Biomedical subjects

Susan A Moore

Publications and source records attributed to Susan A Moore.

3 recordsLinked to original sources

PubMed2007

Defining indicators and standards for tourism impacts in protected areas: Cape Range National Park, Australia.

Visitors' perceptions of impacts and acceptable standards for environmental conditions can provide essential information for the sustainable management of tourist destinations, especially protected areas. To this end, visitor surveys were administered during the peak visitor season in Cape Range National Park, on the northwest coast of Western Australia and adjacent to the iconic Ningaloo Reef. The central focus was visitors' perceptions regarding environmental conditions and standards for potential indicators. Conditions considered of greatest importance in determining visitors' quality of experience included litter, inadequate disposal of human waste, presence of wildlife, levels of noise, and access to beach and ocean. Standards were determined, based on visitors' perceptions, for a range of site-specific and non-site-specific indicators, with standards for facilities (e.g., acceptable number of parking bays, signs) and for negative environmental impacts (e.g., levels of littering, erosion) sought. The proposed standards varied significantly between sites for the facilities indicators; however, there was no significant difference between sites for environmental impacts. For the facilities, the standards proposed by visitors were closely related to the existing situation, suggesting that they were satisfied with the status quo. These results are considered in the context of current research interest in the efficacy of visitor-derived standards as a basis for protected area management.

Data Collection↗

PubMed2006

Do we all face the same risk when bathing in the estuary?

With the development of coastal areas, microbial water quality is an emerging public health issue though few studies have focused on risks according to age. A survey was undertaken of faecal contamination in relation to recreational activities in the Peel Harvey estuarine system, Western Australia. Levels of exposure to contaminated water were estimated though social surveys. Follow-up was also conducted to estimate the incidence of disease associated with bathing in the estuary. Pathogen levels exceeded the guideline values recommended by the World Health Organisation (WHO) at most locations throughout the year. The social survey provided information about exposure of the population in age groups. Only 31% of the recreational users belonged to the healthy adult group upon which the WHO quantitative microbial risk assessment model is based. A correlation was established between microbial water quality and incidence of respiratory diseases for children as well as for adults. Exposure to recreational water increased the incidence of respiratory illnesses for the whole population almost by a factor 2. Behaviours which resulted in increased exposures were associated with increased incidence of illnesses were observed, particularly among children aged 11-15 yr, who exhibited the highest odd ratio (OR 4.23 [2.44-6.01], CI 95%, p=0.05). There is a need for combining epidemiology studies with risk assessment processes and complementing them with social surveys for understanding the risk of recreational activities to public health.

Adolescent↗

PubMed2004

Both the D-(+) and L-(-) enantiomers of nicotine inhibit Abeta aggregation and cytotoxicity.

The underlying cause of Alzheimer's disease is thought to be the aggregation of monomeric beta-amyloid (Abeta), through a series of toxic oligomers, which forms the mature amyloid fibrils that accumulate at the center of senile plaques. It has been reported that L-(-)-nicotine prevents Abeta aggregation and toxicity, and inhibits senile plaque formation. Previous NMR studies have suggested that this could be due to the specific binding of L-(-)-nicotine to histidine residues (His6, His13, and His14) in the peptide. Here, we have looked at the effects of both of the L-(-) and D-(+) optical enantiomers of nicotine on the aggregation and cytotoxicity of Abeta(1-40). Surprisingly, both enantiomers inhibited aggregation of the peptide and reduced the toxic effects of the peptide on cells. In NMR studies with Abeta(1-40), both enantiomers of nicotine were seen to interact with the three histidine residues. Overall, our data indicate that nicotine can delay Abeta fibril formation and maintain a population of less toxic Abeta species. This effect cannot be due to a highly specific binding interaction between nicotine and Abeta, as previously thought, but could be due instead to weaker, relatively nonspecific binding, or to the antioxidant or metal chelating properties of nicotine. D-(+)-nicotine, being biologically much less active than L-(-)-nicotine, might be a useful therapeutic agent.

Amyloid beta-Peptides↗