Louise, Parnell, Grant, Stewart, Graeme, McKay, Fiona, Kilpatrick, Trevor, Butzkueven, Helmut, Booth, David, Brown, Matthew, other, and, Field, Judith, Shahijanian, Fernando, Schibeci, Stephen, Johnson, Laura, Gresle, Melissa, Laverick, Louise, Parnell, Grant, Stewart, Graeme, McKay, Fiona, Kilpatrick, Trevor, Butzkueven, Helmut, Booth, David, Brown, Matthew, and other, and

Abstract

Human genetic and animal studies have implicated the costimulatory molecule CD40 in the development of multiple sclerosis (MS). We investigated the cell specific gene and protein expression variation controlled by the CD40 genetic variant(s) associated with MS, i.e. the T-allele at rs1883832. Previously we had shown that the risk allele is expressed at a lower level in whole blood, especially in people with MS. Here, we have defined the immune cell subsets responsible for genotype and disease effects on CD40 expression at the mRNA and protein level. In cell subsets in which CD40 is most highly expressed, B lymphocytes and dendritic cells, the MS-associated risk variant is associated with reduced CD40 cell-surface protein expression. In monocytes and dendritic cells, the risk allele additionally reduces the ratio of expression of full-length versus truncated CD40 mRNA, the latter encoding secreted CD40. We additionally show that MS patients, regardless of genotype, express significantly lower levels of CD40 cell-surface protein compared to unaffected controls in B lymphocytes. Thus, both genotype-dependent and independent down-regulation of cell-surface CD40 is a feature of MS. Lower expression of a co-stimulator of T cell activation, CD40, is therefore associated with increased MS risk despite the same CD40 variant being associated with reduced risk of other inflammatory autoimmune diseases. Our results highlight the complexity and likely individuality of autoimmune pathogenesis, and could be consistent with antiviral and/or immunoregulatory functions of CD40 playing an important role in protection from MS.

Published
2015

167. Analytical bias in the measurement of serum 25-hydroxyVitamin D concentrations impairs assessment of Vitamin D status in clinical and research settings

Author

Black, Lucinda, Anderson, Denise, Clarke, Michael, Ponsonby, Anne-Louise, Chapman, C, Coulthard, Alan, Dear, Keith, Dwyer, Terry, Kilpatrick, Trevor J, Lucas, Robyn, Black, Lucinda, Anderson, Denise, Clarke, Michael, Ponsonby, Anne-Louise, Chapman, C, Coulthard, Alan, Dear, Keith, Dwyer, Terry, Kilpatrick, Trevor J, and Lucas, Robyn

Abstract

Measured serum 25-hydroxyvitamin D concentrations vary depending on the type of assay used and the specific laboratory undertaking the analysis, impairing the accurate assessment of vitamin D status. We investigated differences in serum 25-hydroxyvitamin D concentrations measured at three laboratories (laboratories A and B using an assay based on liquid chroma-tography-tandem mass spectrometry and laboratory C using a DiaSorin Liaison assay), against a laboratory using an assay based on liquid chromatography-tandem mass spectrome-try that is certified to the standard reference method developed by the National Institute of Standards and Technology and Ghent University (referred to as the 'certified laboratory'). Separate aliquots from the same original serum sample for a subset of 50 participants from the Ausim-mune Study were analysed at the four laboratories. Bland-Altman plots were used to visually check agreement between each laboratory against the certified laboratory. Compared with the certified laboratory, serum 25-hydroxyvitamin D concentrations were on average 12.4 nmol/L higher at laboratory A (95% limits of agreement: -17.8,42.6); 12.8 nmol/L higher at laboratory B (95% limits of agreement: 0.8,24.8); and 10.6 nmol/L lower at laboratory C (95% limits of agreement: -484,27.1). The prevalence of vitamin D deficiency (defined here as 25-hydroxyvitamin D <50 nmol/L) was 24%, 16%, 12% and 41% at the certified laboratory, and laboratories A, B, and C, respectively. Our results demonstrate considerable differences in the measurement of 25-hydroxyvitamin D concentrations compared with a certified laboratory, even between laboratories using assays based on liquid chromatography-tandem mass spectrometry, which is often considered the gold-standard assay. To ensure accurate and reliable measurement of serum 25-hydroxyvitamin D concentrations, all laboratories should use an accuracy-based quality assurance system and, ideally, comply with international standardisation

Published
2015

168. Inhibitory saccadic dysfunction is associated with cerebellar injury in multiple sclerosis

Author

Kolbe, Scott C., Kilpatrick, Trevor J., Mitchell, Peter J., White, Owen, Egan, Gary F., and Fielding, Joanne

Subjects
Adult, Male, Brain Mapping, Multiple Sclerosis, Middle Aged, Neuropsychological Tests, Disability Evaluation, Diffusion Magnetic Resonance Imaging, Ocular Motility Disorders, Brain Injuries, Cerebellum, Image Processing, Computer-Assisted, Humans, Female, Cognition Disorders, Research Articles
Abstract

Cognitive dysfunction is common in patients with multiple sclerosis (MS). Saccadic eye movement paradigms such as antisaccades (AS) can sensitively interrogate cognitive function, in particular, the executive and attentional processes of response selection and inhibition. Although we have previously demonstrated significant deficits in the generation of AS in MS patients, the neuropathological changes underlying these deficits were not elucidated. In this study, 24 patients with relapsing–remitting MS underwent testing using an AS paradigm. Rank correlation and multiple regression analyses were subsequently used to determine whether AS errors in these patients were associated with: (i) neurological and radiological abnormalities, as measured by standard clinical techniques, (ii) cognitive dysfunction, and (iii) regionally specific cerebral white and gray‐matter damage. Although AS error rates in MS patients did not correlate with clinical disability (using the Expanded Disability Status Score), T2 lesion load or brain parenchymal fraction, AS error rate did correlate with performance on the Paced Auditory Serial Addition Task and the Symbol Digit Modalities Test, neuropsychological tests commonly used in MS. Further, voxel‐wise regression analyses revealed associations between AS errors and reduced fractional anisotropy throughout most of the cerebellum, and increased mean diffusivity in the cerebellar vermis. Region‐wise regression analyses confirmed that AS errors also correlated with gray‐matter atrophy in the cerebellum right VI subregion. These results support the use of the AS paradigm as a marker for cognitive dysfunction in MS and implicate structural and microstructural changes to the cerebellum as a contributing mechanism for AS deficits in these patients. Hum Brain Mapp 35:2310–2319, 2014. © 2013 Wiley Periodicals, Inc.

Published
2013

169. Reported Changes in Dietary Behavior Following a First Clinical Diagnosis of Central Nervous System Demyelination.

Author

Russell, Rebecca D., Lucas, Robyn M., Brennan, Vanessa, Sherriff, Jill L., Begley, Andrea, Black, Lucinda J., Chapman, Caron, Coulthard, Alan, Dear, Keith, Dwyer, Terry, Kilpatrick, Trevor, Lucas, Robyn, McMichael (dec), Tony, Pender, Michael P., Ponsonby, Anne-Louise, Taylor, Bruce, Valery, Patricia, van der Mei, Ingrid, and Williams, David

