As part of a need to understand myelin repair mechanisms, molecular pathways underlying oligodendrocyte behavior and central nervous system (CNS) remyelination are currently key topics in multiple sclerosis (MS). In the present study, we report expression of a chemoattractant receptor of the immune system, the chemokine receptor, CXCR2, on normal and proliferating oligodendrocytes in active MS lesions. Proliferating oligodendrocytes were occasionally associated with reactive astrocytes positive for CXCL1 (GRO-alpha), the ligand for CXCR2. CXCL1 expression was not seen on astrocytes in control and normal CNS tissue, while CXCR2 expression was constitutive on oligodendrocytes. At the functional level, following stimulation with the proinflammatory cytokine, interleukin-1beta (IL-1beta), we found high-level synthesis of CXCL1 by human fetal astrocytes in vitro. In contrast, human oligodendrocytes in culture expressed the receptor, CXCR2, constitutively. We propose that the concurrence of CXCR2 on oligodendrocytes and induced CXCL1 on hypertrophic astrocytes in MS provides a novel mechanism for recruitment of oligodendrocytes to areas of damage, an essential prerequisite for lesion repair in this devastating human condition.
Data from studies of 337 children and 1606 young adults are summarized to identify the major causes of stroke in these age groups. In children under 15 years of age, stroke occurs in patients with congenital heart disease, nonatherosclerotic vasculopathies, infection, and hematologic defects like sickle cell disease. In patients 15 to 35 years of age, dissection, cardioembolism, nonatheroslerotic vasculopathies, and prothrombotic states cause a significant percentage of strokes. In adults over 35 years of age, traditional atherosclerotic risk factors predominate. Lifestyle choices (e.g., cigarette smoking, alcohol consumption, and illicit drug use) can significantly increase the rate of stroke among young adults in a community. Limited access to healthcare may increase the role of infectious disease and peripartum complications.
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