Artificial reefs and marine protected areas: a study in willingness to pay to access Folkestone Marine Reserve, Barbados, West Indies

Artificial reefs in marine protected areas provide additional habitat for biodiversity viewing, and therefore may offer an innovative management solution for managing for coral reef recovery and resilience. Marine park user fees can generate revenue to help manage and maintain natural and artificial reefs. Using a stated preference survey, this study investigates the present consumer surplus associated with visitor use of a marine protected area in Barbados. Two hypothetical markets were presented to differentiate between respondents use values of either: (a) natural reefs within the marine reserve or (b) artificial reef habitat for recreational enhancement. Information was also collected on visitors’ perceptions of artificial reefs, reef material preferences and reef conservation awareness. From a sample of 250 visitors on snorkel trips, we estimate a mean willingness to pay of US$18.33 (median—US$15) for natural reef use and a mean value of US$17.58 (median—US$12.50) for artificial reef use. The number of marine species viewed, age of respondent, familiarity with the Folkestone Marine Reserve and level of environmental concern were statistically significant in influencing willingness to pay. Regression analyses indicate visitors are willing to pay a significant amount to view marine life, especially turtles. Our results suggest that user fees could provide a considerable source of income to aid reef conservation in Barbados. In addition, the substantial use value reported for artificial reefs indicates a reef substitution policy may be supported by visitors to the Folkestone Marine Reserve. We discuss our findings and highlight directions for future research that include the need to collect data to establish visitors’ non-use values to fund reef management

Telomere structure and maintenance gene variants and risk of five cancer types.

Telomeres cap chromosome ends, protecting them from degradation, double-strand breaks, and end-to-end fusions. Telomeres are maintained by telomerase, a reverse transcriptase encoded by TERT, and an RNA template encoded by TERC. Loci in the TERT and adjoining CLPTM1L region are associated with risk of multiple cancers. We therefore investigated associations between variants in 22 telomere structure and maintenance gene regions and colorectal, breast, prostate, ovarian, and lung cancer risk. We performed subset-based meta-analyses of 204,993 directly-measured and imputed SNPs among 61,851 cancer cases and 74,457 controls of European descent. Independent associations for SNP minor alleles were identified using sequential conditional analysis (with gene-level p value cutoffs ≤3.08 × 10-5 ). Of the thirteen independent SNPs observed to be associated with cancer risk, novel findings were observed for seven loci. Across the DCLRE1B region, rs974494 and rs12144215 were inversely associated with prostate and lung cancers, and colorectal, breast, and prostate cancers, respectively. Across the TERC region, rs75316749 was positively associated with colorectal, breast, ovarian, and lung cancers. Across the DCLRE1B region, rs974404 and rs12144215 were inversely associated with prostate and lung cancers, and colorectal, breast, and prostate cancers, respectively. Near POT1, rs116895242 was inversely associated with colorectal, ovarian, and lung cancers, and RTEL1 rs34978822 was inversely associated with prostate and lung cancers. The complex association patterns in telomere-related genes across cancer types may provide insight into mechanisms through which telomere dysfunction in different tissues influences cancer risk.Funding for the iCOGS infrastructure came from: the European Community’s Seventh Framework Programme under grant agreement n° 223175 (HEALTH-F2-2009-223175) (COGS), Cancer Research UK (C1287/A10118, C1287/A 10710, C12292/A11174, C1281/A12014, C5047/A8384, C5047/A15007, C5047/A10692, C8197/A16565), the National Institutes of Health (CA128978) and Post-Cancer GWAS initiative (1U19 CA148537, 1U19 CA148065 and 1U19 CA148112 – the GAME-ON initiative), the Department of Defense (W81XWH-10-1-0341), the Canadian Institutes of Health Research (CIHR) for the CIHR Team in Familial Risks of Breast Cancer, Komen Foundation for the Cure, the Breast Cancer Research Foundation, and the Ovarian Cancer Research Fund.This is the author accepted manuscript. The final version is available from Wiley via http://dx.doi.org/10.1002/ijc.3028

Investigating Pseudorabies Virus as a Mortality Factor for California Mountain Lions

Wild pigs in North America carry multiple pathogens capable of causing diseases in wildlife, people, and domestic animals. Wild pigs are the reservoir host of pseudorabies virus (PrV) which is a fatal infection in wild carnivores. We previously conducted surveillance for PrV in wild pigs from Kern County, California where the distribution of wild pigs overlaps with native mountain lion. We found that 100% of wild pigs were exposed to PrV, and 6% were shedding the virus. Black bears and pumas have been observed preying on wild pigs in the region suggesting that they are vulnerable to exposure to PrV from pigs. We conducted retrospective, post-mortem surveillance for PrV on 16 pumas from five counties in south central California. None of the pumas tested positive for PrV. In Florida, PrV is attributed to one-third of the deaths in Florida panthers. Wild pigs are a large portion of the diet of panthers in Florida, but studies in California suggest pigs may not be utilized as frequently. This difference in diet could account for the lack of evidence that PrV causes measurable mortality in California pumas. Nonetheless, in management areas with carnivores, wild pig management should be carefully considered

Investigating Pseudorabies Virus as a Mortality Factor for California Mountain Lions

Wild pigs in North America carry multiple pathogens capable of causing diseases in wildlife, people, and domestic animals. Wild pigs are the reservoir host of pseudorabies virus (PrV) which is a fatal infection in wild carnivores. We previously conducted surveillance for PrV in wild pigs from Kern County, California where the distribution of wild pigs overlaps with native mountain lion. We found that 100% of wild pigs were exposed to PrV, and 6% were shedding the virus. Black bears and pumas have been observed preying on wild pigs in the region suggesting that they are vulnerable to exposure to PrV from pigs. We conducted retrospective, post-mortem surveillance for PrV on 16 pumas from five counties in south central California. None of the pumas tested positive for PrV. In Florida, PrV is attributed to one-third of the deaths in Florida panthers. Wild pigs are a large portion of the diet of panthers in Florida, but studies in California suggest pigs may not be utilized as frequently. This difference in diet could account for the lack of evidence that PrV causes measurable mortality in California pumas. Nonetheless, in management areas with carnivores, wild pig management should be carefully considered

2012 Update to the 2005 Town of Middletown Comprehensive Plan

This document is an update to the 2005 Town of Middletown Comprehensive Plan and serves as a guide for Middletown’s land use decisions and annexation policy. It also serves as a consolidated reference containing demographic, housing, economic, environmental, and historical information about Middletown.Town of Middletow

Extending Voice and Autonomy through Participatory Action Research: Ethical and Practical Issues

Participatory action research always operates in the tension of extending the voice of people who are marginalised and unheard in the society. A workshop, ‘Extending Voice and Autonomy through Participatory Action Research: Ethical and Practical Issues’, was therefore organised to look at the issues arising from this tension. The workshop aimed to examine critically the potential of participatory action research to enable people whose voices are seldom heard and choices are often restricted to be seen, heard and to influence practice and policy relevant to their lives. The paper first outlines the rationale for the workshop and then demonstrates how ‘co-impact’ of participatory action research projects can be achieved through having conversations and reflecting on the ideas of ‘voice and autonomy’, ‘knowledge’, ‘vulnerability’, ‘user involvement and participation’. Through reflecting on the experience of preparing for and delivering the workshop, we seek ways to transform the relationship(s) between service users/community partners and academic and service professionals in the hope of generating practical knowledge ethically

Conditional disruption of hepatic carbamoyl phosphate synthetase 1 in mice results in hyperammonemia without orotic aciduria and can be corrected by liver-directed gene therapy

Carbamoyl phosphate synthetase 1 (CPS1) is a urea cycle enzyme that forms carbamoyl phosphate from bicarbonate, ammonia and ATP. Bi-allelic mutations of the CPS1 gene result in a urea cycle disorder presenting with hyperammonemia, often with reduced citrulline, and without orotic aciduria. CPS1 deficiency is particularly challenging to treat and lack of early recognition typically results in early neonatal death. Therapeutic interventions have limited efficacy and most patients develop long-term neurologic sequelae. Using transgenic techniques, we generated a conditional Cps1 knockout mouse. By loxP/Cre recombinase technology, deletion of the Cps1 locus was achieved in adult transgenic animals using a Cre recombinase-expressing adeno-associated viral vector. Within four weeks from vector injection, all animals developed hyperammonemia without orotic aciduria and died. Minimal CPS1 protein was detectable in livers. To investigate the efficacy of gene therapy for CPS deficiency following knock-down of hepatic endogenous CPS1 expression, we injected these mice with a helper-dependent adenoviral vector (HDAd) expressing the large murine CPS1 cDNA under control of the phosphoenolpyruvate carboxykinase promoter. Liver-directed HDAd-mediated gene therapy resulted in survival, normalization of plasma ammonia and glutamine, and 13% of normal Cps1 expression. A gender difference in survival suggests that female mice may require higher hepatic CPS1 expression. We conclude that this conditional murine model recapitulates the clinical and biochemical phenotype detected in human patients with CPS1 deficiency and will be useful to investigate ammonia-mediated neurotoxicity and for the development of cell- and gene-based therapeutic approaches

Generalized dermatophytosis caused by Trichophyton equinum in 8 juvenile black bears in California

From 2014-2019, 8 juvenile black bears (Ursus americanus) from different geographic regions were presented to the California Department of Fish and Wildlife because of emaciation, alopecia, and exfoliative dermatitis that resulted in death or euthanasia. Autopsy and histopathology revealed that all 8 bears had generalized hyperkeratotic dermatitis, folliculitis, and furunculosis. Skin structures were heavily colonized by fungal hyphae and arthrospores; fungal cultures of skin from 7 bears yielded Trichophyton equinum, a zoophilic dermatophyte reported only rarely in non-equid species. Additional skin conditions included mites (5), ticks (2), and coagulase-negative Staphylococcus sp. infections (2). No other causes of morbidity or mortality were identified. Molecular comparisons performed at the University of Texas Fungal Reference Laboratory determined that all isolates produced identical banding patterns, potentially representing a clonal population. Dermatophytosis is commonly localized and limited to the stratum corneum of the epidermis and hair follicles. Generalized disease with dermal involvement is rare in immunocompetent individuals; illness, malnutrition, age, or immunosuppression may increase susceptibility. Underlying causes for the severe disease impact in these bears were not evident after physical or postmortem examination. The mechanism by which bears from different geographic locations had severe, T. equinum-associated dermatophytosis from a potentially clonal dermatophyte could not be explained and warrants further investigation