Data_Sheet_1_Feasibility of hemispatial neglect rehabilitation with virtual reality-based visual exploration therapy among patients with stroke: randomised controlled trial.docx

BackgroundHemispatial neglect (HSN) was diagnosed using a virtual reality-based test (FOPR test) that explores the field of perception (FOP) and field of regard (FOR). Here, we developed virtual reality-visual exploration therapy (VR-VET) combining elements from the FOPR test and visual exploration therapy (VET) and examined its efficacy for HSN rehabilitation following stroke.MethodsEleven participants were randomly assigned to different groups, training with VR-VET first then waiting without VR-VET training (TW), or vice versa (WT). The TW group completed 20 sessions of a VR-VET program using a head-mounted display followed by 4 weeks of waiting, while the WT group completed the opposite regimen. Clinical HSN measurements [line bisection test (LBT), star cancellation test (SCT), Catherine Bergego Scale (CBS), CBS perceptual-attentional (CBS-PA), and CBS motor-explanatory (CBS-ME)] and FOPR tests [response time (RT), success rate (SR), and head movement (HM) for both FOP and FOR] were assessed by blinded face-to-face assessments.ResultsFive and six participants were allocated to the TW and WT groups, respectively, and no dropout occurred throughout the study. VR-VET considerably improved LBT scores, FOR variables (FOR-RT, FOR-SR), FOP-LEFT variables (FOP-LEFT-RT, FOP-LEFT-SR), and FOR-LEFT variables (FOR-LEFT-RT, FOR-LEFT-SR) compared to waiting without VR-VET. Additionally, VR-VET extensively improved FOP-SR, CBS, and CBS-PA, where waiting failed to make a significant change. The VR-VET made more improvements in the left hemispace than in the right hemispace in FOP-RT, FOP-SR, FOR-RT, and FOR-SR.ConclusionThe observed improvements in clinical assessments and FOPR tests represent the translatability of these improvements to real-world function and the multi-dimensional effects of VR-VET training.Clinical trial registrationhttps://clinicaltrials.gov/ct2/show/NCT03463122, identifier NCT03463122.</p

Particulate matter 2.5 promotes inflammation and cellular dysfunction <i>via</i> reactive oxygen species/p38 MAPK pathway in primary rat corneal epithelial cells

Numerous studies have linked particulate matter2.5 (PM2.5) to ocular surface diseases, but few studies have been conducted on the biological effect of PM2.5 on the cornea. The objective of this study was to evaluate the harmful effect of PM2.5 on primary rat corneal epithelial cells (RCECs) in vitro and identify the toxic mechanism involved. Primary cultured RCECs were characterized by pan-cytokeratin (CK) staining. In PM2.5-exposed RCECs, cell viability, microarray gene expression, inflammatory cytokine levels, mitochondrial damage, DNA double-strand break, and signalling pathway were investigated. Exposure to PM2.5 induced cytotoxicity and morphological changes in RCECs. In addition, PM2.5 markedly up-regulated pro-inflammatory mediators but down-regulated the wound healing-related transforming growth factor-β. Furthermore, PM2.5 promoted mitochondrial reactive oxygen species (ROS) production and mediated cellular damage to mitochondria and DNA, whereas these cellular alterations induced by PM2.5 were markedly suppressed by a potential ROS scavenger. Noteworthy, removal of ROS selectively down-regulated the phosphorylation of p38 mitogen-activated protein kinase (MAPK) and the activation of the nuclear factor-κB (NF-κB) p65 in PM2.5-stimulated cells. Additionally, SB203580, a p38 MAPK inhibitor, markedly suppressed these PM2.5-mediated cellular dysfunctions. Taken together, our findings show that PM2.5 can promote the ROS/p38 MAPK/NF-κB signalling pathway and lead to mitochondrial damage and DNA double-strand break, which is ultimately caused inflammation and cytotoxicity in RCECs. These findings indicate that the ROS/p38 MAPK/NF-κB signalling pathway is one mechanism involved in PM2.5-induced ocular surface disorders.</p