Funding Nonprofit Radio Technology Initiatives in Canada

Media organizations worldwide are struggling to find sustainable financial models since the arrival of the internet. Nonprofit radio is no different. Using a thematic analysis of 62 Canadian nonprofit stations’ financial statements from 2012–2015, this study examines the impact of the Community Radio Fund of Canada’s Radiometers’ grant competition. Although results show a small financial gain for those who received funding, the study fails to determine the value of relying on such a grant for long-term technological sustainability. This study also shows the classic income effect by demonstrating how stations continued spending on technology whether they received grants or not. Recommendations include creating a matching fund program to encourage stations to find alternative sources of income to sustain their projects and increase accountability.Les organisations de médias à travers le monde luttent pour trouver des modèles financiers durables depuis l’arrivée d’internet. La radio à but non lucratif n’y échappe pas non plus. En effectuant une analyse thématique des états financiers de 62 stations canadiennes à but non lucratif de 2012-2015, cette étude examine l’impact de la compétition Radiomètres du Fonds canadien de la radio communautaire. Malgré le fait que les résultats démontrent un petit gain financier pour ceux ayant reçu du financement, l’étude ne parvient pas à démontrer la valeur de ce type de subvention pour une durabilité technologique à long terme. Cette étude valide aussi l’effet de revenu classique en démontrant que les stations continuent à effectuer des dépenses en technologie, peu importe s’ils ont obtenu ou non une subvention. Les recommandations comprennent la création d’un programme de fonds de contrepartie, afin d’encourager les stations à trouver des sources alternatives de revenus afin de soutenir leurs projets et d’accroître l’imputabilité

Search for dark matter produced in association with bottom or top quarks in √s = 13 TeV pp collisions with the ATLAS detector

A search for weakly interacting massive particle dark matter produced in association with bottom or top quarks is presented. Final states containing third-generation quarks and miss- ing transverse momentum are considered. The analysis uses 36.1 fb−1 of proton–proton collision data recorded by the ATLAS experiment at √s = 13 TeV in 2015 and 2016. No significant excess of events above the estimated backgrounds is observed. The results are in- terpreted in the framework of simplified models of spin-0 dark-matter mediators. For colour- neutral spin-0 mediators produced in association with top quarks and decaying into a pair of dark-matter particles, mediator masses below 50 GeV are excluded assuming a dark-matter candidate mass of 1 GeV and unitary couplings. For scalar and pseudoscalar mediators produced in association with bottom quarks, the search sets limits on the production cross- section of 300 times the predicted rate for mediators with masses between 10 and 50 GeV and assuming a dark-matter mass of 1 GeV and unitary coupling. Constraints on colour- charged scalar simplified models are also presented. Assuming a dark-matter particle mass of 35 GeV, mediator particles with mass below 1.1 TeV are excluded for couplings yielding a dark-matter relic density consistent with measurements

Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018.

Over the past decade, the Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for the definition and interpretation of cell death from morphological, biochemical, and functional perspectives. Since the field continues to expand and novel mechanisms that orchestrate multiple cell death pathways are unveiled, we propose an updated classification of cell death subroutines focusing on mechanistic and essential (as opposed to correlative and dispensable) aspects of the process. As we provide molecularly oriented definitions of terms including intrinsic apoptosis, extrinsic apoptosis, mitochondrial permeability transition (MPT)-driven necrosis, necroptosis, ferroptosis, pyroptosis, parthanatos, entotic cell death, NETotic cell death, lysosome-dependent cell death, autophagy-dependent cell death, immunogenic cell death, cellular senescence, and mitotic catastrophe, we discuss the utility of neologisms that refer to highly specialized instances of these processes. The mission of the NCCD is to provide a widely accepted nomenclature on cell death in support of the continued development of the field

Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)1.

In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field