Sinemurian–Pliensbachian calcareous nannofossil biostratigraphy and organic carbon isotope stratigraphy in the Paris Basin: Calibration to the ammonite biozonation of NW Europe

This is the author accepted manuscript. The final version is available from the publisher via the DOI in this record.Available online 12 December 2016The biostratigraphy of Sinemurian to lower Toarcian calcareous nannofossils has been investigated in the Sancerre-Couy core (Paris Basin), which contains a mixed assemblage of species with affinities to the northern and southern areas of the peri-tethyan realm, thus allowing for the use and calibration of the Mediterranean Province (Italy/S France) and NW Europe (UK) biozonation schemes. This study is based on semi-quantitative analyses of the calcareous nannofossil assemblage performed on 145 samples and the recorded bioevents are calibrated to the NW European Ammonite Zonation and to a new organic carbon isotope curve based on 385 data points. The main bioevents, i.e. the first occurrences of Parhabdolithus liasicus, Crepidolithus pliensbachensis, Crepidolithus crassus, Mitrolithus lenticularis, Similiscutum cruciulus sensu lato, Lotharingius hauffii, Crepidolithus cavus and Lotharingius sigillatus as well as the last occurrence of Parhabdolithus robustus, have been identified. However, we show that a large number of standard biostratigraphic markers show inconsistent occurrences at the base and top of their range, possibly accounting for some of the significant discrepancies observed between the different domains. In addition to the nine main bioevents used for the biozonation of the core, we document an additional 50 distinct bioevents, evaluate their reliability and discuss their potential significance by comparison to previous studies. A total of five significant negative organic carbon isotope excursions are identified and defined in the Paris Basin including the well-documented Sinemurian–Pliensbachian boundary event. One positive excursion is further defined in the Pliensbachian interval. Our calibration of high-resolution calcareous nannofossil biostratigraphy to ammonite biostratigraphy and organic carbon isotopes represents a new stratigraphic reference for the Lower Jurassic series

Climatic and palaeoceanographic changes during the Pliensbachian (Early Jurassic) 2 inferred from clay mineralogy and stable isotope (C-O) geochemistry (NW Europe)

This is the author accepted manuscript. The final version is available from the publisher via the DOI in this record.Available online 17 January 2017The Early Jurassic was broadly a greenhouse climate period that was punctuated by short warm and cold climatic events, positive and negative excursions of carbon isotopes, and episodes of enhanced organic matter burial. Clay minerals from Pliensbachian sediments recovered from two boreholes in the Paris Basin, are used here as proxies of detrital supplies, runoff conditions, and palaeoceanographic changes. The combined use of these minerals with ACCEPTED MANUSCRIPT ACCEPTED MANUSCRIPT stable isotope data (C-O) from bulk carbonates and organic matter allows palaeoclimatic reconstructions to be refined for the Pliensbachian. Kaolinite/illite ratio is discussed as a reliable proxy of the hydrological cycle and runoff from landmasses. Three periods of enhanced runoff are recognised within the Pliensbachian. The first one at the SinemurianPliensbachian transition shows a significant increase of kaolinite concomitant with the negative carbon isotope excursion at the so-called Sinemurian Pliensbachian Boundary Event (SPBE). The Early/Late Pliensbachian transition was also characterised by more humid conditions. This warm interval is associated with a major change in oceanic circulation during the Davoei Zone, likely triggered by sea-level rise; the newly created palaeogeography, notably the flooding of the London-Brabant Massif, allowed boreal detrital supplies, including kaolinite and chlorite, to be exported to the Paris Basin. The last event of enhanced runoff occurred during the late Pliensbachian (Subdonosus Subzone of the Margaritatus Zone), which occurred also during a warm period, favouring organic matter production and preservation. Our study highlights the major role of the London Brabant Massif in influencing oceanic circulation of the NW European area, as a topographic barrier (emerged lands) during periods of lowstand sea-level and its flooding during period of high sea-level. This massif was the unique source of smectite in the Paris Basin. Two episodes of smectite-rich sedimentation (‘smectite events’), coincide with regressive intervals, indicating emersion of the London Brabant Massif and thus suggesting that an amplitude of sea-level change high enough to be linked to glacio-eustasy. This mechanism is consistent with sedimentological and geochemical evidences of continental ice growth notably during the Latest Pliensbachian (Spinatum Zone), and possibly during the Early Pliensbachian (late Jamesoni/early Ibex Zones).The study was supported by the “Agence Nationale pour la Gestion des Déchets Radioactifs” (Andra––French National Radioactive Waste Management Agency)

