Comparison of organic and conventional dairy farm economic and environmental performances throughout North West Europe

From an environmental point of view, organic farming (OF) systems have been identified as beneficial thanks to a system allowing fewer losses of nitrogen (N) per ha and lower green house gases (GHG) emissions per ha and per ton of milk (TM). From an economic point of view, milk coming from these OF systems is sold at a higher prize. However, incomes provided by both systems are similar (for similar amount of milk produced). This may be explained by higher input costs per unit of product for OF systems and by more incomes coming from sold crops for conventional farming (CF) systems. Therefore, on the one hand CF systems may improve their environmental performances by reducing the amount of inputs brought into the system, for example through a better forage and fertilisation management. On the other hand, the valorisation of milk through a differentiated production or market (price premium due to a label and/or on-farm transformation and/or sale) may bring them higher incomes. OF system may increase their incomes by selling one cash crop destined for human consumption and by finding the good balance between intensivity and extensivity in order to better valorise the inputs brought into the system

Soluble beta-amyloid1-40 induces NMDA-dependent degradation of postsynaptic density-95 at glutamatergic synapses

Amyloid-beta (Abeta) has been implicated in memory loss and disruption of synaptic plasticity observed in early-stage Alzheimer\u27s disease. Recently, it has been shown that soluble Abeta oligomers target synapses in cultured rat hippocampal neurons, suggesting a direct role of Abeta in the regulation of synaptic structure and function. Postsynaptic density-95 (PSD-95) is a postsynaptic scaffolding protein that plays a critical role in synaptic plasticity and the stabilization of AMPA (AMPARs) and NMDA (NMDARs) receptors at synapses. Here, we show that exposure of cultured cortical neurons to soluble oligomers of Abeta(1-40) reduces PSD-95 protein levels in a dose- and time-dependent manner and that the Abeta1(1-40)-dependent decrease in PSD-95 requires NMDAR activity. We also show that the decrease in PSD-95 requires cyclin-dependent kinase 5 activity and involves the proteasome pathway. Immunostaining analysis of cortical cultured neurons revealed that Abeta treatment induces concomitant decreases in PSD-95 at synapses and in the surface expression of the AMPAR glutamate receptor subunit 2. Together, these data suggest a novel pathway by which Abeta triggers synaptic dysfunction, namely, by altering the molecular composition of glutamatergic synapses

Response: Commentary: Analysis of SUMO1-conjugation at synapses

Wilkinson et al. (2017) commented in this forum on a study of ours (Daniel et al., 2017), in which we report that the evidence for SUMO1-conjugation at synapses and of several synaptic proteins is equivocal. We present here—due to length restrictions—an abbreviated version of a response to Wilkinson et al. that appeared in the comments section of our original publication (Daniel et al., 2017).</p

An intellectual-disability-associated mutation of the transcriptional regulator NACC1 impairs glutamatergic neurotransmission

Advances in genome sequencing technologies have favored the identification of rare de novo mutations linked to neurological disorders in humans. Recently, a de novo autosomal dominant mutation in NACC1 was identified (NM_052876.3: c.892C &gt; T, NP_443108.1; p.Arg298Trp), associated with severe neurological symptoms including intellectual disability, microcephaly, and epilepsy. As NACC1 had never before been associated with neurological diseases, we investigated how this mutation might lead to altered brain function. We examined neurotransmission in autaptic glutamatergic mouse neurons expressing the murine homolog of the human mutant NACC1, i.e., Nacc1-R284W. We observed that expression of Nacc1-R284W impaired glutamatergic neurotransmission in a cell-autonomous manner, likely through a dominant negative mechanism. Furthermore, by screening for Nacc1 interaction targets in the brain, we identified SynGAP1, GluK2A, and several SUMO E3 ligases as novel Nacc1 interaction partners. At a biochemical level, Nacc1-R284W exhibited reduced binding to SynGAP1 and GluK2A, and also showed greatly increased SUMOylation. Ablating the SUMOylation of Nacc1-R284W partially restored its interaction with SynGAP1 but did not restore binding to GluK2A. Overall, these data indicate a role for Nacc1 in regulating glutamatergic neurotransmission, which is substantially impaired by the expression of a disease-associated Nacc1 mutant. This study provides the first functional insights into potential deficits in neuronal function in patients expressing the de novo mutant NACC1 protein

Aldo Keto Reductase 1B7 and Prostaglandin F2α Are Regulators of Adrenal Endocrine Functions

