42 research outputs found

    How others\u27 behaviours affect visitors\u27 pro-environmental behavioural intention : a research model based on the case of beach cleaning

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    This study proposed a model that could elucidate the effects of othersā€™ pro-environmental behaviour on visitorsā€™ proenvironmental behavioural intention, using beach cleaning as othersā€™ behaviour. The model relied on knowledge of tourism studies and environmental psychology, especially the concept of Motivation Towards the Environment (MTE) as well as the effects of othersā€™ pro-environmental behaviour, as suggested with reference to social dilemma theory and the concept of social norm. The model aimed to examine the effects of information regarding othersā€™ pro-environmental behaviour on visitorsā€™ MTE and ā€˜desire to be awayā€™, effects of the motivations on visitorsā€™ pro-environmental behavioural intention, and indirect effects of the intervention on visitorsā€™ pro-environmental behavioural intention

    Suppressing TGFĪ² signaling in regenerating epithelia in an inflammatory microenvironment is sufficient to cause invasive intestinal cancer

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    Genetic alterations in the TGFĪ² signaling pathway in combination with oncogenic alterations lead to cancer development in the intestines. However, the mechanisms of TGFĪ² signaling suppression in malignant progression of intestinal tumors have not yet been fully understood. We have examined ApcĪ”716 TGFĪ²r2Ī”IEC compound mutant mice that carry mutations in Apc and TGFĪ²r2 genes in the intestinal epithelial cells. We found inflammatory microenvironment only in the invasive intestinal adenocarcinomas but not in noninvasive benign polyps of the same mice. We thus treated simple TGFĪ²r2Ī”IEC mice with dextran sodium sulfate (DSS) that causes ulcerative colitis. Importantly, these TGFĪ²r2Ī”IEC mice developed invasive colon cancer associated with chronic inflammation.Wealso found that TGFĪ² signaling is suppressed in human colitis-associated colon cancer cells. In the mouse invasive tumors, macrophages infiltrated and expressed MT1-MMP, causingMMP2activation. These results suggest that inflammatory microenvironment contributes to submucosal invasion of TGFĪ² signaling-repressed epithelial cells through activation of MMP2. We further found that regeneration was impaired in TGFĪ²r2Ī”IEC mice for intestinal mucosa damaged by DSS treatment or X-ray irradiation, resulting in the expansion of undifferentiated epithelial cell population. Moreover, organoids of intestinal epithelial cells cultured from irradiated TGFĪ²r2Ī”IEC mice formed "long crypts" in Matrigel, suggesting acquisition of an invasive phenotype into the extracellular matrix. These results, taken together, indicate that a simple genetic alteration in the TGFĪ² signaling pathway in the inflamed and regenerating intestinal mucosa can cause invasive intestinal tumors. Such a mechanism may play a role in the colon carcinogenesis associated with inflammatory bowel disease in humans
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