Is it time to talk? Interpreter services use in general practice within Canterbury

INTRODUCTION: Effective communication is fundamental to successful health care service delivery, and has a positive impact on access, quality of care, health outcomes, and patient satisfaction. Although there are a growing number of New Zealanders who do not speak English proficiently, underutilisation of trained interpreter services appears to be common in primary health care settings. AIMS: To describe the pattern of interpreter service need and utilisation by general practice services, and to identify key barriers and enabling factors to the use of trained interpreters. METHODS: A mixed methods study was employed. Census and Partnership Health Canterbury Te Kei o Te Waka (PHC) databases were combined, and quantitative analysis used to derive interpreter service need and utilisation patterns. Transcripts of focus groups and interviews from general practitioners, practice nurses and practice administration staff within the PHC were analysed, using qualitative methods to identify barriers and enablers to interpreter service use. RESULTS: For the years 2008-2010, approximately 10 742 consultations per year involved a non-Englishspeaking patient, yet in only approximately 74.8 (0.7%) consultations per year were interpreter services utilised. Analysis of focus groups and interviews identified four global themes that represented barriers for interpreter service utilisation; namely, practicalities, expectations, knowledge of service, and systems. DISCUSSION: The current use of interpreter services in PHC general practice appears to be significantly less than the need. In order to maximise health outcomes and reduce risk, strategies must be initiated to counter the barriers currently inhibiting interpreter service use, including adopting best practice policies

Improving the evidence-base for access to primary health care in Canterbury: a panel study

Objective: Despite many reforms and initiatives, inequities in access to primary health care remain. However, the concept of ‘access’ and its measurement is complex. This paper aims to provide estimates of general practice visit frequencies for ‘attenders’ (those who seek consultation) and the proportion of ‘non-attenders’ (those who never seek consultation) of primary health care services. Methods: A panel study of people enrolled within a large primary health care organisation of affiliated general practices. Standard and zero-inflated regression models were assessed. Results: 980,918 visits were made by 388,424 people, averaging 2.64 visits/person/year. The zero-inflated negative binomial model was superior, and significant age, gender and ethnic differences were observed in attender and non-attender profiles. More Asian (21.0%), Pacific (19.6%) and Maori (17.1%) people were non-attenders than European/Other (9.0%) people. Among attenders, males, Asian and Pacific people, and young to middle-aged adults, generally had relatively lower visit rates. Conclusions: Interpretation of utilisation data must be made with caution because of two distinct characteristics: the differential rates of non-attenders and the highly dispersed distribution of attenders. Implications: Improved understanding of differential non-attender rates and attender visit distributions by demographic factors needs to be considered when addressing improved access to general practice services

Structural basis of receptor sulfotyrosine recognition by a cc chemokine: The n-terminal region of CCR3 bound to CCL11/eotaxin-1

© 2014 Elsevier Ltd. Trafficking of leukocytes in immune surveillance and inflammatory responses is activated by chemokines engaging their receptors. Sulfation of tyrosine residues in peptides derived from the eosinophil chemokine receptor CCR3 dramatically enhances binding to cognate chemokines. We report the structural basis of this recognition and affinity enhancement. We describe the structure of a CC chemokine (CCL11/eotaxin-1) bound to a fragment of a chemokine receptor: residues 8-23 of CCR3, including two sulfotyrosine residues. We also show that intact CCR3 is sulfated and sulfation enhances receptor activity. The CCR3 sulfotyrosine residues form hydrophobic, salt bridge and cation-π interactions with residues that are highly conserved in CC chemokines. However, the orientation of the chemokine relative to the receptor N terminus differs substantially from those observed for two CXC chemokines, suggesting that initial binding of the receptor sulfotyrosine residues guides subsequent steps in receptor activation, thereby influencing the receptor conformational changes and signaling

Novel drivers and modifiers of MPL-dependent oncogenic transformation identified by deep mutational scanning.

The single transmembrane domain (TMD) of the human thrombopoietin receptor (TpoR/myeloproliferative leukemia [MPL] protein), encoded by exon 10 of the MPL gene, is a hotspot for somatic mutations associated with myeloproliferative neoplasms (MPNs). Approximately 6% and 14% of JAK2 V617F- essential thrombocythemia and primary myelofibrosis patients, respectively, have "canonical" MPL exon 10 driver mutations W515L/K/R/A or S505N, which generate constitutively active receptors and consequent loss of Tpo dependence. Other "noncanonical" MPL exon 10 mutations have also been identified in patients, both alone and in combination with canonical mutations, but, in almost all cases, their functional consequences and relevance to disease are unknown. Here, we used a deep mutational scanning approach to evaluate all possible single amino acid substitutions in the human TpoR TMD for their ability to confer cytokine-independent growth in Ba/F3 cells. We identified all currently recognized driver mutations and 7 novel mutations that cause constitutive TpoR activation, and a much larger number of second-site mutations that enhance S505N-driven activation. We found examples of both of these categories in published and previously unpublished MPL exon 10 sequencing data from MPN patients, demonstrating that some, if not all, of the new mutations reported here represent likely drivers or modifiers of myeloproliferative disease