Recent evidence have suggested that neuroinflammation and ischemia induce the activation of two different types of reactive astrocytes, termed A1 and A2. Additionally, A1 astrocytes contribute to the death of neurons and oligodendrocytes in neurodegenerative diseases, such as Alzheimer's disease (AD). In the current study, we constructed an Aβ42-activated microglia-conditioned medium to induce A1 astrocytic activation via secretion of interleukin 1α, tumor necrosis factor, and complement component 1q in vitro, and indicated the regulatory role of milk fat globule epidermal growth factor 8 (MFG-E8) on A1/A2 astrocytic alteration through the downregulation of nuclear factor-κB and the upregulation of PI3K-Akt. This study showed that MFG-E8 suppressed A1 astrocytes and holds great potential for the treatment of AD.
Flunarizine, topiramate, and the combination of flunarizine with topiramate are all effective and have good tolerability in migraine prophylaxis. Adding topiramate to flunarizine may reduce the latter's impact on body weight.
Four cases with previously unidentified X-chromosome abnormalities were studied by standard cytogenetic techniques and FISH in order to demonstrate the origin of the extra segment on the abnormal X chromosomes. All cases were identified as X-chromosome duplications by using a chromosome-specific painting probe. Application of appropriate locus-specific DNA probes as an adjunct to GTG- and RBG-banding proved useful in defining the breakpoints and the extent of the duplications. Although the duplicated X chromosome in female cases was selectively inactivated, as demonstrated by its late-replicating pattern, abnormal clinical findings were manifested in 3 female patients.
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