Controlled Deposition of Tin Oxide and Silver Nanoparticles Using Microcontact Printing

This report describes extensive studies of deposition processes involving tin oxide (SnOx) nanoparticles on smooth glass surfaces. We demonstrate the use of smooth films of these nanoparticles as a platform for spatially-selective electroless deposition of silver by soft lithographic stamping. The edge and height roughness of the depositing metallic films are 100 nm and 20 nm, respectively, controlled by the intrinsic size of the nanoparticles. Mixtures of alcohols as capping agents provide further control over the size and shape of nanoparticles clusters. The distribution of cluster heights obtained by atomic force microscopy (AFM) is modeled through a modified heterogeneous nucleation theory as well as Oswald ripening. The thermodynamic modeling of the wetting properties of nanoparticles aggregates provides insight into their mechanism of formation and how their properties might be further exploited in wide-ranging applications

Facile Pyrolytic Synthesis of Silicon Nanowires

One-dimensional nanostructures such as silicon nanowires (SiNW) are attractive candidates for low power density electronic and optoelectronic devices including sensors. A new simple method for SiNW bulk synthesis[1, 2] is demonstrated in this work, which is inexpensive and uses low toxicity materials, thereby offering a safe, energy efficient and green approach. The method uses low flammability liquid phenylsilanes, offering a safer avenue for SiNW growth compared with using silane gas. A novel, duo-chamber glass vessel is used to create a low-pressure environment where SiNWs are grown through vapor-liquid-solid mechanism using gold nanoparticles as a catalyst. The catalyst decomposes silicon precursor vapors of diphenylsilane and triphenylsilane and precipitates single crystal SiNWs, which appear to grow parallel to the substrate surface. This opens up possibilities for synthesizing nano-junctions amongst wires which is important for the grid architecture of nanoelectronics proposed by Likharev[3]. Even bulk synthesis of SiNW is feasible using sacrificial substrates such as CaCO(3) that can be dissolved post-synthesis. Furthermore, by dissolving appropriate dopants in liquid diphenylsilane, a controlled doping of the nanowires is realized without the use of toxic gases and expensive mass flow controllers. Upon boron doping, we observe a characteristic red shift in photoluminescence spectra. In summary, an inexpensive and versatile method for SiNW is presented that makes these exotic materials available to any lab at low cost

Do Clawback Adoptions Influence Capital Investments?

We present evidence that clawback provision adoptions influence capital investment mix via managerial compensation incentives. Specifically, we find for a propensity-matched sample of 931 voluntary clawback adoptions that capital investments shift away from R&D and toward capital expenditures, and for firms with enabling liquidity toward acquisitions, consistent with clawback effects on earnings-linked compensation. Corroborating evidence confirms that these effects are positively related to performance-based pay, growth opportunities, and invariant to risk-toleration incentives, with firms adopting clawbacks also exhibiting capital over-investment. This evidence is timely given a pending SEC rule that would mandate clawbacks for all firms listing on US exchanges.postprin

APE1 Promotes Pancreatic Cancer Proliferation through GFRα1/Src/ERK Axis-Cascade Signaling in Response to GDNF

Pancreatic cancer is the worst exocrine gastrointestinal cancer leading to the highest mortality. Recent studies reported that aberrant expression of apurinic/apyrimidinic endodeoxyribonuclease 1 (APE1) is involved in uncontrolled cell growth. However, the molecular mechanism of APE1 biological role remains unrevealed in pancreatic cancer progression. Here, we demonstrate that APE1 accelerates pancreatic cancer cell proliferation through glial cell line-derived neurotrophic factor (GDNF)/glial factor receptor α1 (GFRα1)/Src/ERK axis-cascade signaling. The proliferation of endogenous APE1 expressed-MIA PaCa-2, a human pancreatic carcinoma cell line, was increased by treatment with GDNF, a ligand of GFRα1. Either of downregulated APE1 or GFRα1 expression using small interference RNA (siRNA) inhibited GDNF-induced cancer cell proliferation. The MEK-1 inhibitor PD98059 decreased GDNF-induced MIA PaCa-2 cell proliferation. Src inactivation by either its siRNA or Src inhibitor decreased ERK-phosphorylation in response to GDNF in MIA PaCa-2 cells. Overexpression of GFRα1 in APE1-deficient MIA PaCa-2 cells activated the phosphorylation of Src and ERK. The expression of both APE1 and GFRα1 was gradually increased as progressing pancreatic cancer grades. Our results highlight a critical role for APE1 in GDNF-induced pancreatic cancer cell proliferation through APE1/GFRα1/Src/ERK axis-cascade signaling and provide evidence for future potential therapeutic drug targets for the treatment of pancreatic cancer

