63 resultados para AFFERENT LIMB

em Deakin Research Online - Australia


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AIMS: To examine the relationship between physiological status at the emergency department-ward interface and emergency calls (medical emergency team or cardiac arrest team activation) during the first 72 hours of hospital admission. BACKGROUND: Ward adverse events are related to abnormal physiology in emergency department however the relationship between physiology at the emergency department-ward interface and ward adverse events is unknown. DESIGN: Descriptive and exploratory design. METHODS: The study involved 1980 patients at three hospitals in Melbourne Australia: i) 660 randomly selected adults admitted via the emergency department to medical or surgical wards during 2012 and who had an emergency call; and ii) 1320 adults without emergency calls matched for gender, triage category, usual residence, admitting unit and age. RESULTS/FINDINGS: The median age was 78 years and 48·8% were males. The median time to the first emergency call was 18·8 hours and ≥1 abnormal parameters were documented in 34·9% of patients during the last hour of ED care and 47·1% of patients during first hour of ward care. Emergency calls were significantly more common in patients with heart rate and conscious state abnormalities during the last hour of emergency care and abnormal oxygen saturation, heart rate or respiratory rate during the first hour of ward care. Medical emergency team afferent limb failure occurred in 55·3% patients with medical emergency team activation criteria during first hour of ward care. CONCLUSION: The use of physiological status at the emergency department-ward interface to guide care planning and reasons for and outcomes of medical emergency team afferent limb failure are important areas for future research.

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Calcineurin activity is essential for successful skeletal muscle regeneration in young mdx mice and in wild type mice following myotoxic injury and cryodamage. In mature myofibres of adult mdx mice, calcineurin stimulation can ameliorate the dystrophic pathology. The aim of this study was to test the hypothesis that the more severe dystrophic pathology of the diaphragm compared with hindlimb muscles of mdx mice could be attributed to aberrant calcineurin signalling and that due to ongoing regeneration calcineurin activity would be greater in muscles of adult mdx than wild type mice. Differences in markers of regeneration between tibialis anterior and diaphragm muscles were also characterised, to determine whether there was an association between regeneration efficacy and calcineurin activity in dystrophic muscles. In diaphragm muscles of adult mdx mice, the proportion of centrally nucleated fibres and developmental myosin heavy chain protein expression was lower and myogenin protein expression was higher than in tibialis anterior muscles. Calcineurin and activated NFATc1 protein content and calcineurin phosphatase activity were higher in muscles from mdx than wild type mice and calcineurin activation was greater in diaphragm than tibialis anterior muscles of mdx mice. Thus, despite greater calcineurin activity in diaphragm compared to hindlimb muscles, regeneration events downstream of myoblast differentiation and mediated by the injured myofibre were severely compromised.

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Little research documents the contribution of upper limb and total body movement to energy expenditure (EE) during active video gaming. To address this, EE, heart rate (HR), and, upper limb and total body movement were assessed in 11- to 17-year-old adolescents whilst playing three active (Nintendo Wii) and one sedentary (XBOX 360) video games. Non-dominant upper limb activity, EE and HR were significantly greater during Wii Sports boxing [mean 267.2 (SD 115.8) J kg−1 min−1; 136.7 (24.5) beats min−1] than tennis or bowling (P ≤ 0.044). For all active games hip activity best predicted EE (R 2 ≥ 0.53), with two-measure models of HR and single-site activity data, and multi-site activity data, similarly explaining the variance in EE (R 2 ≥ 0.64). The physiological cost of upper-body orientated active video games increased when movement of both upper limbs was encouraged. Improvements in EE explanatory power provide support for multi-site activity monitoring during unique, non-ambulatory activities.

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The contralateral transfer of strength following unilateral strength training (ULS) is thought to be due to changes within the nervous system. Using transcranial magnetic stimulation (TMS) we compared corticospinal responses following ULS of the right biceps brachii (BB) projecting to the untrained left BB. Motor evoked potentials (MEPs) were recorded from both BB of 23 individuals pre and post 4 weeks heavy load (80% of 1RM) ULS of right BB. TMS was delivered at intensities below active motor threshold (AMT) to saturation of the MEP (MEPmax). ULS resulted in a 28% increase in 1RM right BB strength, resulting in a 19.2% increase in contralateral strength of the left BB (p = .0001). There was a significant increase in MEP amplitude of 30.3% (p = .03), 33% (p = .05), and 26.5% (p = .01) at AMT, 20% above AMT and MEPmax respectively. No significant differences in silent period were seen at AMT, 20% above AMT or MEPmax. This study has demonstrated increased corticospinal excitability projecting to the untrained arm following heavy load ULS.

