14 research outputs found

    Can We Accurately Measure Axial Segment Coordination during Turning Using Inertial Measurement Units (IMUs)?

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    Camera-based 3D motion analysis systems are considered to be the gold standard for movement analysis. However, using such equipment in a clinical setting is prohibitive due to the expense and time-consuming nature of data collection and analysis. Therefore, Inertial Measurement Units (IMUs) have been suggested as an alternative to measure movement in clinical settings. One area which is both important and challenging is the assessment of turning kinematics in individuals with movement disorders. This study aimed to validate the use of IMUs in the measurement of turning kinematics in healthy adults compared to a camera-based 3D motion analysis system. Data were collected from twelve participants using a Vicon motion analysis system which were compared with data from 4 IMUs placed on the; forehead, middle thorax, and feet in order to determine accuracy and reliability. The results demonstrated that IMUs sensors produced reliable kinematic measures and showed excellent reliability (ICCs 0.80–0.98) and no significant differences were seen in paired t-tests in all parameters when comparing the two systems. This suggests that IMU sensors provide a viable alternative to camera-based motion capture that could be used in isolation to gather data from individuals with movement disorders in clinical settings and real-life situations

    The Effects of Constraining Head Rotation on Eye and Whole-Body Coordination During Standing Turns at Different Speeds.

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    A limitation of the ability to rotate the head with respect to the upper body has been associated with turning problems; however, the extent of head constraints on whole-body coordination has not been fully determined. The aim of this study was to limit head on body rotation and observe the effects on whole-body coordination during standing turns at various speeds. Twelve participants completed standing turns at 180°. A Vicon motion system and a BlueGain Electrooculography system were used to record movement kinematics and measure horizontal eye movements, respectively. All participants were tested at 3 randomized speeds, and under 2 conditions with or without their head constrained using a head, neck, and chest brace which restricted neck movement. A repeated-measures analysis of variance found a significant main effect of turning speed on the onset latency of all segments, peak head-thorax angular separation, and step characteristics. Constraining the head rotation had multiple significant effects including delayed onset latency and decreased intersegmental coordination defined as peak head segmental angular separations, increased total step and step duration, and decreased step size. This indicates the contribution of speed, head, and neck constraints, which have been associated with falls during turning and whole-body coordination

    Low Concentrations of Methamphetamine Can Protect Dopaminergic Cells against a Larger Oxidative Stress Injury: Mechanistic Study

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    Mild stress can protect against a larger insult, a phenomenon termed preconditioning or tolerance. To determine if a low intensity stressor could also protect cells against intense oxidative stress in a model of dopamine deficiency associated with Parkinson disease, we used methamphetamine to provide a mild, preconditioning stress, 6-hydroxydopamine (6-OHDA) as a source of potentially toxic oxidative stress, and MN9D cells as a model of dopamine neurons. We observed that prior exposure to subtoxic concentrations of methamphetamine protected these cells against 6-OHDA toxicity, whereas higher concentrations of methamphetamine exacerbated it. The protection by methamphetamine was accompanied by decreased uptake of both [3H] dopamine and 6-OHDA into the cells, which may have accounted for some of the apparent protection. However, a number of other effects of methamphetamine exposure suggest that the drug also affected basic cellular survival mechanisms. First, although methamphetamine preconditioning decreased basal pERK1/2 and pAkt levels, it enhanced the 6-OHDA-induced increase in these phosphokinases. Second, the apparent increase in pERK1/2 activity was accompanied by increased pMEK1/2 levels and decreased activity of protein phosphatase 2. Third, methamphetamine upregulated the pro-survival protein Bcl-2. Our results suggest that exposure to low concentrations of methamphetamine cause a number of changes in dopamine cells, some of which result in a decrease in their vulnerability to subsequent oxidative stress. These observations may provide insights into the development of new therapies for prevention or treatment of PD

    Differences in the epigenetic regulation of MT-3 gene expression between parental and Cd<sup>+2 </sup>or As<sup>+3 </sup>transformed human urothelial cells

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    <p>Abstract</p> <p>Background</p> <p>Studies have shown that metallothionein 3 (MT-3) is not expressed in normal urothelium or in the UROtsa cell line, but is expressed in urothelial cancer and in tumors generated from the UROtsa cells that have been transformed by cadmium (Cd<sup>+2</sup>) or arsenite (As<sup>+3</sup>).The present study had two major goals. One, to determine if epigenetic modifications control urothelial MT-3 gene expression and if regulation is altered by malignant transformation by Cd<sup>+2 </sup>or As<sup>+3</sup>. Two, to determine if MT-3 expression might translate clinically as a biomarker for malignant urothelial cells released into the urine.</p> <p>Results</p> <p>The histone deacetylase inhibitor MS-275 induced MT-3 mRNA expression in both parental UROtsa cells and their transformed counterparts. The demethylating agent, 5-Aza-2'-deoxycytidine (5-AZC) had no effect on MT-3 mRNA expression. ChIP analysis showed that metal-responsive transformation factor-1 (MTF-1) binding to metal response elements (MRE) elements of the MT-3 promoter was restricted in parental UROtsa cells, but MTF-1 binding to the MREs was unrestricted in the transformed cell lines. Histone modifications at acetyl H4, trimethyl H3K4, trimethyl H3K27, and trimethyl H3K9 were compared between the parental and transformed cell lines in the presence and absence of MS-275. The pattern of histone modifications suggested that the MT-3 promoter in the Cd<sup>+2 </sup>and As<sup>+3 </sup>transformed cells has gained bivalent chromatin structure, having elements of being "transcriptionally repressed" and "transcription ready", when compared to parental cells. An analysis of MT-3 staining in urinary cytologies showed that a subset of both active and non-active patients with urothelial cancer shed positive cells in their urine, but that control patients only rarely shed MT-3 positive cells.</p> <p>Conclusion</p> <p>The MT-3 gene is silenced in non-transformed urothelial cells by a mechanism involving histone modification of the MT-3 promoter. In contrast, transformation of the urothelial cells with either Cd<sup>+2 </sup>or As<sup>+3 </sup>modified the chromatin of the MT-3 promoter to a bivalent state of promoter readiness. Urinary cytology for MT-3 positive cells would not improve the diagnosis of urothelial cancer, but might have potential as a biomarker for tumor progression.</p
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