Comparing the DNA Hypermethylome with Gene Mutations in Human Colorectal Cancer

We have developed a transcriptome-wide approach to identify genes affected by promoter CpG island DNA hypermethylation and transcriptional silencing in colorectal cancer. By screening cell lines and validating tumor-specific hypermethylation in a panel of primary human colorectal cancer samples, we estimate that nearly 5% or more of all known genes may be promoter methylated in an individual tumor. When directly compared to gene mutations, we find larger numbers of genes hypermethylated in individual tumors, and a higher frequency of hypermethylation within individual genes harboring either genetic or epigenetic changes. Thus, to enumerate the full spectrum of alterations in the human cancer genome, and to facilitate the most efficacious grouping of tumors to identify cancer biomarkers and tailor therapeutic approaches, both genetic and epigenetic screens should be undertaken

Severe acute respiratory syndrome coronavirus protein 7a interacts with hSGT

Severe acute respiratory syndrome coronavirus (SARS-CoV) 7a is an accessory protein with no known homologues. In this study, we report the interaction of a SARS-CoV 7a and small glutamine-rich tetratricopeptide repeat-containing protein (SGT). SARS-CoV 7a and human SGT interaction was identified using a two-hybrid system screen and confirmed with interaction screens in cell culture and cellular co-localization studies. The SGT domain of interaction was mapped by deletion mutant analysis and results indicated that tetratricopeptide repeat 2 (aa 125-158) was essential for interaction. We also showed that 7a interacted with SARS-CoV structural proteins M (membrane) and E (envelope), which have been shown to be essential for virus-like particle formation. Taken together, our results coupled with data from studies of the interaction between SGT and HIV-1 vpu indicated that SGT could be involved in the life-cycle, possibly assembly of SARS-CoV.IS

Minor Physical Anomalies in Patients with Schizophrenia, Unaffected First-Degree Relatives, and Healthy Controls: A Meta-Analysis

Background: Minor physical anomalies (MPAs) have been found to be more prevalent in schizophrenia than control participants in numerous studies and may index a potential endophenotype for schizophrenia.</p

NADPH Oxidase Limits Innate Immune Responses in the Lungs in Mice

Background: Chronic granulomatous disease (CGD), an inherited disorder of the NADPH oxidase in which phagocytes are defective in generating superoxide anion and downstream reactive oxidant intermediates (ROIs), is characterized by recurrent bacterial and fungal infections and by excessive inflammation (e.g., inflammatory bowel disease). The mechanisms by which NADPH oxidase regulates inflammation are not well understood. Methodology/Principal Findings: We found that NADPH oxidase restrains inflammation by modulating redox-sensitive innate immune pathways. When challenged with either intratracheal zymosan or LPS, NADPH oxidase-deficient p47phox-/- mice and gp91phox-deficient mice developed exaggerated and progressive lung inflammation, augmented NF-kB activation, and elevated downstream pro-inflammatory cytokines (TNF-α, IL-17, and G-CSF) compared to wildtype mice. Replacement of functional NADPH oxidase in bone marrow-derived cells restored the normal lung inflammatory response. Studies in vivo and in isolated macrophages demonstrated that in the absence of functional NADPH oxidase, zymosan failed to activate Nrf2, a key redox-sensitive anti-inflammatory regulator. The triterpenoid, CDDO-Im, activated Nrf2 independently of NADPH oxidase and reduced zymosan-induced lung inflammation in CGD mice. Consistent with these findings, zymosan-treated peripheral blood mononuclear cells from X-linked CGD patients showed impaired Nrf2 activity and increased NF-kB activation. Conclusions/Significance: These studies support a model in which NADPH oxidase-dependent, redox-mediated signaling is critical for termination of lung inflammation and suggest new potential therapeutic targets for CGD