462 research outputs found

    What Is the Risk Posed to the Lateral Femoral Cutaneous Nerve During the Use of the Anterior Portal of Supine Hip Arthroscopy and the Minimally Invasive Anterior Approach for Total Hip Arthroplasty?

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    PURPOSE: To determine: (1) What is the proximity of the lateral femoral cutaneous nerve (LFCN) to the anterior portal (AP) used in supine hip arthroscopy? (2) What is the proximity of the LCFN to the incision in the minimally invasive anterior approach (MIAA) for total hip arthroplasty? (3) What effect does lateralizing the AP have on the likelihood of nerve injury? (4) What branching patterns are observable in the LFCN? METHODS: Forty-five hemipelves were dissected. The LFCN was identified and its path dissected. The positions of the nerve in relation to the AP and the MIAA incision were measured. RESULTS: The AP intersected with 38% of nerves. In the remainder, the LFCN was located 5.7 ± 4.5 mm from the portal's edge. In addition, 44% of nerves crossed the incision of the MIAA. Of those that did not, the average minimum distance from the incision was 14.4 ± 7.0 mm. We found a significant reduction in risk if the AP is moved medially by 5 mm or laterally by 15 mm (P = .0054 and P = .0002). The LFCN showed considerable variation with 4 branching variants. CONCLUSIONS: These results show that the LFCN is at high risk during supine hip arthroscopy and the MIAA, emphasizing the need for meticulous dissection. We suggest that relocation of the AP 5 mm medially or 15 mm laterally will reduce the risk to the LFCN. CLINICAL RELEVANCE: These findings should aid surgeons in minimizing the risk to the LCFN during hip arthroscopy and the minimally invasive anterior approach to the hip

    Exercise-induced cell signalling responses of human skeletal responses of human skeletal muscle: the effects of reduced carbohydrate availability

