Adversarial learning has been embedded into deep networks to learn disentangled and transferable representations for domain adaptation. Existing adversarial domain adaptation methods may not effectively align different domains of multimodal distributions native in classification problems. In this paper, we present conditional adversarial domain adaptation, a principled framework that conditions the adversarial adaptation models on discriminative information conveyed in the classifier predictions. Conditional domain adversarial networks (CDANs) are designed with two novel conditioning strategies: multilinear conditioning that captures the crosscovariance between feature representations and classifier predictions to improve the discriminability, and entropy conditioning that controls the uncertainty of classifier predictions to guarantee the transferability. With theoretical guarantees and a few lines of codes, the approach has exceeded state-of-the-art results on five datasets.

Metal-organic frameworks (MOFs) have been used for photodynamic therapy (PDT) of cancers by integrating photosensitizers, which cause cytotoxic effects on cancer cells by converting tumor oxygen into reactive singlet oxygen (O). However, the PDT efficiency of MOFs is severely limited by tumor hypoxia. Herein, by decorating platinum nanozymes on photosensitizer integrated MOFs, we report a simple yet versatile strategy for enhanced PDT. The platinum nanoparticles homogeneously immobilized on MOFs possess high stability and catalase-like activity. Thus, our nanoplatform can facilitate the formation of O in hypoxic tumor site via HO-activated evolvement of O, which can cause more serious damage to cancer cells. Our finding highlights that the composites of nanozymes and MOFs have the potential to serve as efficient agents for cancer therapy, which will open an avenue of nanozymes and MOFs toward biological applications.

Atherosclerosis is a chronic inflammatory disease; unstable atherosclerotic plaque rupture, vascular stenosis, or occlusion caused by platelet aggregation and thrombosis lead to acute cardiovascular disease. Atherosclerosis-related inflammation is mediated by proinflammatory cytokines, inflammatory signaling pathways, bioactive lipids, and adhesion molecules. This review discusses the effects of inflammation and the systemic inflammatory signaling pathway on atherosclerosis, the role of related signaling pathways in inflammation, the formation of atherosclerosis plaques, and the prospects of treating atherosclerosis by inhibiting inflammation.