Considering the potential hazardous effects of disinfectant residues on environment, organisms and biodiversity, the sharp rise in use of disinfectants during COVID-19 pandemic has been considered highly likely to cause worldwide secondary disasters in ecosystems and human health. This questionnaire-based survey investigated the impact of COVID-19 outbreak on household disinfectant product consumption levels and behaviour of 3667 Chinese residents. In particular, in the context that no strategy is currently available to minimize the disinfectant pollution, based on the similarities between disinfectants and pharmaceuticals, we proposed a perspective of ecopharmacovigilance (EPV), which is an effective measure to minimize the environmental risks posed by pharmaceuticals using drug administration protocols, for disinfectant environmental risk management. The public’s environmental perceptions, attitudes and the related practices regarding household disinfectant consumption from an EPV perspective were also included in the study. The results showed that the COVID-19 outbreak caused a tremendous rise in the public’s household disinfectant consumption and usage levels in China. After the COVID-19 outbreak, the chlorine-based and alcohol-based disinfectants were considered as the most preferred products for household disinfection and hand sanitization, respectively. Importantly, the Chinese public’s environmental perceptions and practice on disinfectants were poor. Less than half respondents had positive attitudes toward the source control of disinfectant pollution. The population groups including females, the middle aged adults, those having healthcare professional background, as well as the higher-educated could be focused on to develop targeted efforts for the future control of disinfectant pollution in environment.
Ulcerative colitis (UC) has closely been associated with an increased risk of colorectal cancer. However, the exact mechanisms underlying colitis-associated cancer (CAC) development remain unclear. As a classic pattern-recognition receptor, Toll like receptor (TLR)4 is a canonical receptor for lipopolysaccharide of Gram-negative bacteria (including two CAC-associated pathogens Fusobacterium nucleatum and Salmonella), and functions as a key bridge molecule linking oncogenic infection to colonic inflammatory and malignant processes. Accumulating studies verified the overexpression of TLR4 in colitis and CAC, and the over-expressed TLR4 might promote colitis-associated tumorigenesis via facilitating cell proliferation, protecting malignant cells against apoptosis, accelerating invasion and metastasis, as well as contributing to the creation of tumor-favouring cellular microenvironment. In recent years, considerable attention has been focused on the regulation of TLR4 signaling in the context of colitis-associated tumorigenesis. MicroRNA (miR)-155 and TLR4 exhibited a similar dynamic expression change during CAC development and shared similar CAC-promoting properties. The available data demonstrated an interplay between TLR4 and miR-155 in the context of different disorders or cell lines. miR-155 could augment TLR4 signaling through targeting negative regulators SOCS1 and SHIP1; and TLR4 activation would induce miR-155 expression via transcriptional and post-transcriptional mechanisms. This possible TLR4-miR-155 positive feedback loop might result in the synergistic accelerating effect of TLR4 and miR-155 on CAC development.
As a pancreatic inflammatory marker, regenerating isletderived protein 3A (Reg3A) plays a key role in inflammationassociated pancreatic carcinogenesis by promoting cell proliferation, inhibiting apoptosis, and regulating cancer cell migration and invasion. This study aimed to reveal a novel immuno-regulatory mechanism by which Reg3A modulates tumour-promoting responses during pancreatic cancer (PC) progression. In an in vitro Transwell system that allowed the direct co-culture of human peripheral blood-derived dendritic cells (DCs) and Reg3A-overexpressing/ silenced human PC cells, PC cell-derived Reg3A was found to downregulate CD80, CD83 and CD86 expression on educated DCs, increase DC endocytic function, inhibit DC-induced T lymphocyte proliferation, reduce IL-12p70 production, and enhance IL-23 production by DCs. The positive effect of tumourderived Reg3A-educated human DCs on PC progression was demonstrated in vivo by intraperitoneally transferring them into PC-implanted severe combined immunodeficiency (SCID) mice reconstituted with human T cells. A Reg3A-JAK2/STAT3 positive feedback loop was identified in DCs educated with Reg3A. In conclusion, as a tumour-derived factor, Reg3A acted to block the differentiation and maturation of the most important antigen-presenting cells, DCs, causing them to limit their potential anti-tumour responses, thus facilitating PC escape and progression.
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