The fact that Internet companies may record our personal data and track our online behavior for commercial or political purpose has emphasized aspects related to online privacy. This has also led to the development of search engines that promise no tracking and privacy. Search engines also have a major role in spreading low-quality health information such as that of anti-vaccine websites. This study investigates the relationship between search engines' approach to privacy and the scientific quality of the information they return. We analyzed the first 30 webpages returned searching “vaccines autism” in English, Spanish, Italian, and French. The results show that not only “alternative” search engines (Duckduckgo, Ecosia, Qwant, Swisscows, and Mojeek) but also other commercial engines (Bing, Yahoo) often return more anti-vaccine pages (10–53%) than
Google.com
(0%). Some localized versions of Google, however, returned more anti-vaccine webpages (up to 10%) than
Google.com
. Health information returned by search engines has an impact on public health and, specifically, in the acceptance of vaccines. The issue of information quality when seeking information for making health-related decisions also impact the ethical aspect represented by the right to an informed consent. Our study suggests that designing a search engine that is privacy savvy and avoids issues with filter bubbles that can result from user-tracking is necessary but insufficient; instead, mechanisms should be developed to test search engines from the perspective of information quality (particularly for health-related webpages) before they can be deemed trustworthy providers of public health information.
z inoculation, rots of about 30mm in diameter appeared on the inoculated wounds, whereas on control no symptoms were observed. F. brachygibbosum was re-isolated from rots. F. brachygibbosum is a fungal plant pathogen associated with a wide range of symptoms on approximately 25 cultivated and non-cultivated plant species; the pathogen has been reported in Italy in soil/marine sediments and in quinoa and durum wheat seeds (EFSA Panel, 2021). F. brachygibbosum was recently reported as a pathogen of potato tubers in Algeria (Azil et al. 2021). To our knowledge, this is the first report of this pathogen on potato tubers in Italy.
The present study used human myeloid leukemia U937 cells, a versatile promonocytic cellular system which, based on its endoplasmic reticulum (ER)/mitochondria functional relationships, respond to low micromolar concentrations of arsenite with a single, defined mechanism of superoxide (O2 -. )formation. Under these conditions, we observe an initial Ca 2+ mobilization from the ER associated with the mitochondrial accumulation of the cation, followed by Ca 2+ -dependent mitochondrial O2 -.(mitoO2 -. ) formation. These events, barely detectable after 3 h were better appreciated at 6 h. We found that remarkably shorter exposure to, and lower concentrations of, arsenite are required to induce extensive O2formation in cells supplemented with inositol-1,4,5-trisphosphate receptor (IP3R) or ryanodine receptor (RyR) agonists. Indeed, nanomolar arsenite induced maximal O2 -. formation after only 10 min of exposure, and this response was uniquely dependent on the enforced mitochondrial Ca 2+ accumulation. The dramatic anticipation of, sensitization to, the effects of arsenite caused by the IP3R or RyR agonists was accompanied by a parallel significant genotoxic response in the absence of detectable mitochondrial dysfunction and cytotoxicity. We conclude that the prolonged, low micromolar arsenite exposure paradigm resulting in mitoO2 -. formation is necessary to affect Ca 2+ homeostasis and accumulate the cation in mitochondria. The arsenite requirements to promote mitoO2 -. formation in the presence of sufficient mitochondrial Ca 2+ were instead remarkably lower in terms of both concentration and time of exposure. These conditions were associated with the induction of extensive DNA strand scission in the absence of detectable signs of toxicity.
Significance StatementIn RP-cells, arsenite causes mitochondrial Ca 2+ accumulation ([Ca 2+ ]m) and Ca 2+ -dependent mitochondrial superoxide formation. We now report that the second event requires remarkably lower concentrations of /time of exposure to the metalloid than the former. Indeed, a brief exposure to nanomolar levels of arsenite produced maximal effects under conditions in which the [Ca 2+ ]m was increased by IP3R or RyR agonists. Hence, specific substances or conditions enhancing the [Ca 2+ ]m,
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