68 research outputs found
Discovery of Extremely Embedded X-ray Sources in the R Coronae Australis Star Forming Core
With the XMM-Newton and Chandra observatories, we detected two extremely
embedded X-ray sources in the R Corona Australis (R CrA) star forming core,
near IRS 7. These sources, designated as XB and XA, have X-ray absorption
columns of ~3e23 cm-2 equivalent to AV ~180 mag. They are associated with the
VLA centimeter radio sources 10E and 10W, respectively. XA is the counterpart
of the near-infrared source IRS 7, whereas XB has no K-band counterpart above
19.4 mag. This indicates that XB is younger than typical Class I protostars,
probably a Class 0 protostar or in an intermediate phase between Class 0 and
Class I. The X-ray luminosity of XB varied between 29<log LX <31.2 ergs s-1 on
timescales of 3-30 months. XB also showed a monotonic increase in X-ray
brightness by a factor of two in 30 ksec during an XMM-Newton observation. The
XMM-Newton spectra indicate emission from a hot plasma with kT ~3-4 keV and
also show fluorescent emission from cold iron. Though the X-ray spectrum from
XB is similar to flare spectra from Class I protostars in luminosity and
temperature, the light curve does not resemble the lightcurves of magnetically
generated X-ray flares because the variability timescale of XB is too long and
because variations in X-ray count rate were not accompanied by variations in
spectral hardness. The short-term variation of XB may be caused by the partial
blocking of the X-ray plasma, while the month-long flux enhancement may be
driven by mass accretion.Comment: 26 pages, 8 figures, To be published in ApJ in April 200
H Emission Nebulosity Associated with KH 15D
An H emission filament is found in close proximity to the unique object
KH 15D using the adaptive optics system of the Subaru Telescope. The morphology
of the filament, the presence of spectroscopic outflow signatures observed by
Hamilton et al., and the detection of extended H emission from KH 15D by
Deming, Charbonneau, & Harrington suggest that this filament arises from
shocked H in an outflow. The filament extends about 15" to the north of KH
15D.Comment: 11 pages, 3 figures, 1 table. Astrophysical Journal Letters, in pres
A Subarcsecond Companion to the T Tauri Star AS 353B
Adaptive optics imaging of the bright visual T Tauri binary AS 353 with the
Subaru Telescope shows that it is a hierarchical triple system. The secondary
component, located 5.6" south of AS 353A, is resolved into a subarcsecond
binary, AS 353Ba and Bb, separated by 0.24". Resolved spectroscopy of the two
close components shows that both have nearly identical spectral types of about
M1.5. Whereas AS 353A and Ba show clear evidence for an infrared excess, AS
353Bb does not. We discuss the possible role of multiplicity in launching the
large Herbig-Haro flow associated with AS 353A.Comment: AASTeXv5.0, 21 pages, 5 figures, Astronomical Journal, in pres
Diffraction-limited 3 μm spectroscopy of IRAS 04296+3429 and IRAS 05341+0852: Spatial extent of hydrocarbon dust emission and dust evolutionary sequence
We present 3 μm spectroscopy of the carbon-rich protoplanetary nebulae IRAS 04296+3429 and IRAS 05341+0852, conducted with the adaptive optics system at the Subaru Telescope. We utilize the nearly diffraction-limited spectroscopy to probe the spatial extent of the hydrocarbon dust emitting zone. We find a hydrocarbon emission core extending up to 100-160 mas from the center of IRAS 04296+3429, corresponding to a physical diameter of 400-640 AU, assuming a distance of 4 kpc. However, we find that IRAS 05341+0852 is not spatially resolved with this instrumentation. The physical extent of these protoplanetary nebulae, along with the reanalyzed data of IRAS 22272+5435 published previously, suggests a correlation between the physical extent of the hydrocarbon dust emission and the spectral evolution of the aliphatic to aromatic features in these post-AGB stars. These measurements represent the first direct test of the proposed chemical synthesis route of carbonaceous dust in the circumstellar environment of evolved stars. © 2007, The American Astronomical Society, Ail rights reserved.published_or_final_versio
Adaptive Optics Spectroscopy of the [Fe II] Outflows from HL Tauri and RW Aurigae
We present new results of [Fe II] 1.644-micron spectroscopy toward the jets
from HL Tau and RW Aur carried out with the Subaru Telescope combined with the
adaptive optics system. We observed the regions within 2" - 3" from the stars
with the sub-arcsecond resolutions of 0."5 and 0."2 for HL Tau and RW Aur,
respectively. In addition to the strong, high velocity emission extended along
each jet, we detected a blueshifted low velocity emission feature seen as a
wing or shoulder of the high velocity emission at each stellar position.
Detailed analysis shows that the position-velocity diagrams (PVDs) of HL Tau
and RW Aur show a characteristic similar to those of the cold disk wind and
X-wind models in that the [Fe II] line width is broad in the vicinity of the
stellar position and is narrower at the extended jet. A closer comparison
suggests, however, that the disk wind model tends to have too large line width
at the jet while the X-wind model has excess emission on the redshifted side at
the stellar position. The narrow velocity width with symmetric line profiles of
the observed high velocity emission supports an X-wind type model where the
launching region is localized in a small radial range, while the low velocity
emission located away from the star favors the presence of a disk wind. The [Fe
II] emission from the HL Tau jet shows a gap of 0."8 between the redshifted jet
and the star, indicating the presence of an optically thick disk of ~ 160 AU in
radius. The [Fe II] emission from the RW Aur jet shows a marked drop from the
redshifted peak at Y ~ -0."2 toward the star, suggesting that its disk radius
is smaller than 40 AU.Comment: Accepted in the ApJ (October 2006, v649n2), AAS LaTEX macros v 5.2,
Total 25 pages with 7 figure
Focal Adhesion Kinase contributes to insulin-induced actin reorganization into a mesh harboring Glucose transporter-4 in insulin resistant skeletal muscle cells
<p>Abstract</p> <p>Background</p> <p>Focal Adhesion Kinase (FAK) is recently reported to regulate insulin resistance by regulating glucose uptake in C2C12 skeletal muscle cells. However, the underlying mechanism for FAK-mediated glucose transporter-4 translocation (Glut-4), responsible for glucose uptake, remains unknown. Recently actin remodeling was reported to be essential for Glut-4 translocation. Therefore, we investigated whether FAK contributes to insulin-induced actin remodeling and harbor Glut-4 for glucose transport and whether downregulation of FAK affects the remodeling and causes insulin resistance.</p> <p>Results</p> <p>To address the issue we employed two approaches: gain of function by overexpressing FAK and loss of function by siRNA-mediated silencing of FAK. We observed that overexpression of FAK induces actin remodeling in skeletal muscle cells in presence of insulin. Concomitant to this Glut-4 molecules were also observed to be present in the vicinity of remodeled actin, as indicated by the colocalization studies. FAK-mediated actin remodeling resulted into subsequent glucose uptake via PI3K-dependent pathway. On the other hand FAK silencing reduced actin remodeling affecting Glut-4 translocation resulting into insulin resistance.</p> <p>Conclusion</p> <p>The data confirms that FAK regulates glucose uptake through actin reorganization in skeletal muscle. FAK overexpression supports actin remodeling and subsequent glucose uptake in a PI3K dependent manner. Inhibition of FAK prevents insulin-stimulated remodeling of actin filaments resulting into decreased Glut-4 translocation and glucose uptake generating insulin resistance. To our knowledge this is the first study relating FAK, actin remodeling, Glut-4 translocation and glucose uptake and their interrelationship in generating insulin resistance.</p
Electrical Pulse Stimulation of Cultured Human Skeletal Muscle Cells as an In Vitro Model of Exercise
Background and Aims
Physical exercise leads to substantial adaptive responses in skeletal muscles and plays a central role in a healthy life style. Since exercise induces major systemic responses, underlying cellular mechanisms are difficult to study in vivo. It was therefore desirable to develop an in vitro model that would resemble training in cultured human myotubes.
