Unlabelled: Electroencephalography-based (EEG) microstate analysis is a promising and widely studied method in which spontaneous cerebral activity is segmented into sub second level quasi-stable states and analyzed. Currently it is being widely explored due to increasing evidence of the association of microstates with cognitive functioning and large-scale brain networks identified by functional magnetic resonance imaging (fMRI). In our study using the four archetypal microstates (A, B, C and D), we investigated the changes in resting state EEG microstate dynamics in persons with temporal lobe epilepsy (TLE) and idiopathic generalized epilepsy (IGE) compared to healthy controls (HC).
View Article and Find Full Text PDFMicrostate analysis is a spatiotemporal method where instantaneous scalp potential topography represents the current state of the brain. The temporal evolution of these scalp topographies gives an understanding of quasi-stable periods of long-range coherence between distant electrodes, reflecting functional coordination within large-scale cortical networks. It has been proven potential in identification and characterization of neurophysiological indicators associated with neuropsychiatric conditions.
View Article and Find Full Text PDFBackground: In the COVID era, medical education has been hit hard. Paradoxically, the need for health professionals has increased. Online methods are being widely used, but its efficacy is rarely measured.
View Article and Find Full Text PDFTwist1, a key transcription factor regulating epithelial-mesenchymal transition and cancer metastasis, is highly expressed in invasive cancers in contrast to the loss of BTG2 expression. Based on our observation that forced expression of BTG2 downregulated Twist1 protein expression without altering mRNA level, we investigated molecular mechanisms of the BTG2-inhibited Twist1 translation in the triple negative breast cancer (TNBC) cells and in vivo BTG2-knockout (KO) mice and human breast cancer tissues. (1) C-terminal domain of Twist1 and Box B of BTG2 interacted with each other, which abrogated Twist1 activity.
View Article and Find Full Text PDFPurpose: It has been reported that PI3K/AKT pathway is altered in various cancers and AKT isoforms specifically regulate cell growth and metastasis of cancer cells; AKT1, but not AKT2, reduces invasion of cancer cells but maintains cancer growth. We propose here a novel mechanism of the tumor suppresser, TIS21, that inhibits both growth and invasion of triple negative breast cancer cells via AKT1 activation by differential regulation of mTORc1 and mTORc2 activity.
Methods: Transduction of adenovirus carrying TIS21 gene and transfection of short interfering RNAs were employed to regulate TIS21 gene expression in various cell lines.