Impact of the Erika oil spill on sea birds: review of post-Erika studies

Le Drean-Quenec’Hdu Sophie, L'Hostis Monique. Impact de la marée noire de l’Erika sur les oiseaux marins : bilan des différentes études post-Erika. In: Bulletin de l'Académie Vétérinaire de France tome 158 n°3, 2005. pp. 313-317

Caring for oiled birds : update since the Erika oil spill

The treatment and management of oiled birds is constantly being improved. Since the oil spill following the wreck of the tanker Erika, in December 1999, the wildlife centre of the National Veterinary School of Nantes has received several hundred of oiled birds. The current rescue protocol is described with the improvements made since the Erika oil spill. This protocol, which covers the period from the time the birds arrive up to their release, must be implemented by properly trained staff, so that the birds are treated as quickly and efficiently as possible. Indeed, reducing the duration of the process reduces the stress level for the birds and the number of secondary infections.Le traitement des oiseaux mazoutés est en constante évolution. Depuis la marée noire consécutive au naufrage du pétrolier Erika, en décembre 1999, le centre vétérinaire de la faune sauvage de l'Ecole Nationale Vétérinaire de Nantes reçoit des centaines d'oiseaux mazoutés. Le protocole de soins actuel est présenté avec les améliorations apportées après la catastrophe de l'Erika, depuis l'entrée des oiseaux jusqu'à leur relâcher. Ce protocole doit être mis en place par des personnes formées pour que chaque étape soit la plus courte possible. En effet, la rapidité permet de réduire le stress et limite l'apparition d'affections secondaires

Population development and breeding success of Dark-bellied Brent Geese Branta b. bernicla from 1991-2011

The Dark-bellied Brent Goose Branta bernicla bernicla is the largest of the six Brent Goose populations, which collectively number around 600,000 birds globally. After a major decline to 16,500 geese in 1958, numbers recovered during the 1970s and 1980s to a peak of c. 330,000 individuals between 1992 and 1994. From 1994 onwards the population declined again to 200,000–250,000. This decline has been attributed to poor breeding, associated with faltering cycles of Siberian Brown Lemming Lemmus sibiricus (predominantly) and Palearctic Collared Lemming Dicrostonyx torquatus abundance on the breeding grounds on the Taimyr Peninsula, where lemmings are a main food resource for potential predators of goslings. Darkbellied Brent Geese only breed well in peak lemming years (Summers & Underhill 1991), and this usually occurs every three years, but the frequent failure since 1994 of lemming numbers to peak (except in 2005) has resulted in the absence of very good breeding years for the geese (Nolet et al. 2013). The mid-winter distribution has shown a marked shift towards France over the last decade. France currently supports 50% of the population in January, Great Britain 35–40%, the Netherlands 15–20%, and Germany and Denmark 2%. In spring, almost the entire population gathers in the Wadden Sea, leaving only 4% of the population in Great Britain, and virtually none in France, with the Dutch part of the Wadden Sea supporting 40–45%, the German section 45–50% and Denmark 6%

The Tyrosine Kinase Pyk-2/Raftk Regulates Natural Killer (Nk) Cell Cytotoxic Response, and Is Translocated and Activated upon Specific Target Cell Recognition and Killing

The compartmentalization of plasma membrane proteins has a key role in regulation of lymphocyte activation and development of immunity. We found that the proline-rich tyrosine kinase-2 (PYK-2/RAFTK) colocalized with the microtubule-organizing center (MTOC) at the trailing edge of migrating natural killer (NK) cells. When polyclonal NK cells bound to K562 targets, PYK-2 translocated to the area of NK–target cell interaction. The specificity of this process was assessed with NK cell clones bearing activatory or inhibitory forms of CD94/NKG2. The translocation of PYK-2, MTOC, and paxillin to the area of NK–target cell contact was regulated upon specific recognition of target cells through NK cell receptors, controlling target cell killing. Furthermore, parallel in vitro kinase assays showed that PYK-2 was activated in response to signals that specifically triggered its translocation and NK cell mediated cytotoxicity. The overexpression of both the wt and a dominant-negative mutant of PYK-2, but not ZAP-70 wt, prevented the specific translocation of the MTOC and paxillin, and blocked the cytotoxic response of NK cells. Our data indicate that subcellular compartmentalization of PYK-2 correlates with effective signal transduction. Furthermore, they also suggest an important role for PYK-2 on the assembly of the signaling complexes that regulate the cytotoxic response

