Use of Robotics to Improve Upper Extremity Function in Adults with Neurological Conditions

Objectives of Presentation: 1. Describe the impact of robotics on upper extremity function among various neurological populations. 2. Differentiate which patients are appropriate for robotics interventions for upper extremity rehabiliation. 3. Defend the feasibility of robotic interventions for upper extremity rehabilitation of neurological populations. PICO: To what extend does robotic-assisted therapy improve UE function in adults with neurological conditions? Note: Handout with references available at bottom of page. Presentation: 37:3

ROCK activity expressed as a phosphorylation of ezrin following ischemia/reperfusion.

<p>(A) Effect of the peroxynitrite decomposition catalyst FeTPPS, the ROCK inhibitor hydroxyfasudil (H.fasudil), remote ischemic preconditioning (RIPerc) and RIPerc+the NOS inhibitor L-NMMA in protocol 1. (B and C) Effect of RIPerC in non-diabetic and diabetic rats of protocol 2. Values are means ± SEM; n = 5–7. ***<i>P</i><0.001 vs. CIR; ^###<i>P</i><0.001 vs. RIPerc and ^††<i>P</i><0.01 vs. ND-CIR.</p

Hemodynamic changes in Protocol 2.

<p>Values are mean ± SEM; n = 6–7. Abbreviations: MABP (mm Hg), mean arterial blood pressure; HR (beats/min), heart rate; ND-CIR, non-diabetic control ischemia/reperfusion; ND-RIPerc, non-diabeic remote ischemic perconditioning; DM-CIR: diabetes mellitus control ischemia/reperfusion; DM-RIPerc, diabetes mellitus remote perconditioning.</p><p>*<i>P</i><0.05 vs. ND-CIR.</p

Myocardial area at risk and infarct size.

<p>Area at risk (A and B) expressed as % of left ventricle and infarct size (C and D) expressed as % of the area at risk following 30 min ischemia and 2 hrs reperfusion in rats included in protocol 1 (A and C) and in non-diabetic and diabetic rats included in protocol 2 (B and D). Values are means ± SEM; n = 6–10. **<i>P</i><0.01, ***<i>P</i><0.001 vs. CIR; ^###<i>P</i><0.001 vs. RIPerc and ^†††<i>P</i><0.001 vs. ND-CIR.</p

The effect of RIPerc on eNOS expression and peroxynitrite formation.

<p>(A and C) Effect of remote ischemic perconditioning (RIPerc) on phosphorylated of eNOS at Ser1177 (p-eNOS), total eNOS and nitrotyrosine (3NT) in protocol 1. (B) Effect of RIPerc on NOS expression in non-diabetic and diabetic rats of protocol 2. Values are means ± SEM; n = 5–8. *<i>P</i><0.05 vs. CIR.</p

Cardiomyocytes from mice with the metabolic syndrome show normal β₁-AR, β₂-AR expression and distribution.

<p><b>(A)</b> Representative Western blots and mean data ± SEM (<b><i>B</i></b>; n = 6) of total expression of β₁- and β₂-ARs in left ventricles from control mice and HFD mice. Immunofluorescence staining of β₁-AR <b>(C)</b> and β₂-AR <b>(D)</b> co-stained with RyR2 in control and HFD cardiomyocytes. Merged (yellow) show the intensity overlap between β-ARs and RyR2 in the dyads. <b><i>E</i></b> and <b><i>F</i></b> show plotted intensity profiles of along the dashed lines in <i>C</i> and <i>D</i> with β-AR (red) and RyR2 (green).</p

The antioxidant NAC has no effect on the β-adrenergic stimulated SR Ca²⁺ release and contractility in cardiomyocytes from mice with the metabolic syndrome.

<p><b>(A)</b> Total body weight of mice after 8–10 weeks on control diet (Ctrl, n = 34) or high fat diet (HFD, n = 40). <b>(B)</b> Total body fat measured with DXA whole-body scan (n = 9–10). <b>(C)</b> Typical example of cross-sectional ORO staining showing fat accumulation (stained red) in left ventricles and mean data of ORO staining; eight sections per left ventricle from each group were analyzed (n = 3). Representative [Ca²⁺]_i transients from ctrl <b>(D)</b>, HFD <b>(E)</b> and <i>ob/ob</i> <b>(F)</b> cardiomyocytes obtained in the absence (full lines) and presence (dashed lines) of ISO (100 nM), and without (black lines) and with (red lines) NAC (5 mM). Average amplitude of Ca²⁺ transients <b>(G)</b>, fractional cell shortening (FS, <b><i>H</i></b>) and [Ca²⁺]_i transient decay time constant (tau) <b>(I)</b> with ISO and/or NAC as indicated from control (white bars), HFD (black bars) and <i>ob/ob</i> (grey bars) cardiomyocytes (n>16 cells from at least three mice). Representative Western blots <b>(J)</b> and mean data (n = 6) of ISO-induced PLB phosphorylation normalized to total PLB expression in left ventricles from control and HFD mice. Data are mean ± SEM; **<i>P</i> < 0.01, ***<i>P</i> < 0.001.</p

The ISO-induced increases in L-type Ca²⁺ current density is ROS-independent in cardiomyocytes with the metabolic syndrome.

<p>Mean data (±SEM; n = 6–8 in each group) of <i>I-V</i> curves of peak current density in the absence and presence of ISO (100nM) and NAC (20 mM) as indicated from control <b>(A, D)</b>, HFD <b>(B, E)</b> and <i>ob/ob</i> <b>(C, F)</b> cardiomyocytes. The <i>I-V</i> relationships were obtained by giving test pulses varying from -80 mV to +50 mV from a holding potential of -80 mV. The mean basal current density (i.e. in the absence of NAC and ISO) was -6.1±0.5 pA/pF and for comparisons between groups each group were normalized its basal current to give a relative current density (relative pA/pF).</p