The outbreak of severe acute respiratory syndrome (SARS) in 2003 marked the explosion of health information seeking online in China and the increasing emergence of Chinese health websites. There are both benefits and potential hazards of people's online health information seeking. This article intended to test part of Wilson's second model of information behavior, including source characteristics and activating mechanisms, and to identify the relationships among perceived access, perceived expertise credibility, reward assessment, Internet self-efficacy, and online health information-seeking behavior. Data were drawn from face-to-face surveys and an online survey of health information seekers (N = 393) in China. The results showed that source characteristics predicted activating mechanisms, which in turn predicted online health information-seeking behavior. Activating mechanisms, that is, reward assessment and Internet self-efficacy, mediated the relationship between source characteristics (i.e., access and credibility) and online health information-seeking behavior. Strategies for improving information access, expertise credibility, and Internet self-efficacy are discussed in order to maximize the benefits of online health information seeking and to minimize the potential harm.
Chronic stress could induce cancer metastasis by constant activation of the sympathetic nervous system, while cellular mechanism remains obscure. The aim of this research is to explore the metastasis associated negative effect of chronic stress. The analysis of transcriptome sequencing implied that activation of STAT3 signaling pathway by downregulated miR-337-3p might be a potential mechanism to induce epithelial to mesenchymal transition (EMT) of cancer cell and promote metastasis under chronic stress. We also verified this biological process in further experiments. Downregulation of miR-337-3p could downregulate E-cadherin expression and upregulate vimentin expression in vitro and in vivo. STAT3, related signal pathways of which are involved in metastasis regulation, was directly targeted by miR-337-3p. In conclusion, the above results denoted that activation of miR-337-3p/STAT3 axis might be a potential pathway for the increasing metastasis of breast cancer under chronic stress.
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