Vegetarian and vegan rights in Europe : chickening out or egging them on?

The recognition of vegetarianism as a protected belief under equality legislation in the UK was denied by an employment tribunal judge in 2019. The judge in question treated vegetarianism as if it were frivolous and whimsical and compared it negatively with veganism. The following year he recognised veganism as a protected belief, which diverges from the norm of protecting both of these beliefs under the same legislative provisions. This article examines a selection of European cases starting in Ireland in the late nineteenth century in which vegetarianism was familiar, respected by eminent courts and protected without much fuss. The purpose is to demonstrate that the tribunal judge erred and that the pending appeal should be successful, failing which legislative intervention may be necessary.El reconocimiento del vegetarianismo como una creencia protegida bajo la legislación de igualdad en el Reino Unido fue denegado por un juez de un tribunal laboral en 2019. El juez en cuestión trató el vegetarianismo como si fuera frívolo y caprichoso y lo comparó negativamente con el veganismo. Al año siguiente reconoció el veganismo como una creencia protegida, lo que difiere de la norma de proteger ambas creencias bajo las mismas disposiciones legislativas. Este artículo examina una selección de casos que comenzaron a finales del siglo XIX en los que el vegetarianismo era familiar, respetado por tribunales eminentes y protegido sin mucho alboroto. El propósito es demostrar que el juez del tribunal incurrió en error y que la apelación pendiente debería ser exitosa, de no ser así, puede ser necesaria la intervención legislativa

Morality patently matters: the case for a universal suffrage for morally controversial biotechnological patents

This thesis is a critique and proposed reform of the decision-making process under the European Patent Convention 1973, Article 53(a) as it relates to morality. It postulates that the manner in which the morality bar is currently managed is inappropriate as it relies on patent officials to make the initial decision as to whether the patent application is morally permissible or not. In a pluralistic world, morality is understood differently by a wide variety of people but this is not currently being acknowledged within the patent system. Whilst there is an option to bring opposition proceedings to challenge patent grants, this onus is considerable on the challenger and any debate is then played out by a very small sector of highly specialised experts, often with very differing views on morality. This thesis seeks to broaden the decision-making process to reflect society’s pluralism. Officials, it will be argued, should instead of trying to decide what constitutes morality in a realm of such importance for humanity as a whole, administer a system which facilitates public participation and a vote. This will be based on existing models of widespread public deliberation and participation, albeit not ones that currently operate in (or near) the patent world. At present, criticisms in the legal literature tend to suggest more deliberation in the patent field and more participation is recommended in science literature but the logistics are unexplored and will be brought together in this work, making an original contribution to knowledge. In order to achieve its aim, the thesis employs a pluralistic methodology which includes doctrinal, socio-legal and interdisciplinary facets which will enable the construction of a model for reform of the patent system in the domain of morality. This will come from outside of traditional legal mechanisms such as legislative, judicial or patent office reform solutions, as a far-reaching paradigm is envisaged. The claim to originality lies in the extraction of principles from deliberative and participatory models of democracy and their application to the decision-making process in morally controversial biotechnological patents

Post-Transcriptional Dysregulation by miRNAs Is Implicated in the Pathogenesis of Gastrointestinal Stromal Tumor [GIST]

peer-reviewedIn contrast to adult mutant gastrointestinal stromal tumors [GISTs], pediatric/wild-type GISTs remain poorly understood overall, given their lack of oncogenic activating tyrosine kinase mutations. These GISTs, with a predilection for gastric origin in female patients, show limited response to therapy with tyrosine kinase inhibitors and generally pursue a more indolent course, but still may prove fatal. Defective cellular respiration appears to underpin tumor development in these wild-type cases, which as a group lack expression of succinate dehydrogenase [SDH] B, a surrogate marker for respiratory chain metabolism. Yet, only a small subset of the wild-type tumors show mutations in the genes coding for the SDH subunits [SDHx]. To explore additional pathogenetic mechanisms in these wild-type GISTs, we elected to investigate posttranscriptional regulation of these tumors by conducting microRNA (miRNA) profiling of a mixed cohort of 73 cases including 18 gastric pediatric wild-type, 25 (20 gastric, 4 small bowel and 1 retroperitoneal) adult wild-type GISTs and 30 gastric adult mutant GISTs. By this approach we have identified distinct signatures for GIST subtypes which correlate tightly with clinico-pathological parameters. A cluster of miRNAs on 14q32 show strikingly different expression patterns amongst GISTs, a finding which appears to be explained at least in part by differential allelic methylation of this imprinted region. Small bowel and retroperitoneal wild-type GISTs segregate with adult mutant GISTs and express SDHB, while adult wildtype gastric GISTs are dispersed amongst adult mutant and pediatric wild-type cases, clustering in this situation on the basis of SDHB expression. Interestingly, global methylation analysis has recently similarly demonstrated that these wild-type, SDHB-immunonegative tumors show a distinct pattern compared with KIT and PDGFRA mutant tumors, which as a rule do express SDHB. All cases with Carney triad within our cohort cluster together tightly.Funding was obtained from the Medical Research Charities Group (http://www.mrcg.ie/) and Health Research Board of Ireland (http://www.hrb.ie) (MO’S), The Children’s Medical and Research Foundation (http://www.cmrf.org) (MO’S), the GIST Cancer Awareness Foundation [GCAF] (http://www. gistawareness.org/)(MO’S), and research grants from the Life Raft Group (http://www.liferaftgroup.org/)(MD-R) and from the Fonds voor Wetenschappelijk Onderzoek Vlaanderen (http://www.fwo.be/)(grant # G.0286.05 MD-R)