Subjects
DIET, MULTIPLE sclerosis, NUTRITION
Abstract

Background/objectives: Although the current evidence is insufficient to recommend a special diet for people with multiple sclerosis (MS), dietary advice for people with MS is prolific online and in the media. This study aimed to describe dietary changes made in the year following a first clinical diagnosis of central nervous system demyelination (FCD), a common precursor to MS. subjects/methods: We used follow-up data from the Ausimmune Study, a multicentre matched case-control study examining the environmental risk factors for a FCD. A total of 244 cases (60 male, 184 female) completed a 1-year follow-up interview, which included a question about dietary changes. We described the number and proportion (%) of participants who reported making dietary changes and the type of change made. We investigated independent predictors of making a dietary change using a multivariable logistic regression model. results: A total of 38% (n = 92) of participants at the 1-year follow-up reported making at least one dietary change over the last year. There were no statistically significant independent associations between any participant characteristic and odds of making a dietary change. Of those who made at least one dietary change, the most common changes were increasing fruit and/or vegetable intake (27%, n = 25) and following a low-fat diet (25%, n = 23). conclusion: A considerable proportion of the study population reported making at least one dietary change in the year following a FCD, with the majority of changes being toward a healthier diet. Further research is warranted to investigate the reasons behind any dietary changes adopted by people with a FCD or with MS, and whether making a dietary change has benefits for the progression of demyelinating diseases, e.g., to a diagnosis of MS, as well as for general health and well-being. [ABSTRACT FROM AUTHOR]

Published
2018
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171. A new era in the treatment of multiple sclerosis

Author

Broadley, Simon A, primary, Barnett, Michael H, additional, Boggild, Mike, additional, Brew, Bruce J, additional, Butzkueven, Helmut, additional, Heard, Robert, additional, Hodgkinson, Suzanne, additional, Kermode, Allan G, additional, Lechner‐Scott, Jeannette, additional, Macdonell, Richard AL, additional, Marriott, Mark, additional, Mason, Deborah F, additional, Parratt, John, additional, Reddel, Stephen W, additional, Shaw, Cameron P, additional, Slee, Mark, additional, Spies, Judith M, additional, Taylor, Bruce V, additional, Carroll, William M, additional, Kilpatrick, Trevor J, additional, King, John, additional, McCombe, Pamela A, additional, Pollard, John D, additional, and Willoughby, Ernest, additional

Published
2015
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174. Stressful life events and the risk of initial central nervous system demyelination.

Author

Saul, Alice, Ponsonby, Anne-Louise, Lucas, Robyn M., Taylor, Bruce V., Simpson, Steve, Valery, Patricia, Dwyer, Terence, Kilpatrick, Trevor J., Pender, Michael P., and van der Mei, Ingrid A. F.

Subjects
LIFE change events, DEMYELINATION, CENTRAL nervous system diseases, MULTIPLE sclerosis, AUTOIMMUNE diseases
Abstract

Background: There is substantial evidence that stress increases multiple sclerosis disease activity, but limited evidence on its association with the onset of multiple sclerosis. Objective: To examine the association between stressful life events and risk of first demyelinating event (FDE). Methods: This was a multicentre incident case–control study. Cases (n = 282 with first diagnosis of central nervous system (CNS) demyelination, including n = 216 with ‘classic FDE’) were aged 18–59 years. Controls without CNS demyelination (n = 558) were matched to cases on age, sex and study region. Stressful life events were assessed using a questionnaire based on the Social Readjustment Rating Scale. Results: Those who suffered from a serious illness in the previous 12 months were more likely to have an FDE (odds ratio (OR) = 2.35 (1.36, 4.06), p = 0.002), and when we limited our reference group to those who had no stressful life events, the magnitude of effect became stronger (OR = 5.41 (1.80, 16.28)). The total stress number and stress load were not convincingly associated with the risk of an FDE. Conclusion: Cases were more likely to report a serious illness in the previous 12 months, which could suggest that a non-specific illness provides an additional strain to an already predisposed immune system. [ABSTRACT FROM AUTHOR]

Published
2017
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178. Ceruloplasmin gene-deficient mice with experimental autoimmune encephalomyelitis show attenuated early disease evolution

Author

Gresle, Melissa M., primary, Schulz, Katrin, additional, Jonas, Anna, additional, Perreau, Victoria M., additional, Cipriani, Tania, additional, Baxter, Alan G., additional, Miranda-Hernandez, Socorro, additional, Field, Judith, additional, Jokubaitis, Vilija G., additional, Cherny, Robert, additional, Volitakis, Irene, additional, David, Samuel, additional, Kilpatrick, Trevor J., additional, and Butzkueven, Helmut, additional

Published
2014
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179. Occupational Exposure and Risk of Central Nervous System Demyelination

Author

Valery, Patricia C., Lucas, Robyn M., Williams, David B., Pender, Michael P., Chapman, Caron, Coulthard, Alan, Dear, Keith, Dwyer, Terence, Kilpatrick, Trevor. J., McMichael, Anthony J., van, der Mei, Ingrid, Taylor, Bruce, Ponsonby, Anne-Louise, Valery, Patricia C., Lucas, Robyn M., Williams, David B., Pender, Michael P., Chapman, Caron, Coulthard, Alan, Dear, Keith, Dwyer, Terence, Kilpatrick, Trevor. J., McMichael, Anthony J., van, der Mei, Ingrid, Taylor, Bruce, and Ponsonby, Anne-Louise

Published
2013

180. Vitamin D status: Multifactorial contribution of environment, genes and other factors in healthy Australian adults across a latitude gradient

Author

Lucas, Robyn M., Ponsonby, Anne-Louise, Dear, Keith, Valery, Patricia C., Taylor, Bruce, van der Mei, Ingrid, McMichael, Anthony J., Pender, Michael P., Chapman, Caron, Coulthard, Alan, Kilpatrick, Trevor J., Stankovich, Jim, Williams, David B., Dwyer, Terence, Lucas, Robyn M., Ponsonby, Anne-Louise, Dear, Keith, Valery, Patricia C., Taylor, Bruce, van der Mei, Ingrid, McMichael, Anthony J., Pender, Michael P., Chapman, Caron, Coulthard, Alan, Kilpatrick, Trevor J., Stankovich, Jim, Williams, David B., and Dwyer, Terence

