Near-infrared and Mid-infrared Spectroscopy with the Infrared Camera (IRC) for AKARI

The Infrared Camera (IRC) is one of the two instruments on board the AKARI satellite. In addition to deep imaging from 1.8-26.5um for the pointed observation mode of the AKARI, it has a spectroscopic capability in its spectral range. By replacing the imaging filters by transmission-type dispersers on the filter wheels, it provides low-resolution (lambda/d_lambda ~ 20-120) spectroscopy with slits or in a wide imaging field-of-view (approximately 10'X10'). The IRC spectroscopic mode is unique in space infrared missions in that it has the capability to perform sensitive wide-field spectroscopic surveys in the near- and mid-infrared wavelength ranges. This paper describes specifications of the IRC spectrograph and its in-orbit performance.Comment: 13 pages, 7 figures, accepted for publication on PAS

Low- and Medium-Dispersion Spectropolarimetry of Nova V475 Sct (Nova Scuti 2003): Discovery of an Asymmetric High-Velocity Wind in a Moderately Fast Nova

We present low-resolution ($R\sim 90$) and medium-resolution ($R\sim 2500$) spectropolarimetry of Nova V475 Sct with the HBS instrument, mounted on the 0.91-m telescope at the Okayama Astrophysical Observatory, and with FOCAS, mounted on the 8.2-m Subaru telescope. We estimated the interstellar polarization toward the nova from the steady continuum polarization components and H$\alpha$ line emission components. After subtracting the interstellar polarization component from the observations, we found that the H$\alpha$ emission seen on 2003 October 7 was clearly polarized. In the polarized flux spectrum, the H$\alpha$ emission had a distinct red wing extending to $\sim +4900$ km s$^{-1}$ and a shoulder around $+3500$ km s$^{-1}$, showing a constant position angle of linear polarization \theta_{\rm *}\simeq 155\arcdeg\pm 15\arcdeg. This suggests that the nova had an asymmetric outflow with a velocity of $v_{\rm wind}\simeq 3500$ km s$^{-1}$ or more, which is six times higher than the expansion velocity of the ionized shell at the same epoch. Such a high-velocity component has not previously been reported for a nova in the `moderately fast' speed class. Our observations suggest the occurrence of violent mass-loss activity in the nova binary system even during the common-envelope phase. The position angle of the polarization in the H$\alpha$ wing is in good agreement with that of the continuum polarization found on 2003 September 26 ($p_{\rm *}\simeq 0.4$--0.6 %), which disappeared within the following 2 d. The uniformity of the PA between the continuum polarization and the wing polarization on October 7 suggests that the axis of the circumstellar asymmetry remained nearly constant during the period of our observations.Comment: 27 pages, 7 figures, accepted for publication in A

XRCC4 deficiency in human subjects causes a marked neurological phenotype but no overt immunodeficiency

Background Nonhomologous end-joining (NHEJ) is the major DNA double-strand break (DSB) repair mechanism in human cells. The final rejoining step requires DNA ligase IV (LIG4) together with the partner proteins X-ray repair cross-complementing protein 4 (XRCC4) and XRCC4-like factor. Patients with mutations in genes encoding LIG4, XRCC4-like factor, or the other NHEJ proteins DNA-dependent protein kinase catalytic subunit and Artemis are DSB repair defective and immunodeficient because of the requirement for NHEJ during V(D)J recombination. Objective We found a patient displaying microcephaly and progressive ataxia but a normal immune response. We sought to determine pathogenic mutations and to describe the molecular pathogenesis of the patient. Methods We performed next-generation exome sequencing. We evaluated the DSB repair activities and V(D)J recombination capacity of the patient's cells, as well as performing a standard blood immunologic characterization. Results We identified causal mutations in the XRCC4 gene. The patient's cells are radiosensitive and display the most severe DSB repair defect we have encountered using patient-derived cell lines. In marked contrast, a V(D)J recombination plasmid assay revealed that the patient's cells did not display the junction abnormalities that are characteristic of other NHEJ-defective cell lines. The mutant protein can interact efficiently with LIG4 and functions normally in in vitro assays and when transiently expressed in vivo. However, the mutation makes the protein unstable, and it undergoes proteasome-mediated degradation. Conclusion Our findings reveal a novel separation of impact phenotype: there is a pronounced DSB repair defect and marked clinical neurological manifestation but no clinical immunodeficiency