MicroRNA-184 inhibits neuroblastoma cell survival through targeting the serine/threonine kinase AKT2

BACKGROUND: Neuroblastoma is a paediatric cancer of the sympathetic nervous system. The single most important genetic indicator of poor clinical outcome is amplification of the MYCN transcription factor. One of many down-stream MYCN targets is miR-184, which is either directly or indirectly repressed by this transcription factor, possibly due to its pro-apoptotic effects when ectopically over-expressed in neuroblastoma cells. The purpose of this study was to elucidate the molecular mechanism by which miR-184 conveys pro-apoptotic effects. RESULTS: We demonstrate that the knock-down of endogenous miR-184 has the opposite effect of ectopic up-regulation, leading to enhanced neuroblastoma cell numbers. As a mechanism of how miR-184 causes apoptosis when over-expressed, and increased cell numbers when inhibited, we demonstrate direct targeting and degradation of AKT2, a major downstream effector of the phosphatidylinositol 3-kinase (PI3K) pathway, one of the most potent pro-survival pathways in cancer. The pro-apoptotic effects of miR-184 ectopic over-expression in neuroblastoma cell lines is reproduced by siRNA inhibition of AKT2, while a positive effect on cell numbers similar to that obtained by the knock-down of endogenous miR-184 can be achieved by ectopic up-regulation of AKT2. Moreover, co-transfection of miR-184 with an AKT2 expression vector lacking the miR-184 target site in the 3\u27UTR rescues cells from the pro-apoptotic effects of miR-184. CONCLUSIONS: MYCN contributes to tumorigenesis, in part, by repressing miR-184, leading to increased levels of AKT2, a direct target of miR-184. Thus, two important genes with positive effects on cell growth and survival, MYCN and AKT2, can be linked into a common genetic pathway through the actions of miR-184. As an inhibitor of AKT2, miR-184 could be of potential benefit in miRNA mediated therapeutics of MYCN amplified neuroblastoma and other forms of cancer

Neonatal scrotal wall necrotizing fasciitis (Fournier gangrene): a case report

<p>Abstract</p> <p>Introduction</p> <p>Necrotizing fasciitis in neonates is rare and is associated with almost 50% mortality. Although more than 80 cases of neonates (under one month of age) with necrotizing fasciitis have been reported in the literature, only six of them are identified as originating in the scrotum.</p> <p>Case presentation</p> <p>We report the case of a four-week-old, full-term, otherwise-healthy Caucasian baby boy who presented with an ulcerating lesion of his scrotal wall. His scrotum was explored because of a provisional diagnosis of missed torsion of the testis. He was found to have necrotizing fasciitis of the scrotum. We were able to preserve the testis and excise the necrotic tissue, and with intravenous antibiotics there was a successful outcome.</p> <p>Conclusions</p> <p>Fournier gangrene is rarely considered as part of the differential diagnosis in the clinical management of the acute scrotum. However, all doctors who care for small babies must be aware of this serious condition and, if it is suspected, should not hesitate in referring the babies to a specialist pediatric surgical center immediately.</p

Seeing lockdown through the eyes of children from around the world: Reflecting on a children's artwork project.

The COVID-19 pandemic created new challenges for children including access to education and limiting social and emotional connections to extended family, friends, and the community. Globally, opportunities for sharing children’s self-reported experiences during lockdown were limited. The primary aim of this project was to create an art-E-Book that reflects children’s experiences of life during the COVID-19 pandemic that could be shared with other children around the world. Secondly, we wanted to reflect on the consultation undertaken within the International Network of Child and Family Centered Care (INCFCC) using Gibbs (1988) reflective cycle framework. Children from around the world were invited to submit a piece of artwork that reflected their experience during the COVID-19 pandemic via a Qualtrics-survey in May 2020. The children’s artwork and written pieces were transcribed verbatim into an E-Book and the artwork was further placed into groups based on similarity of meaning. Fifty-five children from 17 countries submitted an artwork piece. Four groups were evident within the children’s artwork including infection control measures, positive experiences and emotions (connection to family, fun activities), negative experiences and emotions (social impact, emotional impact), and uniting children globally. The E-Book is available to download free of charge via the INCFCC website. The E-Book illustrates how children of all ages can provide meaningful insightful commentary and valuable information on their experiences during an unprecedented pandemic

SMARCB1 loss induces druggable cyclin D1 deficiency via upregulation of MIR17HG in atypical teratoid rhabdoid tumors

Atypical teratoid rhabdoid tumor (ATRT) is a fatal pediatric malignancy of the central neural system lacking effective treatment options. It belongs to the rhabdoid tumor family and is usually caused by biallelic inactivation of SMARCB1, encoding a key subunit of SWI/SNF chromatin remodeling complexes. Previous studies proposed that SMARCB1 loss drives rhabdoid tumor by promoting cell cycle through activating transcription of cyclin D1 while suppressing p16. However, low cyclin D1 protein expression is observed in most ATRT patient tumors. The underlying mechanism and therapeutic implication of this molecular trait remain unknown. Here, we show that SMARCB1 loss in ATRT leads to the reduction of cyclin D1 expression by upregulating MIR17HG, a microRNA (miRNA) cluster known to generate multiple miRNAs targeting CCND1. Furthermore, we find that this cyclin D1 deficiency in ATRT results in marked in vitro and in vivo sensitivity to the CDK4/6 inhibitor palbociclib as a single agent. Our study identifies a novel genetic interaction between SMARCB1 and MIR17HG in regulating cyclin D1 in ATRT and suggests a rationale to treat ATRT patients with FDA- approved CDK4/6 inhibitors. © 2020 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/156416/2/path5493.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/156416/1/path5493_am.pd