Biosecurity assessment of Argentinian pig farms

The pig industry is growing very fast in Argentina with an increasing need for replacement animals, feedstuff and transportation of animals. One of the main competitive advantages of the Argentinian pig industry is its being free of most major pig diseases. Within this context, applying measures aimed to reduce the risk of introduction and spread of pathogens is critical. The aim of the present study was to assess the biosecurity of Argentinian pig farms. Two types of farms were assessed: firstly, all official suppliers of high-genetic-value (n = 110) and secondly, a sample from commercial farms (n = 192). Data on the external and internal biosecurity practices applied on the farms was collected with a questionnaire. Data was analysed using a correspondence analysis and a hierarchical clustering analysis, which allowed identification of types of farms with regard to the biosecurity measures applied. Key variables characterizing the clusters were identified through an indicator value analysis. In addition, the external biosecurity of the farms was evaluated by using risk assessment tools with respect to the potential introduction of porcine epidemic diarrhoea virus. Results made evident three clusters: the first one which, amongst other measures, applied several barriers to prevent the entry of people, trucks and other vehicles, and could be considered as a group of high biosecurity, and the two other groups which applied a lower number of external and internal biosecurity measures. The results of the risk assessment showed that the routes with the highest risk of disease introduction were: replacement animals, vehicles transporting feed or animals, and visitors. The assessment of the external biosecurity showed that most Argentinian farms were not prepared for the contingency of a pathogen such as porcine epidemic diarrhoea virus. Special efforts should be made in official suppliers of high-genetic-value farms with poor biosecurity scores since they are at the top of the pig production chain and can be key for the spread of diseases.info:eu-repo/semantics/acceptedVersio

Improved Optoelectronic Properties of Rapid Thermally Annealed Dilute Nitride GaInNAs Photodetectors

We investigate the optical and electrical characteristics of GaInNAs/GaAs long-wavelength photodiodes grown under varying conditions by molecular beam epitaxy and subjected to postgrowth rapid thermal annealing (RTA) at a series of temperatures. It is found that the device performance of the nonoptimally grown GaInNAs p-i-n structures, with nominal compositions of 10% In and 3.8% N, can be improved significantly by the RTA treatment to match that of optimally grown structures. The optimally annealed devices exhibit overall improvement in optical and electrical characteristics, including increased photoluminescence brightness, reduced density of deep-level traps, reduced series resistance resulting from the GaAs/GaInNAs heterointerface, lower dark current, and significantly lower background doping density, all of which can be attributed to the reduced structural disorder in the GaInNAs alloy.© 2012 TMS

Methodologies for <i>in vitro</i> and <i>in vivo</i> evaluation of efficacy of antifungal and antibiofilm agents and surface coatings against fungal biofilms.

Unlike superficial fungal infections of the skin and nails, which are the most common fungal diseases in humans, invasive fungal infections carry high morbidity and mortality, particularly those associated with biofilm formation on indwelling medical devices. Therapeutic management of these complex diseases is often complicated by the rise in resistance to the commonly used antifungal agents. Therefore, the availability of accurate susceptibility testing methods for determining antifungal resistance, as well as discovery of novel antifungal and antibiofilm agents, are key priorities in medical mycology research. To direct advancements in this field, here we present an overview of the methods currently available for determining (i) the susceptibility or resistance of fungal isolates or biofilms to antifungal or antibiofilm compounds and compound combinations; (ii) the &lt;i&gt;in vivo&lt;/i&gt; efficacy of antifungal and antibiofilm compounds and compound combinations; and (iii) the &lt;i&gt;in vitro&lt;/i&gt; and &lt;i&gt;in vivo&lt;/i&gt; performance of anti-infective coatings and materials to prevent fungal biofilm-based infections

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease