Agile training to help enable standardisation of phytoplankton sampling and gross gill terminology across the Scottish sector

Current aquaculture operations in the UK are dominated by finfish farming in Scotland, contributing over £1.8 billion to the Scottish economy with the ambition to double this value by 2030. Finfish health is the top priority across the sector as healthy fish enjoy higher survival rates. One of the most important threats is the occurrence of gill disease, e.g. due to HABs, with potentially devastating impacts on fish health resulting in mortality, reduced welfare, and associated losses in profit on the rise. To understand this threat better, high-quality data generation for reporting is essential. For example, a significant body of work – catalysed by the Scottish Government’s Farmed Fish Health Framework and involving SAIC, agencies, regulators, and a large representation from producers within the sector – acknowledged the need for procedures for sustained and standardised surveillance and reporting of algal blooms, and a standardised operating procedure was developed. The sector representatives are unanimous in the need for developing specific skills to operate under the HABs SOP and in fish health generally. Two courses have been funded by Defra, UK, in the area of aquaculture operators’ skills development. The first course aims for standardisation of HABs sampling and classification, and understanding of the data and modelling associated with mitigation and management of HABs events, and will be delivered through a partnership between SAIC, the Scottish Association for Marine Science (SAMS) and Lantra. The second course is under the health framework and aims to improve the skills and knowledge of technicians and veterinary professionals currently working in, or interested in diversifying into, the seafood sector. An initial aim of the latter course, a partnership between SRUC and SSF, is to standardise salmon gross gill health monitoring terminology

Agile training to help enable standardisation of phytoplankton sampling and gross gill terminology across the Scottish sector

Current aquaculture operations in the UK are dominated by finfish farming in Scotland, contributing over £1.8 billion to the Scottish economy with the ambition to double this value by 2030. Finfish health is the top priority across the sector as healthy fish enjoy higher survival rates. One of the most important threats is the occurrence of gill disease, e.g. due to HABs, with potentially devastating impacts on fish health resulting in mortality, reduced welfare, and associated losses in profit on the rise. To understand this threat better, high-quality data generation for reporting is essential. For example, a significant body of work – catalysed by the Scottish Government’s Farmed Fish Health Framework and involving SAIC, agencies, regulators, and a large representation from producers within the sector – acknowledged the need for procedures for sustained and standardised surveillance and reporting of algal blooms, and a standardised operating procedure was developed. The sector representatives are unanimous in the need for developing specific skills to operate under the HABs SOP and in fish health generally. Two courses have been funded by Defra, UK, in the area of aquaculture operators’ skills development. The first course aims for standardisation of HABs sampling and classification, and understanding of the data and modelling associated with mitigation and management of HABs events, and will be delivered through a partnership between SAIC, the Scottish Association for Marine Science (SAMS) and Lantra. The second course is under the health framework and aims to improve the skills and knowledge of technicians and veterinary professionals currently working in, or interested in diversifying into, the seafood sector. An initial aim of the latter course, a partnership between SRUC and SSF, is to standardise salmon gross gill health monitoring terminology

Defining hereditary alpha-tryptasemia as a risk/modifying factor for anaphylaxis: are we there yet?

Hereditary a-tryptasemia (HaT) is a common autosomal dominant genet-ic trait with variable penetrance associated with increased serum baseline tryptase (SBT) levels. Clinical manifestations may range from an absence of symptoms to overtly severe and recurrent anaphylaxis. Symptoms have been claimed to result from excessive activation of EGF-like module -con-taining mucin-like hormone receptor-like 2 (EMR2) and protease activat-ed receptor 2 (PAR-2) receptors by a/13-tryptase heterotetramers. Herein, we aimed to review the evidence on whether HaT can be considered a hereditary risk factor or a modifying factor for anaphylaxis. Increased SBT levels have been linked to an increased risk of anaphylaxis. Likewise, recent studies have shown that HaT might be associated with a higher risk of developing anaphylaxis and more severe anaphylaxis. The same has also been shown for patients with clonal mast cell disorders, in whom the co-existence of HaT might lead to a greater propensity for se-vere, potentially life-threatening anaphylaxis. However, studies leading to such conclusions are generally limited in sample size, while other studies have shown opposing results. As such, further studies investigating the po-tential association of HaT with anaphylaxis caused by different triggers, and different severity grades, in both patients with clonal mast cell activa-tion syndromes and the general population are still needed

