PirABVP toxin binds to epithelial cells of the digestive tract and produce pathognomonic AHPND lesions in germ-free brine shrimp

Acute hepatopancreatic necrosis disease (AHPND), a newly emergent farmed penaeid shrimp bacterial disease originally known as early mortality syndrome (EMS), is causing havoc in the shrimp industry. The causative agent of AHPND was found to be a specific strain of bacteria, e.g., Vibrio and Shewanella sps., that contains pVA1 plasmid (63–70 kb) encoding the binary PirAVP and PirBVP toxins. The PirABVP and toxins are the primary virulence factors of AHPND-causing bacteria that mediates AHPND and mortality in shrimp. Hence, in this study using a germ-free brine shrimp model system, we evaluated the PirABVP toxin-mediated infection process at cellular level, including toxin attachment and subsequent toxin-induced damage to the digestive tract. The results showed that, PirABVP toxin binds to epithelial cells of the digestive tract of brine shrimp larvae and produces characteristic symptoms of AHPND. In the PirABVP-challenged brine shrimp larvae, shedding or sloughing of enterocytes in the midgut and hindgut regions was regularly visualized, and the intestinal lumen was filled with moderately electron-dense cells of variable shapes and sizes. In addition, the observed cellular debris in the intestinal lumen of the digestive tract was found to be of epithelial cell origin. The detailed morphology of the digestive tract demonstrates further that the PirABVP toxin challenge produces focal to extensive necrosis and damages epithelial cells in the midgut and hindgut regions, resulting in pyknosis, cell vacuolisation, and mitochondrial and rough endoplasmic reticulum (RER) damage to different degrees. Taken together, our study provides substantial evidence that PirABVP toxins bind to the digestive tract of brine shrimp larvae and seem to be responsible for generating characteristic AHPND lesions and damaging enterocytes in the midgut and hindgut regions

Organiser un débat argumenté en troisième (« Découverte professionnelle six heures »)

L’article offre aux praticiens de l’orientation un cadre d’intervention relatif à la pratique de débats argumentés en classe de troisième – « Découverte professionnelle six heures » –, dont l’objectif est d’enrichir les représentations des élèves sur l’école et le travail, mais aussi sur eux-mêmes et ainsi les aider à construire un point de vue argumenté sur leur orientation. Après nous être arrêtés, dans une première partie, sur la notion de débat (cadre général et objectifs), nous présentons, dans une seconde partie, le déroulé des trois séances formalisées à partir d’expérimentations de terrain.The article provides the experts of professional guidance with a framework of intervention for argumentative debates in fourth form classes –‘six hours of professional discovery’–, the aim of which is to enrich pupils’ representations of school and work, but also of themselves, and thus to help them build an argued point of view of their own orientation. In a first part, we focus on the concept of debate (general framework and objectives) and, in a second part, we present the method used for the three meetings based on practical experimentations

Depletion of embryonic macrophages leads to a reduction in Angiogenesis in the Ex OVO chick Chorioallantoic membrane assay

Macrophages play an important but poorly understood role in angiogenesis. To investigate their role in vessel formation, relevant in vivo models are crucial. Although the chick chorioallantoic membrane (CAM) model has been frequently used as an angiogenesis assay, limited data are available on the involvement of chicken macrophages in this process. Here, we describe a method to deplete macrophages in the ex ovo chick CAM assay by injection of clodronate liposomes and show that this depletion directly affects vascularisation of collagen onplants. Chicken embryos were injected intravenously with either clodronate or phosphate-buffered saline (PBS) liposomes, followed by placement of collagen type I plugs on the CAM to quantify angiogenic ingrowth. Clodronate liposome injection led to a significant 3.4-fold reduction of macrophages compared with control embryos as measured by immunohistochemistry and flow cytometry. Furthermore, analysis of vessel ingrowth into the collagen plugs revealed a significantly lower angiogenic response in macrophage-depleted embryos compared with control embryos, indicating that chicken embryonic macrophages play an essential function in the development of blood vessels. These results demonstrate that the chick CAM assay provides a promising model to investigate the role of macrophages in angiogenesis

A Refreshing Take: Analysing Accident Scenarios through Causal Network Topology Metrics

PresentationAccident causation investigation and even more hazard scenario identification are troubled by the complexity of interactions between three elements in a process facility: People, Plant and Procedures. Interactions are of various nature, such as physical change and information transfer, all influencing the process. To facilitate investigation the digraph network was applied as the most flexible visual aid to describe a causal structure. Such structure consists of nodes and edges representing an event or condition in the accident scenario and a causal link respectively. Attributing the nodes and edges to the type of interaction, numbers of the same type can be counted, and so two metrics are developed: The P3 Interaction Contribution (PIC). This is the proportion of nodes and edges associated with an interaction between People, Plant and Procedures. The Average Edge Weight. This relates to the proportion of events in the scenario that are associated with the logical AND gate conjunction from its causes (incident nodes), where the event requires more than one simultaneous cause. The technique was tried on four CSB accident descriptions. Interesting differences are seen. Also, in view of a paper accepted to be published in Safety Science the approach seems quite helpful in process hazard analysis

Methicillin-resistant Staphylococcus aureus Toxic Shock Syndrome

Case ReportsLetterSCOPUS: le.jinfo:eu-repo/semantics/publishe

A study of carry-over and histopathological effects after chronic dietary intake of citrinin in pigs, broiler chickens and laying hens

Citrinin (CIT) is a polyketide mycotoxin occurring in a variety of food and feedstuff, among which cereal grains are the most important contaminated source. Pigs and poultry are important livestock animals frequently exposed to mycotoxins, including CIT. Concerns are rising related to the toxic, and especially the potential nephrotoxic, properties of CIT. The purpose of this study was to clarify the histopathological effects on kidneys, liver, jejunum and duodenum of pigs, broiler chickens and laying hens receiving CIT contaminated feed. During 3 weeks, pigs (n = 16) were exposed to feed containing 1 mg CIT/kg feed or to control feed (n = 4), while 2 groups of broiler chickens and laying hens (n = 8 per group) received 0.1 mg CIT/kg feed (lower dose group) and 3 or 3.5 mg CIT/kg feed (higher dose group), respectively, or control feed (n = 4). CIT concentrations were quantified in plasma, kidneys, liver, muscle and eggs using a validated ultra-high performance liquid chromatography-tandem mass spectrometry (UHPLC-MS/MS) method. Kidneys, liver, duodenum and jejunum were evaluated histologically using light microscopy, while the kidneys were further examined using transmission electron microscopy (TEM). Histopathology did not reveal major abnormalities at the given contamination levels. However, a significant increase of swollen and degenerated mitochondria in renal cortical cells from all test groups were observed (p < 0.05). These observations could be related to oxidative stress, which is the major mechanism of CIT toxicity. Residues of CIT were detected in all collected tissues, except for muscle and egg white from layers in the lowest dose group, and egg white from layers in the highest dose group. CIT concentrations in plasma ranged between 0.1 (laying hens in lower dose group) and 20.8 ng/mL (pigs). In tissues, CIT concentrations ranged from 0.6 (muscle) to 20.3 µg/kg (liver) in pigs, while concentrations in chickens ranged from 0.1 (muscle) to 70.2 µg/kg (liver). Carry-over ratios from feed to edible tissues were between 0.1 and 2% in pigs, and between 0.1 and 6.9% in chickens, suggesting a low contribution of pig and poultry tissue-derived products towards the total dietary CIT intake for humans