The Maori social science academy and evidence-based policy

This paper focuses on recent moves to forge stronger linkages between the Māori social science academy and the policy industry. A critical appraisal of this development is offered, with particular attention given to the desirability of enhancing the academy’s role in the policy process, given the policy industry’s continued privileging of Eurocentric theory and research methodologies within the developing evidence-based environment. The paper ends with a discussion of the possibilities and problems associated with engagement with the policy industry, particularly as these relate to the various roles members can (or are forced to) take; either as ‘insiders’ (such as policy workers and contract researchers), or independent, critical ‘outsiders’. The author concludes that the best that insiders can hope for are incremental, largely ineffective changes to Māori policy, while independent members of the academy are best placed to speak on behalf of Māori, Māori communities, hapu and iwi.

Ambient temperature and morbidity: A review of epidemiological evidence

OBJECTIVE: This paper reviews the epidemiological evidence on the relationship between ambient temperature and morbidity. It assesses the methodological issues in previous studies, and proposes future research directions. DATA SOURCES AND DATA EXTRACTION: We searched the PubMed database for epidemiological studies on ambient temperature and morbidity of non-communicable diseases published in refereed English journals prior to June 2010. 40 relevant studies were identified. Of these, 24 examined the relationship between ambient temperature and morbidity, 15 investigated the short-term effects of heatwave on morbidity, and 1 assessed both temperature and heatwave effects. DATA SYNTHESIS: Descriptive and time-series studies were the two main research designs used to investigate the temperature–morbidity relationship. Measurements of temperature exposure and health outcomes used in these studies differed widely. The majority of studies reported a significant relationship between ambient temperature and total or cause-specific morbidities. However, there were some inconsistencies in the direction and magnitude of non-linear lag effects. The lag effect of hot temperature on morbidity was shorter (several days) compared to that of cold temperature (up to a few weeks). The temperature–morbidity relationship may be confounded and/or modified by socio-demographic factors and air pollution. CONCLUSIONS: There is a significant short-term effect of ambient temperature on total and cause-specific morbidities. However, further research is needed to determine an appropriate temperature measure, consider a diverse range of morbidities, and to use consistent methodology to make different studies more comparable.

Evidence for u.v. induction of CDKN2 mutations in melanoma cell lines

The CDKN2 gene, encoding the cyclin dependent kinase inhibitor p16, is a tumour suppressor gene involved in melanoma and maps to chromosome band 9p22. Mutations or interstitial deletions of this gene have been found both in the germline of familial melanoma cases and somatically in melanoma cell lines. Previous mutation analyses of melanoma cell lines have indicated a high frequency of C:G to T:A transitions, with all of these mutations occurring at dipyrimidine sites. Including three melanoma cell lines carrying tandem CC to TT mutations, the spectrum of mutations so far reported indicates a possible role for u.v. radiation in the mutagenesis of this gene in some tumours. To further examine this hypothesis we have characterised mutations of the CDKN2 gene in 30 melanoma cell lines. Nineteen lines carried complete or partial homozygous deletions of the gene. Of the remaining cell lines, eight were shown by direct sequencing of PCR products from exon 1 and exon 2 to carry a total of nine different mutations of CDKN2. Two cell lines carried tandem CC to TT mutations and a high rate of C:G to T:A transitions was observed. This study provides further evidence for the role of u.v. light in the genesis of melanoma, with one target being the CDKN2 tumour suppressor gene.

Haplotype analysis of two recurrent CDKN2A mutations in 10 melanoma families : evidence for common founders and independent mutations

Germ-line mutations in CDKN2A have been shown to predispose to cutaneous malignant melanoma. We have identified 2 new melanoma kindreds which carry a duplication of a 24bp repeat present in the 5' region of CDKN2A previously identified in melanoma families from Australia and the United States. This mutation has now been reported in 5 melanoma families from 3 continents: Europe, North America, and Australasia. The M53I mutation in exon 2 of CDKN2A has also been documented in 5 melanoma families from Australia and North America. The aim of this study was to determine whether the occurrence of the mutations in these families from geographically diverse populations represented mutation hotspots within CDKN2A or were due to common ancestors. Haplotypes of 11 microsatellite markers flanking CDKN2A were constructed in 5 families carrying the M53I mutation and 5 families carrying the 24bp duplication. There were some differences in the segregating haplotypes due primarily to recombinations and mutations within the short tandem-repeat markers; however, the data provide evidence to indicate that there were at least 3 independent 24bp duplication events and possibly only 1 original M53I mutation. This is the first study to date which indicates common founders in melanoma families from different continents.