Designing and Analyzing In-Place Motor Tasks in Virtual Reality With Goal Functions.

Goal functions make virtual goal-oriented motor tasks easier to analyze and manipulate by explicitly linking movement to outcome. However, they have only been used to study constrained (e.g., planar) upper limb movements. We present a design framework for integrating goal functions with unconstrained postural and upper limb movements in a virtual reality (VR) device. VR tasks designed with the framework can mimic unconstrained natural motions and thus train a range of functional movements yet remain analytically tractable. We created three in-place VR motor tasks: a bow-and-arrow, a reach-and-strike, and a punching bag task. Each task was adjusted to subject-specific workspace limits and anthropometrics. We studied the effects of 3 days of practice and 3 reach/lean distances on task performance in 12 healthy adults. Subjects performed all tasks on day 1 with moderate proficiency and improved with practice at all reach/lean distances. Task-specific results showed that performance decreased and movement variability increased near the edge of the reaching workspace; viewing angles and the imperfect depth cues in VR likely led to biases in performance and practice could attenuate the former effect; in reach-and-strike, subjects learned movement patterns similar to those seen in a real-world striking sport. These results show that our framework can deliver tasks useful for analyzing and training motor performance and can guide future in-place motor training. Post-hoc, we demonstrated the feasibility of generalizable methods that adjust required movement speeds and task difficulty for impaired populations.

Association between uric acid and the risk of hemorrhagic transformation in patients with acute ischemic stroke: a systematic review and meta-analysis.

Background: The relationship between hemorrhagic transformation (HT) and uric acid (UA) remains controversial. This study aimed to investigate the relationship between UA concentrations and the risk of HT following acute ischemic stroke (AIS). Methods: Electronic databases were searched for studies on HT and UA from inception to October 31, 2023. Two researchers independently reviewed the studies for inclusion. STATA Software 16.0 was used to compute the standardized mean difference (SMD) and 95% confidence interval (CI) for the pooled and post-outlier outcomes. Heterogeneity was evaluated using the I2 statistic and the Galbraith plot. Additionally, sensitivity analysis was performed. Lastly, Begg's funnel plot and Egger's test were used to assess publication bias. Results: A total of 11 studies involving 4,608 patients were included in the meta-analysis. The pooled SMD forest plot (SMD = -0.313, 95% CI = -0.586--0.039, p = 0.025) displayed that low UA concentrations were linked to a higher risk of HT in post-AIS patients. However, heterogeneity (I2 = 89.8%, p < 0.001) was high among the studies. Six papers fell outside the Galbraith plot regression line, and there exclusive resulted in the absence of heterogeneity (I2 = 52.1%, p = 0.080). Meanwhile, repeated SMD analysis (SMD = -0.517, 95% CI = -0.748--0.285, p = 0.000) demonstrated that the HT group had lower UA concentrations. Finally, Begg's funnel plot and Egger's test indicated the absence of publication bias in our meta-analysis. Conclusion: This meta-analysis illustrated a substantial connection between UA concentrations and HT, with lower UA concentrations independently linked with a higher risk of HT post-AIS. These results lay a theoretical reference for future studies.Systematic review registration:https://www.crd.york.ac.uk/PROSPERO/CRD42023485539.

Pathological mechanisms and future therapeutic directions of thrombin in intracerebral hemorrhage: a systematic review.

Intracerebral hemorrhage (ICH), a common subtype of hemorrhagic stroke, often causes severe disability or death. ICH induces adverse events that might lead to secondary brain injury (SBI), and there is currently a lack of specific effective treatment strategies. To provide a new direction for SBI treatment post-ICH, the systematic review discussed how thrombin impacts secondary injury after ICH through several potentially deleterious or protective mechanisms. We included 39 studies and evaluated them using SYRCLE's ROB tool. Subsequently, we explored the potential molecular mechanisms of thrombin-mediated effects on SBI post-ICH in terms of inflammation, iron deposition, autophagy, and angiogenesis. Furthermore, we described the effects of thrombin in endothelial cells, astrocytes, pericytes, microglia, and neurons, as well as the harmful and beneficial effects of high and low thrombin concentrations on ICH. Finally, we concluded the current research status of thrombin therapy for ICH, which will provide a basis for the future clinical application of thrombin in the treatment of ICH.

Revisiting the role of the complement system in intracerebral hemorrhage and therapeutic prospects.

Intracerebral hemorrhage (ICH) is a stroke subtype characterized by non-traumatic rupture of blood vessels in the brain, resulting in blood pooling in the brain parenchyma. Despite its lower incidence than ischemic stroke, ICH remains a significant contributor to stroke-related mortality, and most survivors experience poor outcomes that significantly impact their quality of life. ICH has been accompanied by various complex pathological damage, including mechanical damage of brain tissue, hematoma mass effect, and then leads to inflammatory response, thrombin activation, erythrocyte lysis, excitatory amino acid toxicity, complement activation, and other pathological changes. Accumulating evidence has demonstrated that activation of complement cascade occurs in the early stage of brain injury, and the excessive complement activation after ICH will affect the occurrence of secondary brain injury (SBI) through multiple complex pathological processes, aggravating brain edema, and pathological brain injury. Therefore, the review summarized the pathological mechanisms of brain injury after ICH, specifically the complement role in ICH, and its related pathological mechanisms, to comprehensively understand the specific mechanism of different complements at different stages after ICH. Furthermore, we systematically reviewed the current state of complement-targeted therapies for ICH, providing a reference and basis for future clinical transformation of complement-targeted therapy for ICH.