http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
DENSE GAS IN MOLECULAR CORES ASSOCIATED WITH<i>PLANCK</i>GALACTIC COLD CLUMPS
Yuan (袁敬华,), Jinghua,Wu, Yuefang,Liu, Tie,Zhang, Tianwei,Li, Jin Zeng,Liu, Hong-Li,Meng, Fanyi,Chen, Ping,Hu, Runjie,Wang, Ke American Astronomical Society 2016 The Astrophysical journal Vol.820 No.1
<P>We present the first survey of dense gas toward Planck Galactic Cold Clumps (PGCCs). Observations in the J = 1-0 transitions of HCO+ and HCN toward 621 molecular cores associated with PGCCs were performed using the Purple Mountain Observatory's 13.7 m telescope. Among them, 250 sources were detected, including 230 cores detected in HCO+. and 158 in HCN. Spectra of the J = 1-0 transitions from (CO)-C-12, (CO)-C-13, and (CO)-O-18 at the centers of the 250 cores were extracted from previous mapping observations to construct a multi-line data set. The significantly low detection rate of asymmetric double-peaked profiles, together with the good consistency among central velocities of CO, HCO+, and HCN spectra, suggests that the CO-selected Planck cores are more quiescent than classical star-forming regions. The small difference between line widths of (CO)-O-18. and HCN indicates that the inner regions of CO-selected Planck cores are no more turbulent than the exterior. The velocity-integrated intensities and abundances of HCO+ are positively correlated with those of HCN, suggesting that these two species are well coupled and chemically connected. The detected abundances of both HCO+ and HCN are significantly lower than values in other low- to high-mass star-forming regions. The low abundances may be due to beam dilution. On the basis of an inspection of the parameters given in the PGCC catalog, we suggest that there may be about 1000 PGCC objects that have a sufficient reservoir of dense gas to form stars.</P>
Kim, Jung‐,Hyun,Kurtz, Andreas,Yuan, Bao‐,Zhu,Zeng, Fanyi,Lomax, Geoff,Loring, Jeanne F.,Crook, Jeremy,Ju, Ji Hyeon,Clarke, Laura,Inamdar, Maneesha S.,Pera, Martin,Firpo, Meri T.,Sheldon, John Wiley and Sons Inc. 2017 Stem cells translational medicine Vol.6 No.11
<P><B>Abstract</B></P><P>This article summarizes the recent activity of the International Stem Cell Banking Initiative (ISCBI) held at the California Institute for Regenerative Medicine (CIRM) in California (June 26, 2016) and the Korean National Institutes for Health in Korea (October 19–20, 2016). Through the workshops, ISCBI is endeavoring to support a new paradigm for human medicine using pluripotent stem cells (hPSC) for cell therapies. Priority considerations for ISCBI include ensuring the safety and efficacy of a final cell therapy product and quality assured source materials, such as stem cells and primary donor cells. To these ends, ISCBI aims to promote global harmonization on quality and safety control of stem cells for research and the development of starting materials for cell therapies, with regular workshops involving hPSC banking centers, biologists, and regulatory bodies. Here, we provide a brief overview of two such recent activities, with summaries of key issues raised. S<SMALL>TEM</SMALL> C<SMALL>ELLS</SMALL> T<SMALL>RANSLATIONAL</SMALL> M<SMALL>EDICINE</SMALL><I>2017;6:1956–1962</I></P>
Jingbin Yan,Yanna Liu,Yuehua Zhang,Zhaorui Ren,Fanyi Zeng 한국분자세포생물학회 2023 Molecules and cells Vol.46 No.4
Down syndrome (DS) is the most common autosomal aneuploidy caused by trisomy of chromosome 21. Previous studies demonstrated that DS affected mitochondrial functions, which may be associated with the abnormal development of the nervous system in patients with DS. Runt-related transcription factor 1 (RUNX1) is an encoding gene located on chromosome 21. It has been reported that RUNX1 may affect cell apoptosis via the mitochondrial pathway. The present study investigated whether RUNX1 plays a critical role in mitochondrial dysfunction in DS and explored the mechanism by which RUNX1 affects mitochondrial functions. Expression of RUNX1 was detected in induced pluripotent stem cells of patients with DS (DS-iPSCs) and normal iPSCs (N-iPSCs), and the mitochondrial functions were investigated in the current study. Subsequently, RUNX1 was overexpressed in N-iPSCs and inhibited in DS-iPSCs. The mitochondrial functions were investigated thoroughly, including reactive oxygen species levels, mitochondrial membrane potential, ATP content, and lysosomal activity. Finally, RNA-sequencing was used to explore the global expression pattern. It was observed that the expression levels of RUNX1 in DS-iPSCs were significantly higher than those in normal controls. Impaired mitochondrial functions were observed in DS-iPSCs. Of note, overexpression of RUNX1 in N-iPSCs resulted in mitochondrial dysfunction, while inhibition of RUNX1 expression could improve the mitochondrial function in DS-iPSCs. Global gene expression analysis indicated that overexpression of RUNX1 may promote the induction of apoptosis in DS-iPSCs by activating the PI3K/Akt signaling pathway. The present findings indicate that abnormal expression of RUNX1 may play a critical role in mitochondrial dysfunction in DS-iPSCs.