Subjects: Biology >> Biophysics >> Neurosciences submitted time 2016-05-11
Wu, Qiong
Xi, Sisi
Wu, Yanhong
Chang, Chi-Fu
Huang, I-Wen
Juan, Chi-Hung
Liu, Zuxiang
Wu, Yanhong
Wu, Yanhong
Fan, Jin
Fan, Jin
Fan, Jin
Fan, Jin
Abstract： Information processing can be biased toward behaviorally relevant and salient stimuli by top-down (goal-directed) and bottom-up (stimulus-driven) attentional control processes respectively. However, the neural basis underlying the integration of these processes is not well understood. We employed functional magnetic resonance imaging (fMRI) and transcranial direct-current stimulation (tDCS) in humans to examine the brain mechanisms underlying the interaction between these two processes. We manipulated the cognitive load involved in top-down processing and stimulus surprise involved in bottom-up processing in a factorial design by combining a majority function task and an oddball paradigm. We found that high cognitive load and high surprise level were associated with prolonged reaction time compared to low cognitive load and low surprise level, with a synergistic interaction effect, which was accompanied by a greater deactivation of bilateral temporoparietal junction (TPJ). In addition, the TPJ displayed negative functional connectivity with right middle occipital gyrus, which is involved in bottom-up processing (modulated by the interaction effect), and the right frontal eye field (FEF), which is involved in top-down control. The enhanced negative functional connectivity between the TPJ and right FEF was accompanied by a larger behavioral interaction effect across subjects. Application of cathodal tDCS over the right TPJ eliminated the interaction effect. These results suggest that the TPJ plays a critical role in processing bottom-up information for top-down control of attention. Hum Brain Mapp 36:4317-4333, 2015. (c) 2015 Wiley Periodicals, Inc.
Peer Review Status:
Awaiting Review
Subjects: Biology >> Biophysics >> Oncology submitted time 2016-05-11
Wang, Huiru
Wu, Yanhong
Zhou, Chunxia
Ma, Wenbo
Zhang, Youhui
Zhang, Shuren
Wang, Huiru
Wu, Yanhong
Zhou, Chunxia
Ma, Wenbo
Zhang, Youhui
Zhang, Shuren
Wang, Huiru
Wu, Yanhong
Wang, Lin
Zhou, Chunxia
Ma, Wenbo
Zhang, Youhui
Zhang, Shuren
Sun, Qing
Abstract： Granzyme M is a serine protease known to be often expressed by natural killer cells and induce target cells apoptosis in combination with perforin. However, we detected granzyme M expression in murine and human cancer cell lines and human tumor samples in our study. Granzyme M increased chemoresistance, colony-formation, cytokine secretion and invasiveness in vitro. Most importantly, granzyme M facilitated tumor growth and metastasis in vivo. Granzyme M induced the epithelial-mesenchymal transition (EMT) in cancer cells associated with STAT3 activation. Our study revealed the role of granzyme M expressed by tumor in chemoresistance, invasion, metastasis and EMT.
Peer Review Status:Awaiting Review
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