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Richard Turner

Publications and source records attributed to Richard Turner.

12 recordsLinked to original sources
PubMed2005

Colorectal carcinoma among Indigenous people: a public hospital-based study in Townsville and Cairns, North Queensland, Australia.

INTRODUCTION: There are very little clinical and pathological data on colorectal cancer among Indigenous people in Australia. METHODS: A retrospective study on Indigenous patients treated for colorectal cancer at the Townsville and Cairns Base Hospitals from 1999 to 2004 was carried out in order to better characterise this disease in the Indigenous population. RESULTS: There were 25 patients (12 M, 13 F) with a median age of 57.3 years. The majority (56%) of the tumours were left-sided, being in the sigmoid colon, rectosigmoid junction and rectum. Of the patients, 60% had American Joint Committee on Cancer (AJCC) staging system Stage I and II disease at presentation. There was a relatively high proportion of poorly differentiated adenocarcinomas (40%). Six patients died of the disease. The median follow-up was 20.5 months (range 2-51). CONCLUSIONS: Comparisons were made with available data on colorectal cancer in the general Australian population. The limitations and deficiencies of the study, as well as problems of data collection on Indigenous people were discussed.

Adult↗
PubMed2005

The processing and perception of size information in speech sounds.

There is information in speech sounds about the length of the vocal tract; specifically, as a child grows, the resonators in the vocal tract grow and the formant frequencies of the vowels decrease. It has been hypothesized that the auditory system applies a scale transform to all sounds to segregate size information from resonator shape information, and thereby enhance both size perception and speech recognition [Irino and Patterson, Speech Commun. 36, 181-203 (2002)]. This paper describes size discrimination experiments and vowel recognition experiments designed to provide evidence for an auditory scaling mechanism. Vowels were scaled to represent people with vocal tracts much longer and shorter than normal, and with pitches much higher and lower than normal. The results of the discrimination experiments show that listeners can make fine judgments about the relative size of speakers, and they can do so for vowels scaled well beyond the normal range. Similarly, the recognition experiments show good performance for vowels in the normal range, and for vowels scaled well beyond the normal range of experience. Together, the experiments support the hypothesis that the auditory system automatically normalizes for the size information in communication sounds.

Humans↗
PubMed2003

MHC recognition by hapten-specific HLA-A2-restricted CD8+ CTL.

T cell recognition by peptide-specific alphabeta TCRs involves not only recognition of the peptide, but also recognition of multiple molecular features on the surface of the MHC molecule to which the peptide has been bound. We have previously shown that TCRs that are specific for five different peptides presented by HLA-A2 recognize similar molecular features on the surface of the alpha1 and alpha2 helices of the HLA-A2 molecule. We next asked whether these same molecular features of the HLA-A2 molecule would be recognized by hapten-specific HLA-A2-restricted TCRs, given that hapten-specific T cells frequently show reduced MHC dependence/restriction. The results show that a panel of CD8+ CTL that are specific for the hapten DNP bound to two different peptides presented by HLA-A2 do the following: 1) show stringent MHC restriction, and 2) are largely affected by the same mutations on the HLA-A2 molecule that affected recognition by peptide-specific CTL. A small subset of this panel of CD8+ CTL can recognize a mutant HLA-A2 molecule in the absence of hapten. These data suggest that TCR recognition of a divergent repertoire of ligands presented by HLA-A2 is largely dependent upon common structural elements in the central portion of the peptide-binding site.

Alanine↗
PubMed2003

Taking myc to the max.

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Basic Helix-Loop-Helix Leucine Zipper Transcriptio↗
PubMed2002

MHC allele-specific molecular features determine peptide/HLA-A2 conformations that are recognized by HLA-A2-restricted T cell receptors.

The structures of alphabeta TCRs bound to complexes of class I MHC molecules and peptide show that the TCRs make multiple contacts with the alpha1 and alpha2 helixes of the MHC. Previously we have shown that the A6 TCR in complex with the HLA-A2/Tax peptide has 15 contact sites on HLA-A2. Single amino acid mutagenesis of these contact sites demonstrated that mutation of only three amino acids clustered on the alpha1 helix (R65, K66, A69) disrupted recognition by the A6 TCR. In the present study we have asked whether TCRs that recognize four other peptides presented by HLA-A2 interact with the MHC in identical, similar, or different patterns as the A6 TCR. Mutants K66A and Q155A had the highest frequency of negative effects on lysis. A subset of peptide-specific CTL also selectively recognized mutants K66A or Q155A in the absence of exogenous cognate peptides, indicating that these mutations affected the presentation of endogenous peptide/HLA-A2 complexes. These findings suggest that most HLA-A2-restricted TCRs recognize surfaces on the HLA-A2/peptide complex that are dependent upon the side chains of K66 and Q155 in the central portion of the peptide binding groove. Crystallographic structures of several peptide/HLA-A2 structures have shown that the side chains of these critical amino acids that make contact with the A6 TCR also contact the bound peptide. Collectively, our results indicate that the generalized effects of changes at these critical amino acids are probably due to the fact that they can be directly contacted by TCRs as well as influence the binding and presentation of the bound peptides.

Alleles↗