An Analysis of Facial Expression Recognition Techniques

In present era of technology , we need applications which could be easy to use and are user-friendly , that even people with specific disabilities use them easily. Facial Expression Recognition has vital role and challenges in communities of computer vision, pattern recognition which provide much more attention due to potential application in many areas such as human machine interaction, surveillance , robotics , driver safety, non- verbal communication, entertainment, health- care and psychology study. Facial Expression Recognition has major importance ration in face recognition for significant image applications understanding and analysis. There are many algorithms have been implemented on different static (uniform background, identical poses, similar illuminations ) and dynamic (position variation, partial occlusion orientation, varying lighting )conditions. In general way face expression recognition consist of three main steps first is face detection then feature Extraction and at last classification. In this survey paper we discussed different types of facial expression recognition techniques and various methods which is used by them and their performance measures

SRF Phosphorylation by Glycogen Synthase Kinase-3 Promotes Axon Growth in Hippocampal Neurons

The growth of axons is an intricately regulated process involving intracellular signaling cascades and gene transcription. We had previously shown that the stimulus-dependent transcription factor, serum response factor (SRF), plays a critical role in regulating axon growth in the mammalian brain. However, the molecular mechanisms underlying SRF-dependent axon growth remains unknown. Here we report that SRF is phosphorylated and activated by GSK-3 to promote axon outgrowth in mouse hippocampal neurons. GSK-3 binds to and directly phosphorylates SRF on a highly conserved serine residue. This serine phosphorylation is necessary for SRF activity and for its interaction with MKL-family cofactors, MKL1 and MKL2, but not with TCF-family cofactor, ELK-1. Axonal growth deficits caused by GSK-3 inhibition could be rescued by expression of a constitutively active SRF. The SRF target gene and actin-binding protein, vinculin, is sufficient to overcome the axonal growth deficits of SRF-deficient and GSK-3-inhibited neurons. Furthermore, short hairpin RNA-mediated knockdown of vinculin also attenuated axonal growth. Thus, our findings reveal a novel phosphorylation and activation of SRF by GSK-3 that is critical for SRF-dependent axon growth in mammalian central neurons