Clinical Application of Virtual Reality for Upper Limb Motor Rehabilitation in Stroke: Review of Technologies and Clinical Evidence

Neurorehabilitation for stroke is important for upper limb motor recovery. Conventional rehabilitation such as occupational therapy has been used, but novel technologies are expected to open new opportunities for better recovery. Virtual reality (VR) is a technology with a set of informatics that provides interactive environments to patients. VR can enhance neuroplasticity and recovery after a stroke by providing more intensive, repetitive, and engaging training due to several advantages, including: (1) tasks with various difficulty levels for rehabilitation, (2) augmented real-time feedback, (3) more immersive and engaging experiences, (4) more standardized rehabilitation, and (5) safe simulation of real-world activities of daily living. In this comprehensive narrative review of the application of VR in motor rehabilitation after stroke, mainly for the upper limbs, we cover: (1) the technologies used in VR rehabilitation, including sensors; (2) the clinical application of and evidence for VR in stroke rehabilitation; and (3) considerations for VR application in stroke rehabilitation. Meta-analyses for upper limb VR rehabilitation after stroke were identified by an online search of Ovid-MEDLINE, Ovid-EMBASE, the Cochrane Library, and KoreaMed. We expect that this review will provide insights into successful clinical applications or trials of VR for motor rehabilitation after stroke

Effect of the carbon nanotube type on the thermoelectric properties of CNT/Nafion nanocomposites

The effect of different carbon nanotube (CNT) types on the thermoelectric performance of CNT/polymer nanocomposites was studied. Three different kinds of CNTs, single( SWCNTs), few-(FWCNTs) and multi-walled CNTs (MWCNTs), were effectively dispersed in an aqueous solution of Nafion. The electrical properties of the CNT/Nafion nanocomposites were primarily affected by the CNTs since the Nafion acts as an electrically non-conducting matrix, while the thermal conductivity of the nanocomposites was dominated by the Nafion mainly due to weak van der Waals interaction. In this way, electrical and thermal transport can be separated. In all three types of CNTs, both the electrical conductivity and Seebeck coefficient increased as the concentration of CNTs was increased. While the electrical conductivity depends on the type of CNT, the behavior of the Seebeck coefficient was relatively insensitive of the CNT type at high CNT loading. This indicates that high-energy-charges can participate in transport processes irrespective of the type of CNT. It is suggested that FWCNTs and MWCNTs are preferred over SWCNTs in CNT/Nafion nanocomposites for thermoelectric applications

Piceatannol Attenuates Renal Fibrosis Induced by Unilateral Ureteral Obstruction via Downregulation of Histone Deacetylase 4/5 or p38-MAPK Signaling.

Piceatannol, a resveratrol metabolite, is a phenolic compound found in red wine and grapes. We investigated the effect of piceatannol on renal fibrosis and histone deacetylase (HDAC) expression in a mouse model of unilateral ureteral obstruction (UUO). Fibrosis was established by UUO and piceatannol was intraperitoneally injected for 2 weeks. Piceatannol suppressed extracellular matrix (ECM) protein deposition including collagen type I and fibronectin as well as connective tissue growth factor (CTGF) and α-smooth muscle actin (α-SMA) in UUO kidneys. However, the expressions of epithelial-mesenchymal transition (EMT) marker genes, such as N-cadherin and E-cadherin, were not changed in the kidneys after UUO. Masson's trichrome staining and fluorescence immunostaining showed that piceatannol administration attenuated collagen deposition in UUO kidneys. HDAC1, HDAC4, HDAC5, HDAC6, and HDAC10 protein expression was upregulated in UUO kidneys, whereas that of HDAC8 was downregulated. Piceatannol treatment significantly reduced HDAC4 and HDAC5 protein expression. Further, piceatannol attenuated phosphorylation of p38 mitogen-activated protein kinase (p38-MAPK) in UUO kidneys, but not that of transforming growth factor beta1-Smad2/3. These results suggest that class I HDACs and class IIa/b HDACs are involved in renal fibrosis development. Piceatannol may be a beneficial therapeutic agent for treating renal fibrosis via reduction of HDAC4 and HDAC5 protein expression or suppression of the p38-MAPK signaling pathway

Class I histone deacetylase inhibitor MS-275 attenuates vasoconstriction and inflammation in angiotensin II-induced hypertension.

OBJECTIVE:Non-selective histone deacetylase (HDAC) inhibitors are known to improve hypertension. Here, we investigated the therapeutic effect and regulatory mechanism of the class I HDAC selective inhibitors, MS-275 and RGFP966, in angiotensin (Ang) II-induced hypertensive mice. METHODS AND RESULTS:MS-275 inhibited the activity of HDAC1, HDAC2, and HDAC3, while RGFP966 weakly inhibited that of HDAC3 in a cell-free system. MS-275 and RGFP966 treatment reduced systolic blood pressure and thickness of the aorta wall in Ang II-induced hypertensive mice. MS-275 treatment reduced aorta collagen deposition, as determined by Masson's trichrome staining. MS-275 decreased the components of the renin angiotensin system and increased vascular relaxation of rat aortic rings via the nitric oxide (NO) pathway. NO levels reduced by Ang II were restored by MS-275 treatment in vascular smooth muscle cells (VSMCs). However, MS-275 dose (3 mg·kg-1·day-1) was not enough to induce NO production in vivo. In addition, MS-275 did not prevent endothelial nitric oxide synthase (eNOS) uncoupling in the aorta of Ang II-induced mice. Treatment with MS-275 failed to inhibit Ang II-induced expression of NADPH oxidase (Nox)1, Nox2, and p47phox. MS-275 treatment reduced proinflammatory cytokines such as tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and monocyte chemoattractant protein (MCP)-1, as well as adhesion molecules. Histological analysis showed that Ang II-induced macrophage infiltration was reduced by MS-275 and RGFP966 administration. CONCLUSIONS:Our results indicate that class I HDAC selective inhibitors may be good therapeutic agents for the treatment of hypertension through the regulation of vascular remodeling and vasoconstriction, as well as inflammation

Pharmacological effects of piceatannol and resveratrol on <i>in vivo</i> models of renal diseases.

<p>Pharmacological effects of piceatannol and resveratrol on <i>in vivo</i> models of renal diseases.</p

HDAC1 protein expression is upregulated in the UUO kidney.

<p>(A) Kidney protein lysates were analyzed using western blotting. Antibodies against HDAC1, HDAC2, HDAC3, and HDAC8 were used. GAPDH was used as a loading control. (B-E) Quantification analysis was performed using densitometry. The data are expressed as the means ± SD of the mice (n = 6 per group). *<i>P</i><0.05 and ***<i>P</i><0.001 compared with the contralateral kidney. NS indicates not significant.</p

Piceatannol suppresses renal fibrosis by downregulation of the p38-MAPK/HDAC4/5 pathway.

<p>Fibrotic stress such as UUO can induce TGF-β1 expression, which causes phosphorylation and upregulation of Smad2/3 or MAPK (JNK2, ERK1/2, or p38) protein expression. It also increases the expression of class II HDACs (HDAC4/5). Piceatannol attenuates the activation of p38-MAPK signaling and the increased HDAC4/5 expression, but not the activation of the TGF-β1/Smad3 signaling pathway. However, whether a direct association between HDAC4/5 and MAPK signaling or between HDAC4/5 and renal fibrosis exists remains unknown. TβRII and TβRI indicate TGFβ receptor II and TGFβ receptor I, respectively.</p