Water at interfaces - some recent experimental results from surface spectroscopy

Journal ArticleFundamental aspects of interfacial phenomena in aqueous systems are determined by the properties of interfacial water It has become evident that interfacial water must be characterized spectroscopically in order to explain the recently identified non DLVO forces observed by atomic force microscopy and with the surface force apparatus. In the past little information was available regarding the spectroscopic characteristics of interfacial water due to the difficulty in differentiating between bulk and interfacial water. However, with the advent of FTIR and Raman internal reflection spectroscopy (IRS) and the recent non-linear optical technique, sum frequency generation (SFG), more information on interfacial water is now available as is evident from the results of recent spectroscopic studies. Thus the non DLVO forces eventually may be explained by the extent of hydrogen bonding as revealed by surface spectroscopic techniques

Characterization of interfacial water at hydrophilic and hydrophobic surfaces by in situ FTIR/internal reflection spectroscopy

Journal ArticleIn-situ FTIR/internal reflection spectroscopy (FTIR/IRS) has been used to spectroscopically characterize interfacial water near hydrophilic (silicon single crystal) and hydrophobic (polymer-coated germanium single crystal) surfaces. Interfacial water was examined spectroscopically over certain distances from the surface by appropriate design of the geometry and optics of the internal reflection system. The in-situ FTIR/IRS spectra were characterized by consideration of the OH stretching region (3000-3800 cm"1) associated with the vibrational spectra of the interfacial water. Preliminary spectral results indicate the prevalence of an ice-like structure at the hydrophilic silicon surface, whereas at the hydrophobic surface the ice like structure is not so prevalent and there appears to be a significant decrease in hydrogen bonding

Effectively Transparent Front Contacts for Optoelectronic Devices

Effectively transparent front contacts for optoelectronic devices achieve a measured transparency of up to 99.9% and a measured sheet resistance of 4.8 Ω sq^(−1). The 3D microscale triangular cross-section grid fingers redirect incoming photons efficiently to the active semiconductor area and can replace standard grid fingers as well as transparent conductive oxide layers in optoelectronic devices

Shocks in supersonic sand

We measure time-averaged velocity, density, and temperature fields for steady granular flow past a wedge and calculate a speed of granular pressure disturbances (sound speed) equal to 10% of the flow speed. The flow is supersonic, forming shocks nearly identical to those in a supersonic gas. Molecular dynamics simulations of Newton's laws and Monte Carlo simulations of the Boltzmann equation yield fields in quantitative agreement with experiment. A numerical solution of Navier-Stokes-like equations agrees with a molecular dynamics simulation for experimental conditions excluding wall friction.Comment: 4 pages, 5 figure

Effectively Transparent Front Contacts for Optoelectronic Devices

Effectively transparent front contacts for optoelectronic devices achieve a measured transparency of up to 99.9% and a measured sheet resistance of 4.8 Ω sq^(−1). The 3D microscale triangular cross-section grid fingers redirect incoming photons efficiently to the active semiconductor area and can replace standard grid fingers as well as transparent conductive oxide layers in optoelectronic devices

Enterovirus 71 3C Protease Cleaves a Novel Target CstF-64 and Inhibits Cellular Polyadenylation