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    It is well documented that regular endurance exercise induces skeletal muscle mitochondrial biogenesis. However, the optimal training stimulus and nutritional intervention for which to maximize mitochondrial adaptations to endurance exercise is not well known. Developments in molecular techniques now permit the examination of the cell signalling responses to acute exercise therefore increasing our understanding of how manipulation of the training protocol and nutrient availability may enhance the training stimulus to a given bout of exercise. The primary aim of this thesis is to therefore characterise the skeletal muscle cell signalling responses thought to regulate mitochondrial biogenesis following an acute bout of high-intensity interval exercise and moderate- intensity continuous exercise. A secondary aim is to subsequently examine how manipulation of carbohydrate (CHa) availability may enhance the activation of key regulatory cell signalling pathways. The aim of the first study (Chapter 4) was to develop two exercise protocols of varied activity profile, which induced comparable total oxygen consumption and energy expenditure after being matched for average intensity, duration and distance ran. In a repeated measures and randomised design, eight active males performed an acute bout of high-intensity interval (HIT) running (6 x 3 min at 90 % V02max interspersed with 6 x 3 min at 50 % V02max also performed with a 7-min warm up and cool down at 70 % V02max) and an acute bout of moderate-intensity continuous (CaNT) running (50-m in continuous running at 70 % V02max). As a result of average intensity (70 % V02max) duration (50-min) and distance ran (9843 ± 176) being equal between protocols, total oxygen consumption (HIT; 162 ± 6, CaNT; 166 ± 10 L) and energy expenditure (HIT; 811 ± 30, CaNT; 832 ± 48 kcal) were matched between protocols (P > 0.05). Despite higher ratings of perceived exertion in HIT compared with CaNT (HIT; 14 ± 0.5, caNT; 13 ± 0.4 AU, P 0.05). Data therefore demonstrate comparable cell signalling responses between HIT and CaNT when matched for work done, average intensity, duration and distance ran. Furthermore, this is the first time exercise is shown to up-regulate p53 phosphorylation in human skeletal muscle therefore highlighting an additional pathway by which exercise may regulate mitochondrial biogenesis. Progressing from the role of the exercise stimulus in initiating mitochondrial biogenesis, the aim of the third study (Chapter 6) was to examine the effects of reduced CHO availability on modulating the exercise-induced activation of the cell signalling pathways as characterised in Chapter 5. Although HIT and CaNT protocols resulted in comparable signalling in Chapter 5, we chose HIT as our chosen exercise model given that it is perceived as more enjoyable than CaNT, has application for improving both human health and performance and also because of its relevance as a training modality for elite athletes in team and endurance sports. In a repeated measures and randomised design, muscle biopsies (vastus lateralis) were obtained from eight active males pre-, post and 3 h after performing an acute bout of high-intensity interval running with either high (HIGH) or low CHO availability (LOW). In LOW, subjects performed a bout of glycogen depleting exercise the night before and reported to the laboratory on the subsequent morning in a fasted state as well as restricting CHO before, during and after exercise. Subjects in HIGH CHO loaded for 24 h before reporting to the laboratory to perform HIT with CHO consumed before, during and after exercise. Resting muscle glycogen (HIGH, 467 ± 19; LOW, 103 ± 9 rnmol.kq" dw) and utilisation (HIGH, 142 ± 34; LOW, and 30 ± 12) was greater in HIGH compared with LOW (P < 0.05). Phosphorylation (P-) of ACCSer79 (HIGH, 1.4 ± 0.4; LOW, 2.9 ± 0.9), a marker for AMPK activity, and p53ser15 (HIGH, 0.9 ± 0.4; LOW, 2.6 ± 0.8) was higher in LOW immediately post- and 3 h post-exercise, respectively (P < 0.05). Before and 3 h post-exercise, mRNA content of PDK4, Tfam, COXIVand PGC-1a were greater in LOW compared with HIGH (P < 0.05) whereas CPT1 showed trend towards significance (P = 0.09). However, only PGC-1a expression was increased by exercise (P < 0.05) where 3-fold increases occurred independent of CHO availability. Data demonstrate that low CHO availability enhances p53 phosphorylation in a manner that may be related to upstream signalling through AMPK. Given the emergence of p53 as a potential molecular regulator of mitochondrial biogenesis, such nutritional modulation of contraction-induced p53 activation may have implications for both athletic and clinical populations. In summary, the work undertaken from the studies in this thesis provides novel information in relation to the regulation of exercise-induced cell signalling responses associated with mitochondrial biogenesis. Specifically, this is first report to examine cell-signalling responses to running exercise where comparable signalling between HIT and CaNT was observed when protocols are matched for average intensity and duration. Furthermore, these data provide the first report of an exercise-induced increase in p53 phosphorylation in which data demonstrate low CHO availability augments the exercise-induced increase in p53 signalling which may be related to upstream signalling through AMPK. Further studies would now benefit from addressing the nuclear and mitochondrial abundance of p53 in response to an acute exercise challenge as well as comprehensively examining how training status, exercise intensity and CHO availability affects p53 regulation and downstream target genes

    Towards photostatistics from photon-number discriminating detectors

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    We study the properties of a photodetector that has a number-resolving capability. In the absence of dark counts, due to its finite quantum efficiency, photodetection with such a detector can only eliminate the possibility that the incident field corresponds to a number of photons less than the detected photon number. We show that such a {\em non-photon} number-discriminating detector, however, provides a useful tool in the reconstruction of the photon number distribution of the incident field even in the presence of dark counts.Comment: 7 pages, 4 figure

    Comparison of random forest and parametric imputation models for imputing missing data using MICE: a CALIBER study.