Prostaglandin F2α (PGF2α), represses ovarian steroidogenesis and initiates parturition in mammals but its impact on adrenal gland is unknown. Prostaglandins biosynthesis depends on the sequential action of upstream cyclooxygenases (COX) and terminal synthases but no PGF2α synthases (PGFS) were functionally identified in mammalian cells. In vitro, the most efficient mammalian PGFS belong to aldo-keto reductase 1B (AKR1B) family. The adrenal gland is a major site of AKR1B expression in both human (AKR1B1) and mouse (AKR1B3, AKR1B7). Thus, we examined the PGF2α biosynthetic pathway and its functional impact on both cortical and medullary zones. Both compartments produced PGF2α but expressed different biosynthetic isozymes. In chromaffin cells, PGF2α secretion appeared constitutive and correlated to continuous expression of COX1 and AKR1B3. In steroidogenic cells, PGF2α secretion was stimulated by adrenocorticotropic hormone (ACTH) and correlated to ACTH-responsiveness of both COX2 and AKR1B7/B1. The pivotal role of AKR1B7 in ACTH-induced PGF2α release and functional coupling with COX2 was demonstrated using over- and down-expression in cell lines. PGF2α receptor was only detected in chromaffin cells, making medulla the primary target of PGF2α action. By comparing PGF2α-responsiveness of isolated cells and whole adrenal cultures, we demonstrated that PGF2α repressed glucocorticoid secretion by an indirect mechanism involving a decrease in catecholamine release which in turn decreased adrenal steroidogenesis. PGF2α may be regarded as a negative autocrine/paracrine regulator within a novel intra-adrenal feedback loop. The coordinated cell-specific regulation of COX2 and AKR1B7 ensures the generation of this stress-induced corticostatic signal

Investigating trophic ecology and dietary niche overlap among morphs of Lake Trout in Lake Superior

Four morphs of Lake Trout (Salvelinus namaycush, Walbaum 1792) have been identified in Lake Superior: leans, siscowets, humpers, and redfins. In this comprehensive study, the trophic ecology of Lake Trout morphs were characterized using stomach content, fatty acid, and stable isotope data. Stomach content results indicated a predominately piscivorous diet for leans, siscowets, and redfins, whereas humper diets were comprised of 50% fish and 50% Mysis by mass. Humper and siscowets were most similar in their dietary fatty acid profiles, whereas redfins had the most distinct dietary fatty acid profile. Results from stable isotope analysis revealed some among-morph differences along a pelagic-profundal consumption gradient (34S), but there were no significant differences in trophic position (15N) or basal carbon sources among morphs (13C). Using the recently developed nicheROVER software package, 4-dimensional trophic niches for each morph were quantified using stable isotope ratios (δ13C, δ15N, and δ34S) and fatty acid profiles (30 dietary fatty acids, condensed to one axis). Humpers had the largest 4-dimensional niche regions of all four morphs, and redfins had the smallest. Pairwise probability of overlap among morphs in these four-dimensional niche regions was determined to be < 50% in most cases. Overall, stomach content results indicate that humpers diets were more planktivorous than the other morphs, consistent with previous research. Results of the niche overlap analysis suggests some degree of generalist feeding for all morphs. Better characterization of seasonal variation in diet using tracers that reflect more recent feeding (e.g., fatty acids, stomach contents, and/or stable isotope analyses performed on tissues that turnover more quickly than muscle) are needed to further elucidate among-morph differences and similarities in diet and trophic ecology

La fourmi Tapinoma nigerrimum, une opportunité pour contenir la fourmi d’Argentine ?

La fourmi d'Argentine (Linepithema humile), originaire d’Amérique du Sud, a envahi en un siècle tous les continents excepté l’Antarctique. En Europe, son expansion s'étend sur tout le pourtour méditerranéen de la péninsule Ibérique à l’Italie en passant par la France. En région PACA, elle envahit tout le littoral provençal et azuréen, par petits foyers centrés autour des zones urbaines côtières.Comment contenir cette invasion, sachant qu’il est devenu nécessaire de se démarquer des approches développées habituellement en matière de lutte contre les fourmis invasives ? En effet, les méthodes de lutte utilisées actuellement sont peu efficaces, non-spécifiques et surtout agressives envers l'environnement. C’est l’objectif de cette thèse qui bénéficie d’une bourse BDE (Région PACA/ EcoMed). Nous avons noté en Corse, la présence d'une fourmi native, Tapinoma, qui semble résister à la fourmi d'Argentine). Ces fourmis peuvent donc constituer un moyen de lutte pour contenir la progression de la fourmi d’argentine. Il s’agit de développer nos connaissances sur le genre Tapinoma et plus particulièrement sur l’espèce nigerrimum (qui bien que présente en région PACA, n’y a jamais été étudié) et sur la structure de leurs colonies. Est-elle unicoloniale, c’est-à-dire forme-t elle des supercolonies au sein desquelles on enregistre une perte plus ou moins importante des manifestations agressives intraspécifiques, comme chez la fourmi d’Argentine ? Quelles sont leurs répartitions respectives en région PACA ? Etablit-elle ses nids à proximité de ceux de la fourmi d’Argentine comme nous l’avons observé en Corse ? Dans l’affirmative, quels types d’interactions agonistiques ont-elles vis-à-vis de la fourmi d’Argentine ? Après des tests éthologiques au laboratoire, peut-on envisager de déplacer un fragment de colonie de Tapinoma à proximité d’un nid de fourmid’argentine (in situ) avec une bonne chance de survie ? Est-il envisageable de transplanter des colonies de Tapinoma en lisière du front d’invasion de la fourmi d’Argentine pour former une barrière contre cette invasion