Drivers for Rift Valley fever emergence in Mayotte: A Bayesian modelling approach

Rift Valley fever (RVF) is a major zoonotic and arboviral hemorrhagic fever. The conditions leading to RVF epidemics are still unclear, and the relative role of climatic and anthropogenic factors may vary between ecosystems. Here, we estimate the most likely scenario that led to RVF emergence on the island of Mayotte, following the 2006–2007 African epidemic. We developed the first mathematical model for RVF that accounts for climate, animal imports and livestock susceptibility, which is fitted to a 12-years dataset. RVF emergence was found to be triggered by the import of infectious animals, whilst transmissibility was approximated as a linear or exponential function of vegetation density. Model forecasts indicated a very low probability of virus endemicity in 2017, and therefore of re-emergence in a closed system (i.e. without import of infected animals). However, the very high proportion of naive animals reached in 2016 implies that the island remains vulnerable to the import of infectious animals. We recommend reinforcing surveillance in livestock, should RVF be reported is neighbouring territories. Our model should be tested elsewhere, with ecosystem-specific data

Psychological stress in adolescent and adult mice increases neuroinflammation and attenuates the response to LPS challenge

<p>Abstract</p> <p>Background</p> <p>There is ample evidence that psychological stress adversely affects many diseases. Recent evidence has shown that intense stressors can increase inflammation within the brain, a known mediator of many diseases. However, long-term outcomes of chronic psychological stressors that elicit a neuroinflammatory response remain unknown.</p> <p>Methods</p> <p>To address this, we have modified previously described models of rat/mouse predatory stress (PS) to increase the intensity of the interaction. We postulated that these modifications would enhance the predator-prey experience and increase neuroinflammation and behavioral dysfunction in prey animals. In addition, another group of mice were subjected to a modified version of chronic unpredictable stress (CUS), an often-used model of chronic stress that utilizes a combination of stressors that include physical, psychological, chemical, and other. The CUS model has been shown to exacerbate a number of inflammatory-related diseases via an unknown mechanism. Using these two models we sought to determine: 1) whether chronic PS or CUS modulated the inflammatory response as a proposed mechanism by which behavioral deficits might be mediated, and 2) whether chronic exposure to a pure psychological stressor (PS) leads to deficits similar to those produced by a CUS model containing psychological and physical stressors. Finally, to determine whether acute PS has neuroinflammatory consequences, adult mice were examined at various time-points after PS for changes in inflammation.</p> <p>Results</p> <p>Adolescent mice subjected to chronic PS had increased basal expression of inflammation within the midbrain. CUS and chronic PS mice also had an impaired inflammatory response to a subsequent lipopolysaccharide challenge and PS mice displayed increased anxiety- and depressive-like behaviors following chronic stress. Finally, adult mice subjected to acute predatory stress had increased gene expression of inflammatory factors.</p> <p>Conclusion</p> <p>Our results demonstrate that predatory stress, an ethologically relevant stressor, can elicit changes in neuroinflammation and behavior. The predatory stress model may be useful in elucidating mechanisms by which psychological stress modulates diseases with an inflammatory component.</p

Neuroprotective Effect of Inhaled Nitric Oxide on Excitotoxic-Induced Brain Damage in Neonatal Rat

BACKGROUND: Inhaled nitric oxide (iNO) is one of the most promising therapies used in neonates. However, little information is known about its impact on the developing brain submitted to excitotoxic challenge. METHODOLOGY/PRINCIPAL FINDINGS: We investigated here the effect of iNO in a neonatal model of excitotoxic brain lesions. Rat pups and their dams were placed in a chamber containing 20 ppm NO during the first week of life. At postnatal day (P)5, rat pups were submitted to intracranial injection of glutamate agonists. At P10, rat pups exposed to iNO exhibited a significant decrease of lesion size in both the white matter and cortical plate compared to controls. Microglia activation and astrogliosis were found significantly decreased in NO-exposed animals. This neuroprotective effect was associated with a significant decrease of several glutamate receptor subunits expression at P5. iNO was associated with an early (P1) downregulation of pCREB/pAkt expression and induced an increase in pAkt protein concentration in response to excitotoxic challenge (P7). CONCLUSION: This study is the first describe and investigate the neuroprotective effect of iNO in neonatal excitotoxic-induced brain damage. This effect may be mediated through CREB pathway and subsequent modulation of glutamate receptor subunits expression