Relation entre la structure et les propriétés d'organisation de nouvelles cyclodextrines amphiphiles

AMIENS-BU Sciences (800212103) / SudocSudocFranceF

On the slow quenching of ℳ* galaxies: heavily obscured AGNs clarify the picture

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LARgE Survey – I. Dead monsters: the massive end of the passive galaxy stellar mass function at cosmic noon

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LARgE survey – III. Environments of ultra-massive passive galaxies at cosmic noon: BCG progenitors growing through mergers

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On the fast quenching of young low-mass galaxies up to z ∼ 0.6: new spotlight on the lead role of environment

14 pages, 5 figures, accepted for publication in MNRAS; published versionInternational audienceWe investigate the connection between environment and the different quenching channels that galaxies are prone to follow in the rest-frame NUVrK colour diagram, as identified by Moutard et al. (2016b). Namely, the fast quenching channel followed by $young$ low-mass galaxies and the slow quenching channel followed by $old$ high-mass ones. We make use of the >22 deg$^2$ covered the VIPERS Multi-Lambda Survey (VIPERS-MLS) to select a galaxy sample complete down to stellar masses of $M_* > 10^{9.4} M_\odot$ at $z 10^{8.8} M_\odot$ at $z < 0.5$) and including 33,500 (43,000) quiescent galaxies properly selected at $0.2 < z < 0.65$, while being characterized by reliable photometric redshifts ($\sigma_{\delta z/(1+z)} \leq 0.04$) that we use to measure galaxy local densities. We find that (1) the quiescence of low-mass [$M_* \leq 10^{9.7} M_\odot$] galaxies requires a strong increase of the local density, which confirms the lead role played by environment in their fast quenching and, therefore, confirms that the low-mass upturn observed in the stellar mass function of quiescent galaxies is due to $environmental$ $quenching$. We also observe that (2) the reservoir of low-mass star-forming galaxies located in very dense regions (prone to environmental quenching) has grown between $z \sim 0.6$ and $z \sim 0.4$ whilst the share of low-mass quiescent galaxies (expected to being environmentally quenched) may have simultaneously increased, which would plead for a rising importance of $environmental$ $quenching$ with cosmic time, compared to $mass$ $quenching$. We finally discuss the composite picture of such environmental quenching of low-mass galaxies and, in particular, how this picture may be consistent with a $delayed$-$then$-$rapid$ quenching scenario

LARgE Survey – II. The dark matter haloes and the progenitors and descendants of ultramassive passive galaxies at cosmic noon

International audienceWe use a 27.6 deg^2 survey to measure the clustering of -selected quiescent galaxies at z ∼ 1.6, focusing on ultramassive quiescent galaxies. We find that z ∼ 1.6 Ultra-Massive Passively Evolving Galaxies (UMPEGs), which have K_s(AB)  = 10^11.5 M_⊙), cluster more strongly than any other known galaxy population at high redshift. Comparing their correlation length, r_0 = 29.77 ± 2.75h^−1Mpc, with the clustering of dark matter (DM) haloes in the Millennium XXL N-body simulation suggests that these z ∼ 1.6 UMPEGs reside in DM haloes of mass M_h ∼ 10^14.1h^−1M_⊙. Such very massive z ∼ 1.6 haloes are associated with the ancestors of z ∼ 0 massive galaxy clusters such as the Virgo and Coma clusters. Given their extreme stellar masses and lack of companions with comparable mass, we surmise that these UMPEGs could be the already-quenched central massive galaxies of their (proto)clusters. We conclude that with only a modest amount of further growth in their stellar mass, z ∼ 1.6 UMPEGs could be the progenitors of some of the massive central galaxies of present-day massive galaxy clusters observed to be already very massive and quiescent near the peak epoch of the cosmic star formation

UV and U-band luminosity functions from CLAUDS and HSC-SSP – I. Using four million galaxies to simultaneously constrain the very faint and bright regimes to z ∼ 3

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WWOX -related encephalopathies: delineation of the phenotypical spectrum and emerging genotype-phenotype correlation

International audienceBACKGROUND:Homozygous mutations in WWOX were reported in eight individuals of two families with autosomal recessive spinocerebellar ataxia type 12 and in two siblings with infantile epileptic encephalopathy (IEE), including one who deceased prior to DNA sampling.METHODS:By combining array comparative genomic hybridisation, targeted Sanger sequencing and next generation sequencing, we identified five further patients from four families with IEE due to biallelic alterations of WWOX.RESULTS:We identified eight deleterious WWOX alleles consisting in four deletions, a four base-pair frameshifting deletion, one missense and two nonsense mutations. Genotype-phenotype correlation emerges from the seven reported families. The phenotype in four patients carrying two predicted null alleles was characterised by (1) little if any psychomotor acquisitions, poor spontaneous motility and absent eye contact from birth, (2) pharmacoresistant epilepsy starting in the 1st weeks of life, (3) possible retinal degeneration, acquired microcephaly and premature death. This contrasted with the less severe autosomal recessive spinocerebellar ataxia type 12 phenotype due to hypomorphic alleles. In line with this correlation, the phenotype in two siblings carrying a null allele and a missense mutation was intermediate.CONCLUSIONS:Our results obtained by a combination of different molecular techniques undoubtedly incriminate WWOX as a gene for recessive IEE and illustrate the usefulness of high throughput data mining for the identification of genes for rare autosomal recessive disorders. The structure of the WWOX locus encompassing the FRA16D fragile site might explain why constitutive deletions are recurrently reported in genetic databases, suggesting that WWOX-related encephalopathies, although likely rare, may not be exceptional