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Biomedical subjects

G Hughes

Publications and source records attributed to G Hughes.

At least 55 records · Page 3Linked to original sources
PubMed2001

Surveillance of sexually transmitted infections in England and Wales.

Surveillance of sexually transmitted infections (STIs) in England and Wales has, in the past, relied principally on aggregated statistical data submitted by all genitourinary medicine clinics to the Communicable Disease Surveillance Centre, supplemented by various laboratory reporting systems. Although these systems provide comparatively robust surveillance data, they do not provide sufficient information on risk factors to target STI control and prevention programmes appropriately. Over recent years, substantial rises in STIs, the emergence of numerous outbreaks of STIs, and changes in gonococcal resistance patterns have necessitated the introduction of more sophisticated surveillance mechanisms. This article describes current STI surveillance systems in England and Wales, including new systems that have recently been introduced or are currently being developed to meet the need for enhanced STI surveillance data.

Chlamydia Infections↗
PubMed2000

Selective targeting of a redox-active ubiquinone to mitochondria within cells: antioxidant and antiapoptotic properties.

With the recognition of the central role of mitochondria in apoptosis, there is a need to develop specific tools to manipulate mitochondrial function within cells. Here we report on the development of a novel antioxidant that selectively blocks mitochondrial oxidative damage, enabling the roles of mitochondrial oxidative stress in different types of cell death to be inferred. This antioxidant, named mitoQ, is a ubiquinone derivative targeted to mitochondria by covalent attachment to a lipophilic triphenylphosphonium cation through an aliphatic carbon chain. Due to the large mitochondrial membrane potential, the cation was accumulated within mitochondria inside cells, where the ubiquinone moiety inserted into the lipid bilayer and was reduced by the respiratory chain. The ubiquinol derivative thus formed was an effective antioxidant that prevented lipid peroxidation and protected mitochondria from oxidative damage. After detoxifying a reactive oxygen species, the ubiquinol moiety was regenerated by the respiratory chain enabling its antioxidant activity to be recycled. In cell culture studies, the mitochondrially localized antioxidant protected mammalian cells from hydrogen peroxide-induced apoptosis but not from apoptosis induced by staurosporine or tumor necrosis factor-alpha. This was compared with untargeted ubiquinone analogs, which were ineffective in preventing apoptosis. These results suggest that mitochondrial oxidative stress may be a critical step in apoptosis induced by hydrogen peroxide but not for apoptosis induced by staurosporine or tumor necrosis factor-alpha. We have shown that selectively manipulating mitochondrial antioxidant status with targeted and recyclable antioxidants is a feasible approach to investigate the role of mitochondrial oxidative damage in apoptotic cell death. This approach will have further applications in investigating mitochondrial dysfunction in a range of experimental models.

Animals↗
PubMed2000

Changes in mitochondrial membrane potential during staurosporine-induced apoptosis in Jurkat cells.

Cytochrome c release from mitochondria is central to apoptosis, but the events leading up to it are disputed. The mitochondrial membrane potential has been reported to decrease, increase or remain unchanged during cytochrome c release. We measured mitochondrial membrane potential in Jurkat cells undergoing apoptosis by the uptake of the radiolabelled lipophilic cation TPMP, enabling small changes in potential to be determined. The ATP/ADP ratio, mitochondrial and cell volumes, plasma membrane potential and the mitochondrial membrane potential in permeabilised cells were also measured. Before cytochrome c release the mitochondrial membrane potential increased, followed by a decrease in potential associated with mitochondrial swelling and the release of cytochrome c and DDP-1, an intermembrane space house keeping protein. Mitochondrial swelling and cytochrome c release were both blocked by bongkrekic acid, an inhibitor of the permeability transition. We conclude that during apoptosis mitochondria undergo an initial priming phase associated with hyperpolarisation which leads to an effector phase, during which mitochondria swell and release cytochrome c.

Apoptosis↗