Damage in porous media due to salt crystallization

We investigate the origins of salt damage in sandstones for the two most common salts: sodium chloride and sulfate. The results show that the observed difference in damage between the two salts is directly related to the kinetics of crystallization and the interfacial properties of the salt solutions and crystals with respect to the stone. We show that, for sodium sulfate, the existence of hydrated and anhydrous crystals and specifically their dissolution and crystallization kinetics are responsible for the damage. Using magnetic resonance imaging and optical microscopy we show that when water imbibes sodium sulfate contaminated sandstones, followed by drying at room temperature, large damage occurs in regions where pores are fully filled with salts. After partial dissolution, anhydrous sodium sulfate salt present in these regions gives rise to a very rapid growth of the hydrated phase of sulfate in the form of clusters that form on or close to the remaining anhydrous microcrystals. The rapid growth of these clusters generates stresses in excess of the tensile strength of the stone leading to the damage. Sodium chloride only forms anhydrous crystals that consequently do not cause damage in the experiments

Simulating Plasmon Resonances of Gold Nanoparticles with Bipyramidal Shapes by Boundary Element Methods

Computational modeling and accurate simulations of localized surface plasmon resonance (LSPR) absorption properties are reported for gold nanobipyramids (GNBs), a class of metal nanoparticle that features highly tunable, geometry-dependent optical properties. GNB bicone models with spherical tips performed best in reproducing experimental LSPR spectra while the comparison with other geometrical models provided a fundamental understanding of base shapes and tip effects on the optical properties of GNBs. Our results demonstrated the importance of averaging all geometrical parameters determined from transmission electron microscopy images to build representative models of GNBs. By assessing the performances of LSPR absorption spectra simulations based on a quasi-static approximation, we provided an applicability range of this approach as a function of the nanoparticle size, paving the way to the theoretical study of the coupling between molecular electron densities and metal nanoparticles in GNB-based nanohybrid systems, with potential applications in the design of nanomaterials for bioimaging, optics and photocatalysis

The lipoatrophic caveolin-1 deficient mouse model reveals autophagy in mature adipocytes

Adipose tissue lipoatrophy caused by caveolin gene deletion in mice is not linked to defective adipocyte differentiation. We show that adipose tissue development cannot be rescued by endothelial specific caveolin-1 re-expression, indicating primordial role of caveolin in mature adipocytes. Partial or total caveolin deficiency in adipocytes induced broad protein expression defects, including but not limited to previously described downregulation of insulin receptor. Global alterations in protein turnover, and accelerated degradation of long-lived proteins were found in caveolin-deficient adipocytes. Lipidation of endogenous LC3 autophagy marker and distribution of GFP-LC3 into aggregates demonstrated activated autophagy in the absence of caveolin-1 in adipocytes. Furthermore, electron microscopy revealed autophagic vacuoles in caveolin-1 deficient but not control adipocytes. Surprisingly, significant levels of lipidated LC3-II were found around lipid droplets of normal adipocytes, maintained in nutrient-rich conditions or isolated from fed mice, which do not display autophagy. Altogether, these data indicate that caveolin deficiency induce autophagy in adipocytes, a feature that is not a physiological response to fasting in normal fat cells. This likely resulted from defective insulin and lipolytic responses that converge in chronic nutrient shortage in adipocytes lacking caveolin-1. This is the first report of a pathological situation with autophagy as an adaptative response to adipocyte failure