Published
2013

181. Analysis of immune-related loci identifies 48 new susceptibility variants for multiple sclerosis

Author

Beecham, Ashley H., Patsopoulos, Nikolaos A., Xifara, Dionysia K., Davis, Mary F., Kemppinen, Anu, Cotsapas, Chris, Shah, Tejas S., Spencer, Chris, Booth, David, Goris, An, Oturai, Annette, Saarela, Janna, Fontaine, Bertrand, Hemmer, Bernhard, Martin, Claes, Zipp, Frauke, DAlfonso, Sandra, Martinelli-Boneschi, Filippo, Taylor, Bruce, Harbo, Hanne F., Kockum, Ingrid, Hillert, Jan, Olsson, Tomas, Ban, Maria, Oksenberg, Jorge R., Hintzen, Rogier, F Barcellos, Lisa, Agliardi, Cristina, Alfredsson, Lars, Alizadeh, Mehdi, Anderson, Carl, Andrews, Robert, Bach Sondergaard, Helle, Baker, Amie, Band, Gavin, Baranzini, Sergio E., Barizzone, Nadia, Barrett, Jeffrey, Bellenguez, Celine, Bergamaschi, Laura, Bernardinelli, Luisa, Berthele, Achim, Biberacher, Viola, Binder, Thomas M C., Blackburn, Hannah, Bomfim, Izaura L., Brambilla, Paola, Broadley, Simon, Brochet, Bruno, Brundin, Lou, Buck, Dorothea, Butzkueven, Helmut, Caillier, Stacy J., Camu, William, Carpentier, Wassila, Cavalla, Paola, Celius, Elisabeth G., Coman, Irene, Comi, Giancarlo, Corrado, Lucia, Cosemans, Leentje, Cournu-Rebeix, Isabelle, Cree, Bruce A C., Cusi, Daniele, Damotte, Vincent, Defer, Gilles, Delgado, Silvia R., Deloukas, Panos, di Sapio, Alessia, Dilthey, Alexander T., Donnelly, Peter, Dubois, Benedicte, Duddy, Martin, Edkins, Sarah, Elovaara, Irina, Esposito, Federica, Evangelou, Nikos, Fiddes, Barnaby, Field, Judith, Franke, Andre, Freeman, Colin, Frohlich, Irene Y., Galimberti, Daniela, Gieger, Christian, Gourraud, Pierre-Antoine, Graetz, Christiane, Graham, Andrew, Grummel, Verena, Guaschino, Clara, Hadjixenofontos, Athena, Hakonarson, Hakon, Halfpenny, Christopher, Hall, Gillian, Hall, Per, Hamsten, Anders, Harley, James, Harrower, Timothy, Hawkins, Clive, Hellenthal, Garrett, Hillier, Charles, Hobart, Jeremy, Hoshi, Muni, Hunt, Sarah E., Jagodic, Maja, Jelcic, Ilijas, Jochim, Angela, Kendall, Brian, Kermode, Allan, Kilpatrick, Trevor, Koivisto, Keijo, Konidari, Ioanna, Korn, Thomas, Kronsbein, Helena, Langford, Cordelia, Larsson, Malin, Lathrop, Mark, Lebrun-Frenay, Christine, Lechner-Scott, Jeannette, Lee, Michelle H., Leone, Maurizio A., Leppa, Virpi, Liberatore, Giuseppe, Lie, Benedicte A., Lill, Christina M., Linden, Magdalena, Link, Jenny, Luessi, Felix, Lycke, Jan, Macciardi, Fabio, Mannisto, Satu, Manrique, Clara P., Martin, Roland, Martinelli, Vittorio, Mason, Deborah, Mazibrada, Gordon, McCabe, Cristin, Mero, Inger-Lise, Mescheriakova, Julia, Moutsianas, Loukas, Myhr, Kjell-Morten, Nagels, Guy, Nicholas, Richard, Nilsson, Petra, Piehl, Fredrik, Pirinen, Matti, Price, Sian E., Quach, Hong, Reunanen, Mauri, Robberecht, Wim, Robertson, Neil P., Rodegher, Mariaemma, Rog, David, Salvetti, Marco, Schnetz-Boutaud, Nathalie C., Sellebjerg, Finn, Selter, Rebecca C., Schaefer, Catherine, Shaunak, Sandip, Shen, Ling, Shields, Simon, Siffrin, Volker, Slee, Mark, Soelberg Sorensen, Per, Sorosina, Melissa, Sospedra, Mireia, Spurkland, Anne, Strange, Amy, Sundqvist, Emilie, Thijs, Vincent, Thorpe, John, Ticca, Anna, Tienari, Pentti, van Duijn, Cornelia, Visser, Elizabeth M., Vucic, Steve, Westerlind, Helga, Wiley, James S., Wilkins, Alastair, Wilson, James F., Winkelmann, Juliane, Zajicek, John, Zindler, Eva, Haines, Jonathan L., Pericak-Vance, Margaret A., Ivinson, Adrian J., Stewart, Graeme, Hafler, David, Hauser, Stephen L., Compston, Alastair, McVean, Gil, De Jager, Philip, Sawcer, Stephen J., McCauley, Jacob L., Beecham, Ashley H., Patsopoulos, Nikolaos A., Xifara, Dionysia K., Davis, Mary F., Kemppinen, Anu, Cotsapas, Chris, Shah, Tejas S., Spencer, Chris, Booth, David, Goris, An, Oturai, Annette, Saarela, Janna, Fontaine, Bertrand, Hemmer, Bernhard, Martin, Claes, Zipp, Frauke, DAlfonso, Sandra, Martinelli-Boneschi, Filippo, Taylor, Bruce, Harbo, Hanne F., Kockum, Ingrid, Hillert, Jan, Olsson, Tomas, Ban, Maria, Oksenberg, Jorge R., Hintzen, Rogier, F Barcellos, Lisa, Agliardi, Cristina, Alfredsson, Lars, Alizadeh, Mehdi, Anderson, Carl, Andrews, Robert, Bach Sondergaard, Helle, Baker, Amie, Band, Gavin, Baranzini, Sergio E., Barizzone, Nadia, Barrett, Jeffrey, Bellenguez, Celine, Bergamaschi, Laura, Bernardinelli, Luisa, Berthele, Achim, Biberacher, Viola, Binder, Thomas M C., Blackburn, Hannah, Bomfim, Izaura L., Brambilla, Paola, Broadley, Simon, Brochet, Bruno, Brundin, Lou, Buck, Dorothea, Butzkueven, Helmut, Caillier, Stacy J., Camu, William, Carpentier, Wassila, Cavalla, Paola, Celius, Elisabeth G., Coman, Irene, Comi, Giancarlo, Corrado, Lucia, Cosemans, Leentje, Cournu-Rebeix, Isabelle, Cree, Bruce A C., Cusi, Daniele, Damotte, Vincent, Defer, Gilles, Delgado, Silvia R., Deloukas, Panos, di Sapio, Alessia, Dilthey, Alexander T., Donnelly, Peter, Dubois, Benedicte, Duddy, Martin, Edkins, Sarah, Elovaara, Irina, Esposito, Federica, Evangelou, Nikos, Fiddes, Barnaby, Field, Judith, Franke, Andre, Freeman, Colin, Frohlich, Irene Y., Galimberti, Daniela, Gieger, Christian, Gourraud, Pierre-Antoine, Graetz, Christiane, Graham, Andrew, Grummel, Verena, Guaschino, Clara, Hadjixenofontos, Athena, Hakonarson, Hakon, Halfpenny, Christopher, Hall, Gillian, Hall, Per, Hamsten, Anders, Harley, James, Harrower, Timothy, Hawkins, Clive, Hellenthal, Garrett, Hillier, Charles, Hobart, Jeremy, Hoshi, Muni, Hunt, Sarah E., Jagodic, Maja, Jelcic, Ilijas, Jochim, Angela, Kendall, Brian, Kermode, Allan, Kilpatrick, Trevor, Koivisto, Keijo, Konidari, Ioanna, Korn, Thomas, Kronsbein, Helena, Langford, Cordelia, Larsson, Malin, Lathrop, Mark, Lebrun-Frenay, Christine, Lechner-Scott, Jeannette, Lee, Michelle H., Leone, Maurizio A., Leppa, Virpi, Liberatore, Giuseppe, Lie, Benedicte A., Lill, Christina M., Linden, Magdalena, Link, Jenny, Luessi, Felix, Lycke, Jan, Macciardi, Fabio, Mannisto, Satu, Manrique, Clara P., Martin, Roland, Martinelli, Vittorio, Mason, Deborah, Mazibrada, Gordon, McCabe, Cristin, Mero, Inger-Lise, Mescheriakova, Julia, Moutsianas, Loukas, Myhr, Kjell-Morten, Nagels, Guy, Nicholas, Richard, Nilsson, Petra, Piehl, Fredrik, Pirinen, Matti, Price, Sian E., Quach, Hong, Reunanen, Mauri, Robberecht, Wim, Robertson, Neil P., Rodegher, Mariaemma, Rog, David, Salvetti, Marco, Schnetz-Boutaud, Nathalie C., Sellebjerg, Finn, Selter, Rebecca C., Schaefer, Catherine, Shaunak, Sandip, Shen, Ling, Shields, Simon, Siffrin, Volker, Slee, Mark, Soelberg Sorensen, Per, Sorosina, Melissa, Sospedra, Mireia, Spurkland, Anne, Strange, Amy, Sundqvist, Emilie, Thijs, Vincent, Thorpe, John, Ticca, Anna, Tienari, Pentti, van Duijn, Cornelia, Visser, Elizabeth M., Vucic, Steve, Westerlind, Helga, Wiley, James S., Wilkins, Alastair, Wilson, James F., Winkelmann, Juliane, Zajicek, John, Zindler, Eva, Haines, Jonathan L., Pericak-Vance, Margaret A., Ivinson, Adrian J., Stewart, Graeme, Hafler, David, Hauser, Stephen L., Compston, Alastair, McVean, Gil, De Jager, Philip, Sawcer, Stephen J., and McCauley, Jacob L.

