## 3 Results  
Biochemical markers have recently gained significance in identifying brain lesions. In this context, our study aimed to assess the expression of immune parameters and biological factors involved in childhood stroke. We analyzed their relationship with the disease severity, infarct size, and long-term clinical outcomes. Additionally, we investigated the correlation between these parameters and their potential early prognostic role in pediatric ischemic stroke (IS). Given the limited data on the role of these markers in the mechanisms of acute childhood stroke--which remains poorly studied--we focused on assessing the expression of interleukin-6 (IL-6), vascular endothelial growth factor (VEGF), ciliary neurotrophic factor (CNTF), the S-100B protein, CD105 (endoglin), and antiphospholipid antibodies (APAs) in peripheral blood. The aim was to understand their role in inflammation at disease onset and in angiogenesis during the onset and progression of the disease. Following the research objectives, a prospective study was conducted during the years 2017-2020 on a sample of 53 children who suffered neonatal or pediatric IS. Also, an equal number of children were included in the control group. Concomitantly with the evaluation of children with acute IS using the PedNIHSS scale, the serum concentrations of IL-6, VEGF, CNTF, S100B, endoglin (CD105), and APAs in patients with acute IS and children in the control group were determined. In addition, the serum VEGF and S100B protein levels were assessed during the acute period of the disease and more than six months after the acute stroke. We considered certain practically determined and scientifically substantiated normal concentration limit levels. The obtained results were characterized by statistically significant variations in the serum concentrations of these biomarkers. Concerning endoglin (ENG) or CD105, it is known to be a membrane glycoprotein that can bind the \(\beta\)1 and \(\beta\)3 isoforms of transforming growth factor beta (TGF\(\beta\)). Endoglin is a TGF\(\beta\)-associated receptor and is required for both vasculogenesis (the formation of an embryonic vascular system) and angiogenesis (the growth of new vessels in an existing vascular system), as the process of new blood vessel formation in an organ or tissue, during which the reorganization of the primary capillary network results in it being reduced to a simpler and more distinct system of capillaries, arteries and veins, is known to be continuous. Normally, angiogenesis processes in the body continue with moderate intensity and are activated only during the regeneration of injured tissues, drainage of blood clots, elimination of inflammatory outbreaks, scar formation, and similar processes of recovery, as well as during the growth and development of the body. However, the impact of ENG on recovery after stroke and brain surgery is unclear. In this study, the serum CD105 concentration was determined to be lower in children with acute stroke, and endoglin deficiency impairs recovery processes after stroke [11]. Thus, ENG-CD105 deficiency may impair recovery after ischemic brain injury. Endoglin deficiency was associated with impaired recovery processes post-stroke, suggesting that ENG-CD105 deficiency might hinder angiogenesis, alter macrophage adhesion, and delay the resolution of inflammation [11; 12; 13; 14]. Experimental studies have indicated that CD105 deficiency exacerbates ischemic brain injury and delays neurobehavioral recovery processes. According to the literature, \"hypoxia-induced CD105\" expression is regulated by hypoxia-inducible factor 1 (HIF-1), which directly binds to the hypoxia response element in the CD105 promoter. HIF-1, an essential factor for cellular adaptation to low oxygen levels, is predominantly found in the brain, heart, and lungs. The activation of HIF in response to hypoxia may facilitate improved recovery from IS in children by improving therapeutic responses.