Electrochemical preparation of free-standing carbon-nanotube/Sn composite paper

Toward achieving Li-ion batteries with high energy density, SWCNT/Sn composite paper was electrochemically prepared and the addition effect of formaldehyde (HCHO) and polyethylene glycol (PEG) on Sn electrodeposition morphology was studied. PEG improved the wettability of electroplating bath to enable inhomogeneous Sn embeddedness inside SWCNT paper, and HCHO delivered more nuclear growth. The synergetic effect resulted in a composite paper in which Sn particles with several-hundred nanometer order were distributed. Compared with a commercially-available Cu foil (18 mu m-thickness) with 32 mg at 2 cm(2) (phi 16 mm), the weight of the SWCNT paper (5 mg) is one sixth of that of the Cu foil. The dramatic reduction of the component greatly contributes to the increase in energy density of batteries. (c) 2018 Elsevier B.V. All rights reserved.ArticleMATERIALS LETTERS.220:182-185(2018)journal articl

Impact of Native Coronary Artery Calcification on Lesion Outcome Following Drug-Coated Balloon Angioplasty for Treatment of In-Stent Restenosis

This study aimed to clarify whether native coronary artery（CA） calcification before index percutaneous coronary intervention（PCI） has an impact on the effectiveness of drug-coated balloon（DCB） angioplasty for the treatment of in-stent restenosis（ISR）. 100consecutive patients with 166ISR lesions underwent quantitative coronary angiography（QCA） before and after index PCI and before and after DCB angioplasty for ISR. CA calcification before index PCI was assessed by angiography and results were analyzed to reveal the predictive values for target lesion revascularization（TLR） and major adverse cardiac events（MACE）. During 1.03±1.03years of follow-up, TLR occurred in 44lesions（26.5%） and MACE in 33 patients（33%）. On multivariate analysis, CA calcification before index PCI（p=0.016）, and % diameter of stenosis（%DS）≥73%（p=0.023） and minimal lumen diameter（MLD）<0.65mm（p=0.001） before DCB angioplasty were independent predictors for TLR after DCB angioplasty. MACE was also associated with CA calcification before index PCI（p=0.01）, and %DS≥73%（p=0.001） and MLD<0.65mm（p=0.01） before DCB angioplasty, but only %DS≥73% before DCB angioplasty was an independent predictor for MACE after DCB angioplasty（p=0.039）. The combination of CA calcification before index PCI and these QCA factors before DCB angioplasty was an independent and more powerful predictor for MACE than the QCA factors alone（p<0.001）. Thereafter, the combination of CA calcification and %DS≥73% before DCB angioplasty stratified the risk of MACE after DCB angioplasty（p<0.05）. CA calcification before index PCI, as well as anatomical information at ISR, have an impact on outcome after DCB angioplasty for ISR

Evi1 is essential for hematopoietic stem cell self-renewal, and its expression marks hematopoietic cells with long-term multilineage repopulating activity

A new mouse in which an IRES-GFP cassette is knocked-in to the Evi1 locus reveals that HSC long-term multilineage repopulating activity specifically segregates with expression of the Evi1 transcription factor

Unique proximal tubular cell injury and the development of acute kidney injury in adult patients with minimal change nephrotic syndrome

Abstract Background Adult patients with minimal change nephrotic syndrome (MCNS) are often associated with acute kidney injury (AKI). To assess the mechanisms of AKI, we examined whether tubular cell injuries unique to MCNS patients exist. Methods We performed a retrospective analysis of clinical data and tubular cell changes using the immunohistochemical expression of vimentin as a marker of tubular injury and dedifferentiation at kidney biopsy in 37 adult MCNS patients. AKI was defined by the criteria of the Kidney Disease: Improving Global Outcomes (KDIGO) Clinical Practice Guidelines for AKI. Results Thirteen patients (35.1%) were designated with AKI at kidney biopsy. No significant differences in age, history of hypertension, chronic kidney disease, diuretics use, proteinuria, and serum albumin were noted between the AKI and non-AKI groups. Urinary N-acetyl-β-D-glucosaminidase (uNAG) and urinary alpha1-microglobulin (uA1MG) as markers of tubular injury were increased in both groups, but the levels were significantly increased in the AKI group compared with the non-AKI group. The incidence of vimentin-positive tubules was comparable between AKI (84.6%) and non-AKI (58.3%) groups, but vimentin-positive tubular area per interstitial area was significantly increased in the AKI group (19.8%) compared with the non-AKI group (6.8%) (p = 0.011). Vimentin-positive injured tubules with tubular simplification (loss of brush-border of the proximal tubule/dilated tubule with flattening of tubular epithelium) were observed in the vicinity of glomeruli in both groups, suggesting that the proximal convoluted tubules were specifically injured. Two patients exhibited relatively severe tubular injuries with vimentin positivity and required dialysis within 2 weeks after kidney biopsy. The percentage of the vimentin-positive tubular area was positively correlated with uNAG but not with uA1MG in the non-AKI group. Conclusions Proximal tubular injuries with increased uNAG exist in MCNS patients without renal dysfunction and were more severe in the AKI group than they were in the non-AKI group. The unique tubular injuries probably due to massive proteinuria might be a predisposing factor for the development of severe AKI in adult MCNS patients

ADAM8 Is an Antigen of Tyrosine Kinase Inhibitor-Resistant Chronic Myeloid Leukemia Cells Identified by Patient-Derived Induced Pluripotent Stem Cells

Summary: Properties of cancer stem cells involved in drug resistance and relapse have significant effects on clinical outcome. Although tyrosine kinase inhibitors (TKIs) have dramatically improved survival of patients with chronic myeloid leukemia (CML), TKIs have not fully cured CML due to TKI-resistant CML stem cells. Moreover, relapse after discontinuation of TKIs has not been predicted in CML patients with the best TKI response. In our study, a model of CML stem cells derived from CML induced pluripotent stem cells identified ADAM8 as an antigen of TKI-resistant CML cells. The inhibition of expression or metalloproteinase activity of ADAM8 restored TKI sensitivity in primary samples. In addition, residual CML cells in patients with optimal TKI response were concentrated in the ADAM8+ population. Our study demonstrates that ADAM8 is a marker of residual CML cells even in patients with optimal TKI response and would be a predictor of relapse and a therapeutic target of TKI-resistant CML cells. : The paucity and heterogeneity of CML stem cells are obstacles for analyses. In our study, a model of CML stem cells derived from CML-iPSCs identified ADAM8 as an antigen of TKI-resistant cells. In CML patients, ADAM8+ cells showed TKI resistance and residual CML cells after TKIs-treatment were concentrated in ADAM8+ population, suggesting that ADAM8 is a marker of TKI-resistant CML cells. Keywords: chronic myeloid leukemia, disease specific iPSCs, TKI-resistant CML stem cell