Abstract

Using the ImmunoChip custom genotyping array, we analyzed 14,498 subjects with multiple sclerosis and 24,091 healthy controls for 161,311 autosomal variants and identified 135 potentially associated regions (P andlt; 1.0 x 10(-4)). In a replication phase, we combined these data with previous genome-wide association study (GWAS) data from an independent 14,802 subjects with multiple sclerosis and 26,703 healthy controls. In these 80,094 individuals of European ancestry, we identified 48 new susceptibility variants (P andlt; 5.0 x 10(-8)), 3 of which we found after conditioning on previously identified variants. Thus, there are now 110 established multiple sclerosis risk variants at 103 discrete loci outside of the major histocompatibility complex. With high-resolution Bayesian fine mapping, we identified five regions where one variant accounted for more than 50% of the posterior probability of association. This study enhances the catalog of multiple sclerosis risk variants and illustrates the value of fine mapping in the resolution of GWAS signals., Funding Agencies|US National Institutes of Health||Wellcome Trust||UK MS Society||UK Medical Research Council||US National MS Society||Cambridge National Institute for Health Research (NIHR) Biomedical Research Centre||DeNDRon||Swedish Brain Foundation||Swedish Research Council||Knut and Alice Wallenberg Foundation||Swedish Heart-Lung Foundation||Foundation for Strategic Research

Published
2013
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182. Sex as a determinant of relapse incidence and progressive course of multiple sclerosis.

Author

UCL - SSS/IONS/CEMO - Pôle Cellulaire et moléculaire, UCL - (SLuc) Service de neurologie, Kalincik, Tomas, Vivek, Vino, Jokubaitis, Vilija, Lechner-Scott, Jeannette, Trojano, Maria, Izquierdo, Guillermo, Lugaresi, Alessandra, Grand'maison, Francois, Hupperts, Raymond, Oreja-Guevara, Celia, Bergamaschi, Roberto, Iuliano, Gerardo, Alroughani, Raed, Van Pesch, Vincent, Amato, Maria Pia, Slee, Mark, Verheul, Freek, Fernandez-Bolanos, Ricardo, Fiol, Marcela, Spitaleri, Daniele La, Cristiano, Edgardo, Gray, Orla, Cabrera-Gomez, Jose Antonio, Shaygannejad, Vahid, Herbert, Joseph, Vucic, Steve, Needham, Merilee, Petkovska-Boskova, Tatjana, Sirbu, Carmen-Adella, Duquette, Pierre, Girard, Marc, Grammond, Pierre, Boz, Cavit, Giuliani, Giorgio, Rio, Maria Edite, Barnett, Michael, Flechter, Shlomo, Moore, Fraser, Singhal, Bhim, Bacile, Elizabeth Alejandra, Saladino, Maria Laura, Shaw, Cameron, Skromne, Eli, Poehlau, Dieter, Vella, Norbert, Spelman, Timothy, Liew, Danny, Kilpatrick, Trevor J, Butzkueven, Helmut, UCL - SSS/IONS/CEMO - Pôle Cellulaire et moléculaire, UCL - (SLuc) Service de neurologie, Kalincik, Tomas, Vivek, Vino, Jokubaitis, Vilija, Lechner-Scott, Jeannette, Trojano, Maria, Izquierdo, Guillermo, Lugaresi, Alessandra, Grand'maison, Francois, Hupperts, Raymond, Oreja-Guevara, Celia, Bergamaschi, Roberto, Iuliano, Gerardo, Alroughani, Raed, Van Pesch, Vincent, Amato, Maria Pia, Slee, Mark, Verheul, Freek, Fernandez-Bolanos, Ricardo, Fiol, Marcela, Spitaleri, Daniele La, Cristiano, Edgardo, Gray, Orla, Cabrera-Gomez, Jose Antonio, Shaygannejad, Vahid, Herbert, Joseph, Vucic, Steve, Needham, Merilee, Petkovska-Boskova, Tatjana, Sirbu, Carmen-Adella, Duquette, Pierre, Girard, Marc, Grammond, Pierre, Boz, Cavit, Giuliani, Giorgio, Rio, Maria Edite, Barnett, Michael, Flechter, Shlomo, Moore, Fraser, Singhal, Bhim, Bacile, Elizabeth Alejandra, Saladino, Maria Laura, Shaw, Cameron, Skromne, Eli, Poehlau, Dieter, Vella, Norbert, Spelman, Timothy, Liew, Danny, Kilpatrick, Trevor J, and Butzkueven, Helmut

Abstract

The aim of this work was to evaluate sex differences in the incidence of multiple sclerosis relapses; assess the relationship between sex and primary progressive disease course; and compare effects of age and disease duration on relapse incidence. Annualized relapse rates were calculated using the MSBase registry. Patients with incomplete data or <1 year of follow-up were excluded. Patients with primary progressive multiple sclerosis were only included in the sex ratio analysis. Relapse incidences over 40 years of multiple sclerosis or 70 years of age were compared between females and males with Andersen-Gill and Tweedie models. Female-to-male ratios stratified by annual relapse count were evaluated across disease duration and patient age and compared between relapse-onset and primary progressive multiple sclerosis. The study cohort consisted of 11 570 eligible patients with relapse-onset and 881 patients with primary progressive multiple sclerosis. Among the relapse-onset patients (82 552 patient-years), 48 362 relapses were recorded. Relapse frequency was 17.7% higher in females compared with males. Within the initial 5 years, the female-to-male ratio increased from 2.3:1 to 3.3:1 in patients with 0 versus ≥4 relapses per year, respectively. The magnitude of this sex effect increased at longer disease duration and older age (P < 10(-12)). However, the female-to-male ratio in patients with relapse-onset multiple sclerosis and zero relapses in any given year was double that of the patients with primary progressive multiple sclerosis. Patient age was a more important determinant of decline in relapse incidence than disease duration (P < 10(-12)). Females are predisposed to higher relapse activity than males. However, this difference does not explain the markedly lower female-to-male sex ratio in primary progressive multiple sclerosis. Decline in relapse activity over time is more closely related to patient age than disease duration.

Published
2013

183. Occupational Exposure and Risk of Central Nervous System Demyelination

Author

Valery, Patricia C, Williams, David, Pender, M P, Chapman, C, Coulthard, Alan, Dear, Keith, Dwyer, Terry, Kilpatrick, Trevor J, McMichael, Anthony, Van Der Mei, Ingrid, Taylor, B V, Ponsonby, Anne-Louise, Lucas, Robyn, Valery, Patricia C, Williams, David, Pender, M P, Chapman, C, Coulthard, Alan, Dear, Keith, Dwyer, Terry, Kilpatrick, Trevor J, McMichael, Anthony, Van Der Mei, Ingrid, Taylor, B V, Ponsonby, Anne-Louise, and Lucas, Robyn

Abstract

Inconsistent evidence exists regarding the association between work-related factors and risk of multiple sclerosis (MS). We examined the association between occupational exposures and risk of a first clinical diagnosis of central nervous system demyelinat

Published
2013

184. The physical anthropology, lifestyle habits and blood pressure presenting with a first class clinical demyelinating event compared to controls: the Ausimmune study

Author

Ponsonby, Anne-Louise, Dear, Keith, Van Der Mei, Ingrid, Taylor, Bruce, Chapman, Caron, Coulthard, Alan, Dwyer, Terry, Kilpatrick, Trevor J, McMichael, Anthony, Pender, M P, Valery, Patricia C., Williams, David, Lucas, Robyn, Ponsonby, Anne-Louise, Dear, Keith, Van Der Mei, Ingrid, Taylor, Bruce, Chapman, Caron, Coulthard, Alan, Dwyer, Terry, Kilpatrick, Trevor J, McMichael, Anthony, Pender, M P, Valery, Patricia C., Williams, David, and Lucas, Robyn

