Building resilience to mosquito-borne diseases in the Caribbean.

Small island developing states in the Caribbean are among the most vulnerable countries on the planet to climate variability and climate change. In the last 3 decades, the Caribbean region has undergone frequent and intense heat waves, storms, floods, and droughts. This has had a detrimental impact on population health and well-being, including an increase in infectious disease outbreaks. Recent advances in climate science have enhanced our ability to anticipate hydrometeorological hazards and associated public health challenges. Here, we discuss progress towards bridging the gap between climate science and public health decision-making in the Caribbean to build health system resilience to extreme climatic events. We focus on the development of climate services to help manage mosquito-transmitted disease epidemics. There are numerous areas of ongoing biological research aimed at better understanding the direct and indirect impacts of climate change on the transmission of mosquito-borne diseases. Here, we emphasise additional factors that affect our ability to operationalise this biological understanding. We highlight a lack of financial resources, technical expertise, data sharing, and formalised partnerships between climate and health communities as major limiting factors to developing sustainable climate services for health. Recommendations include investing in integrated climate, health and mosquito surveillance systems, building regional and local human resource capacities, and designing national and regional cross-sectoral policies and national action plans. This will contribute towards achieving the Sustainable Development Goals (SDGs) and maximising regional development partnerships and co-benefits for improved health and well-being in the Caribbean.

Insulin promoter factor-1 mutations and diabetes in Trinidad: identification of a novel diabetes-associated mutation (E224K) in an Indo-Trinidadian family.

This study investigated the prevalence of insulin promoter factor-1(IPF-1) mutations in familial early-onset diabetes mellitus in Trinidad. We screened 264 unrelated subjects with type 2 diabetes diagnosed before 40 yr of age and a family history of diabetes for mutations in the minimal promoter and coding region of the IPF-1 gene (IPF1). This study population included 169 patients of East Indian descent (Indo-Trinidadians), 66 of African descent (Afro-Trinidadians), and 29 of mixed ancestry. We identified five IPF1 variants, including one new missense mutation E224K, the previously described diabetes-associated duplication P242 P243dupP, two silent mutations in the codons for Leu54 (c.162G>A) and Ala256 (c.768C>A), and a substitution in the 5'-untranslated region (c.-18C>T). The E224K mutation was found in two unrelated diabetic Indo-Trinidadians and 0 of 60 controls. It was present on the same haplotype in both patients suggesting a founder effect. The E224K mutation cosegregated with early-onset diabetes or impaired glucose tolerance in a large family, suggestive of the type 4 form of maturity-onset diabetes of the young rather than type 2 diabetes. Functional studies of E224K showed reduced transactivation activity. IPF1 mutations leading to synthesis of a mutant protein may contribute to the development of familial early-onset diabetes/maturity-onset diabetes of the young in Indo-Trinidadians.

Insulin promoter factor-1 mutations and diabetes in Trinidad: Identification of a novel diabetes-associated mutation (E224K) in an Indo-Trinidadian family

This study investigated the prevalence of insulin promoter factor-1 (IPF-1) mutations in familial early-onset diabetes mellitus in Trinidad. We screened 264 unrelated subjects with type 2 diabetes diagnosed before 40yr of age and a family history of diabetes for mutations in the minimal promoter and coding region of the IPF-1 gene (IPF1). This study population included 169 patients of East Indian descent (Indo-Trinidadians) 66 of African descent (Afro-Trinidadians), and 29 of mixed ancestry. We identified five IPF1 variants, including one new missense mutation E224K, the previously described diabetes-associated duplication P242 P243dupP, two silent mutations in the codons for Leu54 (c.162G>A) and Ala256 (c.768C>A), and a substitution in the 5'-untranslated region (c.-18C>T). The E224K mutation was found in two unrelated diabetic Indo-Trinidadians and 0 of 60 controls. It was present on the same haplotype in both patients suggesting a founder effect. The E224K mutation cosegregated with early-onset diabetes or impaired glucose tolerance in a large family, suggestive of the type 4 form of maturity-onset diabetes of the young rather than type 2 diabetes. Functional studies of E224K showed reduced transactivation activity. IPF1 mutations leading to synthesis of a mutant protein may contribute to the development of familial early-oneset diabetes/maturity-onset diabetes of the young in Indo-Trinidadians (AU)