Ring Gap Structure around Class I Protostar WL 17

WL 17 is a Class I object and was considered to have a ring-hole structure. We analyzed the structure around WL 17 to investigate the detailed properties of WL 17. We used ALMA archival data, which have a higher angular resolution than previous observations. We investigated the WL 17 system with the 1.3 mm dust continuum and 12CO and C18O (J = 2-1) line emissions. The dust continuum emission showed a clear ring structure with inner and outer edges of ~11 and ~21 au, respectively. In addition, we detected an inner disk of < 5 au radius enclosing the central star within the ring, the first observation of this structure. Thus, WL 17 has a ring-gap structure, not a ring-hole structure. We did not detect any marked emission in either the gap or inner disk, indicating that there is no sign of a planet, circumplanetary disk, or binary companion. We identified the base of both blue-shifted and red-shifted outflows based on the 12CO emission, which is clearly associated with the disk around WL 17. The outflow mass ejection rate is ~3.6x10^-7 Msun yr-1 and the dynamical timescale is as short as ~ 10^4 yr. The C18O emission showed that an inhomogeneous infalling envelope, which can induce episodic mass accretion, is distributed in the region within ~1000 au from the central protostar. With these new findings, we can constrain the planet formation and dust growth scenarios in the accretion phase of star formation.Comment: 22 pages, 9 figures, Accepted for publication in the Astrophysical Journa

In Vivo Analysis of Extracellular Proteins in Rat Brains with a Newly Developed Intracerebral Microdialysis Probe

Peptides and proteins in the extracellular space in the central nervous system were investigated in vivo using an intracerebral microdialysis probe. The molecular cut-off of the hollow fiber which was used for the probe was approximately 100 kDa. We examined recovery rates of several compounds in vitro. The recovery rates of proteins and peptides were between 7-28%, with the exceptions of substance P and insulin-like growth factor I. The recovery rates of monoamines and their metabolites were 22-40%. In in vivo studies, two major proteins with apparent molecular weights of 62 kDa and 12 kDa, and several minor proteins (28 kDa, 43 kDa, 52 kDa and 70 kDa) were detected by SDS-polyacrylamide gel electrophoresis in the dialysate from a probe implanted in the striatum of anesthetized rats. These results suggest that the newly developed, intracerebral microdialysis probe might be useful for investigating the dynamic changes of peptides and proteins in the central nervous system.</p

The Role of the p38 MAPK Signaling Pathway in High Glucose-Induced Epithelial-Mesenchymal Transition of Cultured Human Renal Tubular Epithelial Cells

Epithelial-mesenchymal transition of tubular epithelial cells, which is characterized by a loss of epithelial cell characteristics and a gain of ECM-producing myofibroblast characteristics, is an essential mechanism that is involved in tubulointerstitial fibrosis, an important component of the renal injury that is associated with diabetic nephropathy. Under diabetic conditions, p38 MAPK activation has been reported in glomeruli and mesangial cells; however, studies on p38 MAPK in TECs are lacking. In this study, the role of p38 MAPK in AP-1 activation and in the EMT in the human proximal tubular epithelial cell line (HK-2) under high glucose concentration conditions is investigated.A vector for small interfering RNA that targets p38 MAPK was constructed; the cells were then either transfected with p38 siRNA or pretreated with a chemical inhibitor of AP-1 and incubated with low glucose plus TGF-β1 or high glucose for 48 h. Cells that were not transfected or pretreated and were exposed to low glucose with or without TGF-β1 or high glucose for 48 h were considered to be the controls. We found that high glucose induced an increase in TGF-β1. And high glucose-induced p38 MAPK activation was inhibited by p38 siRNA (P<0.05). A significant decline in E-cadherin and CK expression and a notable increase in vimentin and α-SMA were detected when exposed to low glucose with TGF-β1 or high glucose, and a significant raise of secreted fibronectin were detected when exposed to high glucose; whereas these changes were reversed when the cells were treated with p38 siRNA or AP-1 inhibitor (P<0.05). AP-1 activity levels and Snail expression were up-regulated under high glucose conditions but were markedly down-regulated through knockdown of p38 MAPK with p38 siRNA or pretreatment with AP-1 inhibitor (P<0.05).This study suggests that p38 MAPK may play an important role in the high glucose-induced EMT by activating AP-1 in tubular epithelial cells