Ranking Port Cities with High Exposure and Vulnerability to Climate Extremes

DOI:10.1787/011766488208This global screening study makes a first estimate of the exposure of the world's large port cities to coastal flooding due to storm surge and damage due to high winds. This assessment also investigates how climate change is likely to impact each port city's exposure to coastal flooding by the 2070s, alongside subsidence and population growth and urbanisation. The study provides a much more comprehensive analysis than earlier assessments, focusing on the 136 port cities around the world that have more than one million inhabitants in 2005. The analysis demonstrates that a large number of people are already exposed to coastal flooding in large port cities. Across all cities, about 40 million people (0.6% of the global population or roughly 1 in 10 of the total port city population in the cities considered here) are exposed to a 1 in 100 year coastal flood event. For present-day conditions (2005), the top ten cities in terms of exposed population are estimated to be Mumbai, Guangzhou, Shanghai, Miami, Ho Chi Minh City, Kolkata, Greater New York, Osaka-Kobe, Alexandria and New Orleans; almost equally split between developed and developing countries. When assets are considered, the current distribution becomes more heavily weighted towards developed countries, as the wealth of the cities becomes important. The top 10 cities in terms of assets exposed are Miami, Greater New York, New Orleans, Osaka-Kobe, Tokyo, Amsterdam, Rotterdam, Nagoya, Tampa-St Petersburg and Virginia Beach. These cities contain 60% of the total exposure, but are from only three (wealthy) countries: USA, Japan and the Netherlands. The total value of assets exposed in 2005 is across all cities considered here is estimated to be US3,000 billion; corresponding to around 5% of global GDP in 2005 (both measured in international USD)... Available at : http://www.oecd-ilibrary.org/environment/ranking-port-cities-with-high-exposure-and-vulnerability-to-climate-extremes_01176648820

Macroeconomic drivers of baseline scenarios in dynamic CGE models: review and guidelines proposal

For dynamic computable general equilibrium (CGE) modeling, long-term baseline construction is key and depends on the applied methods and the sources of projections considered. For dynamic CGE models, baseline assumptions and base data are both important determinants of results. This paper reviews the assumptions made by 24 modeling teams on baseline macroeconomic drivers, understood as factor accumulation and gross domestic product (GDP) growth. We critically review the various methods, identifying state-of-the-art practices and propose simple guidelines, particularly focusing on consistency between data sources and models, which is intended to help dynamic CGE modelers build their own baselines

Biogenesis of Pro-senescent Microparticles by Endothelial Colony Forming Cells from Premature Neonates is driven by SIRT1-Dependent Epigenetic Regulation of MKK6.

Senescent cells may exert detrimental effect on microenvironment through the secretion of soluble factors and the release of extracellular vesicles, such as microparticles, key actors in ageing and cardiovascular diseases. We previously reported that sirtuin-1 (SIRT1) deficiency drives accelerated senescence and dysfunction of endothelial colony-forming cells (ECFC) in PT neonates. Because preterm birth (PT) increases the risk for cardiovascular diseases during neonatal period as well as at adulthood, we hypothesized that SIRT1 deficiency could control the biogenesis of microparticles as part of a senescence-associated secretory phenotype (SASP) of PT-ECFC and investigated the related molecular mechanisms. Compared to control ECFC, PT-ECFC displayed a SASP associated with increased release of endothelial microparticles (EMP), mediating a paracrine induction of senescence in naïve endothelial cells. SIRT1 level inversely correlated with EMP release and drives PT-ECFC vesiculation. Global transcriptomic analysis revealed changes in stress response pathways, specifically the MAPK pathway. We delineate a new epigenetic mechanism by which SIRT1 deficiency regulates MKK6/p38 <sup>MAPK</sup> /Hsp27 pathway to promote EMP biogenesis in senescent ECFC. These findings deepen our understanding of the role of ECFC senescence in the disruption of endothelial homeostasis and provide potential new targets towards the control of cardiovascular risk in individuals born preterm

Multi-time-over-threshold technique for photomultiplier signal processing: Description and characterization of the SCOTT ASIC

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First Report of Root and Collar Rot Caused by Fusarium tricinctum and Fusarium avenaceum on Carrot in France

