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i-Minds 2.0 : how and why constant connectivity is rewiring our brains and what to do about it
\"Engaging and scientifically rigorous, this fully updated edition of i-Minds explores screen-based technology's assimilation into our lives, pondering them as both godsend and plague, demonstrating how constant connectivity is changing our brains and exploring positive steps to take to embrace new technologies.\"-- Provided by publisher.
Book
Beer in health and disease prevention
Beer in Health and Disease Prevention is the single comprehensive volume needed to understand beer and beer-related science.Presenting both the concerns and problems of beer consumption as well as the emerging evidence of benefit, this book offers a balanced view of today's findings and the potential of tomorrow's research.Just as wine in.
eBook
Agrochemicals interact synergistically to increase bee mortality
Global concern over widely documented declines in pollinators
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has led to the identification of anthropogenic stressors that, individually, are detrimental to bee populations
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. Synergistic interactions between these stressors could substantially amplify the environmental effect of these stressors and could therefore have important implications for policy decisions that aim to improve the health of pollinators
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. Here, to quantitatively assess the scale of this threat, we conducted a meta-analysis of 356 interaction effect sizes from 90 studies in which bees were exposed to combinations of agrochemicals, nutritional stressors and/or parasites. We found an overall synergistic effect between multiple stressors on bee mortality. Subgroup analysis of bee mortality revealed strong evidence for synergy when bees were exposed to multiple agrochemicals at field-realistic levels, but interactions were not greater than additive expectations when bees were exposed to parasites and/or nutritional stressors. All interactive effects on proxies of fitness, behaviour, parasite load and immune responses were either additive or antagonistic; therefore, the potential mechanisms that drive the observed synergistic interactions for bee mortality remain unclear. Environmental risk assessment schemes that assume additive effects of the risk of agrochemical exposure may underestimate the interactive effect of anthropogenic stressors on bee mortality and will fail to protect the pollinators that provide a key ecosystem service that underpins sustainable agriculture.
A meta-analysis of studies in which bees were exposed to combinations of agrochemicals, nutritional stressors and/or parasites revealed evidence for synergistic effects on mortality when bees were exposed to multiple agrochemicals at field-realistic levels.
Journal Article
Automotive ergonomics : driver-vehicle interaction
\"The name of Karl Benz, one of the father figures in the automotive industry, is quoted more than once in this book. This is not only because of his undoubted contribution during the initial phase of developments, but also because of the contrast of expectations by key figures such as himself against the established beliefs and practices of today. Common perception of what the automobile is and whom it is addressed to was significantly different back then. From the very few who could afford and the handful of those skilled enough to control such machines, within a few decades we were led to the generalization of the automobile, first in the US, then in Europe and post-WWII Japan\"-- Provided by publisher.
Book
Mitochondrial stress is relayed to the cytosol by an OMA1–DELE1–HRI pathway
In mammalian cells, mitochondrial dysfunction triggers the integrated stress response, in which the phosphorylation of eukaryotic translation initiation factor 2α (eIF2α) results in the induction of the transcription factor ATF4
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. However, how mitochondrial stress is relayed to ATF4 is unknown. Here we show that HRI is the eIF2α kinase that is necessary and sufficient for this relay. In a genome-wide CRISPR interference screen, we identified factors upstream of HRI: OMA1, a mitochondrial stress-activated protease; and DELE1, a little-characterized protein that we found was associated with the inner mitochondrial membrane. Mitochondrial stress stimulates OMA1-dependent cleavage of DELE1 and leads to the accumulation of DELE1 in the cytosol, where it interacts with HRI and activates the eIF2α kinase activity of HRI. In addition, DELE1 is required for ATF4 translation downstream of eIF2α phosphorylation. Blockade of the OMA1–DELE1–HRI pathway triggers an alternative response in which specific molecular chaperones are induced. The OMA1–DELE1–HRI pathway therefore represents a potential therapeutic target that could enable fine-tuning of the integrated stress response for beneficial outcomes in diseases that involve mitochondrial dysfunction.
A genome-wide CRISPR interference screen shows that a signalling pathway involving OMA1, DELE1 and the eIF2α kinase HRI relays mitochondrial stress to the cytosol to trigger the integrated stress response.
Journal Article
The immunological and metabolic landscape in primary and metastatic liver cancer
The liver is the sixth most common site of primary cancer in humans, and generally arises in a background of cirrhosis and inflammation. Moreover, the liver is frequently colonized by metastases from cancers of other organs (particularly the colon) because of its anatomical location and organization, as well as its unique metabolic and immunosuppressive environment. In this Review, we discuss how the hepatic microenvironment adapts to pathologies characterized by chronic inflammation and metabolic alterations. We illustrate how these immunological or metabolic changes alter immunosurveillance and thus hinder or promote the development of primary liver cancer. In addition, we describe how inflammatory and metabolic niches affect the spreading of cancer metastases into or within the liver. Finally, we review the current therapeutic options in this context and the resulting challenges that must be surmounted.This Review discusses the unique and complex immunological and metabolic features of the liver, from the precancerous stage through to oncological transformation and metastasis. Strategies for targeting this niche are also considered.
Journal Article
Hypoxia-inducible factors: cancer progression and clinical translation
Hypoxia-inducible factors (HIFs) are master regulators of oxygen homeostasis that match O2 supply and demand for each of the 50 trillion cells in the adult human body. Cancer cells co-opt this homeostatic system to drive cancer progression. HIFs activate the transcription of thousands of genes that mediate angiogenesis, cancer stem cell specification, cell motility, epithelial-mesenchymal transition, extracellular matrix remodeling, glucose and lipid metabolism, immune evasion, invasion, and metastasis. In this Review, the mechanisms and consequences of HIF activation in cancer cells are presented. The current status and future prospects of small-molecule HIF inhibitors for use as cancer therapeutics are discussed.
Journal Article
Population genomics of bacterial host adaptation
Some bacteria can transfer to new host species, and this poses a risk to human health. Indeed, an estimated 60% of all human pathogens have originated from other animal species. Similarly, human-to-animal transitions are recognized as a major threat to sustainable livestock production, and emerging pathogens impose an increasing burden on crop yield and global food security. Recent advances in high-throughput sequencing technologies have enabled comparative genomic analyses of bacterial populations from multiple hosts. Such studies are providing new insights into the evolutionary processes that underpin the establishment of bacteria in new host niches. A better understanding of the genetic and mechanistic basis for bacterial host adaptation may reveal novel targets for controlling infection or inform the design of approaches to limit the emergence of new pathogens.
Journal Article
Epigenetic and chromatin-based mechanisms in environmental stress adaptation and stress memory in plants
Plants frequently have to weather both biotic and abiotic stressors, and have evolved sophisticated adaptation and defense mechanisms. In recent years, chromatin modifications, nucleosome positioning, and DNA methylation have been recognized as important components in these adaptations. Given their potential epigenetic nature, such modifications may provide a mechanistic basis for a stress memory, enabling plants to respond more efficiently to recurring stress or even to prepare their offspring for potential future assaults. In this review, we discuss both the involvement of chromatin in stress responses and the current evidence on somatic, intergenerational, and transgenerational stress memory.
Journal Article