Renormalization group improved pQCD prediction for Υ(1S)\Upsilon(1S) leptonic decay

The complete next-to-next-to-next-to-leading order short-distance and bound-state QCD corrections to $\Upsilon(1S)$ leptonic decay rate $\Gamma(\Upsilon(1S)\to \ell^+\ell^-)$ has been finished by Beneke {\it et al.} \cite{Beneke:2014qea}. Based on those improvements, we present a renormalization group (RG) improved pQCD prediction for $\Gamma(\Upsilon(1S)\to \ell^+\ell^-)$ by applying the principle of maximum conformality (PMC). The PMC is based on RG-invariance and is designed to solve the pQCD renormalization scheme and scale ambiguities. After applying the PMC, all known-type of $\beta$-terms at all orders, which are controlled by the RG-equation, are resummed to determine optimal renormalization scale for its strong running coupling at each order. We then achieve a more convergent pQCD series, a scheme- independent and more accurate pQCD prediction for $\Upsilon(1S)$ leptonic decay, i.e. $\Gamma_{\Upsilon(1S) \to e^+ e^-}|_{\rm PMC} = 1.270^{+0.137}_{-0.187}$ keV, where the uncertainty is the squared average of the mentioned pQCD errors. This RG-improved pQCD prediction agrees with the experimental measurement within errors.Comment: 11 pages, 4 figures. Numerical results and discussions improved, references updated, to be published in JHE

Reconsideration of Second Harmonic Generation from neat Air/Water Interface: Broken of Kleinman Symmetry from Dipolar Contribution

It has been generally accepted that there are significant quadrupolar and bulk contributions to the second harmonic generation (SHG) reflected from the neat air/water interface, as well as common liquid interfaces. Because there has been no general methodology to determine the quadrupolar and bulk contributions to the SHG signal from a liquid interface, this conclusion was reached based on the following two experimental phenomena. Namely, the broken of the macroscopic Kleinman symmetry, and the significant temperature dependence of the SHG signal from the neat air/water interface. However, because sum frequency generation vibrational spectroscopy (SFG-VS) measurement of the neat air/water interface observed no apparent temperature dependence, the temperature dependence in the SHG measurement has been reexamined and proven to be an experimental artifact. Here we present a complete microscopic analysis of the susceptibility tensors of the air/water interface, and show that dipolar contribution alone can be used to address the issue of broken of the macroscopic Kleinman symmetry at the neat air/water interface. Using this analysis, the orientation of the water molecules at the interface can be obtained, and it is consistent with the measurement from SFG-VS. Therefore, the key rationales to conclude significantly quadrupolar and bulk contributions to the SHG signal of the neat air/water interface can no longer be considered as valid as before. This new understanding of the air/water interface can shed light on our understanding of the nonlinear optical responses from other molecular interfaces as well

Participation of Tom1L1 in EGF-stimulated endocytosis of EGF receptor

Although many proteins have been shown to participate in ligand-stimulated endocytosis of EGF receptor (EGFR), the adaptor protein responsible for interaction of activated EGFR with endocytic machinery remains elusive. We show here that EGF stimulates transient tyrosine phosphorylation of Tom1L1 by the Src family kinases, resulting in transient interaction of Tom1L1 with the activated EGFR bridged by Grb2 and Shc. Cytosolic Tom1L1 is recruited onto the plasma membrane and subsequently redistributes into the early endosome. Mutant forms of Tom1L1 defective in Tyr-phosphorylation or interaction with Grb2 are incapable of interaction with EGFR. These mutants behave as dominant-negative mutants to inhibit endocytosis of EGFR. RNAi-mediated knockdown of Tom1L1 inhibits endocytosis of EGFR. The C-terminal tail of Tom1L1 contains a novel clathrin-interacting motif responsible for interaction with the C-terminal region of clathrin heavy chain, which is important for exogenous Tom1L1 to rescue endocytosis of EGFR in Tom1L1 knocked-down cells. These results suggest that EGF triggers a transient Grb2/Shc-mediated association of EGFR with Tyr-phosphorylated Tom1L1 to engage the endocytic machinery for endocytosis of the ligand–receptor complex

