49 research outputs found

    The short-term effect of swimming training load on shoulder rotational range of motion, shoulder joint position sense and pectoralis minor length

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    Background: Shoulder pain or injury is the most common issue facing elite competitive swimmers and the most frequent reason for missed or modified training. Literature suggests that highly repetitive upper limb loading leads to inappropriate adaptations within the shoulder complex. The most likely maladaptations to occur are variations in shoulder rotational range of motion, reduction in joint position sense and shortened pectoralis minor length. This has yet to have been confirmed in experimental studies. The aim of this study was to investigate the short-term effects of swimming training load upon internal and external rotation range of motion, joint position sense and pectoralis minor length. Method: Sixteen elite swimmers training in the British Swimming World Class programme participated. Measures of internal and external range of motion, joint position sense error score and pectoralis minor length were taken before and after a typical 2h swimming session. Results: Following swimming training shoulder external rotation range of motion and pectoralis minor length reduced significantly (-3.4°,p=<0.001 and -0.7cm, p=<0.001, respectively), joint position sense error increased significantly (+2.0° error angle, p=<0.001). Internal rotation range of motion demonstrated no significant change (-0.6, p=0.53). Discussion: This study determined that elite level swimming training results in short-term maladaptive changes in shoulder performance that could potentially predispose them to injury

    Radiation induced pulmonary fibrosis as a model of progressive fibrosis: Contributions of DNA damage, inflammatory response and cellular senescence genes

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    <p><b>Purpose/Aim of Study</b>: Studies of pulmonary fibrosis (PF) have resulted in DNA damage, inflammatory response, and cellular senescence being widely hypothesized to play a role in the progression of the disease. Utilizing these aforementioned terms, genomics databases were interrogated along with the term, “pulmonary fibrosis,” to identify genes common among all 4 search terms. Findings were compared to data derived from a model of radiation-induced progressive pulmonary fibrosis (RIPF) to verify that these genes are similarly expressed, supporting the use of radiation as a model for diseases involving PF, such as human idiopathic pulmonary fibrosis (IPF). <b>Materials and Methods</b>: In an established model of RIPF, C57BL/6J mice were exposed to 12.5 Gy thorax irradiation and sacrificed at 24 hours, 1, 4, 12, and 32 weeks following exposure, and lung tissue was compared to age-matched controls by RNA sequencing. <b>Results</b>: Of 176 PF associated gene transcripts identified by database interrogation, 146 (>82%) were present in our experimental model, throughout the progression of RIPF. Analysis revealed that nearly 85% of PF gene transcripts were associated with at least 1 other search term. Furthermore, of 22 genes common to all four terms, 16 were present experimentally in RIPF. <b>Conclusions</b>: This illustrates the validity of RIPF as a model of progressive PF/IPF based on the numbers of transcripts reported in both literature and observed experimentally. Well characterized genes and proteins are implicated in this model, supporting the hypotheses that DNA damage, inflammatory response and cellular senescence are associated with the pathogenesis of PF.</p

    Cerebral PET with florbetapir compared with neuropathology at autopsy for detection of neuritic amyloid-β plaques: A prospective cohort study

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    Background: Results of previous studies have shown associations between PET imaging of amyloid plaques and amyloid-β pathology measured at autopsy. However, these studies were small and not designed to prospectively measure sensitivity or specificity of amyloid PET imaging against a reference standard. We therefore prospectively compared the sensitivity and specificity of amyloid PET imaging with neuropathology at autopsy. Methods: This study was an extension of our previous imaging-to-autopsy study of participants recruited at 22 centres in the USA who had a life expectancy of less than 6 months at enrolment. Participants had autopsy within 2 years of PET imaging with florbetapir (18F). For one of the primary analyses, the interpretation of the florbetapir scans (majority interpretation of five nuclear medicine physicians, who classified each scan as amyloid positive or amyloid negative) was compared with amyloid pathology (assessed according to the Consortium to Establish a Registry for Alzheimer\u27s Disease standards, and classed as amyloid positive for moderate or frequent plaques or amyloid negative for no or sparse plaques); correlation of the image analysis results with amyloid burden was tested as a coprimary endpoint. Correlation, sensitivity, and specificity analyses were also done in the subset of participants who had autopsy within 1 year of imaging as secondary endpoints. The study is registered with ClinicalTrials.gov, number NCT 01447719 (original study NCT 00857415). Findings: We included 59 participants (aged 47-103 years; cognitive status ranging from normal to advanced dementia). The sensitivity and specificity of florbetapir PET imaging for detection of moderate to frequent plaques were 92% (36 of 39; 95% CI 78-98) and 100% (20 of 20; 80-100%), respectively, in people who had autopsy within 2 years of PET imaging, and 96% (27 of 28; 80-100%) and 100% (18 of 18; 78-100%), respectively, for those who had autopsy within 1 year. Amyloid assessed semiquantitatively with florbetapir PET was correlated with the post-mortem amyloid burden in the participants who had an autopsy within 2 years (Spearman ρ=0·76; p\u3c0·0001) and within 12 months between imaging and autopsy (0·79; p\u3c0·0001). Interpretation: The results of this study validate the binary visual reading method approved in the USA for clinical use with florbetapir and suggest that florbetapir could be used to distinguish individuals with no or sparse amyloid plaques from those with moderate to frequent plaques. Additional research is needed to understand the prognostic implications of moderate to frequent plaque density. Funding: Avid Radiopharmaceuticals. © 2012 Elsevier Ltd
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