Searching for a Companion Star of Tycho's Type Ia Supernova with Optical Spectroscopic Observations

We report our first results of photometric and spectroscopic observations for Tycho's supernova remnant (SNR Tycho) to search for the companion star of a type Ia supernova (SN Ia). From photometric observations using Suprime-Cam on the Subaru Telescope, we have picked up stars brighter than 22 mag (in $V$-band) for spectroscopy, which are located within a circular region with the radius of 30" around the center of SNR Tycho. If the ejecta of young supernova remnants, such as SNR Tycho, have a sufficient amount of Fe I, we should be able to detect absorption lines at 3720 \AA and 3860 \AA associated with transitions from the ground state of Fe I in the spectrum of the companion star. To identify the companion star of a SN Ia using these characteristic absorption lines of Fe I, we made optical low-resolution spectroscopy of their targets using FOCAS on the Subaru Telescope. In our spectroscopic observations, we obtained spectra of 17 stars in the SNR Tycho region and compare them with template stellar spectra. We detect significant absorption lines from two stars at 3720 \AA. Since widths of their absorption lines are broad, it is likely that the detected absorptions are due to Fe I in the expanding ejecta of SNR Tycho. However, none of stars exhibits a clear red wing in the observed profiles of the absorption, though a star in the background of the SNR should show it. Hence, we suggest another interpretation that the detected absorption lines might be caused by the peculiarity of stars. A star named Tycho(E) has the absorption line at 3720 \AA and its projected position is close to the center of SNR Tycho. Based on our observations, Tycho(E) is a new candidate as the companion star of Tycho's supernova.Comment: 17 pages, 28 figures, accepted for publication in PAS

The Stellar Abundances for Galactic Archaeology (SAGA) Database II - Implications for Mixing and Nucleosynthesis in Extremely Metal-Poor Stars and Chemical Enrichment of the Galaxy

We discuss the characteristics of known extremely metal-poor (EMP) stars in the Galaxy using the Stellar Abundances for Galactic Archaeology (SAGA) database (Suda et al. 2008, PASJ, 60, 1159).The analyses of carbon-enhanced stars in our sample suggest that the nucleosynthesis in AGB stars can contribute to the carbon enrichment in a different way depending on whether the metallicity is above or below [Fe/H] ~ -2.5, which is consistent with the current models of stellar evolution at low metallicity. We find the transition of the initial mass function at [Fe/H] ~ -2 in the viewpoint of the distribution of carbon abundance and the frequency of carbon-enhanced stars. For observed EMP stars, we confirmed that some, not all, of observed stars might have undergone at least two types of extra mixing to change their surface abundances. One is to deplete the lithium abundance during the early phase of red giant branch. Another is to decrease the C/N ratio by one order of magnitude during the red giant branch phase. Observed small scatters of abundances for alpha-elements and iron-group elements suggest that the chemical enrichment of our Galaxy takes place in a well-mixed interstellar medium. We find that the abundance trends of alpha-elements are highly correlated with each other, while the abundances of iron-group elements are subject to different slopes relative to the iron abundance. This implies that the supernova yields of alpha-elements are almost independent of mass and metallicity, while those of iron-group elements have a metallicity dependence or mass dependence with the variable initial mass function.The occurrence of the hot bottom burning in the mass range of 5 <~ M / Msun <~ 6 is consistent with the initial mass function of the Galaxy peaked at ~ 10 - 12 Msun to be compatible with the statistics of carbon enhanced stars with and without s-process element (truncated)Comment: 35 pages, 27 figures, 6 tables, accepted by MNRAS, database to reproduce figures is available at http://saga.sci.hokudai.ac.j

The Origin of Carbon-Enhancement and Initial Mass Function of Extremely Metal-Poor Stars in the Galactic Halo

It is known that the carbon-enhanced, extremely metal-poor (CEMP) stars constitute a substantial proportion in the extremely metal-poor (EMP) stars of the Galactic Halo, by far larger than CH stars in Population II stars. We investigate their origin with taking into account an additional evolutionary path to the surface carbon-enrichment, triggered by hydrogen engulfment by the helium flash convection, in EMP stars of $[Fe/H] \lesssim -2.5$. This process is distinct from the third dredge-up operating in more metal-rich stars and also in EMP stars. In binary systems of EMP stars, the secondary stars become CEMP stars through mass transfer from the primary stars of low and intermediate masses, which have developed the surface carbon-enhancement. Our binary scenario can predict the variations in the abundances not only for carbon but also for nitrogen and s-process elements and reasonably explain the observed properties such as the stellar distributions with respect to the carbon abundances, the binary periods, and the evolutionary stages. Furthermore, from the observed frequencies of CEMP stars with and without s-process element enhancement, we demonstrate that the initial mass function of EMP stars need to give the mean mass ~10\msun under the reasonable assumptions on the distributions of orbital separations and mass ratio of binary components. This also indicates that the currently observed EMP stars were exclusively born as the secondary members of binaries, making up $\sim 10$ remnants of EMP binary systems of mass ~10^8\msun in total; in addition to CEMP stars with white dwarf companions, a significant fraction of them have experienced supernova explosions of their companions. We discuss the implications of the present results in relation to the formation of Galactic halo.Comment: 66 pages, 12 figures, 2 tables Accepted for publication in Ap

