Zero-Shot Visual Recognition using Semantics-Preserving Adversarial Embedding Networks

We propose a novel framework called Semantics-Preserving Adversarial Embedding Network (SP-AEN) for zero-shot visual recognition (ZSL), where test images and their classes are both unseen during training. SP-AEN aims to tackle the inherent problem --- semantic loss --- in the prevailing family of embedding-based ZSL, where some semantics would be discarded during training if they are non-discriminative for training classes, but could become critical for recognizing test classes. Specifically, SP-AEN prevents the semantic loss by introducing an independent visual-to-semantic space embedder which disentangles the semantic space into two subspaces for the two arguably conflicting objectives: classification and reconstruction. Through adversarial learning of the two subspaces, SP-AEN can transfer the semantics from the reconstructive subspace to the discriminative one, accomplishing the improved zero-shot recognition of unseen classes. Comparing with prior works, SP-AEN can not only improve classification but also generate photo-realistic images, demonstrating the effectiveness of semantic preservation. On four popular benchmarks: CUB, AWA, SUN and aPY, SP-AEN considerably outperforms other state-of-the-art methods by an absolute performance difference of 12.2\%, 9.3\%, 4.0\%, and 3.6\% in terms of harmonic mean value

Fatigue Deformation Mechanisms of Zirconia Ceramics

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/65237/1/j.1151-2916.1992.tb05558.x.pd

Fatigue of Yttria-Stabilized Zirconia: I, Fatigue Damage, Fracture Origins, and Lifetime Prediction

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/65792/1/j.1151-2916.1991.tb04088.x.pd

Regulation of axon repulsion by MAX-1 SUMOylation and AP-3.

During neural development, growing axons express specific surface receptors in response to various environmental guidance cues. These axon guidance receptors are regulated through intracellular trafficking and degradation to enable navigating axons to reach their targets. In Caenorhabditis elegans, the UNC-5 receptor is necessary for dorsal migration of developing motor axons. We previously found that MAX-1 is required for UNC-5-mediated axon repulsion, but its mechanism of action remained unclear. Here, we demonstrate that UNC-5-mediated axon repulsion in C. elegans motor axons requires both max-1 SUMOylation and the AP-3 complex β subunit gene, apb-3 Genetic interaction studies show that max-1 is SUMOylated by gei-17/PIAS1 and acts upstream of apb-3 Biochemical analysis suggests that constitutive interaction of MAX-1 and UNC-5 receptor is weakened by MAX-1 SUMOylation and by the presence of APB-3, a competitive interactor with UNC-5. Overexpression of APB-3 reroutes the trafficking of UNC-5 receptor into the lysosome for protein degradation. In vivo fluorescence recovery after photobleaching experiments shows that MAX-1 SUMOylation and APB-3 are required for proper trafficking of UNC-5 receptor in the axon. Our results demonstrate that SUMOylation of MAX-1 plays an important role in regulating AP-3-mediated trafficking and degradation of UNC-5 receptors during axon guidance