Canine models of copper toxicosis for understanding mammalian copper metabolism

Hereditary forms of copper toxicosis exist in man and dogs. In man, Wilson’s disease is the best studied disorder of copper overload, resulting from mutations in the gene coding for the copper transporter ATP7B. Forms of copper toxicosis for which no causal gene is known yet are recognized as well, often in young children. Although advances have been made in unraveling the genetic background of disorders of copper metabolism in man, many questions regarding disease mechanisms and copper homeostasis remain unanswered. Genetic studies in the Bedlington terrier, a dog breed affected with copper toxicosis, identified COMMD1, a gene that was previously unknown to be involved in copper metabolism. Besides the Bedlington terrier, a number of other dog breeds suffer from hereditary copper toxicosis and show similar phenotypes to humans with copper storage disorders. Unlike the heterogeneity of most human populations, the genetic structure within a purebred dog population is homogeneous, which is advantageous for unraveling the molecular genetics of complex diseases. This article reviews the work that has been done on the Bedlington terrier, summarizes what was learned from studies into COMMD1 function, describes hereditary copper toxicosis phenotypes in other dog breeds, and discusses the opportunities for genome-wide association studies on copper toxicosis in the dog to contribute to the understanding of mammalian copper metabolism and copper metabolism disorders in man

Monitoring timber beam bridge structural reliability in regional Australia

There are many thousands of timber beam bridges throughout regional Australia, which are monitored primarily by visual inspection. Experience gained from historical failures has led to the clear realisation that visual inspection at intervals of many months or years is insufficient to identify potential failure caused by overloading and biological degradation. A bridge overloaded today can fail tomorrow and there is a need to implement structural health monitoring (SHM) so that the incidence of overloading can be identified soon after it occurs. This need is becoming more vital with the increased expectation to cater for the increased loads during periods of transporting seasonal produce. The measurement mid-span displacement of girders can be used to determine safety indices for the evaluation of structural safety. The detection of real-time damage in timber girder bridges by the use of high-speed camera and laser-based methods offer unique advantages and can lead to low cost measurement techniques. This work reports on the use of continuous monitoring methods for determining the structural reliability of timber-beam bridge girders. Some applications of the use of laser-based displacement sensing systems are discussed in relation to the monitoring of the structural reliability of two older timber beam bridges in regional New South Wales, Australia. Experimental and analytical approaches are presented and used to demonstrate that the probability of failure can be readily determined on a continuous basis using an SHM system

Does smoking or alcohol modify the risk of Epstein-Barr Virus-Positive or -Negative Hodgkin Lymphoma?

BACKGROUND: The aim was to investigate whether 2 subgroups of Hodgkin lymphoma (Epstein-Barr virus-positive and Epstein-Barr virus-negative) are associated with smoking or alcohol. METHODS: Patients with lymphoma diagnosed between age 16 and 69 years in geographically defined areas of England were recruited between 1998 and 2003. One control, matched to each lymphoma case on sex, date of birth, and area of residence, was randomly selected from population registers. Self-reported histories of tobacco and alcohol use were collected during face-to-face interviews with cases and controls. RESULTS: Compared with lifelong nonsmokers, ever-smokers were at increased risk of Hodgkin lymphoma (odds ratio =1.4; 95% confidence interval = 1.1–1.9). This excess was among current smokers, defined as smoking 2 years before diagnosis (1.7; 1.2–2.3). An increasing trend was observed with rising numbers of years smoked. Risks fell as the number of years stopped smoking increased, becoming equivalent to that of a nonsmoker 10 or more years after quitting. Associations were suggested for Epstein-Barr virus-positive Hodgkin lymphoma, but less so for Epstein-Barr negative Hodgkin lymphoma. No associations between Hodgkin lymphoma and alcohol consumption were observed. CONCLUSIONS: The association between smoking and Hodgkin lymphoma in general, and Epstein-Barr-positive Hodgkin lymphoma in particular, is consistent with previous studies. Further exploration of the relationship between Hodgkin lymphoma and smoking and of the potential mechanisms by which smoking could interact with Epstein-Barr virus status to increase Hodgkin lymphoma risk are required