Give CRISPR a chance : the GeneSprout Initiative

Did you know that a group of early-career researchers launched an initiative enabling open dialog on new plant breeding techniques, such as genome editing? We developed a wide-ranging initiative that aims to facilitate public engagement and provide a platform for young plant scientists to encourage participation in science communication

Participatory Design for Whom? Designing Conversational User Interfaces for Sensitive Settings and Vulnerable Populations

Conversational User Interfaces (CUIs) are becoming increasingly applied in a broad range of sensitive settings to address the needs and struggles of vulnerable or marginalized users. Sensitive settings include, for instance, CUIs mediating the communication difficulties of people with dementia or supporting refugees to cope with new cultural practices as a chatbot on a government website. While researchers are increasingly designing CUIs for such sensitive set tings, methods and participatory design approaches to address vulnerable user groups’ highly sensitive needs and struggles are sparse in research thus far. This workshop aims to explore how we can design CUIs for and in sensitive settings with vulnerable users in mind through the participatory design process. We aim to establish a working definition of vulnerability, sensitive settings, and how practice-oriented design of CUIs can be inclusive of diverse users

Enriching everyday lived experiences in dementia care

Research in HCI is increasingly investigating the role of technology in supporting meaningful and social activities to enhance the lived experiences of people with dementia. However, to further enrich the daily experiences in care, more insight is needed into how technology can directly promote social participation and pleasurable experiences in everyday care situations. This paper discusses the deployment of VITA and SAM: two research products that address the social and emotional needs of residents in day-to-day dementia care. We report how both products offered aesthetic and sensory enrichment, created new experiences in the everyday, and were integrated into the care environment. Furthermore, we identify implications for design to provide: 1) aesthetics in care, 2) authentic experiences, 3) reinforcing everyday life, and 4) community-driven use in practice. We contribute to existing research by demonstrating how technology for dementia care can transcend instrumental use and culminate in warm-felt everyday experiences

1-Aminocyclopropane-1-Carboxylic Acid Oxidase (ACO): The Enzyme That Makes the Plant Hormone Ethylene

The volatile plant hormone ethylene regulates many plant developmental processes and stress responses. It is therefore crucial that plants can precisely control their ethylene production levels in space and time. The ethylene biosynthesis pathway consists of two dedicated steps. In a first reaction, S-adenosyl-L-methionine (SAM) is converted into 1-aminocyclopropane-1-carboxylic acid (ACC) by ACC-synthase (ACS). In a second reaction, ACC is converted into ethylene by ACC-oxidase (ACO). Initially, it was postulated that ACS is the rate-limiting enzyme of this pathway, directing many studies to unravel the regulation of ACS protein activity, and stability. However, an increasing amount of evidence has been gathered over the years, which shows that ACO is the rate-limiting step in ethylene production during certain dedicated processes. This implies that also the ACO protein family is subjected to a stringent regulation. In this review, we give an overview about the state-of-the-art regarding ACO evolution, functionality and regulation, with an emphasis on the transcriptional, post-transcriptional, and post-translational control. We also highlight the importance of ACO being a prime target for genetic engineering and precision breeding, in order to control plant ethylene production levels

The role of hazard- and risk-based approaches in ensuring food safety

AbstractBackgroundFood legislation in the European Union and elsewhere includes both hazard- and risk-based approaches for ensuring safety. In hazard-based approaches, simply the presence of a potentially harmful agent at a detectable level in food is used as a basis for legislation and/or risk management action. Risk-based approaches allow consideration of exposure in assessing whether there may be unacceptable risks to health.Scope and approachThe advantages and disadvantages of hazard- and risk-based approaches for ensuring the safety of food chemicals, allergens, ingredients and microorganisms were explored at an ILSI Europe workshop.Key findings and conclusionsIt was concluded that both types of approach have their place, depending on the context. However, problems can arise when both types of approach are used in regulation by separate agencies that address different aspects of the same agent/substance present in food. This separation of decision-making can result in hazard-based restrictions on marketing and use, whereas risk-based assessments for those exposed show there is reasonable certainty no harm will result. This in turn can lead to contradictory, confusing and ultimately unnecessary actions. Use of hazard-based approaches for foods also means that comparisons with benefits for nutrition and food security cannot be undertaken. This has the potential to lead to bias in the overall conclusions of regulators and risk managers, who may not have been presented with the benefits of particular foods. The value of risk-based approaches is becoming increasingly recognised

Bi-allelic variants in NAE1 cause intellectual disability, ischiopubic hypoplasia, stress-mediated lymphopenia and neurodegeneration

Neddylation has been implicated in various cellular pathways and in the pathophysiology of numerous diseases. We identified four individuals with bi-allelic variants in NAE1, which encodes the neddylation E1 enzyme. Pathogenicity was supported by decreased NAE1 abundance and overlapping clinical and cellular phenotypes. To delineate how cellular consequences of NAE1 deficiency would lead to the clinical phenotype, we focused primarily on the rarest phenotypic features, based on the assumption that these would best reflect the pathophysiology at stake. Two of the rarest features, neuronal loss and lymphopenia worsening during infections, suggest that NAE1 is required during cellular stress caused by infections to protect against cell death. In support, we found that stressing the proteasome system with MG132—requiring upregulation of neddylation to restore proteasomal function and proteasomal stress—led to increased cell death in fibroblasts of individuals with NAE1 genetic variants. Additionally, we found decreased lymphocyte counts after CD3/CD28 stimulation and decreased NF-κB translocation in individuals with NAE1 variants. The rarest phenotypic feature—delayed closure of the ischiopubic rami—correlated with significant downregulation of RUN2X and SOX9 expression in transcriptomic data of fibroblasts. Both genes are involved in the pathophysiology of ischiopubic hypoplasia. Thus, we show that NAE1 plays a major role in (skeletal) development and cellular homeostasis during stress. Our approach suggests that a focus on rare phenotypic features is able to provide significant pathophysiological insights in diseases caused by mutations in genes with pleiotropic effects.</p

Bi-allelic variants in NAE1 cause intellectual disability, ischiopubic hypoplasia, stress-mediated lymphopenia and neurodegeneration

Neddylation has been implicated in various cellular pathways and in the pathophysiology of numerous diseases. We identified four individuals with bi-allelic variants in NAE1, which encodes the neddylation E1 enzyme. Pathogenicity was supported by decreased NAE1 abundance and overlapping clinical and cellular phenotypes. To delineate how cellular consequences of NAE1 deficiency would lead to the clinical phenotype, we focused primarily on the rarest phenotypic features, based on the assumption that these would best reflect the pathophysiology at stake. Two of the rarest features, neuronal loss and lymphopenia worsening during infections, suggest that NAE1 is required during cellular stress caused by infections to protect against cell death. In support, we found that stressing the proteasome system with MG132—requiring upregulation of neddylation to restore proteasomal function and proteasomal stress—led to increased cell death in fibroblasts of individuals with NAE1 genetic variants. Additionally, we found decreased lymphocyte counts after CD3/CD28 stimulation and decreased NF-κB translocation in individuals with NAE1 variants. The rarest phenotypic feature—delayed closure of the ischiopubic rami—correlated with significant downregulation of RUN2X and SOX9 expression in transcriptomic data of fibroblasts. Both genes are involved in the pathophysiology of ischiopubic hypoplasia. Thus, we show that NAE1 plays a major role in (skeletal) development and cellular homeostasis during stress. Our approach suggests that a focus on rare phenotypic features is able to provide significant pathophysiological insights in diseases caused by mutations in genes with pleiotropic effects.</p