Consumer attitudes to vaccination of food-producing animals

Summary The 2001 outbreak of foot and mouth disease in the United Kingdom was unprecedented, with the need to develop a vaccination policy at the height of the epidemic. The extent of consumer concerns about eating products derived from vaccinated animals was unknown as survey results were equivocal. A recent survey on avian influenza reveals that the European public are well informed about the disease and its control, but over 50% of respondents would be reluctant to consume meat from vaccinated birds. There is little specific information available on consumer views about routine vaccination for other diseases. Their concerns appear to increase in an emergency situation when there is heightened awareness through the media. With the development of newer types of vaccines consumers will need more assurance about the safety and use of these products. This article examines these issues and makes practical recommendations for ensuring public confidence when emergency vaccination for disease control is proposed

Medical Doctrines of Heredity.

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Can athletes be tough yet compassionate to themselves? Practical implications for NCAA mental health best practice no. 4

Recent tragic events and data from official NCAA reports suggest student-athletes’ wellbeing is compromised by symptoms of mental health (MH) disorders. Self-compassion (SC) and mental toughness (MT) are two psychological constructs that have been shown effective against stressors associated with sports. The purpose of this study was to investigate SC, MT, and MH in a NCAA environment for the first time and provide practical suggestions for MH best practice No.4. In total, 542 student-athletes participated across Divisions (Mage = 19.84, SD = 1.7). Data were collected through Mental Toughness Index, Self-Compassion Scale, and Mental Health Continuum–Short Form. MT, SC (including mindfulness), and MH were positively correlated. Males scored higher than females on all three scales. No differences were found between divisions. SC partially mediated the MT-MH relationship, but moderation was not significant. Working towards NCAA MH best practice should include training athletes in both MT and SC skills (via mindfulness)

Shared Ageing Research Models (ShARM) : a new facility to support ageing research

In order to manage the rise in life expectancy and the concomitant increased occurrence of age-related diseases, research into ageing has become a strategic priority. Mouse models are commonly utilised as they share high homology with humans and show many similar signs and diseases of ageing. However, the time and cost needed to rear aged cohorts can limit research opportunities. Sharing of resources can provide an ethically and economically superior framework to overcome some of these issues but requires dedicated infrastructure. Shared Ageing Research Models (ShARM) (www.ShARMUK.org) is a new, not-for-profit organisation funded by Wellcome Trust, open to all investigators. It collects, stores and distributes flash frozen tissues from aged murine models through its biorepository and provides a database of live ageing mouse colonies available in the UK and abroad. It also has an online environment (MICEspace) for collation and analysis of data from communal models and discussion boards on subjects such as the welfare of ageing animals and common endpoints for intervention studies. Since launching in July 2012, thanks to the generosity of researchers in UK and Europe, ShARM has collected more than 2,500 tissues and has in excess of 2,000 mice registered in live ageing colonies. By providing the appropriate support, ShARM has been able to bring together the knowledge and experience of investigators in the UK and Europe to maximise research outputs with little additional cost and minimising animal use in order to facilitate progress in ageing research

HOIL-1 ubiquitin ligase activity targets unbranched glucosaccharides and is required to prevent polyglucosan accumulation

HOIL‐1, a component of the linear ubiquitin chain assembly complex (LUBAC), ubiquitylates serine and threonine residues in proteins by esterification. Here, we report that mice expressing an E3 ligase‐inactive HOIL‐1[C458S] mutant accumulate polyglucosan in brain, heart and other organs, indicating that HOIL‐1’s E3 ligase activity is essential to prevent these toxic polysaccharide deposits from accumulating. We found that HOIL‐1 monoubiquitylates glycogen and α1:4‐linked maltoheptaose in vitro and identify the C6 hydroxyl moiety of glucose as the site of ester‐linked ubiquitylation. The monoubiquitylation of maltoheptaose was accelerated > 100‐fold by the interaction of Met1‐linked or Lys63‐linked ubiquitin oligomers with the RBR domain of HOIL‐1. HOIL‐1 also transferred pre‐formed ubiquitin oligomers to maltoheptaose en bloc, producing polyubiquitylated maltoheptaose in one catalytic step. The Sharpin and HOIP components of LUBAC, but not HOIL‐1, bound to unbranched and infrequently branched glucose polymers in vitro, but not to highly branched mammalian glycogen, suggesting a potential function in targeting HOIL‐1 to unbranched glucosaccharides in cells. We suggest that monoubiquitylation of unbranched glucosaccharides may initiate their removal from cells, preventing precipitation as polyglucosan

Pandemic Strain of Foot-and-Mouth Disease Virus Serotype O

The PanAsia strain is spreading explosively in Asia and extending to parts of Africa and Europe

Intrauterine death following intraamniotic triiodothyronine and thyroxine therapy for fetal goitrous hypothyroidism associated with polyhydramnios and caused by a thyroglobulin mutation

