Objective-Intracellular tumor necrosis factor receptor-associated factors (TRAFs) translocation to lipid rafts is a key element in CD40-induced signaling. The purpose of this study was to investigate the influence of anthocyanin on CD40-mediated proinflammatory events in human endothelial cells and the underlying possible molecular mechanism. Methods and Results-Treatment of endothelial cells with anthocyanin prevented from CD40-induced proinflammatory status, measured by production of IL-6, IL-8, and monocyte chemoattractant protein-1 through inhibiting CD40-induced nuclear factor-B (NF-B) activation. TRAF-2 played pivotal role in CD40 -NF-B pathway as TRAF-2 small interference RNA (siRNA) diminished CD40-induced NF-B activation and inflammation. TRAF-2 overexpression increased CD40-mediated NF-B activation. Moreover, TRAF-2 almost totally recruited to lipid rafts after stimulation by CD40 ligand and depletion of cholesterol diminished CD40-mediated NF-B activation. Exposure to anthocyanin not only interrupted TRAF-2 recruitment to lipid rafts but also decreased cholesterol content in Triton X-100 insoluble lipid rafts. However, anthocyanin did not influence the interaction between CD40 ligand and CD40 receptor. Conclusions-Our findings suggest that anthocyanin protects from CD40-induced proinflammatory signaling by preventing TRAF-2 translocation to lipid rafts through regulation of cholesterol distribution, which thereby may represent a mechanism that would explain the anti-inflammatory response of anthocyanin.

Humans can learn a new language task efficiently with only few examples, by leveraging their knowledge obtained when learning prior tasks. In this paper, we explore whether and how such cross-task generalization ability can be acquired, and further applied to build better few-shot learners across diverse NLP tasks. We introduce CROSSFIT , a problem setup for studying cross-task generalization ability, which standardizes seen/unseen task partitions, data access during different learning stages, and the evaluation protocols. To instantiate different seen/unseen task partitions in CROSS-FIT and facilitate in-depth analysis, we present the NLP Few-shot Gym, a repository of 160 diverse few-shot NLP tasks created from openaccess NLP datasets and converted to a unified text-to-text format. Our analysis reveals that the few-shot learning ability on unseen tasks can be improved via an upstream learning stage using a set of seen tasks. We also observe that the selection of upstream learning tasks can significantly influence few-shot performance on unseen tasks, asking further analysis on task similarity and transferability. 1

Humans can learn a new language task more efficiently than machines, conceivably by leveraging their prior experience and knowledge in learning other tasks. In this paper, we explore whether such cross-task generalization ability can be acquired, and further applied to build better few-shot learners across diverse NLP tasks. We introduce CROSSFIT, a task setup for studying cross-task few-shot learning ability, which standardizes seen/unseen task splits, data access during different learning stages, and the evaluation protocols. In addition, we present NLP Few-shot Gym, a repository of 160 few-shot NLP tasks, covering diverse task categories and applications, and converted to a unified text-to-text format.Our empirical analysis reveals that the fewshot learning ability on unseen tasks can be improved via an upstream learning stage using a set of seen tasks. Additionally, the advantage lasts into medium-resource scenarios when thousands of training examples are available. We also observe that selection of upstream learning tasks can significantly influence few-shot performance on unseen tasks, asking further analysis on task similarity and transferability. 1

In cultured Kupffer cell, using CMZ as inhibitor, ethanol-induced CYP2E1 overexpression was proved to contribute to the sensitization of Kupffer cells to LPS stimuli, with amplification of ROS production and activation of NF-κB, resulting in increased TNF-α production.