Radiosensitization with an inhibitor of poly(ADP-ribose) glycohydrolase: A comparison with the PARP1/2/3 inhibitor olaparib

Upon DNA binding the poly(ADP-ribose) polymerase family of enzymes (PARPs) add multiple ADP-ribose subunits to themselves and other acceptor proteins. Inhibitors of PARPs have become an exciting and real prospect for monotherapy and as sensitizers to ionising radiation (IR). The action of PARPs are reversed by poly(ADP-ribose) glycohydrolase (PARG). Until recently studies of PARG have been limited by the lack of an inhibitor. Here, a first in class, specific, and cell permeable PARG inhibitor, PDD00017273, is shown to radiosensitize. Further, PDD00017273 is compared with the PARP1/2/3 inhibitor olaparib. Both olaparib and PDD00017273 altered the repair of IR-induced DNA damage, resulting in delayed resolution of RAD51 foci compared with control cells. However, only PARG inhibition induced a rapid increase in IR-induced activation of PRKDC (DNA-PK) and perturbed mitotic progression. This suggests that PARG has additional functions in the cell compared with inhibition of PARP1/2/3, likely via reversal of tankyrase activity and/or that inhibiting the removal of poly(ADP-ribose) (PAR) has a different consequence to inhibiting PAR addition. Overall, our data are consistent with previous genetic findings, reveal new insights into the function of PAR metabolism following IR and demonstrate for the first time the therapeutic potential of PARG inhibitors as radiosensitizing agents

Deoxynivalenol-Induced Proinflammatory Gene Expression: Mechanisms and Pathological Sequelae

The trichothecene mycotoxin deoxynivalenol (DON) is commonly encountered in human cereal foods throughout the world as a result of infestation of grains in the field and in storage by the fungus Fusarium. Significant questions remain regarding the risks posed to humans from acute and chronic DON ingestion, and how to manage these risks without imperiling access to nutritionally important food commodities. Modulation of the innate immune system appears particularly critical to DON’s toxic effects. Specifically, DON induces activation of mitogen-activated protein kinases (MAPKs) in macrophages and monocytes, which mediate robust induction of proinflammatory gene expression—effects that can be recapitulated in intact animals. The initiating mechanisms for DON-induced ribotoxic stress response appear to involve the (1) activation of constitutive protein kinases on the damaged ribosome and (2) autophagy of the chaperone GRP78 with consequent activation of the ER stress response. Pathological sequelae resulting from chronic low dose exposure include anorexia, impaired weight gain, growth hormone dysregulation and aberrant IgA production whereas acute high dose exposure evokes gastroenteritis, emesis and a shock-like syndrome. Taken together, the capacity of DON to evoke ribotoxic stress in mononuclear phagocytes contributes significantly to its acute and chronic toxic effects in vivo. It is anticipated that these investigations will enable the identification of robust biomarkers of effect that will be applicable to epidemiological studies of the human health effects of this common mycotoxin

Comprehensive overview of the structure and regulation of the glucocorticoid receptor

Glucocorticoids are among the most prescribed drugs worldwide for the treatment of numerous immune and inflammatory disorders. They exert their actions by binding to the glucocorticoid receptor (GR), a member of the nuclear receptor superfamily. There are several GR isoforms resulting from alternative RNA splicing and translation initiation of the GR transcript. Additionally, these isoforms are all subject to several transcriptional, post-transcriptional, and post-translational modifications, all of which affect the protein's stability and/or function. In this review, we summarize recent knowledge on the distinct GR isoforms and the processes that generate them. We also review the importance of all known transcriptional, post-transcriptional, and post-translational modifications, including the regulation of GR by microRNAs. Moreover, we discuss the crucial role of the putative GR-bound DNA sequence as an allosteric ligand influencing GR structure and activity. Finally, we describe how the differential composition and distinct regulation at multiple levels of different GR species could account for the wide and diverse effects of glucocorticoids