Inspection of Refinery Vessels for Hydrogen Attack Using Ultrasonic Techniques

Hydrogen attack is a damage mechanism occurring in steels exposed to high pressure hydrogen at elevated temperatures. Under such conditions, hydrogen atoms diffuse into steels and react with carbides. The reaction leads to formation of methane and, subsequently, intergranular fissuring and losses of material strength and toughness

Gap modification of atomically thin boron nitride by phonon mediated interactions

A theory is presented for the modification of bandgaps in atomically thin boron nitride (BN) by attractive interactions mediated through phonons in a polarizable substrate, or in the BN plane. Gap equations are solved, and gap enhancements are found to range up to 70% for dimensionless electron-phonon coupling \lambda=1, indicating that a proportion of the measured BN bandgap may have a phonon origin

Investigation of USP30 inhibition to enhance Parkin-mediated mitophagy: tools and approaches

Mitochondrial dysfunction is implicated in Parkinson disease (PD). Mutations in Parkin, an E3 ubiquitin ligase, can cause juvenile-onset Parkinsonism probably through impairment of mitophagy. Inhibition of the de-ubiquitinating enzyme USP30 may counter this effect to enhance mitophagy. Using different tools and cellular approaches, we wanted to independently confirm this claimed role for USP30. Pharmacological characterization of additional tool compounds that selectively inhibit USP30 are reported. The consequence of USP30 inhibition by these compounds, siRNA knockdown and overexpression of dominant-negative USP30 in the mitophagy pathway in different disease-relevant cellular models was explored. Knockdown and inhibition of USP30 showed increased p-Ser65-ubiquitin levels and mitophagy in neuronal cell models. Furthermore, patient-derived fibroblasts carrying pathogenic mutations in Parkin showed reduced p-Ser65-ubiquitin levels compared to wild-type cells, levels that could be restored using either USP30 inhibitor or dominant-negative USP30 expression. Our data provide additional support for USP30 inhibition as a regulator of the mitophagy pathway

Exceptionally large migration length of carbon and topographically-facilitated self-limiting molecular beam epitaxial growth of graphene on hexagonal boron nitride

This is the author accepted manuscript. The final version is available from the publisher via the DOI in this record.Available online 18 December 2016We demonstrate growth of single-layer graphene (SLG) on hexagonal boron nitride (h-BN) by molecular beam epitaxy (MBE), only limited in area by the finite size of the h-BN flakes. Using atomic force microscopy and micro-Raman spectroscopy, we show that for growth over a wide range of temperatures (500◦C – 1000◦C) the deposited carbon atoms spill off the edge of the h-BN flakes. We attribute this spillage to the very high mobility of the carbon atoms on the BN basal plane, consistent with van der Waals MBE. The h-BN flakes vary in size from 30 µm to 100 µm, thus demonstrating that the migration length of carbon atoms on h-BN is greater than 100 µm. When sufficient carbon is supplied to compensate for this loss, which is largely due to this fast migration of the carbon atoms to and off the edges of the h-BN flake, we find that the best growth temperature for MBE SLG on h-BN is ∼950◦C. Self-limiting graphene growth appears to be facilitated by topographic h-BN surface features: We have thereby grown MBE self-limited SLG on an h-BN ridge. This opens up future avenues for precisely tailored fabrication of nano- and hetero-structures on pre-patterned h-BN surfaces for device applications.This work is supported by ONR (N000140610138 and Graphene MURI), AFOSR (FA9550-11-1-0010), EFRC Center for Re-Defining Photovoltaic Efficiency through Molecule Scale Control (award DE-SC0001085), NSF (CHE-0641523), NYSTAR and Spanish Government (AIC-B-2011-0806, MAT2014-54231, MAT2015-67021-R). S.W. and A.P. were supported by the US Department of Energy Office of Science, Division of Materials Science and Engineering (award DE-SC0010695)

Differentiation of Glioma and Radiation Injury in Rats Using In Vitro Produce Magnetically Labeled Cytotoxic T-Cells and MRI