mTOR pathway overactivation in BRAF mutated papillary thyroid carcinoma

CONTEXT: There are several genetic and molecular evidences suggesting dysregulation of the mammalian target of rapamycin (mTOR) pathway in thyroid neoplasia. Activation of the phosphatidylinositol-3-kinase/AKT pathway by RET/PTC and mutant RAS has already been demonstrated, but no data have been reported for the BRAF(V600E) mutation. OBJECTIVE: The aim of this study was to evaluate the activation pattern of the mTOR pathway in malignant thyroid lesions and whether it may be correlated with known genetic alterations, as well as to explore the mechanisms underlying mTOR pathway activation in these neoplasias. RESULTS: We observed, by immunohistochemical evaluation, an up-regulation/activation of the mTOR pathway proteins in thyroid cancer, particularly in conventional papillary thyroid carcinoma (cPTC). Overactivation of the mTOR signaling was particularly evident in cPTC samples harboring the BRAF(V600E) mutation. Transfection assays with BRAF expression vectors as well as BRAF knockdown by small interfering RNA revealed a positive association between BRAF expression and mTOR pathway activation, which appears to be mediated by pLKB1 Ser428, and emerged as a possible mechanism contributing to the association between BRAF mutation and mTOR pathway up-regulation. When we evaluated the rapamycin in the growth of thyroid cancer cell lines, we detected that cell lines with activating mutations in the MAPK pathway show a higher sensitivity to this drug. CONCLUSIONS: We determined that the AKT/mTOR pathway is particularly overactivated in human cPTC harboring the BRAF(V600E) mutation. Moreover, our results suggest that the mTOR pathway could be a good target to enhance therapy effects in certain types of thyroid carcinoma, namely in those harboring the BRAF(V600E) mutation

Cardiosphere-derived cells suppress allogeneic lymphocytes by production of PGE2 acting via the EP4 receptor

derived cells (CDCs) are a cardiac progenitor cell population, which have been shown to possess cardiac regenerative properties and can improve heart function in a variety of cardiac diseases. Studies in large animal models have predominantly focussed on using autologous cells for safety, however allogeneic cell banks would allow for a practical, cost-effective and efficient use in a clinical setting. The aim of this work was to determine the immunomodulatory status of these cells using CDCs and lymphocytes from 5 dogs. CDCs expressed MHC I but not MHC II molecules and in mixed lymphocyte reactions demonstrated a lack of lymphocyte proliferation in response to MHC-mismatched CDCs. Furthermore, MHC-mismatched CDCs suppressed lymphocyte proliferation and activation in response to Concanavalin A. Transwell experiments demonstrated that this was predominantly due to direct cell-cell contact in addition to soluble mediators whereby CDCs produced high levels of PGE2 under inflammatory conditions. This led to down-regulation of CD25 expression on lymphocytes via the EP4 receptor. Blocking prostaglandin synthesis restored both, proliferation and activation (measured via CD25 expression) of stimulated lymphocytes. We demonstrated for the first time in a large animal model that CDCs inhibit proliferation in allo-reactive lymphocytes and have potent immunosuppressive activity mediated via PGE2

Responses of marine benthic microalgae to elevated CO<inf>2</inf>

Increasing anthropogenic CO2 emissions to the atmosphere are causing a rise in pCO2 concentrations in the ocean surface and lowering pH. To predict the effects of these changes, we need to improve our understanding of the responses of marine primary producers since these drive biogeochemical cycles and profoundly affect the structure and function of benthic habitats. The effects of increasing CO2 levels on the colonisation of artificial substrata by microalgal assemblages (periphyton) were examined across a CO2 gradient off the volcanic island of Vulcano (NE Sicily). We show that periphyton communities altered significantly as CO2 concentrations increased. CO2 enrichment caused significant increases in chlorophyll a concentrations and in diatom abundance although we did not detect any changes in cyanobacteria. SEM analysis revealed major shifts in diatom assemblage composition as CO2 levels increased. The responses of benthic microalgae to rising anthropogenic CO2 emissions are likely to have significant ecological ramifications for coastal systems. © 2011 Springer-Verlag

Involvement of Noradrenergic Neurotransmission in the Stress- but not Cocaine-Induced Reinstatement of Extinguished Cocaine-Induced Conditioned Place Preference in Mice: Role for β-2 Adrenergic Receptors

The responsiveness of central noradrenergic systems to stressors and cocaine poses norepinephrine as a potential common mechanism through which drug re-exposure and stressful stimuli promote relapse. This study investigated the role of noradrenergic systems in the reinstatement of extinguished cocaine-induced conditioned place preference by cocaine and stress in male C57BL/6 mice. Cocaine- (15 mg/kg, i.p.) induced conditioned place preference was extinguished by repeated exposure to the apparatus in the absence of drug and reestablished by a cocaine challenge (15 mg/kg), exposure to a stressor (6-min forced swim (FS); 20–25°C water), or administration of the α-2 adrenergic receptor (AR) antagonists yohimbine (2 mg/kg, i.p.) or BRL44408 (5, 10 mg/kg, i.p.). To investigate the role of ARs, mice were administered the nonselective β-AR antagonist, propranolol (5, 10 mg/kg, i.p.), the α-1 AR antagonist, prazosin (1, 2 mg/kg, i.p.), or the α-2 AR agonist, clonidine (0.03, 0.3 mg/kg, i.p.) before reinstatement testing. Clonidine, prazosin, and propranolol failed to block cocaine-induced reinstatement. The low (0.03 mg/kg) but not high (0.3 mg/kg) clonidine dose fully blocked FS-induced reinstatement but not reinstatement by yohimbine. Propranolol, but not prazosin, blocked reinstatement by both yohimbine and FS, suggesting the involvement of β-ARs. The β-2 AR antagonist ICI-118551 (1 mg/kg, i.p.), but not the β-1 AR antagonist betaxolol (10 mg/kg, i.p.), also blocked FS-induced reinstatement. These findings suggest that stress-induced reinstatement requires noradrenergic signaling through β-2 ARs and that cocaine-induced reinstatement does not require AR activation, even though stimulation of central noradrenergic neurotransmission is sufficient to reinstate