Hunter Medical Research Institute Research Articles

IL‐21 comes of age

IL‐21 comes of age

Cerebral asymmetry in electrophysiological (mismatch negativity) measures of temporal processing determines performance on a between-channel gap detection task

Event Abstract Back to Event Cerebral asymmetry in electrophysiological (mismatch negativity) measures of temporal processing determines performance on a between-channel gap detection task Juanita Todd1, 2, 3, 4*, U. Schall2, 3, 4, 5 and T. B. Budd1, 2, 3, 4 1 School of Psychology, University of Newcastle, Australia 2 Brain and Mental Health Priority Research Centre, University of Newcastle, Australia 3 Hunter Medical Research Institute, Australia 4 Schizophrenia Research Institute, Australia 5 School of Medicine and Population Health, University of Newcastle, Australia There is evidence of a left-hemisphere advantage for processing temporal information in sound that can be observed as a right-ear advantage on auditory tasks. This study was designed to determine whether a right-ear advantage could be observed in mismatch negativity (MMN) measures of central auditory temporal discrimination, and the extent to which this is related to behavioral measures of temporal discrimination ability. Forty-seven adults (18-73 years) completed behavioral and MMN measures of temporal discrimination for sounds presented monaurally to the left and right ear. Temporal discrimination was assessed using between-channel gap-detection - the ability to detect a gap between non-overlapping frequency bands of sound. Temporal discrimination performance showed a positive function of MMN measures of gap-detection, where larger right-ear advantage in MMN to gap sounds correlated with better temporal discrimination ability (rs= -.51, p<.005). Furthermore, only participants with low gap-detection thresholds exhibited significant right-ear advantage in MMN to gap sounds. The association between right-ear advantage in MMN and temporal discrimination ability may reflect the importance of the left-hemisphere in determining the resolution of auditory temporal processing. The results raise the possibility that groups showing impaired temporal processing (e.g. aged, schizophrenia, language disorders) may exhibit altered functional asymmetry in temporal processing. Conference: MMN 09 Fifth Conference on Mismatch Negativity (MMN) and its Clinical and Scientific Applications, Budapest, Hungary, 4 Apr - 7 Apr, 2009. Presentation Type: Poster Presentation Topic: Poster Presentations Citation: Todd J, Schall U and Budd TB (2009). Cerebral asymmetry in electrophysiological (mismatch negativity) measures of temporal processing determines performance on a between-channel gap detection task. Conference Abstract: MMN 09 Fifth Conference on Mismatch Negativity (MMN) and its Clinical and Scientific Applications. doi: 10.3389/conf.neuro.09.2009.05.045 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 24 Mar 2009; Published Online: 24 Mar 2009. * Correspondence: Juanita Todd, School of Psychology, University of Newcastle, Newcastle, Australia, Juanita.Todd@newcastle.edu.au Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Juanita Todd U. Schall T. B Budd Google Juanita Todd U. Schall T. B Budd Google Scholar Juanita Todd U. Schall T. B Budd PubMed Juanita Todd U. Schall T. B Budd Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

DNA mismatch repair genes and hereditary non-polyposis colorectal cancer.

Journal of Gastroenterology and HepatologyVolume 19, Issue 4 p. 465-466 DNA mismatch repair genes and hereditary non-polyposis colorectal cancer RODNEY J SCOTT, RODNEY J SCOTT Discipline of Medical Genetics, Faculty of Health, University of Newcastle and The Hunter Medical Research Institute, Newcastle, NSW, Australia. Email: rodney.scott@newcastle.edu.auSearch for more papers by this author RODNEY J SCOTT, RODNEY J SCOTT Discipline of Medical Genetics, Faculty of Health, University of Newcastle and The Hunter Medical Research Institute, Newcastle, NSW, Australia. Email: rodney.scott@newcastle.edu.auSearch for more papers by this author First published: 10 March 2004 https://doi.org/10.1111/j.1440-1746.2004.03425.x Contributions to the Genetic Disorders in Gastroenterology and Hepatology Section are welcomed and should be submitted to Professor IC Roberts-Thomson, Department of Gastroenterology, The Queen Elizabeth Hospital, Woodville South, South Australia 5011, Australia. Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article. Volume19, Issue4April 2004Pages 465-466 RelatedInformation

29 Erythropoletin improves the oxygen carrying capacity of mouse blood without changing hypoxia in a murine tumour model

Surrogate endpoints for prostate cancer-specific mortality after curative primary treatment are not well established. We sought to assess time to biochemical failure (TTBF) and prostate-specific antigen doubling time (PSADT) after failure of curative treatment as candidates for this endpoint.PSA and survival data from the Trans-Tasman Radiation Oncology Group (TROG) 96.01 trial were used to assess surrogate candidates. Between June 28, 1996, and Feb 16, 2000, 802 eligible men with locally advanced prostate cancer were randomly allocated to prostatic irradiation alone, or to 3 or 6 months of maximum short-term androgen deprivation (STAD) before and during radiation. Successful surrogates were required to satisfy the Prentice criteria and to predict the trial finding. The TROG 96.01 trial is registered with the Australian New Zealand Clinical Trials Registry, number ACTRN12607000237482.6 months of STAD was shown to significantly decrease prostate cancer-specific mortality compared with radiation alone, but 3 months of STAD did not result in a decrease. Relative to radiation alone, the hazard ratio of prostate cancer-specific mortality from randomisation was 0·95 (95% CI 0·63–1·41; p=0·79) in the 3-month STAD treatment arm and 0·56 (0·36–0·88; p=0·01) in the 6-month arm. PSADT predicted the trial finding and satisfied all four Prentice criteria at the cutpoints of less than 12 months and less than 15 months, with proportion of treatment effect ratios between 0·36 and 0·56. Time to biochemical failure was better than PSADT at predicting the trial finding and satisfying all four Prentice criteria at cutpoints of less than 1·5, less than 2, and less than 2·5 years, with proportion of treatment effect ratios between 0·45 and 0·64.This study provides proof of principle that TTBF and PSADT can be useful as surrogate endpoints for prostate cancer-specific mortality and offer potential to substantially reduce follow up in clinical trials. These endpoints now require assessment in multi-trial meta-analyses before use in clinical trials.National Health and Medical Research Council (Australia; Project Grant Applications 9936572, 209801, 455520); Hunter Medical Research Institute (Newcastle, NSW, Australia); AstraZeneca (Sydney, NSW, Australia); and Schering-Plough (Sydney, NSW, Australia).