12 research outputs found

    Reliability of Achilles Tendon Resting Angle and Calf Circumference measurement techniques.

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    BACKGROUND:The resting angle of the ankle joint may be altered following apparently successful management of Achilles tendon rupture. The reliability of the Achilles Tendon Resting Angle and Calf Circumference measurements was determined. METHODS: Three test-retest measurements for reliability assessment were performed on 16 healthy subjects: 10 males and 6 females. RESULTS: The mean left Achilles Tendon Resting Angle was mean 50.1° (range [26-61]), ICC 0.92 (CI [0.83-0.97]), SEM 2.4°. The mean right Achilles tendon resting angle was mean 49.9° (range [26-60]), ICC 0.91 (CI [0.80-0.96]), SEM 2.6°. The mean left calf circumference was mean 38.5cm (range [33.3-44.2]), ICC 0.97 (CI [0.94-0.98]), SEM 0.6cm, and the mean right calf circumference was mean 38.4cm (range [33.3-43.6]), ICC 0.97 (CI [0.94-0.99]), SEM 0.5cm. CONCLUSIONS: The Achilles Tendon Resting Angle and Calf Circumference at 15cm from the antero-medial joint line had excellent test-retest reliability. These are simple, quick and inexpensive measurements, which have the potential to correlate with tendon elongation and functional outcome. The Achilles tendon resting angle may be used as a guide to tendon length during intra-operative repair and rehabilitation

    Blue light therapy improves circadian dysfunction as well as motor symptoms in two mouse models of Huntington's disease.

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    Patients with Huntington's disease (HD) exhibit movement disorders, psychiatric disturbance and cognitive impairments as the disease progresses. Abnormal sleep/wake cycles are common among HD patients with reports of delayed sleep onset, fatigue during the day, and a delayed pattern of melatonin secretion all of which suggest circadian dysfunction. Mouse models of HD confirm disrupted circadian rhythms with pathophysiology found in the central circadian clock (suprachiasmatic nucleus). Importantly, circadian dysfunction manifests early in disease, even before the classic motor symptoms, in both patients and mouse models. Therefore, we hypothesize that the circadian dysfunction may interact with the disease pathology and exacerbate the HD symptoms. If correct, early intervention may benefit patients and delay disease progression. One test of this hypothesis is to determine whether light therapy designed to strengthen this intrinsic timing system can delay the disease progression in mouse models. Therefore, we determined the impact of blue wavelength-enriched light on two HD models: the BACHD and Q175 mice. Both models received 6 h of blue-light at the beginning of their daily light cycle for 3 months. After treatment, both genotypes showed improvements in their locomotor activity rhythm without significant change to their sleep behavior. Critically, treated mice of both lines exhibited improved motor performance compared to untreated controls. Focusing on the Q175 genotype, we sought to determine whether the treatment altered signaling pathways in brain regions known to be impacted by HD using NanoString gene expression assays. We found that the expression of several HD relevant markers was altered in the striatum and cortex of the treated mice. Our study demonstrates that strengthening the circadian system can delay the progression of HD in pre-clinical models. This work suggests that lighting conditions should be considered when managing treatment of HD and other neurodegenerative disorders
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