In 2017, carrot (Daucus carota L.) seed production represented around 22% of the area devoted to the production of vegetable fine seeds. Since 2015, symptoms of root and collar rot have been observed in carrot seed parcels located in the Central Region, one of the most important production zone in France. Diseased plants became dried prematurely, compromising seed development. Depending on the year and the climatic conditions, the disease in a same field can be considered as epidemic (rate losses between 30 to 100% of plants in 2016) or can impact plants more sporadically (less than 10% in 2017 and 2018). Sixteen diseased carrot samples (Nantaise type) were collected from five fields of seed production in the Central Region: two fields in 2016 and 2017, one field in 2018. Seven fungal isolates, obtained from lesions, were grown on Potato Dextrose Agar (PDA) medium and incubated for one week at 20°C in darkness. From the colony top, fluffy mycelium pigmented in pink, red, purple or orange was observed, with a red color at the reverse. To induce sporulation, isolates were grown on Synthetischer Nährstoffarmer Agar (SNA) medium during three weeks at 24°C in near-UV radiations under a 12h-photoperiod. Four isolates (FT001, FT003, FT007, FT017) developed orange sporodochia with lunar or crescent-shaped macroconidia (40.3 ± 0.8 × 5.9 ± 0.1 µm; n=90) and lime or pear-shaped microconidia (10.7 ± 0.2 × 7.7 ± 0.2 µm; n=60), as described in Fusarium tricinctum (Leslie and Summerell 2006). Three isolates (FA001, FA002, FA006) developed orange sporodochia with sickle-shaped macroconidia (50.5 ± 1.1 × 5.0 ± 0.1 µm; n= 60), but no microconidia, as observed in Fusarium avenaceum (Leslie and Summerell 2006). To confirm the identification, DNA was extracted from the mycelium of the seven isolates and molecular markers (ATP citrate lyase, ACL1; RNA polymerase II, RPB2) were used for PCR amplification (Gräfenhan et al. 2011; O’Donnell et al. 2013). The ACL1 sequences from the seven field isolates (GenBank Accession numbers MK183788-MK183791; MK181528-MK181530) were 99-100% identical with the ACL1 sequence of a reference F. tricinctum isolate (query coverages 99-100%; E-values of 0.0) and a reference F. avenaceum isolate (query coverages 98-99%; E-values of 0.0) [respectively DAOM 235630 isolate, GenBank Acc. No. JX397813 and BBA64135 isolate, GenBank Acc. No. JX397768, Niessen et al. 2012]. Using RPB2, sequences from field isolates (GenBank Acc. No. MK183109-MK183115) were 98.5-99.9% identical with the RPB2 sequence of a reference F. tricinctum isolate (query coverages 96-100%; E-values of 0.0) and a reference F. avenaceum isolate (query coverages 95-100%; E-values of 0.0) [respectively MRC 1895 isolate, GenBank Acc. No. MH582113 and MRC 1413 isolate, GenBank Acc. No. MH582082, O’Donnell et al. 2018]. To confirm pathogenicity, FT001 and FA002 were inoculated on collars of 10-weeks old carrot plants in the greenhouse. Forty plants per isolate and 40 control plants were used. Ten microliters of a conidial suspension (105 conidia.mL-1) - or sterile water for the controls - were deposited at the collar, previously wounded using a scalpel blade. Necrotic lesions developed at 20 dpi (FT001) and at 30 dpi (FA002). Fusarium tricinctum and F. avenaceum were re-isolated from the lesions and identified by sequencing using ACL1 and RPB2 markers. No isolation of Fusarium was obtained from the controls. To our knowledge, this is the first report of F. tricinctum and F. avenaceum in carrot in France

HRAS is a therapeutic target in malignant chemo-resistant adenomyoepithelioma of the breast

Abstract Malignant adenomyoepithelioma (AME) of the breast is an exceptionally rare form of breast cancer, with a significant metastatic potential. Chemotherapy has been used in the management of advanced AME patients, however the majority of treatments are not effective. Recent studies report recurrent mutations in the HRAS Q61 hotspot in small series of AMEs, but there are no preclinical or clinical data showing H-Ras protein as a potential therapeutic target in malignant AMEs. We performed targeted sequencing of tumours’ samples from new series of 13 AMEs, including 9 benign and 4 malignant forms. Samples from the breast tumour and the matched axillary metastasis of one malignant HRAS mutated AME were engrafted and two patient-derived xenografts (PDX) were established that reproduced the typical AME morphology. The metastasis-derived PDX was treated in vivo by different chemotherapies and a combination of MEK and BRAF inhibitors (trametinib and dabrafenib). All malignant AMEs presented a recurrent mutation in the HRAS G13R or G12S hotspot. Mutation of PIK3CA were found in both benign and malignant AMEs, while AKT1 mutations were restricted to benign AMEs. Treatment of the PDX by the MEK inhibitor trametinib, resulted in a marked anti-tumor activity, in contrast to the BRAF inhibitor and the different chemotherapies that were ineffective. Overall, these findings further expand on the genetic features of AMEs and suggest that patients carrying advanced HRAS-mutated AMEs could potentially be treated with MEK inhibitors