Abstract

Introduction: Lifestyle factors prior to a first clinical demyelinating event (FCD), a disorder often preceding the development of clinically definite multiple sclerosis (MS), have not previously been examined in detail. Past tobacco smoking has been cons

Published
2013

185. Vitamin D status: multifactorial contribution of environment, genes and other factors in healthy Australian adults across a latitude gradient

Author

Ponsonby, Anne-Louise, Dear, Keith, Valery, Patricia C., Taylor, Bruce, Van Der Mei, Ingrid, McMichael, Anthony, Pender, M P, Chapman, Caron, Coulthard, Alan, Kilpatrick, Trevor J, Stankovich, James, Williams, David, Dwyer, Terry, Lucas, Robyn, Ponsonby, Anne-Louise, Dear, Keith, Valery, Patricia C., Taylor, Bruce, Van Der Mei, Ingrid, McMichael, Anthony, Pender, M P, Chapman, Caron, Coulthard, Alan, Kilpatrick, Trevor J, Stankovich, James, Williams, David, Dwyer, Terry, and Lucas, Robyn

Abstract

Vitamin D deficiency is common and implicated in risk of several human diseases. Evidence on the relative quantitative contribution of environmental, genetic and phenotypic factors to vitamin D status (assessed by the serum concentration of 25-hydroxyvita

Published
2013

186. Analysis of immune-related loci identifies 48 new susceptibility variants for multiple sclerosis

Author

Beecham, Ashley H, Patsopoulos, Nikolaos A, Xifara, Dionysia K, Davis, Mary F, Kemppinen, Anu, Cotsapas, Chris, Shah, Tejas S, Spencer, Chris, Booth, David, Goris, An, Oturai, Annette, Saarela, Janna, Fontaine, Bertrand, Hemmer, Bernhard, Martin, Claes, Zipp, Frauke, D'Alfonso, Sandra, Martinelli-Boneschi, Filippo, Taylor, Bruce, Harbo, Hanne F, Kockum, Ingrid, Hillert, Jan, Olsson, Tomas, Ban, Maria, Oksenberg, Jorge R, Hintzen, Rogier, Barcellos, Lisa F, Agliardi, Cristina, Alfredsson, Lars, Alizadeh, Mehdi, Anderson, Carl, Andrews, Robert, Søndergaard, Helle Bach, Baker, Amie, Band, Gavin, Baranzini, Sergio E, Barizzone, Nadia, Barrett, Jeffrey, Bellenguez, Céline, Bergamaschi, Laura, Bernardinelli, Luisa, Berthele, Achim, Biberacher, Viola, Binder, Thomas, Blackburn, Hannah, Bomfim, Izaura L, Brambilla, Paola, Broadley, Simon, Brochet, Bruno, Brundin, Lou, Buck, Dorothea, Butzkueven, Helmut, Caillier, Stacy J, Camu, William, Carpentier, Wassila, Cavalla, Paola, Celius, Elisabeth G, Coman, Irène, Comi, Giancarlo, Corrado, Lucia, Cosemans, Leentje, Cournu-Rebeix, Isabelle, Cree, Bruce A C, Cusi, Daniele, Damotte, Vincent, Defer, Gilles, Delgado, Silvia R, Deloukas, Panos, di Sapio, Alessia, Dilthey, Alexander T, Donnelly, Peter, Dubois, Bénédicte, Duddy, Martin, Edkins, Sarah, Elovaara, Irina, Esposito, Federica, Evangelou, Nikos, Fiddes, Barnaby, Field, Judith, Franke, Andre, Freeman, Colin, Frohlich, Irene Y, Galimberti, Daniela, Gieger, Christian, Gourraud, Pierre-Antoine, Graetz, Christiane, Graham, Andrew, Grummel, Verena, Guaschino, Clara, Hadjixenofontos, Athena, Hakonarson, Hakon, Halfpenny, Christopher, Hall, Gillian, Hall, Per, Hamsten, Anders, Harley, James, Harrower, Timothy, Hawkins, Clive, Hellenthal, Garrett, Hillier, Charles, Hobart, Jeremy, Hoshi, Muni, Hunt, Sarah E, Jagodic, Maja, Jel?i?, Ilijas, Jochim, Angela, Kendall, Brian, Kermode, Allan, Kilpatrick, Trevor, Koivisto, Keijo, Konidari, Ioanna, Korn, Thomas, Kronsbein, Helena, Langford, Cordelia, Larsson, Malin, Lathrop, Mark, Lebrun-Frenay, Christine, Lechner-Scott, Jeannette, Lee, Michelle H, Leone, Maurizio A, Leppä, Virpi, Liberatore, Giuseppe, Lie, Benedicte A, Lill, Christina M, Lindén, Magdalena, Link, Jenny, Luessi, Felix, Lycke, Jan, Macciardi, Fabio, Männistö, Satu, Manrique, Clara P, Martin, Roland, Martinelli, Vittorio, Mason, Deborah, Mazibrada, Gordon, McCabe, Cristin, Mero, Inger-Lise, Mescheriakova, Julia, Moutsianas, Loukas, Myhr, Kjell-Morten, Nagels, Guy, Nicholas, Richard, Nilsson, Petra, Piehl, Fredrik, Pirinen, Matti, Price, Siân E, Quach, Hong, Reunanen, Mauri, Robberecht, Wim, Robertson, Neil P, Rodegher, Mariaemma, Rog, David, Salvetti, Marco, Schnetz-Boutaud, Nathalie C, Sellebjerg, Finn, Selter, Rebecca C, Schaefer, Catherine, Shaunak, Sandip, Shen, Ling, Shields, Simon, Siffrin, Volker, Slee, Mark, Sorensen, Per Soelberg, Sorosina, Melissa, Sospedra, Mireia, Spurkland, Anne, Strange, Amy, Sundqvist, Emilie, Thijs, Vincent, Thorpe, John, Ticca, Anna, Tienari, Pentti, van Duijn, Cornelia, Visser, Elizabeth M, Vucic, Steve, Westerlind, Helga, Wiley, James S, Wilkins, Alastair, Wilson, James, Winkelmann, Juliane, Zajicek, John, Zindler, Eva, Haines, Jonathan L, Pericak-Vance, Margaret A, Ivinson, Adrian J, Stewart, Graeme, Hafler, David, Hauser, Stephen L, Compston, Alastair, McVean, Gil, De Jager, Philip, Sawcer, Stephen J, McCauley, Jacob L, (IMSGC), International Multiple Sclerosis Genetics Consortium, Beecham, Ashley H, Patsopoulos, Nikolaos A, Xifara, Dionysia K, Davis, Mary F, Kemppinen, Anu, Cotsapas, Chris, Shah, Tejas S, Spencer, Chris, Booth, David, Goris, An, Oturai, Annette, Saarela, Janna, Fontaine, Bertrand, Hemmer, Bernhard, Martin, Claes, Zipp, Frauke, D'Alfonso, Sandra, Martinelli-Boneschi, Filippo, Taylor, Bruce, Harbo, Hanne F, Kockum, Ingrid, Hillert, Jan, Olsson, Tomas, Ban, Maria, Oksenberg, Jorge R, Hintzen, Rogier, Barcellos, Lisa F, Agliardi, Cristina, Alfredsson, Lars, Alizadeh, Mehdi, Anderson, Carl, Andrews, Robert, Søndergaard, Helle Bach, Baker, Amie, Band, Gavin, Baranzini, Sergio E, Barizzone, Nadia, Barrett, Jeffrey, Bellenguez, Céline, Bergamaschi, Laura, Bernardinelli, Luisa, Berthele, Achim, Biberacher, Viola, Binder, Thomas, Blackburn, Hannah, Bomfim, Izaura L, Brambilla, Paola, Broadley, Simon, Brochet, Bruno, Brundin, Lou, Buck, Dorothea, Butzkueven, Helmut, Caillier, Stacy J, Camu, William, Carpentier, Wassila, Cavalla, Paola, Celius, Elisabeth G, Coman, Irène, Comi, Giancarlo, Corrado, Lucia, Cosemans, Leentje, Cournu-Rebeix, Isabelle, Cree, Bruce A C, Cusi, Daniele, Damotte, Vincent, Defer, Gilles, Delgado, Silvia R, Deloukas, Panos, di Sapio, Alessia, Dilthey, Alexander T, Donnelly, Peter, Dubois, Bénédicte, Duddy, Martin, Edkins, Sarah, Elovaara, Irina, Esposito, Federica, Evangelou, Nikos, Fiddes, Barnaby, Field, Judith, Franke, Andre, Freeman, Colin, Frohlich, Irene Y, Galimberti, Daniela, Gieger, Christian, Gourraud, Pierre-Antoine, Graetz, Christiane, Graham, Andrew, Grummel, Verena, Guaschino, Clara, Hadjixenofontos, Athena, Hakonarson, Hakon, Halfpenny, Christopher, Hall, Gillian, Hall, Per, Hamsten, Anders, Harley, James, Harrower, Timothy, Hawkins, Clive, Hellenthal, Garrett, Hillier, Charles, Hobart, Jeremy, Hoshi, Muni, Hunt, Sarah E, Jagodic, Maja, Jel?i?, Ilijas, Jochim, Angela, Kendall, Brian, Kermode, Allan, Kilpatrick, Trevor, Koivisto, Keijo, Konidari, Ioanna, Korn, Thomas, Kronsbein, Helena, Langford, Cordelia, Larsson, Malin, Lathrop, Mark, Lebrun-Frenay, Christine, Lechner-Scott, Jeannette, Lee, Michelle H, Leone, Maurizio A, Leppä, Virpi, Liberatore, Giuseppe, Lie, Benedicte A, Lill, Christina M, Lindén, Magdalena, Link, Jenny, Luessi, Felix, Lycke, Jan, Macciardi, Fabio, Männistö, Satu, Manrique, Clara P, Martin, Roland, Martinelli, Vittorio, Mason, Deborah, Mazibrada, Gordon, McCabe, Cristin, Mero, Inger-Lise, Mescheriakova, Julia, Moutsianas, Loukas, Myhr, Kjell-Morten, Nagels, Guy, Nicholas, Richard, Nilsson, Petra, Piehl, Fredrik, Pirinen, Matti, Price, Siân E, Quach, Hong, Reunanen, Mauri, Robberecht, Wim, Robertson, Neil P, Rodegher, Mariaemma, Rog, David, Salvetti, Marco, Schnetz-Boutaud, Nathalie C, Sellebjerg, Finn, Selter, Rebecca C, Schaefer, Catherine, Shaunak, Sandip, Shen, Ling, Shields, Simon, Siffrin, Volker, Slee, Mark, Sorensen, Per Soelberg, Sorosina, Melissa, Sospedra, Mireia, Spurkland, Anne, Strange, Amy, Sundqvist, Emilie, Thijs, Vincent, Thorpe, John, Ticca, Anna, Tienari, Pentti, van Duijn, Cornelia, Visser, Elizabeth M, Vucic, Steve, Westerlind, Helga, Wiley, James S, Wilkins, Alastair, Wilson, James, Winkelmann, Juliane, Zajicek, John, Zindler, Eva, Haines, Jonathan L, Pericak-Vance, Margaret A, Ivinson, Adrian J, Stewart, Graeme, Hafler, David, Hauser, Stephen L, Compston, Alastair, McVean, Gil, De Jager, Philip, Sawcer, Stephen J, McCauley, Jacob L, and (IMSGC), International Multiple Sclerosis Genetics Consortium

