90 research outputs found

    P1_1 Resting On The Shoulders Of Giants

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    This paper investigates the concept of a ’World Turtle’ as imagined in Terry Pratchett’s Diskworld series. The giant astronomical elephants which stand upon the turtle’s shell support the Diskworld. By assuming that the elephants have the same anatomy as terrestrial elephants, the dimensions of these animals is found. Each of the elephants would have to be 230km tall to be able to support the mass of the disk. It was also found that the size of the elephants to support a flat Earth would be 420km tall. A relationship between the radius of a disk and the height of the elephant was also found

    The Royal Blackburn Hospital, Acute Stroke Unit

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    Traumatic fracture of central venous catheter resulting in potential migration of distal fragment: a case report

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    We report a surgical retrieval of an indwelling portion of a traumatic rupture of the Central venous catheter following hair cutting by a confused patient secondary to Postoperative cognitive dysfunction. He had a dynamic compression screw for fixation of fractured neck of femur after previously failed surgical procedure. The second procedure was complicated with major blood loss, which required central venous and arterial line insertion for intra-operative and post-operative management. The patient was discharged to the ward following an uneventful stay on intensive care. While on the ward, he decided to trim his hair and in the process he inadvertently cut through the right internal jugular catheter. Complications and management resulting from embolisation of central line are reviewed

    Evidence of Long-Distance Coastal Sea Migration of Atlantic Salmon, Salmo Salar, Smolts from Northwest England (River Derwent).

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    Publication history: Accepted - 10 January 2022; Published online - 26 January 2022Background Combining data from multiple acoustic telemetry studies has revealed that west coast England Atlantic salmon (Salmo salar L.) smolts used a northward migration pathway through the Irish Sea to reach their feeding grounds. Hundred Atlantic salmon smolts were captured and tagged in May 2020 in the River Derwent, northwest England as part of an Environment Agency/Natural England funded project. Results Three tagged smolts were detected on marine acoustic receivers distributed across two separate arrays from different projects in the Irish Sea. One fish had migrated approximately 262 km in 10 days from the river mouth at Workington Harbour, Cumbria to the northernmost receiver array operated by the SeaMonitor project; this is the longest tracked marine migration of an Atlantic salmon smolt migrating from the United Kingdom. This migrating fish displayed behaviours which resulted in fast northward migration. The remaining two fish were detected on a receiver array operated by a third project: the Collaborative Oceanography and Monitoring for Protected Areas and Species (COMPASS). Conclusion These detections further provide evidence that migration to reach marine feeding grounds of at least a proportion of salmon smolts from rivers draining into the Irish Sea is northerly, though without a southern marine array it is impossible to conclude that this is the only route. The pattern of these detections would not have been possible without the collaborative efforts of three distinct and separately funded projects to share data. Further work is required to fully understand migration trajectories in this species on the west coast of the British Isles.The main Funding bodies for this project were the Environment Agency, Cumbria and Natural England, Cumbria. Additional funding was provided by The Derwent Owners Association and Bowland Game: Isel Fishings

    Mitochondrial Uncoupling Protein-2 (UCP2) Mediates Leptin Protection Against MPP+ Toxicity in Neuronal Cells

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    Mitochondrial dysfunction is involved in the pathogenesis of neurodegenerative diseases, including Parkinson’s disease (PD). Uncoupling proteins (UCPs) delink ATP production from biofuel oxidation in mitochondria to reduce oxidative stress. UCP2 is expressed in brain, and has neuroprotective effects under various toxic insults. We observed induction of UCP2 expression by leptin in neuronal cultures, and hypothesize that leptin may preserve neuronal survival via UCP2. We showed that leptin preserved cell survival in neuronal SH-SY5Y cells against MPP+ toxicity (widely used in experimental Parkinsonian models) by maintaining ATP levels and mitochondrial membrane potential (MMP); these effects were accompanied by increased UCP2 expression. Leptin had no effect in modulating reactive oxygen species levels. Stable knockdown of UCP2 expression reduced ATP levels, and abolished leptin protection against MPP+-induced mitochondrial depolarization, ATP deficiency, and cell death, indicating that UCP2 is critical in mediating these neuroprotective effects of leptin against MPP+ toxicity. Interestingly, UCP2 knockdown increased UCP4 expression, but not of UCP5. Our findings show that leptin preserves cell survival by maintaining MMP and ATP levels mediated through UCP2 in MPP+-induced toxicity

    Uncoupling Protein-4 (UCP4) Increases ATP Supply by Interacting with Mitochondrial Complex II in Neuroblastoma Cells

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    Mitochondrial uncoupling protein-4 (UCP4) protects against Complex I deficiency as induced by 1-methyl-4-phenylpyridinium (MPP+), but how UCP4 affects mitochondrial function is unclear. Here we investigated how UCP4 affects mitochondrial bioenergetics in SH-SY5Y cells. Cells stably overexpressing UCP4 exhibited higher oxygen consumption (10.1%, p<0.01), with 20% greater proton leak than vector controls (p<0.01). Increased ATP supply was observed in UCP4-overexpressing cells compared to controls (p<0.05). Although state 4 and state 3 respiration rates of UCP4-overexpressing and control cells were similar, Complex II activity in UCP4-overexpressing cells was 30% higher (p<0.05), associated with protein binding between UCP4 and Complex II, but not that of either Complex I or IV. Mitochondrial ADP consumption by succinate-induced respiration was 26% higher in UCP4-overexpressing cells, with 20% higher ADP:O ratio (p<0.05). ADP/ATP exchange rate was not altered by UCP4 overexpression, as shown by unchanged mitochondrial ADP uptake activity. UCP4 overexpression retained normal mitochondrial morphology in situ, with similar mitochondrial membrane potential compared to controls. Our findings elucidate how UCP4 overexpression increases ATP synthesis by specifically interacting with Complex II. This highlights a unique role of UCP4 as a potential regulatory target to modulate mitochondrial Complex II and ATP output in preserving existing neurons against energy crisis
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