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Hoyer, S.,Ló,pez-Morales, M.,Rojo, P.,Nascimbeni, V.,Hidalgo, S.,Astudillo-Defru, N.,Concha, F.,Contreras, Y.,Servajean, E.,Hinse, T. C. Oxford University Press 2013 Monthly notices of the Royal Astronomical Society Vol.434 No.1
<P>We report 12 new transit observations of the exoplanet WASP-4b from the Transit Monitoring in the South (TraMoS) project. These transits are combined with all previously published transit data for this planet to provide an improved radius measurement of R-p = 1.395 +/- 0.022R(jup) and improved transit ephemerides. In a new homogeneous analysis in search for transit timing variations (TTVs) we find no evidence of those with rms amplitudes larger than 20 s over a 4-yr time span. This lack of TTVs rules out the presence of additional planets in the system with masses larger than about 2.5, 2.0 and 1.0 M-circle plus around the 1:2, 5:3 and 2:1 orbital resonances. Our search for the variation of other parameters, such as orbital inclination and transit depth, also yields negative results over the total time span of the transit observations. Finally, we perform a simple study of stellar spots configurations of the system and conclude that the star rotational period is about 34 d.</P>
Garbes, L.,Kim, K.,Riesz, A.,Hoyer-Kuhn, H.,Beleggia, F.,Bevot, A.,Kim, M.,Huh, Y.,Kweon, H.S.,Savarirayan, R.,Amor, D.,Kakadia, Purvi M.,Lindig, T.,Kagan, K.,Becker, J.,Boyadjiev, Simeon A.,Wollnik, University of Chicago Press [etc.] 2015 American journal of human genetics Vol.96 No.3
As a result of a whole-exome sequencing study, we report three mutant alleles in SEC24D, a gene encoding a component of the COPII complex involved in protein export from the ER: the truncating mutation c.613C>T (p.Gln205<SUP>*</SUP>) and the missense mutations c.3044C>T (p.Ser1015Phe, located in a cargo-binding pocket) and c.2933A>C (p.Gln978Pro, located in the gelsolin-like domain). Three individuals from two families affected by a similar skeletal phenotype were each compound heterozygous for two of these mutant alleles, with c.3044C>T being embedded in a 14 Mb founder haplotype shared by all three. The affected individuals were a 7-year-old boy with a phenotype most closely resembling Cole-Carpenter syndrome and two fetuses initially suspected to have a severe type of osteogenesis imperfecta. All three displayed a severely disturbed ossification of the skull and multiple fractures with prenatal onset. The 7-year-old boy had short stature and craniofacial malformations including macrocephaly, midface hypoplasia, micrognathia, frontal bossing, and down-slanting palpebral fissures. Electron and immunofluorescence microscopy of skin fibroblasts of this individual revealed that ER export of procollagen was inefficient and that ER tubules were dilated, faithfully reproducing the cellular phenotype of individuals with cranio-lentico-sutural dysplasia (CLSD). CLSD is caused by SEC23A mutations and displays a largely overlapping craniofacial phenotype, but it is not characterized by generalized bone fragility and presented with cataracts in the original family described. The cellular and morphological phenotypes we report are in concordance with the phenotypes described for the Sec24d-deficient fish mutants vbi (medaka) and bulldog (zebrafish).