28 research outputs found

    External versus internal fixation for bicondylar tibial plateau fractures: systematic review and meta-analysis.

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    BACKGROUND: It is uncertain whether external fixation or open reduction internal fixation (ORIF) is optimal for patients with bicondylar tibial plateau fractures. MATERIALS AND METHODS: A systematic review using Ovid MEDLINE, Embase Classic, Embase, AMED, the Cochrane Library, Open Grey, Orthopaedic Proceedings, WHO International Clinical Trials Registry Platform, Current Controlled Trials, US National Institute for Health Trials Registry, and the Cochrane Central Register of Controlled Trials. The search was conducted on 3rd October 2014 and no language limits were applied. Inclusion criteria were all clinical study designs comparing external fixation with open reduction internal fixation of bicondylar tibial plateau fractures. Studies of only one treatment modality were excluded, as were those that included unicondylar tibial plateau fractures. Treatment effects from studies reporting dichotomous outcomes were summarised using odds ratios. Continuous outcomes were converted to standardized mean differences to assess the treatment effect, and inverse variance methods used to combine data. A fixed effect model was used for meta-analyses. RESULTS: Patients undergoing external fixation were more likely to have returned to preinjury activities by six and twelve months (P = 0.030) but not at 24 months follow-up. However, external fixation was complicated by a greater number of infections (OR 2.59, 95 % CI 1.25-5.36, P = 0.01). There were no statistically significant differences in the rates of deep infection, venous thromboembolism, compartment syndrome, or need for re-operation between the two groups. CONCLUSION: Although external fixation and ORIF are associated with different complication profiles, both are acceptable strategies for managing bicondylar tibial plateau fractures

    Structure of the human DNA repair gene HAP1

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    A role for the human DNA repair enzyme HAP1 in cellular protection against DNA damaging agents and hypoxic stress.

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    The HAP1 protein (also known as APE/Ref-1) is a bifunctional human nuclear enzyme required for repair of apurinic/apyrimidinic sites in DNA and reactivation of oxidized proto-oncogene products. To gain insight into the biological roles of HAP1, the effect of expressing antisense HAP1 RNA in HeLa cells was determined. The constructs for antisense RNA expression consisted of either a full-length HAP1 cDNA or a genomic DNA fragment cloned downstream of the CMV promoter in pcDNAneo. Stable HeLa cell transfectants expressing HAP1 antisense RNA were found to express greatly reduced levels of the HAP1 protein compared to equivalent sense orientation and vector-only control transfectants. The antisense HAP1 transfectants exhibited a normal growth rate, cell morphology and plating efficiency, but were hypersensitive to killing by a wide range of DNA damaging agents, including methyl methanesulphonate, hydrogen peroxide, menadione, and paraquat. However, survival after UV irradiation was unchanged. The antisense transfectants were strikingly sensitive to changes in oxygen tension, exhibiting increased killing compared to controls following exposure to both hypoxia (1% oxygen) and hyperoxia (100% oxygen). Consistent with a requirement for HAP1 in protection against hypoxic stress, expression of the HAP1 protein was found to be induced in a time-dependent manner in human cells during growth under 1% oxygen. The possible involvement of a depletion of cellular glutathione being linked to the hypoxic stress-sensitive phenotype of the antisense HAP1 transfectants came from the finding that they also exhibited hypersensitivity to buthionine sulphoximine, an inhibitor of glutathione biosynthesis. We conclude that the HAP1 protein is a key factor in cellular protection against a wide variety of cellular stresses, including DNA damage and a change in oxygen tension

    The effect of endurance exercise on muscle force generating capacity of the lower limbs

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    The purpose of this study was to investigate the recovery of muscle force generating capacity (FGC) of the lower limbs following a session of cycle exercise (CE). Fourteen male cyclists (mean ± SD age 25± 4 yrs and V̇O2max 65.8 ± 5 ml.kg−1min−1) performed tests assessing lower limb muscle FGC at rest (pre-test). as well as 6 and 24 hrs following CE performed on a mechanically-braked cycle ergometer. The CE consisted of 30 min at a workload corresponding to the lactate (Dmax) threshold (±15 W), and four 60 s rides at 120 % V̇O2max with one min rest between each ride. At the completion of the CE a 6 or 24 hr recovery period was initiated, after which, each subject\u27s muscle FGC was measured. The analysis of lower limb muscle FGC included, (1) 6 s all-out cycle test; (2) a maximal isokinetic leg extension at 60, 120 and 180°·s−1; and (3) a maximal concentric squat jump. Statistical analysis showed that compared to pre-test levels, a significant reduction in both isokinetic peak torque at 60°·s−1 and isoinertial maximum force occurred after 6 hrs of recovery. Although not significant, reductions also occurred at 6 hrs of recovery in isokinetic peak torque at 120 and 180°·s−1, as well as maximum rate of force development (RFD) during the squat jumps. No significant differences were observed between isokinetic peak torque, maximum force or RFD pre-test and following the 24 hr recovery period, indicating these tests had returned to normal by this time. No significant differences were found between peak power (PP) during the 6 s cycle test, pre-test and following either 6 or 24 hrs of recovery. These findings confirm earlier research that maximal voluntary strength is reduced for at least 6 hours following exhaustive dynamic exercise. The reduction in muscle FGC should be considered when resistance training is scheduled after endurance exercise
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