Identification of novel cellular proteins as substrates to viral proteases would provide a new insight into the mechanism of cell–virus interplay. Eight nuclear proteins as potential targets for enterovirus 71 (EV71) 3C protease (3Cpro) cleavages were identified by 2D electrophoresis and MALDI-TOF analysis. Of these proteins, CstF-64, which is a critical factor for 3′ pre-mRNA processing in a cell nucleus, was selected for further study. A time-course study to monitor the expression levels of CstF-64 in EV71-infected cells also revealed that the reduction of CstF-64 during virus infection was correlated with the production of viral 3Cpro. CstF-64 was cleaved in vitro by 3Cpro but neither by mutant 3Cpro (in which the catalytic site was inactivated) nor by another EV71 protease 2Apro. Serial mutagenesis was performed in CstF-64, revealing that the 3Cpro cleavage sites are located at position 251 in the N-terminal P/G-rich domain and at multiple positions close to the C-terminus of CstF-64 (around position 500). An accumulation of unprocessed pre-mRNA and the depression of mature mRNA were observed in EV71-infected cells. An in vitro assay revealed the inhibition of the 3′-end pre-mRNA processing and polyadenylation in 3Cpro-treated nuclear extract, and this impairment was rescued by adding purified recombinant CstF-64 protein. In summing up the above results, we suggest that 3Cpro cleavage inactivates CstF-64 and impairs the host cell polyadenylation in vitro, as well as in virus-infected cells. This finding is, to our knowledge, the first to demonstrate that a picornavirus protein affects the polyadenylation of host mRNA

C-Terminal Region of EBNA-2 Determines the Superior Transforming Ability of Type 1 Epstein-Barr Virus by Enhanced Gene Regulation of LMP-1 and CXCR7

Type 1 Epstein-Barr virus (EBV) strains immortalize B lymphocytes in vitro much more efficiently than type 2 EBV, a difference previously mapped to the EBNA-2 locus. Here we demonstrate that the greater transforming activity of type 1 EBV correlates with a stronger and more rapid induction of the viral oncogene LMP-1 and the cell gene CXCR7 (which are both required for proliferation of EBV-LCLs) during infection of primary B cells with recombinant viruses. Surprisingly, although the major sequence differences between type 1 and type 2 EBNA-2 lie in N-terminal parts of the protein, the superior ability of type 1 EBNA-2 to induce proliferation of EBV-infected lymphoblasts is mostly determined by the C-terminus of EBNA-2. Substitution of the C-terminus of type 1 EBNA-2 into the type 2 protein is sufficient to confer a type 1 growth phenotype and type 1 expression levels of LMP-1 and CXCR7 in an EREB2.5 cell growth assay. Within this region, the RG, CR7 and TAD domains are the minimum type 1 sequences required. Sequencing the C-terminus of EBNA-2 from additional EBV isolates showed high sequence identity within type 1 isolates or within type 2 isolates, indicating that the functional differences mapped are typical of EBV type sequences. The results indicate that the C-terminus of EBNA-2 accounts for the greater ability of type 1 EBV to promote B cell proliferation, through mechanisms that include higher induction of genes (LMP-1 and CXCR7) required for proliferation and survival of EBV-LCLs

Cigarette smoke induces β2-integrin-dependent neutrophil migration across human endothelium

<p>Abstract</p> <p>Background</p> <p>Cigarette smoking induces peripheral inflammatory responses in all smokers and is the major risk factor for neutrophilic lung disease such as chronic obstructive pulmonary disease. The aim of this study was to investigate the effect of cigarette smoke on neutrophil migration and on β₂-integrin activation and function in neutrophilic transmigration through endothelium.</p> <p>Methods and results</p> <p>Utilizing freshly isolated human PMNs, the effect of cigarette smoke on migration and β₂-integrin activation and function in neutrophilic transmigration was studied. In this report, we demonstrated that cigarette smoke extract (CSE) dose dependently induced migration of neutrophils <it>in vitro</it>. Moreover, CSE promoted neutrophil adherence to fibrinogen. Using functional blocking antibodies against CD11b and CD18, it was demonstrated that Mac-1 (CD11b/CD18) is responsible for the cigarette smoke-induced firm adhesion of neutrophils to fibrinogen. Furthermore, neutrophils transmigrated through endothelium by cigarette smoke due to the activation of β₂-integrins, since pre-incubation of neutrophils with functional blocking antibodies against CD11b and CD18 attenuated this transmigration.</p> <p>Conclusion</p> <p>This is the first study to describe that cigarette smoke extract induces a direct migratory effect on neutrophils and that CSE is an activator of β₂-integrins on the cell surface. Blocking this activation of β₂-integrins might be an important target in cigarette smoke induced neutrophilic diseases.</p