Immune gene expression profiling of Proliferative Kidney Disease in rainbow trout Oncorhynchus mykiss reveals a dominance of anti-inflammatory, antibody and T helper cell-like activities

Peer reviewedPublisher PD

What is authorship, and what should it be? A survey of prominent guidelines for determining authorship in scientific publications

Before the mid 20th century most scientific writing was solely authored (Claxton, 2005; Greene, 2007) and thus it is only relatively recently, as science has grown more complex, that the ethical and procedural issues around authorship have arisen. Fields as diverse as medicine (International Committee of Medical Journal Editors, 2008), mathematics (e.g., American Statistical Association, 1999), the physical sciences (e.g., American Chemical Society, 2006), and the social sciences (e.g., American Psychological Association, 2002) have, in recent years, wrestled with what constitutes authorship and how to eliminate problematic practices such as honorary authorship and ghost authorship (e.g., Anonymous, 2004; Claxton, 2005; Manton & English, 2008). As authorship is the coin of the realm in academia (Louis, Holdsworth, Anderson, & Campbell, 2008), it is an ethical issue of singular importance. The goal of this paper is to review prominent and diverse guidelines concerning scientific authorship and to attempt to synthesize existing guidelines into recommendations that represent ethical practices for ensuring credit where (and only where) credit is due. Accessed 16,706 times on https://pareonline.net from July 20, 2009 to December 31, 2019. For downloads from January 1, 2020 forward, please click on the PlumX Metrics link to the right

Characterization of BAFF and APRIL subfamily receptors in rainbow trout (Oncorhynchus mykiss). Potential role of the BAFF/APRIL axis in the pathogenesis of proliferative kidney disease

We would like to thank Lucia González for technical assistance and Rosario Castro for producing some of the cDNAs used in this study. This work was supported by the European Research Council (ERC Starting Grant 2011 280469) and by the European Commission under the 7th Framework Programme for Research and Technological Development (FP7) of the European Union (Grant Agreement 311993 TARGETFISH) and under the Horizon H2020 research and innovation programme (Grant H2020-634429 ParaFishControl). This work was also partially funded by project AGL2014-54456-JIN from the Spanish Ministry of Economy and Competitiveness (MINECO). JWH was supported by the Swiss National Science Foundation (grant reference CRSII3_147649-1).Peer reviewedPublisher PD

Immune response modulation upon sequential heterogeneous co-infection with Tetracapsuloides bryosalmonae and VHSV in brown trout (Salmo trutta)

This work was supported by DEFRA [grant number F1198] in a joint project between SFIRC in Aberdeen, Scotland and CEFAS laboratory in Weymouth, England. Further funding to present this work at international conferences was granted to BG by European Association of Fish Pathologists (EAFP), British Society for Immunology (BSI), Fisheries Society of the British Isles (FSBI), European Society of Veterinary Virology (ESVV), and Aberdeen University Principal’s Excellence Fund. JWH was supported by the BBSRC (BB/K009125/1).Peer reviewedPostprin

Molecular characterization and expression analysis of four fish-specific CC chemokine receptors CCR4La, CCR4Lc1, CCR4Lc2 and CCR11 in rainbow trout (Oncorhynchus mykiss)

ZQ was supported financially by the “Qinglan” project of Jiangsu Province and the Overseas Training Plan for Young and Middle-aged Teachers and Principals of College and Universities in Jiangsu Province, China. This work was partially supported by grants from the National Natural Science Foundation of China (31302221 and 31272666) and Jiangsu Province (BK2011418 and BK20151297). TW received funding from the Marine Alliance for Science and Technology for Scotland (MASTS), a pooling initiative funded by the Scottish Funding Council (grant reference HR09011), and JWH was supported by the Swiss National Science Foundation (grant reference CRSII3_147649-1).Peer reviewedPostprin

Loss of ATM/Chk2/p53 Pathway Components Accelerates Tumor Development and Contributes to Radiation Resistance in Gliomas

SummaryMaintenance of genomic integrity is essential for adult tissue homeostasis and defects in the DNA-damage response (DDR) machinery are linked to numerous pathologies including cancer. Here, we present evidence that the DDR exerts tumor suppressor activity in gliomas. We show that genes encoding components of the DDR pathway are frequently altered in human gliomas and that loss of elements of the ATM/Chk2/p53 cascade accelerates tumor formation in a glioma mouse model. We demonstrate that Chk2 is required for glioma response to ionizing radiation in vivo and is necessary for DNA-damage checkpoints in the neuronal stem cell compartment. Finally, we observed that the DDR is constitutively activated in a subset of human GBMs, and such activation correlates with regions of hypoxia

Characterisation of arginase paralogues in salmonids and their modulation by immune stimulation/ infection

Acknowledgements OB was supported by a PhD studentship from the Marine Collaboration Research Forum (MarCRF), which is a collaboration between the University of Aberdeen and Marine Scotland Science, Marine Laboratory (MSS), and through Scottish Government project AQ0080. EW was supported by a PhD studentship from the Ministry of Science and Technology of Thailand and Mahasarakham University. TW received funding from the Marine Alliance for Science and Technology for Scotland (MASTS), a pooling initiative funded by the Scottish Funding Council (grant reference HR09011), and JWH was supported by the Swiss National Science Foundation (grant reference CRSII3_147649-1).Peer reviewedPostprin

Fish Suppressors of Cytokine Signaling (SOCS): Gene Discovery, Modulation of Expression and Function

The intracellular suppressors of cytokine signaling (SOCS) family members, including CISH and SOCS1 to 7 in mammals, are important regulators of cytokine signaling pathways. So far, the orthologues of all the eight mammalian SOCS members have been identified in fish, with several of them having multiple copies. Whilst fish CISH, SOCS3, and SOCS5 paralogues are possibly the result of the fish-specific whole genome duplication event, gene duplication or lineage-specific genome duplication may also contribute to some paralogues, as with the three trout SOCS2s and three zebrafish SOCS5s. Fish SOCS genes are broadly expressed and also show species-specific expression patterns. They can be upregulated by cytokines, such as IFN-γ, TNF-α, IL-1β, IL-6, and IL-21, by immune stimulants such as LPS, poly I:C, and PMA, as well as by viral, bacterial, and parasitic infections in member- and species-dependent manners. Initial functional studies demonstrate conserved mechanisms of fish SOCS action via JAK/STAT pathways

Sequence and expression analysis of rainbow trout CXCR2, CXCR3a and CXCR3b aids interpretation of lineage-specific conversion, loss and expansion of these receptors during vertebrate evolution

Copyright © 2014 The Authors. Published by Elsevier Ltd.. All rights reserved. Open Access funded by Biotechnology and Biological Sciences Research Council This work received funding from the MASTS pooling initiative (The Marine Alliance for Science and Technology for Scotland). MASTS is funded by the Scottish Funding Council (grant reference HR09011) and contributing institutions. Q.X. and Y.J. were supported financially by the National Scholarship Council of China, J.W.H by the Biotechnology and Biological Sciences Research Council (BB/K009125/1), and M.M.M. by European Commision LIFECYCLE project (222919).Peer reviewedPublisher PD

Immune-modulation of two BATF3 paralogues in rainbow trout Oncorhynchus mykiss

This work was supported by the Royal Society of Edinburgh and the National Natural Science Foundation of China (Grant Nos., 31511130137 and 31372568). Dr Jun Wang’s visit to the Scottish Fish Immunology Research Centre was funded by the China Scholarship Council (CSC).Peer reviewedPostprin