Sinkhorn Adversarial Attack and Defense.

Adversarial attacks have been extensively investigated in the recent past. Quite interestingly, a majority of these attacks primarily work in the lp space. In this work, we propose a novel approach for generating adversarial samples using Wasserstein distance. Unlike previous approaches, we use an unbalanced optimal transport formulation which is naturally suited for images. We first compute an adversarial sample using a gradient step and then project the resultant image into Wasserstein ball with respect to original sample. The attack introduces perturbation in the form of pixel mass distribution which is guided by a cost metric. Elaborate experiments on MNIST, Fashion-MNIST, CIFAR-10 and Tiny ImageNet demonstrate a sharp decrease in the performance of state-of-art classifiers. We also perform experiments with adversarially trained classifiers and show that our system achieves superior performance in terms of adversarial defense against several state-of-art attacks. Our code and pre-trained models are available at https://bit.ly/2SQBR4E.

Anti-leukemic effects of gallic acid on human leukemia K562 cells: downregulation of COX-2, inhibition of BCR/ABL kinase and NF-κB inactivation.

Gallic acid (GA) induces apoptosis in various cancer cell lines. In this study, we investigated the apoptotic activity induced by GA on chronic myeloid leukemia (CML) cell line-K562 and the underlying mechanism. GA reduced the viability of K562 cells in a dose and time dependent manner. GA led to G0/G1 phase arrest in K562 cells by promoting p21 and p27 and inhibiting the levels of cyclin D and cyclin E. Further studies indicated apoptosis with impaired mitochondrial function as a result of deranged Bcl-2/Bax ratio, leakage of cytochrome c and PARP cleavage along with DNA fragmentation and by up-regulating the expression of caspase-3. GA also activated the protein expressions of fatty acid synthase ligand and caspase-8. GA is more effective in imatinib resistant-K562 (IR-K562) cells (IC50 4 µM) than on K562 cells (IC50 33 µM). GA inhibited cyclooxygenase-2 (COX-2) in K562 as well as IR-K562 cells appears to be COX-2 involved in the suppression of growth. Interestingly, GA also inhibited BCR/ABL tyrosine kinase and NF-κB. In conclusion, GA induced apoptosis in K562 cells involves death receptor and mitochondrial-mediated pathways by inhibiting BCR/ABL kinase, NF-κB activity and COX-2.