Biomedical subjects

Mark Osborne

Publications and source records attributed to Mark Osborne.

3 recordsLinked to original sources

PubMed2003

A comparison of two methods for the calculation of accumulated oxygen deficit.

The aim of this study was to compare accumulated oxygen deficit data derived using two different exercise protocols with the aim of producing a less time-consuming test specifically for use with athletes. Six road and four track male endurance cyclists performed two series of cycle ergometer tests. The first series involved five 10 min sub-maximal cycle exercise bouts, a VO2peak test and a 115% VO2peak test. Data from these tests were used to estimate the accumulated oxygen deficit according to the calculations of Medbø et al. (1988). In the second series of tests, participants performed a 15 min incremental cycle ergometer test followed, 2 min later, by a 2 min variable resistance test in which they completed as much work as possible while pedalling at a constant rate. Analysis revealed that the accumulated oxygen deficit calculated from the first series of tests was higher (P < 0.02) than that calculated from the second series: 52.3 +/- 11.7 and 43.9 +/- 6.4 ml x kg(-1), respectively (mean +/- s). Other significant differences between the two protocols were observed for VO2peak, total work and maximal heart rate; all were higher during the modified protocol (P < 0.01 and P < 0.02, respectively). Oxygen kinetics were also significantly faster during the modified 2 min maximal test. We conclude that the difference in accumulated oxygen deficit between protocols was probably due to a reduced oxygen uptake, possibly caused by a slower oxygen on-response during the 115% VO2peak test in the first series, and VO2-power output regression differences caused by an elevated VO2 during the early stages of the second series.

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PubMed2003

Computational knowledge integration in biopharmaceutical research.

An initiative to increase biopharmaceutical research productivity by capturing, sharing and computationally integrating proprietary scientific discoveries with public knowledge is described. This initiative involves both organisational process change and multiple interoperating software systems. The software components rely on mutually supporting integration techniques. These include a richly structured ontology, statistical analysis of experimental data against stored conclusions, natural language processing of public literature, secure document repositories with lightweight metadata, web services integration, enterprise web portals and relational databases. This approach has already begun to increase scientific productivity in our enterprise by creating an organisational memory (OM) of internal research findings, accessible on the web. Through bringing together these components it has also been possible to construct a very large and expanding repository of biological pathway information linked to this repository of findings which is extremely useful in analysis of DNA microarray data. This repository, in turn, enables our research paradigm to be shifted towards more comprehensive systems-based understandings of drug action.

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PubMed2001

A mutation in the LDL receptor-related protein 5 gene results in the autosomal dominant high-bone-mass trait.

Osteoporosis is a complex disease that affects >10 million people in the United States and results in 1.5 million fractures annually. In addition, the high prevalence of osteopenia (low bone mass) in the general population places a large number of people at risk for developing the disease. In an effort to identify genetic factors influencing bone density, we characterized a family that includes individuals who possess exceptionally dense bones but are otherwise phenotypically normal. This high-bone-mass trait (HBM) was originally localized by linkage analysis to chromosome 11q12-13. We refined the interval by extending the pedigree and genotyping additional markers. A systematic search for mutations that segregated with the HBM phenotype uncovered an amino acid change, in a predicted beta-propeller module of the low-density lipoprotein receptor-related protein 5 (LRP5), that results in the HBM phenotype. During analysis of >1,000 individuals, this mutation was observed only in affected individuals from the HBM kindred. By use of in situ hybridization to rat tibia, expression of LRP5 was detected in areas of bone involved in remodeling. Our findings suggest that the HBM mutation confers a unique osteogenic activity in bone remodeling, and this understanding may facilitate the development of novel therapies for the treatment of osteoporosis.

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