A limitation with current imaging strategies of recurrent glioma undergoing radiotherapy is that tumor and radiation injury cannot be differentiated with post contrast CT or MRI, or with PET or other more complex parametric analyses of MRI data. We propose to address the imaging limitation building on emerging evidence indicating that effective therapy for recurrent glioma can be attained by sensitized T-cells following vaccination of primed dendritic cells (DCs). The purpose of this study was to determine whether cord blood T-cells can be sensitized against glioma cells (U-251) and if these sensitized cytotoxic T-cells (CTLs) can be used as cellular magnetic resonance imaging probes to identify and differentiate glioma from radiation necrosis in rodent models.Cord blood T and CD14+ cells were collected. Isolated CD14+ cells were then converted to dendritic cells (DCs), primed with glioma cell lysate and used to sensitize T-cells. Phenotypical expression of the generated DCs were analyzed to determine the expression level of CD14, CD86, CD83 and HLA-DR. Cells positive for CD25, CD4, CD8 were determined in generated CTLs. Specificity of cytotoxicity of the generated CTLs was also determined by lactate dehydrogenase (LDH) release assay. Secondary proliferation capacity of magnetically labeled and unlabeled CTLs was also determined. Generated CTLs were magnetically labeled and intravenously injected into glioma bearing animals that underwent MRI on days 3 and 7 post- injection. CTLs were also administered to animals with focal radiation injury to determine whether these CTLs accumulated non-specifically to the injury sites. Multi-echo T2- and T2*-weighted images were acquired and R2 and R2* maps created. Our method produced functional, sensitized CTLs that specifically induced U251 cell death in vitro. Both labeled and unlabeled CTLs proliferated equally after the secondary stimulation. There were significantly higher CD25 positive cells (p = <0.006) in CTLs. In addition, T2- and T2*-weighted MR images showed increased low signal intensity areas in animals that received labeled CTLs as compared to the images from animals that received control cells. Histological analysis confirmed the presence of iron positive cells in sites corresponding to MRI low signal intensity regions. Significant differences (p = <0.001) in tumor R2 and R2* values were observed among the groups of animals. Animals with radiation injury exhibited neither MRI hypointense areas nor presence of iron positive cells.Our results indicate that T-cells can be effectively sensitized by in vitro methods and used as cellular probes to identify and differentiate glioma from radiation necrosis

Mild forms of hypophosphatasia mostly result from dominant negative effect of severe alleles or from compound heterozygosity for severe and moderate alleles

<p>Abstract</p> <p>Background</p> <p>Mild hypophosphatasia (HPP) phenotype may result from <it>ALPL </it>gene mutations exhibiting residual alkaline phosphatase activity or from severe heterozygous mutations exhibiting a dominant negative effect. In order to determine the cause of our failure to detect a second mutation by sequencing in patients with mild HPP and carrying on a single heterozygous mutation, we tested the possible dominant effect of 35 mutations carried by these patients.</p> <p>Methods</p> <p>We tested the mutations by site-directed mutagenesis. We also genotyped 8 exonic and intronic <it>ALPL </it>gene polymorphisms in the patients and in a control group in order to detect the possible existence of a recurrent intronic mild mutation.</p> <p>Results</p> <p>We found that most of the tested mutations exhibit a dominant negative effect that may account for the mild HPP phenotype, and that for at least some of the patients, a second mutation in linkage disequilibrium with a particular haplotype could not be ruled out.</p> <p>Conclusion</p> <p>Mild HPP results in part from compound heterozygosity for severe and moderate mutations, but also in a large part from heterozygous mutations with a dominant negative effect.</p

The limited usefulness of real-time 3-dimensional echocardiography in obtaining normal reference ranges for right ventricular volumes

<p>Abstract</p> <p>Background</p> <p>To obtain normal reference ranges and intraobserver variability for right ventricular (RV) volume indexes (VI) and ejection fraction (EF) from apical recordings with real-time 3-dimensional echocardiography (RT3DE), and similarly for RV area indexes (AI) and area fraction (AF) with 2-dimensional echocardiography (2DE).</p> <p>Methods</p> <p>166 participants; 79 males and 87 females aged between 29–79 years and considered free from clinical and subclinical cardiovascular disease. Normal ranges are defined as 95% reference values and reproducibility as coefficients of variation (CV) for repeated measurements.</p> <p>Results</p> <p>None of the apical recordings with RT3DE and 2DE included the RV outflow tract. Upper reference values were 62 ml/m²for RV end-diastolic (ED) VI and 24 ml/m²for RV end-systolic (ES) VI. Lower normal reference value for RVEF was 41%. The respective reference ranges were 17 cm²/m²for RVEDAI, 11 cm²/m²for RVESAI and 27% for RVAF. Males had higher upper normal values for RVEDVI, RVESVI and RVEDAI, and a lower limit than females for RVEF and RVAF. Weak but significant negative correlations between age and RV dimensions were found with RT3DE, but not with 2DE. CVs for repeated measurements ranged between 10% and 14% with RT3DE and from 5% to 14% with 2DE.</p> <p>Conclusion</p> <p>Although the normal ranges for RVVIs and RVAIs presented in this study reflect RV inflow tract dimensions only, the data presented may still be regarded as a useful tool in clinical practice, especially for RVEF and RVAF.</p