Peter john Bennett - Academia.edu (original) (raw)

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Papers by Peter john Bennett

Research paper thumbnail of Isolation and Charaeterisation of Deletion Mutants Involving the Transfer Genes of P-group Plasmids in Pseudomonas aeruginosa

Research paper thumbnail of Preliminary analysis of the genetic basis for vancomycin resistance in Staphylococcus aureus strain Mu50

Journal of Antimicrobial Chemotherapy, 2002

Background Staphylococcus aureus has long been recognized as a major cause of hospital-acquired i... more Background Staphylococcus aureus has long been recognized as a major cause of hospital-acquired infection. Over the last decade, methicillin-resistant S. aureus (MRSA) strains have become endemic in hospitals worldwide, including in the UK. Accordingly, the frequency of MRSA isolation has increased dramatically. 1 Glycopeptides, such as vancomycin, are often the therapeutic drugs of choice for serious MRSA infections. However, failures of vancomycin therapy against S. aureus, due to the emergence of strains that are significantly less susceptible to vancomycin [vancomycinresistant S. aureus (VRSA)], are now well established. 2-4 The first clinical VRSA, Mu50, was isolated in Japan in 1997. 2 The VRSA phenotype of Mu50 is the result of changes to the cell wall structure. In comparison with MRSA strains, Mu50 and Mu50-like strains have a thickened cell wall, release more cell wall material into the culture medium and have increased rates of autolysis. 5-7 The fine structure of the Mu50 cell wall is similar to that of an MRSA strain such as N315, except that the Mu50 peptidoglycan chains show significantly less cross-linking, and an increased content of pentapeptide chains. 6,7 The amount of glutamine-non-amidated muropeptide subunits (i.e. those containing D-glutamate rather than D-glutamine) in the Mu50 cell wall increases, and it has been proposed that the reason for decreased cross-linking is that non-amidated muropeptides are poorer substrates for transpeptidases than amidated ones, although this is yet to be confirmed. 6-8 It is believed that the reason such changes in cell wall thickness and cross-linking result in vancomycin resistance is that the modified cell wall binds more vancomycin, due to the increased amount of terminal D-alanyl-D-alanine dipeptide. 5-7 To understand the mechanism of vancomycin resistance in VRSA strains, it is obviously necessary first to understand how these microbes synthesize peptidoglycan.

Research paper thumbnail of Smart bridges, smart tunnels: Transforming wireless sensor networks from research prototypes into robust engineering infrastructure

AD HOC NETWORKS, 2010

We instrumented large civil engineering infrastructure items, such as bridges and tunnels, with s... more We instrumented large civil engineering infrastructure items, such as bridges and tunnels, with sensors that monitor their operational performance and deterioration. In so doing we discovered that commercial oerings of Wireless Sensor Networks (WSNs) are still geared towards research prototypes and are currently not yet mature for deployment in practical scenarios. We distill the experience gained during this three-year interdisciplinary project into specic advice for researchers and developers. We discuss problems and solutions in a variety of areas including sensor hardware, radio propagation, node deployment, system security and data visualization. We also point out the problems that are still open and that the community needs to address to enable widespread adoption of WSNs outside the research lab.

Research paper thumbnail of Isolation and Charaeterisation of Deletion Mutants Involving the Transfer Genes of P-group Plasmids in Pseudomonas aeruginosa

Research paper thumbnail of Preliminary analysis of the genetic basis for vancomycin resistance in Staphylococcus aureus strain Mu50

Journal of Antimicrobial Chemotherapy, 2002

Background Staphylococcus aureus has long been recognized as a major cause of hospital-acquired i... more Background Staphylococcus aureus has long been recognized as a major cause of hospital-acquired infection. Over the last decade, methicillin-resistant S. aureus (MRSA) strains have become endemic in hospitals worldwide, including in the UK. Accordingly, the frequency of MRSA isolation has increased dramatically. 1 Glycopeptides, such as vancomycin, are often the therapeutic drugs of choice for serious MRSA infections. However, failures of vancomycin therapy against S. aureus, due to the emergence of strains that are significantly less susceptible to vancomycin [vancomycinresistant S. aureus (VRSA)], are now well established. 2-4 The first clinical VRSA, Mu50, was isolated in Japan in 1997. 2 The VRSA phenotype of Mu50 is the result of changes to the cell wall structure. In comparison with MRSA strains, Mu50 and Mu50-like strains have a thickened cell wall, release more cell wall material into the culture medium and have increased rates of autolysis. 5-7 The fine structure of the Mu50 cell wall is similar to that of an MRSA strain such as N315, except that the Mu50 peptidoglycan chains show significantly less cross-linking, and an increased content of pentapeptide chains. 6,7 The amount of glutamine-non-amidated muropeptide subunits (i.e. those containing D-glutamate rather than D-glutamine) in the Mu50 cell wall increases, and it has been proposed that the reason for decreased cross-linking is that non-amidated muropeptides are poorer substrates for transpeptidases than amidated ones, although this is yet to be confirmed. 6-8 It is believed that the reason such changes in cell wall thickness and cross-linking result in vancomycin resistance is that the modified cell wall binds more vancomycin, due to the increased amount of terminal D-alanyl-D-alanine dipeptide. 5-7 To understand the mechanism of vancomycin resistance in VRSA strains, it is obviously necessary first to understand how these microbes synthesize peptidoglycan.

Research paper thumbnail of Smart bridges, smart tunnels: Transforming wireless sensor networks from research prototypes into robust engineering infrastructure

AD HOC NETWORKS, 2010

We instrumented large civil engineering infrastructure items, such as bridges and tunnels, with s... more We instrumented large civil engineering infrastructure items, such as bridges and tunnels, with sensors that monitor their operational performance and deterioration. In so doing we discovered that commercial oerings of Wireless Sensor Networks (WSNs) are still geared towards research prototypes and are currently not yet mature for deployment in practical scenarios. We distill the experience gained during this three-year interdisciplinary project into specic advice for researchers and developers. We discuss problems and solutions in a variety of areas including sensor hardware, radio propagation, node deployment, system security and data visualization. We also point out the problems that are still open and that the community needs to address to enable widespread adoption of WSNs outside the research lab.