Ablation of TSC2 Enhances Insulin Secretion by Increasing the Number of Mitochondria through Activation of mTORC1

) mice. The present study examines the effects of TSC2 ablation on insulin secretion from pancreatic beta cells. mice and TSC2 knockdown insulin 1 (INS-1) insulinoma cells treated with small interfering ribonucleic acid were used to investigate insulin secretion, ATP content and the expression of mitochondrial genes. mice exhibit hyperinsulinemia due to an increase in the number of mitochondria as well as enlargement of individual beta cells via activation of mTORC1.Activation of mTORC1 by TSC2 ablation increases mitochondrial biogenesis and enhances insulin secretion from pancreatic beta cells

A case of pituitary metastasis discovered when diabetes insipidus developed in a patient 20 years after breast cancer treatment

The patient was a 52-year-old woman. She had a history of left breast cancer at age 32 years, with no recurrences. She was examined for a feeling of oral dryness and nocturia, and central diabetes insipidus was diagnosed. A mass was seen in the posterior pituitary on magnetic resonance imaging, and multiple pulmonary nodules were seen on computed tomography. Breast cancer metastases were diagnosed in both tissues. Since this patient had no cancer other than the breast cancer treated 20 years earlier, it was difficult to reach a diagnosis of pituitary metastasis with pituitary gland imaging alone. In estrogen receptor-positive breast cancer, there may be recurrences after a long period of time. It may be that recommending a full body examination could be useful in the differential diagnosis of metastasis even in patients who have had a long disease-free period, if they had undergone surgery for breast cancer

Biphasic Response of Pancreatic β-Cell Mass to Ablation of Tuberous Sclerosis Complex 2 in Mice▿

Recent studies have demonstrated the importance of insulin or insulin-like growth factor 1 (IGF-1) for regulation of pancreatic β-cell mass. Given the role of tuberous sclerosis complex 2 (TSC2) as an upstream molecule of mTOR (mammalian target of rapamycin), we examined the effect of TSC2 deficiency on β-cell function. Here, we show that mice deficient in TSC2, specifically in pancreatic β cells (βTSC2−/− mice), manifest increased IGF-1-dependent phosphorylation of p70 S6 kinase and 4E-BP1 in islets as well as an initial increased islet mass attributable in large part to increases in the sizes of individual β cells. These mice also exhibit hypoglycemia and hyperinsulinemia at young ages (4 to 28 weeks). After 40 weeks of age, however, the βTSC2−/− mice develop progressive hyperglycemia and hypoinsulinemia accompanied by a reduction in islet mass due predominantly to a decrease in the number of β cells. These results thus indicate that TSC2 regulates pancreatic β-cell mass in a biphasic manner

Ablation of C/EBPβ alleviates ER stress and pancreatic β cell failure through the GRP78 chaperone in mice

Pancreatic β cell failure is thought to underlie the progression from glucose intolerance to overt diabetes, and ER stress is implicated in such β cell dysfunction. We have now shown that the transcription factor CCAAT/enhancer-binding protein β (C/EBPβ) accumulated in the islets of diabetic animal models as a result of ER stress before the onset of hyperglycemia. Transgenic overexpression of C/EBPβ specifically in β cells of mice reduced β cell mass and lowered plasma insulin levels, resulting in the development of diabetes. Conversely, genetic ablation of C/EBPβ in the β cells of mouse models of diabetes, including Akita mice, which harbor a heterozygous mutation in Ins2 (Ins2WT/C96Y), and leptin receptor–deficient (Lepr–/–) mice, resulted in an increase in β cell mass and ameliorated hyperglycemia. The accumulation of C/EBPβ in pancreatic β cells reduced the abundance of the molecular chaperone glucose-regulated protein of 78 kDa (GRP78) as a result of suppression of the transactivation activity of the transcription factor ATF6α, thereby increasing the vulnerability of these cells to excess ER stress. Our results thus indicate that the accumulation of C/EBPβ in pancreatic β cells contributes to β cell failure in mice by enhancing susceptibility to ER stress