Published
2013

187. Optic Nerve Diffusion Tensor Imaging after Acute Optic Neuritis Predicts Axonal and Visual Outcomes

Author

van der Walt, Anneke, primary, Kolbe, Scott C., additional, Wang, Yejun E., additional, Klistorner, Alexander, additional, Shuey, Neil, additional, Ahmadi, Gelareh, additional, Paine, Mark, additional, Marriott, Mark, additional, Mitchell, Peter, additional, Egan, Gary F., additional, Butzkueven, Helmut, additional, and Kilpatrick, Trevor J., additional

Published
2013
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188. Offspring number, pregnancy, and risk of a first clinical demyelinating event: the AusImmune Study

Author

Ponsonby, Anne-Louise, Lucas, Robyn M., van der Mei, Ingrid, Dear, Keith, Valery, Patricia C., Pender, Mchael P., Taylor, Bruce, Kilpatrick, Trevor. J., Coulthard, Alan, Chapman, Caron, Williams, David B., McMichael, Anthony. J., Dwyer, Terence, Ponsonby, Anne-Louise, Lucas, Robyn M., van der Mei, Ingrid, Dear, Keith, Valery, Patricia C., Pender, Mchael P., Taylor, Bruce, Kilpatrick, Trevor. J., Coulthard, Alan, Chapman, Caron, Williams, David B., McMichael, Anthony. J., and Dwyer, Terence

Published
2012

189. Interleukin-6 gene promoter-572 C allele may play a role in rate of disease progression in multiple sclerosis

Author

Yan, Jun, Liu, Jia, Lin, Clement Yihao, Scott, Rodney J., Lechner-Scott, Jeannette, Booth, David R., Stewart, Graeme J., Broadley, Simon, Mason, Deborah, Griffiths, Lyn, Moscato, Pablo, Slee, Mark, Taylor, Bruce, Wiley, James, Field, Judith, Butzkueven, Helmut, Kilpatrick, Trevor J., Csurhes, Peter A., Pender, Michael P., McCombe, Pamela A., Greer, Judith M., Yan, Jun, Liu, Jia, Lin, Clement Yihao, Scott, Rodney J., Lechner-Scott, Jeannette, Booth, David R., Stewart, Graeme J., Broadley, Simon, Mason, Deborah, Griffiths, Lyn, Moscato, Pablo, Slee, Mark, Taylor, Bruce, Wiley, James, Field, Judith, Butzkueven, Helmut, Kilpatrick, Trevor J., Csurhes, Peter A., Pender, Michael P., McCombe, Pamela A., and Greer, Judith M.

Abstract

Multiple sclerosis (MS) is an inflammatory demyelinating disease affecting the central nervous system. Although the exact pathogenesis of MS is unknown, it is generally considered to be an autoimmune disease, with numerous genetic and environmental factors determining disease susceptibility and severity. One important mediator of immune responses and inflammation is interleukin-6 (IL-6). Previously, elevated levels of IL-6 in mononuclear cells in blood and in brain tissue from MS patients have been reported. Various polymorphisms in the promoter region of the IL6 gene have also been linked with IL-6 protein levels. In MS, several small studies have investigated whether two IL6 promoter polymorphisms (-597 G>A and -174 G>C) correlate with MS susceptibility, but with varying results. In the present study, we analyzed these polymorphisms, together with an additional polymorphism (-572 G>C) in 279 healthy controls and 509 patients with MS. We found no significant differences between MS patients and healthy controls for the different -597 or -174 IL6 promoter alleles or genotypes. There was a slight reduction in the percentage of individuals with MS who carried a C allele at position -572, although this was not significant after correction for multiple comparisons. Interestingly, however, the -572 C allele showed a significant correlation with the MS severity score, suggesting a possible role in disease progression.