Methods
Electrical pulse stimulation (EPS) was applied to adherent human myotubes. Cellular contents of ATP, phosphocreatine (PCr) and lactate were determined. Glucose and oleic acid metabolism were studied using radio-labeled substrates, and gene expression was analyzed using real-time RT-PCR. Mitochondrial content and function were measured by live imaging and determination of citrate synthase activity, respectively. Protein expression was assessed by electrophoresis and immunoblotting.
Results
High-frequency, acute EPS increased deoxyglucose uptake and lactate production, while cell contents of both ATP and PCr decreased. Chronic, low-frequency EPS increased oxidative capacity of cultured myotubes by increasing glucose metabolism (uptake and oxidation) and complete fatty acid oxidation. mRNA expression level of pyruvate dehydrogenase complex 4 (PDK4) was significantly increased in EPS-treated cells, while mRNA expressions of interleukin 6 (IL-6), cytochrome C and carnitin palmitoyl transferase b (CPT1b) also tended to increase. Intensity of MitoTracker®Red FM was doubled after 48 h of chronic, low-frequency EPS. Protein expression of a slow fiber type marker (MHCI) was increased in EPS-treated cells.
Conclusions
Our results imply that in vitro EPS (acute, high-frequent as well as chronic, low-frequent) of human myotubes may be used to study effects of exercise.This work was funded by the University of Oslo, Oslo University College, the Norwegian Diabetes Foundation, the Freia Chocolade Fabriks Medical Foundation and the Anders Jahre’s Foundation. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript
A Novel, Low-Volume Method for Organ Culture of Embryonic Kidneys That Allows Development of Cortico-Medullary Anatomical Organization
Here, we present a novel method for culturing kidneys in low volumes of medium that offers more organotypic development compared to conventional methods. Organ culture is a powerful technique for studying renal development. It recapitulates many aspects of early development very well, but the established techniques have some disadvantages: in particular, they require relatively large volumes (1–3 mls) of culture medium, which can make high-throughput screens expensive, they require porous (filter) substrates which are difficult to modify chemically, and the organs produced do not achieve good cortico-medullary zonation. Here, we present a technique of growing kidney rudiments in very low volumes of medium–around 85 microliters–using silicone chambers. In this system, kidneys grow directly on glass, grow larger than in conventional culture and develop a clear anatomical cortico-medullary zonation with extended loops of Henle
Renal tubular Sirt1 attenuates diabetic albuminuria by epigenetically suppressing Claudin-1 overexpression in podocytes
Sirtuin 1 (Sirt1), a NAD[superscript +]-regulated deacetylase with numerous known positive effects on cellular and whole-body metabolism, is expressed in the renal cortex and medulla. It is known to have protective effects against age-related disease, including diabetes. Here we investigated the protective role of Sirt1 in diabetic renal damage. We found that Sirt1 in proximal tubules (PTs) was downregulated before albuminuria occurred in streptozotocin-induced or obese (db/db) diabetic mice. PT-specific SIRT1 transgenic and Sirt1 knockout mice showed prevention and aggravation of the glomerular changes that occur in diabetes, respectively, and nondiabetic knockout mice exhibited albuminuria, suggesting that Sirt1 in PTs affects glomerular function. Downregulation of Sirt1 and upregulation of the tight junction protein Claudin-1 by SIRT1-mediated epigenetic regulation in podocytes contributed to albuminuria. We did not observe these phenomena in 5/6 nephrectomized mice. We also demonstrated retrograde interplay from PTs to glomeruli using nicotinamide mononucleotide (NMN) from conditioned medium, measurement of the autofluorescence of photoactivatable NMN and injection of fluorescence-labeled NMN. In human subjects with diabetes, the levels of SIRT1 and Claudin-1 were correlated with proteinuria levels. These results suggest that Sirt1 in PTs protects against albuminuria in diabetes by maintaining NMN concentrations around glomeruli, thus influencing podocyte function.Japan. Ministry of Education, Culture, Sports, Science and Technology (Grant 22790800
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