## 3 Results
In this context, based on elevated values of 0.6-1.4 pg/mL, the astroglial-derived serum protein S100B was considered not only a potential clinical marker for assessing the degree of IS manifestation in children, but also a screening marker for evaluating the prognosis of long-term neurological sequelae. Figure 2: Serum endoglin levels in children with IS compared to those of controls (ng/mL). Next, markers from the vascular endothelial growth factor (VEGF) family were evaluated due to their known role in regulating vascularization and stimulating blood vessel formation. In the brain, VEGFs are crucial for regulating vascul- and angiogenesis, neuroprotection, and neurogenesis. VEGF may enhance collateral ischemic remodeling and has recently been recognized as a biomarker for stroke. VEGF is a signaling protein produced by cells to stimulate vasculogenesis (the formation of an embryonic vascular system) and angiogenesis (the growth of new blood vessels within an existing vascular system). Several factors within the VEGF family (a subclass of a larger class of growth factors) have been identified. VEGF proteins are part of the system that restores oxygen supply to tissues during periods of inadequate blood circulation, such as during a stroke. The main functions of VEGF include the formation of new blood vessels during embryonic development and following various diseases, as well as facilitating collateral circulation to form new vessels when existing ones are blocked. Increased VEGF activity is associated with various diseases, including solid cancers, and its overexpression is linked to vascular diseases and epilepsy. Drugs designed to inhibit VEGF, such as bevacizumab, have recently been developed. Controlling or slowing the progression of such diseases remains a critical goal. The current research indicates that VEGF proteins are not the sole activators of angiogenesis. During the acute phase of ischemic stroke (IS), elevated VEGF levels increase the blood-brain barrier permeability and vessel injuries, leading to disruptions in homeostasis, peripheral immune cell infiltration, and localized edema. While VEGF has adverse effects on vascular integrity in the acute phase, these effects are transient. Beyond the acute phase, VEGF exhibits neuroprotective properties when maintained at subthreshold levels. Literature reports consistently indicate elevated serum VEGF levels during the acute phase of IS. In our study, significantly increased mean serum VEGF levels were observed in children during Disability-Adjusted Life Years (DALYs) associated with the acute phase of the disease. The study group demonstrated mean VEGF levels of 613.41 \(\pm\) 39.299 pg/mL, with a range from 296.23 pg/mL to 1705.81 pg/mL. In contrast, the control group showed a mean VEGF level of 185.50 \(\pm\) 12.039 pg/mL, with a maximum of 287.44 pg/mL--significantly lower than the minimum VEGF levels observed in the  
Figure 3: Serum level of the S100B protein during the acute period of stroke in children in comparison with controls (ng/mL) [15]. study group. The difference between the groups was statistically significant (\(p\) < 0.001) (Figure 4). Recently, vascular endothelial growth factor (VEGF) has been linked with ciliary neurotrophic factor (CNTF) as an important biomarker in stroke. CNTF, a pleiotropic cytokine from the neurokinin family, is expressed primarily in gray matter, including the cortex, hippocampus, and astrocytes. Its biological effects are mediated through CNTF receptors. CNTF plays a vital role in maintaining nerve cell survival in neurodegenerative diseases and promoting axonal growth. It significantly contributes to the development and maintenance of the nervous system, as well as the health of cardiomyocytes, osteoblasts, immune cells, adipocytes, and skeletal muscle cells. CNTF exerts multiple beneficial effects on the central nervous system (CNS) and peripheral nervous system, offering potent neuroprotective and neurotrophic actions across various neuron classes, particularly motor neurons.