Published
2012

192. Polymorphisms in the receptor tyrosine kinase MERTK gene are associated with multiple sclerosis susceptibility

Author

Ma, Gerry, Stankovich, Jim, Kilpatrick, Trevor, Binder, Michele, Field, Judith, Griffiths, Lyn, Brown, Matthew, other, and, Ma, Gerry, Stankovich, Jim, Kilpatrick, Trevor, Binder, Michele, Field, Judith, Griffiths, Lyn, Brown, Matthew, and other, and

Abstract

Multiple sclerosis (MS) is a debilitating, chronic demyelinating disease of the central nervous system affecting over 2 million people worldwide. The TAM family of receptor tyrosine kinases (TYRO3, AXL and MERTK) have been implicated as important players during demyelination in both animal models of MS and in the human disease. We therefore conducted an association study to identify single nucleotide polymorphisms (SNPs) within genes encoding the TAM receptors and their ligands associated with MS. Analysis of genotype data from a genome-wide association study which consisted of 1618 MS cases and 3413 healthy controls conducted by the Australia and New Zealand Multiple Sclerosis Genetics Consortium (ANZgene) revealed several SNPs within the MERTK gene (Chromosome 2q14.1, Accession Number NG_011607.1) that showed suggestive association with MS. We therefore interrogated 28 SNPs in MERTK in an independent replication cohort of 1140 MS cases and 1140 healthy controls. We found 12 SNPs that replicated, with 7 SNPs showing p-values of less than 10-5 when the discovery and replication cohorts were combined. All 12 replicated SNPs were in strong linkage disequilibrium with each other. In combination, these data suggest the MERTK gene is a novel risk gene for MS susceptibility. © 2011 Ma et al.

Published
2011

193. State-level differences in the oral health of Australian preschool and early primary school-age children

Author

Lucas, Nina, Neumann, A, Kilpatrick, Trevor, Nicholson, Jan, Lucas, Nina, Neumann, A, Kilpatrick, Trevor, and Nicholson, Jan

Abstract

Background: This study compares oral health outcomes and behaviours for young Australian children by residential state or territory to determine whether state differences arise from individual exposures to risk factors. Methods: Cross-sectional data for 4606 2-3 year olds and 4464 6-7 year olds were obtained from the Longitudinal Study of Australian Children. Outcome measures were parent-reports of children's caries experience, frequency of toothbrushing and dental services use. Results: For 2-3 year olds, children from the Australian Capital Territory were less likely to have parent-reported caries than children from other states, and more likely to brush their teeth twice daily and to have used dental services. For 6-7 year olds, optimal outcomes were observed in New South Wales for lowest caries experience, Western Australia for highest toothbrushing, and South Australia for highest dental services use. Adjustments for socio-demographic predictors did not eliminate state differences in oral health. Conclusions: Large state differences in the oral health of young children persisted after adjustment for individual sociodemographic determinants, suggesting these arise from variations in the systems to promote and care for children's oral health. Several states would benefit from a stronger emphasis on oral health promotion in young children, and disparities from a young age suggest the need for better engagement of early childhood professionals in oral health promotion.

Published
2011

194. Current and past Epstein-Barr virus infection in risk of initial CNS demyelination

Author

Ponsonby, Anne-Louise, Dear, Keith, Valery, Patricia C, Pender, M P, Burrows, J M, Burrows, Scott, Chapman, Caron, Coulthard, Alan, Dwyer, Dominic E, Dwyer, Terry, Kilpatrick, Trevor J, Lay, Meav-Lang, McMichael, Anthony, Taylor, B V, Van Der Mei, Ingrid, Williams, David, Lucas, Robyn, Ponsonby, Anne-Louise, Dear, Keith, Valery, Patricia C, Pender, M P, Burrows, J M, Burrows, Scott, Chapman, Caron, Coulthard, Alan, Dwyer, Dominic E, Dwyer, Terry, Kilpatrick, Trevor J, Lay, Meav-Lang, McMichael, Anthony, Taylor, B V, Van Der Mei, Ingrid, Williams, David, and Lucas, Robyn

Abstract

Objectives: To assess risk of a first clinical diagnosis of CNS demyelination (FCD) in relation to measures of Epstein-Barr virus (EBV) infection within the context of other known risk factors. Methods: This was a multicenter incident case-control study.

Published
2011

195. Multiple sclerosis susceptibility-associated SNPs do not influence disease severity measures in a cohort of Australian MS patients

Author

Jensen, Cathy, Stankovich, Jim, van der Walt, Anneke, Bahlo, Melanie, Taylor, Bruce, Van der Mei, Ingrid, Foote, Simon, Kilpatrick, Trevor, Johnson, Laura, Wilkins, Ella, Field, Judith, Danoy, Patrick, Brown, Matthew, Rubio, Justin, Butzkueven, Helmut, Griffiths, Lyn, other, and, Jensen, Cathy, Stankovich, Jim, van der Walt, Anneke, Bahlo, Melanie, Taylor, Bruce, Van der Mei, Ingrid, Foote, Simon, Kilpatrick, Trevor, Johnson, Laura, Wilkins, Ella, Field, Judith, Danoy, Patrick, Brown, Matthew, Rubio, Justin, Butzkueven, Helmut, Griffiths, Lyn, and other, and

Abstract

Recent association studies in multiple sclerosis (MS) have identified and replicated several single nucleotide polymorphism (SNP) susceptibility loci including CLEC16A, IL2RA, IL7R, RPL5, CD58, CD40 and chromosome 12q13–14 in addition to the well established allele HLA-DR15. There is potential that these genetic susceptibility factors could also modulate MS disease severity, as demonstrated previously for the MS risk allele HLA-DR15. We investigated this hypothesis in a cohort of 1006 well characterised MS patients from South-Eastern Australia. We tested the MS-associated SNPs for association with five measures of disease severity incorporating disability, age of onset, cognition and brain atrophy. We observed trends towards association between the RPL5 risk SNP and time between first demyelinating event and relapse, and between the CD40 risk SNP and symbol digit test score. No associations were significant after correction for multiple testing. We found no evidence for the hypothesis that these new MS disease risk-associated SNPs influence disease severity.

Published
2010

196. A polymorphism in the HLA-DPB1 gene is associated with susceptibility to multiple sclerosis

Author

Field, Judith, Browning, Sharon, Johnson, Laura, Danoy, Patrick, Varney, Michael, Tait, Brian, Gandhi, Kaushal, Charlesworth, Jac, Heard, Robert, Stewart, Graeme, Kilpatrick, Trevor, Foote, Simon, Bahlo, Melanie, Butzkueven, Helmut, Wiley, James, Booth, David, Taylor, Bruce, Brown, Matthew, Rubio, Justin, Stankovich, Jim, Griffiths, Lyn, other, and, Field, Judith, Browning, Sharon, Johnson, Laura, Danoy, Patrick, Varney, Michael, Tait, Brian, Gandhi, Kaushal, Charlesworth, Jac, Heard, Robert, Stewart, Graeme, Kilpatrick, Trevor, Foote, Simon, Bahlo, Melanie, Butzkueven, Helmut, Wiley, James, Booth, David, Taylor, Bruce, Brown, Matthew, Rubio, Justin, Stankovich, Jim, Griffiths, Lyn, and other, and

Abstract

We conducted an association study across the human leukocyte antigen (HLA) complex to identify loci associated with multiple sclerosis (MS). Comparing 1927 SNPs in 1618 MS cases and 3413 controls of European ancestry, we identified seven SNPs that were independently associated with MS conditional on the others (each ). All associations were significant in an independent replication cohort of 2212 cases and 2251 controls () and were highly significant in the combined dataset (). The associated SNPs included proxies for HLA-DRB1*15:01 and HLA-DRB1*03:01, and SNPs in moderate linkage disequilibrium (LD) with HLA-A*02:01, HLA-DRB1*04:01 and HLA-DRB1*13:03. We also found a strong association with rs9277535 in the class II gene HLA-DPB1 (discovery set , replication set , combined ). HLA-DPB1 is located centromeric of the more commonly typed class II genes HLA-DRB1, -DQA1 and -DQB1. It is separated from these genes by a recombination hotspot, and the association is not affected by conditioning on genotypes at DRB1, DQA1 and DQB1. Hence rs9277535 represents an independent MS-susceptibility locus of genome-wide significance. It is correlated with the HLA-DPB1*03:01 allele, which has been implicated previously in MS in smaller studies. Further genotyping in large datasets is required to confirm and resolve this association.

