Genetic population structure of the blue sea star (<i>Linckia laevigata</i>) and the boring giant clam (<i>Tridacna crocea</i>) across Malaysia

Various studies on population genetics in the Indo-Pacific that include the Coral Triangle region have revealed phylogeographic patterns in marine species populations. However, little is known about the population structure and connectivity pattern among the coral reefs in four seas surrounding Malaysia: the Strait of Malacca (Andaman Sea), the South China Sea, the Sulu Sea, and the Sulawesi Sea. In view of this, we examined the genetic population structure of two invertebrate species: the blue sea star (Linckia laevigata) and the boring clam (Tridacna crocea) from seven localities across Malaysia, including Pulau Layang-Layang in the Spratly Islands. Additional samples of L. laevigata were obtained from the Davao Gulf, the Philippines. The analyses were based on partial mitochondrial cytochrome oxidase I sequences of L. laevigata and T. crocea. Populations of L. laevigata and T. crocea showed departure from neutrality, indicating selection or population expansion. However, a mismatch analysis suggested population expansion. Lack of genetic population structure in L. laevigata (ΦST = − 0.001, P = 0.399) implies high connectivity among the sampled reef sites. There was subtle genetic structuring in populations of T. crocea (ΦST = 0.032, P = 0.009), but AMOVA did not detect any structure in the a priori groupings. The genetic population structure and scale in connectivity are most likely attributed to the life history traits of the sea star and giant clam species, and also to the geological history and seasonal current patterns of the region

Sovereign bond yield spreads and sustainability : an empirical analysis of OECD countries

Patricia Crifo acknowledges the support of the chair for Sustainable Finance and Responsible Investment (chair FDIR – Toulouse IDEI & Ecole Polytechnique), the chair for Energy and prosperity, finance and evaluation of energy transition, and the Research program Investissements d'Avenir (ANR-11-IDEX-0003/Labex Ecodec/ANR-11- LABX-0047).We study whether and how a country's environmental, social, and governance (ESG) performance relates to its sovereign borrowing costs in international capital markets. We hypothesize that good ESG performance plays an economic role: It signals a country's commitment to sustainability and long-term orientation and is a buffer against negative shocks, leading to lower sovereign bond yield spreads. Using a sample of 20 OECD countries over the period 1996–2012, we show that countries with good ESG performance are associated with lower default risk and lower sovereign bond yield spreads. Moreover, we show that the social and governance dimensions have a significant negative association with sovereign bond yield spreads, whereas the environmental dimension does not.PostprintPeer reviewe

Host stress drives Salmonella recrudescence

Host stress is well known to result in flare-ups of many bacterial, viral and parasitic infections. The mechanism by which host stress is exploited to increase pathogen loads, is poorly understood. Here we show that Salmonella enterica subspecies enterica serovar Typhimurium employs a dedicated mechanism, driven by the scsA gene, to respond to the host stress hormone cortisol. Through this mechanism, cortisol increases Salmonella proliferation inside macrophages, resulting in increased intestinal infection loads in DBA/2J mice. ScsA directs overall Salmonella virulence gene expression under conditions that mimic the intramacrophagic environment of Salmonella, and stimulates the host cytoskeletal alterations that are required for increased Salmonella proliferation inside cortisol exposed macrophages. We thus provide evidence that in a stressed host, the complex interplay between a pathogen and its host endocrine and innate immune system increases intestinal pathogen loads to facilitate pathogen dispersal

Toxicological evaluation of a novel umami flavour compound: 2-(((3-(2,3-Dimethoxyphenyl)-1H -1,2,4-triazol-5-yl)thio)methyl)pyridine

A toxicological evaluation of a umami flavour compound, 2-(((3-(2, 3-dimethoxyphenyl)-1H -1, 2, 4-triazol-5-yl)thio)methyl)pyridine (S3643, CAS 902136-79-2), was completed for the purpose of assessing its safety for use in food and beverage applications. S3643 undergoes extensive oxidative metabolism in vitro with rat microsomes producing the S3643-sulfoxide and 4′-hydroxy-S3643 as the major metabolites. In incubations with human microsomes, the O -demethyl-S3643 and S3643-sulfoxide were produced as the major metabolites. In pharmacokinetic studies in rats, the S3643-sulfoxide represents the dominant biotransformation product. S3643 was not found to be mutagenic or clastogenic in vitro, and did not induce micronuclei in CHO-WBL cells. In subchronic oral toxicity studies in rats, the no-observed-adverse-effect-level (NOAEL) for S3643 was 100 mg/kg bw/day (highest dose tested) when administered in the diet for 90 consecutive days

Lifting the spin-momentum locking in ultra-thin topological insulator films

Three-dimensional (3D) topological insulators (TIs) are known to carry 2D Dirac-like topological surface states in which spin-momentum locking prohibits backscattering. When thinned down to a few nanometers, the hybridization between the topological surface states at the top and bottom surfaces results in a topological quantum phase transition, which can lead to the emergence of a quantum spin Hall phase. Here, we study the thickness-dependent transport properties across the quantum phase transition on the example of (Bi$_{0.16}$Sb$_{0.84}$)$_2$Te$_3$ films, with a four-tip scanning tunnelling microscope. Our findings reveal an exponential drop of the conductivity below the critical thickness. The steepness of this drop indicates the presence of spin-conserving backscattering between the top and bottom surface states, effectively lifting the spin-momentum locking and resulting in the opening of a gap at the Dirac point. Our experiments provide crucial steps towards the detection of quantum spin Hall states in transport measurements

A vicious cycle of β amyloid-dependent neuronal hyperactivation

beta-amyloid (A beta)-dependent neuronal hyperactivity is believed to contribute to the circuit dysfunction that characterizes the early stages of Alzheimer's disease (AD). Although experimental evidence in support of this hypothesis continues to accrue, the underlying pathological mechanisms are not well understood. In this experiment, we used mouse models of A beta-amyloidosis to show that hyperactivation is initiated by the suppression of glutamate reuptake. Hyperactivity occurred in neurons with preexisting baseline activity, whereas inactive neurons were generally resistant to A beta-mediated hyperactivation. A beta-containing AD brain extracts and purified A beta dimers were able to sustain this vicious cycle. Our findings suggest a cellular mechanism of A beta-dependent neuronal dysfunction that can be active before plaque formation