8 research outputs found
Chandra X-ray observations of Young Clusters II. Orion Flanking Fields Data
We present results of Chandra observations of two flanking fields (FF) in
Orion, outside the Orion Nebula Cluster (ONC). The observations were taken with
the ACIS-I camera with an exposure time of about 48 ks each field. We present a
catalog of 417 sources, which includes X-ray luminosity, optical and infrared
photometry and X-ray variability information. We have found 91 variable
sources, 33 of which have a flare-like light curve, and 11 of which have a
pattern of a steady increase or decrease over a 10 hour period. The optical and
infrared photometry for the stars identified as X-ray sources are consistent
with most of these objects being pre-main sequence stars with ages younger than
10 Myr. We present evidence for an age difference among the X-ray selected
samples of NGC 2264, Orion FF, and ONC, with NGC 2264 being the oldest, and ONC
being the youngest.Comment: AJ in press, 32 pages, 13 figures in total, 5 figures available at
http://spider.ipac.caltech.edu/staff/solange/ramirez07_figs.p
Extending the ICRF into the Infrared: 2MASS - UCAC Astrometry
An external comparison between the infrared 2MASS and the optical UCAC positions was performed, both being on the same system, the ICRS. About 48 million sources in common were identified. Random errors of the 2MASS catalog positions are about 60 to 70 mas per coordinate for the Ks = 4 to 14 range, increasing to about 100 to 150 mas for saturated and very faint stars. Systematic position differences between the 2 catalogs are very small, about 5 to 10 mas as a function of magnitude and color, with somewhat larger errors as a function of right ascension and declination. The extension of the ICRF into the infrared has become a reality
Chandra X-ray Observations of Young Clusters
We present results of Chandra observations of two flanking fields (FFs) in Orion, outside the Orion Nebula Cluster (ONC). The observations were taken with the ACIS-I camera with an exposure time of about 48 ks each field. We present a catalog of 417 sources, which includes X-ray luminosity, optical and infrared photometry, and X-ray variability information. We have found 91 variable sources, 33 of which have a flarelike light curve and 11 of which have a pattern of a steady increase or decrease over a 10 hr period. The optical and infrared photometry for the stars identified as X-ray sources are consistent with most of these objects being pre-main-sequence stars with ages younger than 10 Myr. We present evidence for an age difference among the X-ray-selected samples of NGC 2264, Orion FFs, and ONC, with NGC 2264 being the oldest and ONC being the youngest
Suppressor Mutations for Presenilin 1 Familial Alzheimer Disease Mutants Modulate γ-Secretase Activities
Nicastrin Is Dispensable for γ-Secretase Protease Activity in the Presence of Specific Presenilin Mutations*S⃞
γ-Secretase is a multisubunit membrane protein complex consisting of
presenilin (PS1), nicastrin (NCT), anterior pharynx-1, and presenilin enhancer
2. To analyze the activity of familial Alzheimer disease mutants and to
understand the roles of the subunits, we established a yeast transcriptional
activator Gal4p system with artificial γ-secretase substrates containing
amyloid precursor protein or Notch fragments. The γ-secretase activities
were evaluated by transcriptional activation of reporter genes upon Gal4p
release from the membrane-bound substrates, i.e. growth of yeast on
histidine and adenine, or β-galactosidase assay. We screened and
evaluated γ-secretase mutants using this reconstitution system in yeast,
which does not possess endogenous γ-secretase activity. When we
introduced familial Alzheimer mutants of PS1 in this system, their activities
were shown to be loss of function. Although the protease activity of wild type
PS1 depends on the other three subunits introduced, we obtained 15 new PS1
mutants, which are active in the absence of NCT. They possessed a S438P
mutation at the ninth transmembrane domain (TM9) together with one missense
mutation distributed through transmembrane and loop regions. These mutations
were not related to familial Alzheimer mutations of PS1 as identified so far.
The S438P mutant was partially active but required other mutations for full
activation. Results of the β-galactosidase assay suggested that they have
wild type protease activities, which were further confirmed by the
endoproteolysis of PS1, amyloid β peptides, and Notch intracellular
domain production in mammalian cells. These results suggest that NCT is
dispensable for the protease activity of γ-secretase
3D modeling of esophageal development using human PSC-Derived basal progenitors reveals a critical role for notch signaling
Pluripotent stem cells (PSCs) could provide a powerful system to model development of the human esophagus, whose distinct tissue organization compared to rodent esophagus suggests that developmental mechanisms may not be conserved between species. We therefore established an efficient protocol for generating esophageal progenitor cells (EPCs) from human PSCs. We found that inhibition of TGF-ß and BMP signaling is required for sequential specification of EPCs, which can be further purified using cell-surface markers. These EPCs resemble their human fetal counterparts and can recapitulate normal development of esophageal stratified squamous epithelium during in vitro 3D cultures and in vivo. Importantly, combining hPSC differentiation strategies with mouse genetics elucidated a critical role for Notch signaling in the formation of this epithelium. These studies therefore not only provide an efficient approach to generate EPCs, but also offer a model system to study the regulatory mechanisms underlying development of the human esophagus.Work in the Que lab is partly supported by R01DK113144, R01DK100342, and R01HL132996 (J.Q.), and the
Price Family Foundation. S.D. acknowledges a fellowship support from the Hastings Center for Pulmonary Research (USC). Flow cytometry was performed in the Columbia Center for Translational Immunology (CCTI) Flow Cytometry Core at Columbia University Medical Center, supported in part by the Office of the Director, NIH under the award S10OD020056.info:eu-repo/semantics/publishedVersio