Treatment of Linear and Nonlinear Dielectric Property of Molecular Monolayer and Submonolayer with Microscopic Dipole Lattice Model: I. Second Harmonic Generation and Sum-Frequency Generation

In the currently accepted models of the nonlinear optics, the nonlinear radiation was treated as the result of an infinitesimally thin polarization sheet layer, and a three layer model was generally employed. The direct consequence of this approach is that an apriori dielectric constant, which still does not have a clear definition, has to be assigned to this polarization layer. Because the Second Harmonic Generation (SHG) and the Sum-Frequency Generation vibrational Spectroscopy (SFG-VS) have been proven as the sensitive probes for interfaces with the submonolayer coverage, the treatment based on the more realistic discrete induced dipole model needs to be developed. Here we show that following the molecular optics theory approach the SHG, as well as the SFG-VS, radiation from the monolayer or submonolayer at an interface can be rigorously treated as the radiation from an induced dipole lattice at the interface. In this approach, the introduction of the polarization sheet is no longer necessary. Therefore, the ambiguity of the unaccounted dielectric constant of the polarization layer is no longer an issue. Moreover, the anisotropic two dimensional microscopic local field factors can be explicitly expressed with the linear polarizability tensors of the interfacial molecules. Based on the planewise dipole sum rule in the molecular monolayer, crucial experimental tests of this microscopic treatment with SHG and SFG-VS are discussed. Many puzzles in the literature of surface SHG and SFG spectroscopy studies can also be understood or resolved in this framework. This new treatment may provide a solid basis for the quantitative analysis in the surface SHG and SFG studies.Comment: 23 pages, 3 figure

Prevention of in-stent restenosis with endothelial progenitor cell (EPC) capture stent placement combined with regional EPC transplantation: An atherosclerotic rabbit model

Background: Even with drug-eluting stents, the risk of in-stent restenosis (ISR) remains high. The goal of this study was to investigate the use of an endothelial progenitor cell (EPC) capture stent plus regional EPC transplantation to reduce the ISR rate. Methods: Endothelial progenitor cell capture stents were fabricated using fibrin gel and anti-CD34 plus anti-VEGFR-2 dual antibodies. Twenty male New Zealand white rabbits established as an atherosclerotic model were randomly divided into two groups: group 1 (n = 10), in which EPC capture stents were deployed into the right iliac artery; and group 2 (n = 10), in which sirolimus-eluting stents were placed. In both groups, EPCs were transplanted into target vessels beyond the stents, with outflow blocked. Radiologic-pathologic correlation outcomes were reviewed after 2 months.  Results: The technical success rate of EPC capture stent placement plus EPC transplantation was 100%. The ISR rate in group 1 was lower than in group 2 (1/10 vs. 4/10; p > 0.05). Minimal luminal diameters were larger in group 1 than in group 2 (computed tomographic angiography, 1.85 ± 0.15 mm vs. 1.50 ± 0.20 mm; duplex ultrasound, 1.90 ± 0.10 mm vs. 1.70 ± 0.30 mm; p > 0.05). Transplanted EPCs were tracked positively only in group 1. Pathologic analysis demonstrated neointimal hyperplasia thickness of 0.21 ± 0.09 mm in group 1 vs. 0.11 ± 0.07 mm in group 2 (p < 0.05).  Conclusion: Endothelial progenitor cell capture stent placement plus local EPC transplant decreases the ISR rate through thrombosis reduction rather than through neointimal hyperplasia inhibition

Mouse hepatocyte overexpression of NF‐κB‐inducing kinase (NIK) triggers fatal macrophage‐dependent liver injury and fibrosis

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/109646/1/hep27348-sup-0001-suppinfo01.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/109646/2/hep27348.pd