Assessing the ecological risk of heavy metal sediment contamination from Port Everglades Florida USA.

Port sediments are often contaminated with metals and organic compounds from anthropogenic sources. Remobilization of sediment during a planned expansion of Port Everglades near Fort Lauderdale, Florida (USA) has the potential to harm adjacent benthic communities, including coral reefs. Twelve sediment cores were collected from four Port Everglades sites and a control site; surface sediment was collected at two nearby coral reef sites. Sediment cores, sampled every 5 cm, were analyzed for 14 heavy metals using inductively coupled plasma-mass spectrometry. Results for all three locations yielded concentration ranges (µg/g): As (0.607-223), Cd (n/d-0.916), Cr (0.155-56.8), Co (0.0238-7.40), Cu (0.004-215), Pb (0.0169-73.8), Mn (1.61-204), Hg (n/d-0.736), Mn (1.61-204), Ni (0.232-29.3), Se (n/d-4.79), Sn (n/d-140), V (0.160-176), and Zn (0.112-603), where n/d = non-detected. The geo-accumulation index shows moderate-to-strong contamination of As and Mo in port sediments, and potential ecological risk indicates moderate-to-significantly high overall metal contamination. All four port sites have sediment core subsamples with As concentrations above both threshold effect level (TEL, 7.24 µg/g) and probable effect level (PEL, 41.6 µg/g), while Mo geometric mean concentrations exceed the background continental crust level (1.5 µg/g) threshold. Control site sediments exceed TEL for As, while the reef sites has low to no overall heavy metal contamination. Results of this study indicate there is a moderate to high overall ecological risk from remobilized sediment due to metal contamination. Due to an imminent dredging at Port Everglades, this could have the potential to harm the threatened adjacent coral communities and surrounding protected habitats.

Methods and rationale used in a matched cohort study of the incidence of new primary cancers following prostate cancer.

OBJECTIVES: We describe several methodological issues that were addressed in conducting a Danish population-based matched cohort study comparing rates of new primary cancers (NPCs) in men with and without prostate cancer (PC). METHODS: We matched 30,220 men with PC to 151,100 men without PC (comparators) on age (±2 years) and PC diagnosis/index date. We focused on several methodological issues: 1) to address survival differences between the cohorts we compared rates with and without censoring comparators on the date their matched PC patient died or was censored; 2) to address diagnostic bias, we excluded men with a history of cancer from the comparator cohort; 3) to address prostate cancer immunity, we graphed the hazard of NPC in both cohorts, with and without prostate cancer as an outcome; 4) we used empirical Bayes methods to explore the effect of adjusting for multiple comparisons. RESULTS: After 18 months of follow-up, cumulative person-time was lower in the PC than comparator cohort due to higher mortality among PC patients. Terminating person-time in comparators at the matched PC patient's death or loss to follow-up resulted in comparable person-time up to 30 months of follow-up and lower person-time among comparators thereafter. The hazard of NPC was lower among men with PC than comparators throughout follow-up. There was little difference in rates beyond the first four years of follow-up after removing PC as an outcome. Empirical Bayes adjustment for multiple comparisons had little effect on the estimates. CONCLUSION: Addressing the issues of competing risks, treatment interference or diagnostic bias, prostate cancer immunity due to radical prostatectomy, and multiple comparisons lowered the deficit rate of NPCs among men with a history of PC compared with those without PC. However, the differing rates of NPCs may also be due to risk factor differences between the cohorts.

A polymorphism (D20S32e) close to the human melanocortin receptor 3 is associated with insulin resistance but not the metabolic syndrome.

Insulin resistance (IR) is postulated to underlie diabetes, the metabolic syndrome (MS) and cardiovascular disease (CVD). The D20S32e marker close to the melanocortin receptor-3 (hMC3-R) has been shown to be associated with IR in a large New Zealand Maori kindred, a population at high risk for MS and CVD. Here we examine the potential association of the D20S32e marker with the MS in this 60 member Maori kindred. There was a significant association between the D20S32e "B" allele and the fasting insulin component under both polygenic (beta=-5.3077; p=0.008) and common sibship effect (beta=-4.2161; p=0.03) models. No significant association between the same allele of D20S32e and the MS was observed after adjusting for age under a polygenic (p=0.103) or sibling (p=0.09) correlation model. We conclude that in this Maori kindred, the D20S32e polymorphism is significantly associated with insulin resistance but not with MS. Our data supports the hypothesis that multiple gene variants are necessary for the development of the MS.

Melanocortin-3 receptor gene variants in a Maori kindred with obesity and early onset type 2 diabetes.

Genetic studies suggest a diabetes susceptibility locus on human chromosome 20, near the melanocortin receptor-3 (MC3-R) gene. We examined the MC3-R as a candidate gene for type 2 diabetes in 12 members of a large Maori kindred with multiple affected members. The coding region of the MC3-R gene was sequenced for both diabetic and non-diabetic individuals. Two separate single base pair substitutions were found in the MC3-R coding sequence and these resulted in amino acid changes, Lysine6Threonine and Isoleucine81Valine. Neither of these MC3-R variants tracked with the presence of diabetes. Furthermore, the variant and wild type MC3-R showed similar functional coupling to adenylyl cyclase. A polymorphic marker (D20S32e) close to the human MC3-R (hMC3-R) coding sequence was investigated in a 60-member pedigree for association with diabetes and other metabolic parameters. There was an association between D20S32e genotype and fasting insulin (P=0.0085) and the insulin resistance index, HOMA-R (P=0.0042). An association was also found between genotype and HDL levels during oral glucose tolerance testing (P=0.0037). These associations were independent of BMI, age, gender and diabetes. Our data do not support a role for variations in the coding region of the hMC3-R in the development of type 2 diabetes in this Maori kindred, but suggest that a locus on chromosome 20 q, close to D20S32e, may contribute to both insulin secretion and action in the Maori kindred.