Published
2010

197. Genome-wide association study identifies new multiple sclerosis susceptibility loci on chromosomes 12 and 20

Author

Bahlo, Melanie, Booth, David, Broadley, Simon, Brown, Matthew, Foote, Simon, Griffiths, Lyn, Kilpatrick, Trevor, Lechner-Scott, Jeannette, Moscato, Pablo, Perreau, Victoria, other, and, Bahlo, Melanie, Booth, David, Broadley, Simon, Brown, Matthew, Foote, Simon, Griffiths, Lyn, Kilpatrick, Trevor, Lechner-Scott, Jeannette, Moscato, Pablo, Perreau, Victoria, and other, and

Abstract

To identify multiple sclerosis (MS) susceptibility loci, we conducted a genome-wide association study (GWAS) in 1,618 cases and used shared data for 3,413 controls. We performed replication in an independent set of 2,256 cases and 2,310 controls, for a total of 3,874 cases and 5,723 controls. We identified risk-associated SNPs on chromosome 12q13-14 (rs703842, P = 5.4 x 10(-11); rs10876994, P = 2.7 x 10(-10); rs12368653, P = 1.0 x 10(-7)) and upstream of CD40 on chromosome 20q13 (rs6074022, P = 1.3 x 10(-7); rs1569723, P = 2.9 x 10(-7)). Both loci are also associated with other autoimmune diseases. We also replicated several known MS associations (HLA-DR15, P = 7.0 x 10(-184); CD58, P = 9.6 x 10(-8); EVI5-RPL5, P = 2.5 x 10(-6); IL2RA, P = 7.4 x 10(-6); CLEC16A, P = 1.1 x 10(-4); IL7R, P = 1.3 x 10(-3); TYK2, P = 3.5 x 10(-3)) and observed a statistical interaction between SNPs in EVI5-RPL5 and HLA-DR15 (P = 0.001).

Published
2009

198. BDNF Exerts Contrasting Effects on Peripheral Myelination of NGF-Dependent and BDNF-Dependent DRG Neurons

Author

Xiao, Junhua, Wong, Agnes W, Willingham, Melanie M, Kaasinen, Selma, Hendry, Ian, Howitt, Jason, Putz, Ulrich, Barrett, Graham L, Kilpatrick, Trevor J, Murray, Simon S, Xiao, Junhua, Wong, Agnes W, Willingham, Melanie M, Kaasinen, Selma, Hendry, Ian, Howitt, Jason, Putz, Ulrich, Barrett, Graham L, Kilpatrick, Trevor J, and Murray, Simon S

Abstract

Although brain-derived neurotrophic factor (BDNF) has been shown to promote peripheral myelination during development and remy-elination after injury, the precise mechanisms mediating this effect remain unknown. Here, we determine that BDNF promotes myelination of nerve growth factor-dependent neurons, an effect dependent on neuronal expression of the p75 neurotrophin receptor, whereas BDNF inhibits myelination of BDNF-dependent neurons via the full-length TrkB receptor. Thus, BDNF exerts contrasting effects on Schwann cell myelination, depending on the complement of BDNF receptors that are expressed by different subpopulations of dorsal root ganglion neurons. These results demonstrate that BDNF exerts contrasting modulatory roles in peripheral nervous system myelination, and that its mechanism of action is acutely regulated and specifically targeted to neurons.

Published
2009

199. Associations between Silicone Skin Cast Score, Cumulative Sun Exposure, and Other Factors in the Ausimmune Study: A Multicenter Australian Study

Author

Ponsonby, Anne-Louise, Dear, Keith, Taylor, Bruce, Dwyer, Terry, McMichael, Anthony, Valery, Patricia C, Van Der Mei, Ingrid, Williams, David, Pender, Michael, Chapman, Caron, Coulthard, Alan, Kilpatrick, Trevor J, Lucas, Robyn, Ponsonby, Anne-Louise, Dear, Keith, Taylor, Bruce, Dwyer, Terry, McMichael, Anthony, Valery, Patricia C, Van Der Mei, Ingrid, Williams, David, Pender, Michael, Chapman, Caron, Coulthard, Alan, Kilpatrick, Trevor J, and Lucas, Robyn

Abstract

Past sun exposure is linked to a wide range of disease outcomes but is difficult to measure accurately. Silicone skin casts measure skin damage, but some studies show that age rather than sun exposure is the most important determinant of cast score. We examined skin damage scores from silicone casts of the back of the hand in a large adult sample (n = 534) with a broad range of past cumulative UV radiation (UVR) doses. Participants were ages 18 to 61 years and resided in one of four locations down the eastern Australian seaboard, spanning 27-43°S. Data were collected by questionnaire and during a nurse-led interview and examination. Silicone casts were graded from 1 to 6, where higher score represents greater damage. Higher skin damage score was associated with lighter skin pigmentation [adjusted odds ratio (AOR), 4.51; 95% confidence interval (95% CI), 2.33-8.75], fairer natural hair color, particularly red hair (AOR, 11.31; 95% CI, 4.08-31.36), and blue/gray eyes (AOR, 1.72; 95% CI, 1.14-2.59). Higher cumulative UVR dose, particularly before age 18 years, was associated with higher skin damage score (AOR, 2.06; 95% CI, 1.15-2.67 per 1,000 KJ/m2), as was number of sunburns, even after adjustment for cumulative UVR dose (AOR, 2.86; 95% CI, 1.50-5.43 for >10 sunburns ever compared with no sunburns ever). Silicone casts of the dorsum of the hand provide a measure of cumulative UVR dose and number of sunburns over the lifetime, which persists after adjustment for chronological age. They can be used as an objective measure of cumulative past sun exposure in epidemiologic studies, but other determinants of skin damage, such as skin pigmentation, should be concurrently evaluated.

Published
2009

200. Sex as a determinant of relapse incidence and progressive course of multiple sclerosis

Author

Kalincik, Tomas, primary, Vivek, Vino, additional, Jokubaitis, Vilija, additional, Lechner-Scott, Jeannette, additional, Trojano, Maria, additional, Izquierdo, Guillermo, additional, Lugaresi, Alessandra, additional, Grand’Maison, Francois, additional, Hupperts, Raymond, additional, Oreja-Guevara, Celia, additional, Bergamaschi, Roberto, additional, Iuliano, Gerardo, additional, Alroughani, Raed, additional, Van Pesch, Vincent, additional, Amato, Maria Pia, additional, Slee, Mark, additional, Verheul, Freek, additional, Fernandez-Bolanos, Ricardo, additional, Fiol, Marcela, additional, Spitaleri, Daniele La, additional, Cristiano, Edgardo, additional, Gray, Orla, additional, Cabrera-Gomez, Jose Antonio, additional, Shaygannejad, Vahid, additional, Herbert, Joseph, additional, Vucic, Steve, additional, Needham, Merilee, additional, Petkovska-Boskova, Tatjana, additional, Sirbu, Carmen-Adella, additional, Duquette, Pierre, additional, Girard, Marc, additional, Grammond, Pierre, additional, Boz, Cavit, additional, Giuliani, Giorgio, additional, Rio, Maria Edite, additional, Barnett, Michael, additional, Flechter, Shlomo, additional, Moore, Fraser, additional, Singhal, Bhim, additional, Bacile, Elizabeth Alejandra, additional, Saladino, Maria Laura, additional, Shaw, Cameron, additional, Skromne, Eli, additional, Poehlau, Dieter, additional, Vella, Norbert, additional, Spelman, Timothy, additional, Liew, Danny, additional, Kilpatrick, Trevor J., additional, and Butzkueven, Helmut, additional

Published
2013
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