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    Multivariate imputation by chained equations (MICE) is commonly used for imputing missing data in epidemiologic research. The "true" imputation model may contain nonlinearities which are not included in default imputation models. Random forest imputation is a machine learning technique which can accommodate nonlinearities and interactions and does not require a particular regression model to be specified. We compared parametric MICE with a random forest-based MICE algorithm in 2 simulation studies. The first study used 1,000 random samples of 2,000 persons drawn from the 10,128 stable angina patients in the CALIBER database (Cardiovascular Disease Research using Linked Bespoke Studies and Electronic Records; 2001-2010) with complete data on all covariates. Variables were artificially made "missing at random," and the bias and efficiency of parameter estimates obtained using different imputation methods were compared. Both MICE methods produced unbiased estimates of (log) hazard ratios, but random forest was more efficient and produced narrower confidence intervals. The second study used simulated data in which the partially observed variable depended on the fully observed variables in a nonlinear way. Parameter estimates were less biased using random forest MICE, and confidence interval coverage was better. This suggests that random forest imputation may be useful for imputing complex epidemiologic data sets in which some patients have missing data

    Infection and telomere length:A systematic review protocol

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    Introduction Telomeres are a measure of cellular ageing with potential links to diseases such as cardiovascular diseases and cancer. Studies have shown that some infections may be associated with telomere shortening, but whether an association exists across all types and severities of infections and in which populations is unclear. Therefore we aim to collate available evidence to enable comparison and to inform future research in this field.Methods and analysis We will search for studies involving telomere length and infection in various databases including MEDLINE (Ovid interface), EMBASE (Ovid interface), Web of Science, Scopus, Global Health and the Cochrane Library. For grey literature, the British Library of electronic theses databases (ETHOS) will be explored. We will not limit by study type, geographical location, infection type or method of outcome measurement. Two researchers will independently carry out study selection, data extraction and risk of bias assessment using the ROB2 and ROBINS-E tools. The overall quality of the studies will be determined using the Grading of Recommendations Assessment, Development and Evaluation criteria. We will also evaluate study heterogeneity with respect to study design, exposure and outcome measurement and if there is sufficient homogeneity, a meta-analysis will be conducted. Otherwise, we will provide a narrative synthesis with results grouped by exposure category and study design

    Enhanced skeletal muscle ribosome biogenesis, yet attenuated mTORC1 and ribosome biogenesis-related signalling, following short-term concurrent versus single-mode resistance training

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    Combining endurance training with resistance training (RT) may attenuate skeletal muscle hypertrophic adaptation versus RT alone; however, the underlying mechanisms are unclear. We investigated changes in markers of ribosome biogenesis, a process linked with skeletal muscle hypertrophy, following concurrent training versus RT alone. Twenty-three males underwent eight weeks of RT, either performed alone (RT group, n = 8), or combined with either high-intensity interval training (HIT+RT group, n = 8), or moderate-intensity continuous training (MICT+RT group, n = 7). Muscle samples (vastus lateralis) were obtained before training, and immediately before, 1 h and 3 h after the final training session. Training-induced changes in basal expression of the 45S ribosomal RNA (rRNA) precursor (45S pre-rRNA), and 5.8S and 28S mature rRNAs, were greater with concurrent training versus RT. However, during the final training session, RT further increased both mTORC1 (p70S6K1 and rps6 phosphorylation) and 45S pre-rRNA transcription-related signalling (TIF-1A and UBF phosphorylation) versus concurrent training. These data suggest that when performed in a training-accustomed state, RT induces further increases mTORC1 and ribosome biogenesis-related signalling in human skeletal muscle versus concurrent training; however, changes in ribosome biogenesis markers were more favourable following a period of short-term concurrent training versus RT performed alon

    Optical one-way quantum computing with a simulated valence-bond solid

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    One-way quantum computation proceeds by sequentially measuring individual spins (qubits) in an entangled many-spin resource state. It remains a challenge, however, to efficiently produce such resource states. Is it possible to reduce the task of generating these states to simply cooling a quantum many-body system to its ground state? Cluster states, the canonical resource for one-way quantum computing, do not naturally occur as ground states of physical systems. This led to a significant effort to identify alternative resource states that appear as ground states in spin lattices. An appealing candidate is a valence-bond-solid state described by Affleck, Kennedy, Lieb, and Tasaki (AKLT). It is the unique, gapped ground state for a two-body Hamiltonian on a spin-1 chain, and can be used as a resource for one-way quantum computing. Here, we experimentally generate a photonic AKLT state and use it to implement single-qubit quantum logic gates.Comment: 11 pages, 4 figures, 8 tables - added one referenc
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