In the absence of maternal thyroid disease or iodine deficiency, fetal goitre is rare and usually attributable to dyshormonogenesis, for which genetic ascertainment is not always undertaken in the UK. Mechanical complications include tracheal and oesophageal compression with resultant polyhydramnios, malpresentation at delivery and neonatal respiratory distress. We report an Indian kindred in which the proband (first-born son) had congenital hypothyroidism (CH) without obvious neonatal goitre. His mother's second pregnancy was complicated by fetal hypothyroid goitre and polyhydramnios, prompting amniotic fluid drainage and intraamniotic therapy (with liothyronine, T3 and levothyroxine, T4). Sadly, intrauterine death occurred at 31 weeks. Genetic studies in the proband demonstrated compound heterozygous novel (c.5178delT, p.A1727Hfs*26) and previously described (c.7123G > A, p.G2375R) thyroglobulin (TG) mutations which are the likely cause of fetal goitre in the deceased sibling. TG mutations rarely cause fetal goitre, and management remains controversial due to the potential complications of intrauterine therapy however an amelioration in goitre size may be achieved with intraamniotic T4, and intraamniotic T3/T4 combination has achieved a favourable outcome in one case. A conservative approach, with surveillance, elective delivery and commencement of levothyroxine neonatally may also be justified, although intubation may be required post delivery for respiratory obstruction. Our observations highlight the lethality which may be associated with fetal goitre. Additionally, although this complication may recur in successive pregnancies, our case highlights the possibility of discordance for fetal goitre in siblings harbouring the same dyshormonogenesis-associated genetic mutations. Genetic ascertainment may facilitate prenatal diagnosis and assist management in familial cases. LEARNING POINTS: CH due to biallelic, loss-of-function TG mutations is well-described and readily treatable in childhood however mechanical complications from associated fetal goitre may include polyhydramnios, neonatal respiratory compromise and neck hyperextension with dystocia complicating delivery.CH due to TG mutations may manifest with variable phenotypes, even within the same kindred.Treatment options for hypothyroid dyshormogenic fetal goitre in a euthyroid mother include intraamniotic thyroid hormone replacement in cases with polyhydramnios or significant tracheal obstruction. Alternatively, cases may be managed conservatively with radiological surveillance, elective delivery and neonatal levothyroxine treatment, although intubation and ventilation may be required to support neonatal respiratory compromise.Genetic ascertainment in such kindreds may enable prenatal diagnosis and anticipatory planning for antenatal management of further affected offspring.This work was supported by funding from the Wellcome Trust (grant number 100585/Z/12/Z to N S) and the National Institute for Health Research Biomedical Research Centre Cambridge (N S). The Genomics/ Transcriptomics Core Facility is supported by the UK Medical Research Council (MRC) Metabolic Disease Unit (MRC_MC_UU_12012/5) and a Wellcome Trust Strategic Award (100574/Z/12/Z)

Stability of DON and OTA during the breadmaking process and determination of process and performance criteria

The fate of deoxynivalenol (DON) and ochratoxin A (OTA) during the breadmaking process was studied. In particular, toxin content was analysed in mixed baking ingredients before kneading, after fermentation and proofing, and finally after baking. Fermentation and proofing were carried out at 30 C for 1 h, while baking was performed at different temperature levels (from 170 to 210 C) and baking times from 45 to 135 min, in a full factorial design. DON increased from unkneaded mix to fermented dough, and decreased due to baking; this trend depended on the initial concentration of DON in the flour. The level in the bread was significantly lower than in the initial mix of ingredients. In contrast, deoxynivalenol-3-glucoside (DON-3-G) content increased both during kneading and fermentation, and also during baking. Moreover, the results confirmed the high stability of OTA as no significant change in its content could be observed as a result of the breadmaking process. As conclusion, the design of bakery product processes may help to control DON in final products, because although quite stable, its levels can be reduced to some extent. However, high levels of DON-3-G were released during baking, and this point should be further investigated. Mycotoxins have been always considered as stable compounds; however, in depth knowledge of the processing steps that may lead to some reduction (although limited) and those which can stimulate their release from conjugated forms, will definitely help in their control in finished foodstuffs.The authors are grateful to the Spanish government (projects AGL2010-22182-C04-04 and AGL2011-24862) for the financial support. A. Vidal thanks the Spanish Government (Ministry of Education) for the pre-doctoral grant. H. Morales is grateful to the Portuguese Government. (Ministerio da Ciecia, Tecnologia e Ensino Superior; FCT Fundacao para a Ciencia e a Tecnologia) Grant ref. SFRH/BPD/38011/2007

Targeting of Slc25a21 is associated with orofacial defects and otitis media due to disrupted expression of a neighbouring gene.

Homozygosity for Slc25a21(tm1a(KOMP)Wtsi) results in mice exhibiting orofacial abnormalities, alterations in carpal and rugae structures, hearing impairment and inflammation in the middle ear. In humans it has been hypothesised that the 2-oxoadipate mitochondrial carrier coded by SLC25A21 may be involved in the disease 2-oxoadipate acidaemia. Unexpectedly, no 2-oxoadipate acidaemia-like symptoms were observed in animals homozygous for Slc25a21(tm1a(KOMP)Wtsi) despite confirmation that this allele reduces Slc25a21 expression by 71.3%. To study the complete knockout, an allelic series was generated using the loxP and FRT sites typical of a Knockout Mouse Project allele. After removal of the critical exon and neomycin selection cassette, Slc25a21 knockout mice homozygous for the Slc25a21(tm1b(KOMP)Wtsi) and Slc25a21(tm1d(KOMP)Wtsi) alleles were phenotypically indistinguishable from wild-type. This led us to explore the genomic environment of Slc25a21 and to discover that expression of Pax9, located 3' of the target gene, was reduced in homozygous Slc25a21(tm1a(KOMP)Wtsi) mice. We hypothesize that the presence of the selection cassette is the cause of the down regulation of Pax9 observed. The phenotypes we observed in homozygous Slc25a21(tm1a(KOMP)Wtsi) mice were broadly consistent with a hypomorphic Pax9 allele with the exception of otitis media and hearing impairment which may be a novel consequence of Pax9 down regulation. We explore the ramifications associated with this particular targeted mutation and emphasise the need to interpret phenotypes taking into consideration all potential underlying genetic mechanisms