Wnt inhibitors Dkk1 and Sost are downstream targets of BMP signaling through the type IA receptor (BMPRIA) in osteoblasts

The bone morphogenetic protein (BMP) and Wnt signaling pathways both contribute essential roles in regulating bone mass. However, the molecular interactions between these pathways in osteoblasts are poorly understood. We recently reported that osteoblast-targeted conditional knockout (cKO) of BMP receptor type IA (BMPRIA) resulted in increased bone mass during embryonic development, where diminished expression of Sost as a downstream effector of BMPRIA resulted in increased Wnt/Β-catenin signaling. Here, we report that Bmpr1a cKO mice exhibit increased bone mass during weanling stages, again with evidence of enhanced Wnt/Β-catenin signaling as assessed by Wnt reporter TOPGAL mice and TOPFLASH luciferase. Consistent with negative regulation of the Wnt pathway by BMPRIA signaling, treatment of osteoblasts with dorsomorphin, an inhibitor of Smad-dependent BMP signaling, enhanced Wnt signaling. In addition to Sost , Wnt inhibitor Dkk1 also was downregulated in cKO bone. Expression levels of Dkk1 and Sost were upregulated by BMP2 treatment and downregulated by Noggin. Moreover, expression of a constitutively active Bmpr1a transgene in mice resulted in the upregulation of both Dkk1 and Sost and partially rescued the Bmpr1a cKO bone phenotype. These effectors are differentially regulated by mitogen-activated protein kinase (MAPK) p38 because pretreatment of osteoblasts with SB202190 blocked BMP2-induced Dkk1 expression but not Sost . These results demonstrate that BMPRIA in osteoblasts negatively regulates endogenous bone mass and Wnt/Β-catenin signaling and that this regulation may be mediated by the activities of Sost and Dkk1 . This study highlights several interactions between BMP and Wnt signaling cascades in osteoblasts that may be amenable to therapeutic intervention for the modification of bone mass density. © 2010 American Society for Bone and Mineral ResearchPeer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/65056/1/90806_ftp.pd

Separation of Sympathomimetic Amines of Abuse and Related Compounds by Micellar Electrokinetic Chromatography

Separation of twelve sympathomimetic amines and related compounds by micellar electrokinetic chromatography (MEKC) with UV absorbance detection is described. These amines were well separated within 25 min using 50 mM sodium tetraborate solution containing 15 mM sodium dodecylsulfate (SDS) of pH 9.3 as a running solution and detected at 210 nm. MEKC was performed with an applied voltage of 13 kV at 25 °C using a fused-silica capillary (50 cm×75 mm i.d.) with effective length of 37.5 cm. The detection limits of these compounds were in the range from 4 to 97 fmol/injection at a signal-to-noise ratio (S/N) of 3. The reproducibility of the method expressed as relative standard deviation (RSD) for within-day (n=6) and between-day (n=5) assays was less than 4.8 and 8.8%, respectively. The proposed method could be applied to the determination of an anorectic drug, phentermine, in Chinese tea with a detection limit of 99 μg/g (105 fmol/injection, S/N=3)

A Mini-Review of Reactive Oxygen Species in Urological Cancer: Correlation with NADPH Oxidases, Angiogenesis, and Apoptosis

Oxidative stress refers to elevated reactive oxygen species (ROS) levels, and NADPH oxidases (NOXs), which are one of the most important sources of ROS. Oxidative stress plays important roles in the etiologies, pathological mechanisms, and treatment strategies of vascular diseases. Additionally, oxidative stress affects mechanisms of carcinogenesis, tumor growth, and prognosis in malignancies. Nearly all solid tumors show stimulation of neo-vascularity, termed angiogenesis, which is closely associated with malignant aggressiveness. Thus, cancers can be seen as a type of vascular disease. Oxidative stress-induced functions are regulated by complex endogenous mechanisms and exogenous factors, such as medication and diet. Although understanding these regulatory mechanisms is important for improving the prognosis of urothelial cancer, it is not sufficient, because there are controversial and conflicting opinions. Therefore, we believe that this knowledge is essential to discuss observations and treatment strategies in urothelial cancer. In this review, we describe the relationships between members of the NOX family and tumorigenesis, tumor growth, and pathological mechanisms in urological cancers including prostate cancer, renal cell carcinoma, and urothelial cancer. In addition, we introduce natural compounds and chemical agents that are associated with ROS-induced angiogenesis or apoptosis