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This study used transcranial magnetic stimulation to measure the corticospinal responses following 8 weeks of unilateral leg strength training. Eighteen healthy, non-strength trained participants (14 male, 4 female; 18–35 years of age) were matched for age, gender, and pre-training strength; and assigned to a training or control group. The trained group participated in unilateral horizontal leg press strength training, progressively overloaded and wave periodised, thrice per week for 8 weeks. Testing occurred prior to the intervention, at the end of 4 weeks and at the completion of training at 8 weeks. Participants were tested in both legs for one repetition maximum strength, muscle thickness, maximal electromyography (EMG) activity, and corticospinal excitability and inhibition. No changes were observed in muscle thickness in either leg. The trained leg showed an increase in strength of 21.2% (P = 0.001) and 29.0% (P = 0.007, compared to pre-testing) whilst the untrained contralateral leg showed 17.4% (P = 0.01) and 20.4% (P = 0.004, compared to pre-testing) increases in strength at 4 and 8 weeks, respectively. EMG and corticospinal excitability did not change; however, corticospinal inhibition was significantly reduced by 17.7 ms (P = 0.003) and 17.3 ms (P = 0.001) at 4 and 8 weeks, respectively, in the trained leg, and 25.1 ms (P = 0.001) and 20.8 ms (P = 0.001) at 4 and 8 weeks, respectively, in the contralateral untrained leg. This data support the theory of corticospinal adaptations underpinning cross-education gains in the lower limbs following unilateral strength training.

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Hyperactive inflammatory responses following cancer initiation have led to cancer being described as a ‘wound that never heals’. These inflammatory responses elicit signals via NFκB leading to IL-6 production, and IL-6 in turn has been shown to induce epithelial to mesenchymal transition in breast cancer cells in vitro, implicating a role for this cytokine in cancer cell invasion. We previously have shown that conditioned medium derived from cancer-associated fibroblasts induced an Epithelial to Mesenchymal transition (EMT) in PMC42-LA breast cancer cells and we have now identify IL-6 as present in this medium. We further show that IL-6 is expressed approximately 100 fold higher in a cancer-associated fibroblast line compared to normal fibroblasts. Comparison of mouse-specific (stroma) and human-specific (tumor) IL-6 mRNA expression from MCF-7, MDA MB 468 and MDA MB 231 xenografts also indicated the stroma rather than tumor as a significantly higher source of IL-6 expression. Mast cells (MCs) feature in inflammatory cancer-associated stroma, and activated MCs secrete IL-6. We observed a higher MC index (average number of mast cells per xenograft section/average tumor size) in MDA MB 468 compared to MDA MB 231 xenografts, where all MC were observed to be active (degranulating). This higher MC index correlated with greater mouse-specific IL-6 expression in the MDA MB 468 xenografts, implicating MC as an important source of stromal IL-6. Furthermore, immunohistochemistry on these xenografts for pSTAT3, which lies downstream of the IL-6 receptor indicated frequent correlations between pSTAT3 and mast cell positive cells. Analysis of publically available databases for IL-6 expression in patient tissue revealed higher IL-6 in laser capture microdissected stroma compared to adjacent tissue epithelium from patients with inflammatory breast cancer (IBC) and invasive non-inflammatory breast cancer (non-IBC) and we show that IL-6 expression was significantly higher in Basal versus Luminal molecular/phenotypic groupings of breast cancer cell lines. Finally, we discuss how afferent and efferent IL-6 pathways may participate in a positive feedback cycle to dictate tumor progression.

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 Objective: This study investigated the relationship between motor performance and social-communicative impairment in children with ADHD-combined type (ADHD-CT). Method: An upper limb Fitts’ aiming task was used as a measure of motor performance and the Social Responsiveness Scale as a measure of social-communicative/autistic impairment in the following groups: ADHD-CT (n = 11) and typically developing (TD) controls (n = 10). Results: Children with ADHD-CT displayed greater variability in their movements, reflected in increased error variance over repeated aiming trials compared with TD controls. Motor performance variability was associated with social-communicative deficits in the ADHD-CT but not in the TD group. Conclusion: Social-communicative impairments further complicate the clinical picture of ADHD-CT; therefore, further research in this area is warranted to ascertain whether a particular pattern of motor disturbance in children with ADHD-CT may be clinically useful in identifying and assessing children with a more complex ADHD presentation. © 2012 SAGE Publications.

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