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.

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.

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.

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.