Effect of water vapor on the spallation of thermal barrier coating systems during laboratory cyclic oxidation testing.

The effect of water and water vapor on the lifetime of Ni-based superalloy samples coated with a typical thermal barrier coating system—b-(Ni,Pt)Al bond coat and yttria stabilized zirconia (YSZ) top coat deposited by electron beam physical vapor deposition (EB-PVD) was studied. Samples were thermally cycled to 1,150 C and subjected to a water-drop test in order to elucidate the effect of water vapor on thermal barrier coating (TBC) spallation. It was shown that the addition of water promotes spallation of TBC samples after a given number of cycles at 1,150 C. This threshold was found to be equal to 170 cycles for the present system. Systems based on b-NiAl bond coat or on Pt-rich c/c0 bond coat were also sensitive to the water-drop test. Moreover, it was shown that water vapor in ambient air after minutes or hours at room temperature, promotes also TBC spallation once the critical number of cycles has been reached. This desktop spalling (DTS) can be prevented by locking up the cycled samples in a dry atmosphere box. These results for TBC systems confirm and document Smialek’s theory about DTS and moisture induced delayed spalling (MIDS) being the same phenomenon. Finally, the mechanisms implying hydrogen embrittlement or surface tension modifications are discussed

CpG Islands: Starting Blocks for Replication and Transcription

International audienc

Charged-Lepton Flavour Physics

This writeup of a talk at the 2011 Lepton-Photon symposium in Mumbai, India, summarises recent results in the charged-lepton flavour sector. I review searches for charged-lepton flavour violation, lepton electric dipole moments and flavour-conserving CP violation. I also discuss recent progress in tau-lepton physics and in the Standard Model prediction of the muon anomalous magnetic moment.Comment: Presented at Lepton-Photon 2011, Mumbai, India; 23 pages, 14 figure

Proposal for new experimental schemes to realize the Avogadro constant

We propose two experimental schemes to determine and so to realize the Avogadro constant $N\_{A}$ at the level of 10$^{-7}$ or better with a watt balance experiment and a cold atom experiment measuring $h/m(X)$ (where $h$ is the Planck constant and $m(X)$ the mass of the atom $X$). We give some prospects about achievable uncertainties and we discuss the opportunity to test the existence of possible unknown correction factors for the Josephson effect and quantum Hall effect

Testing new physics with the electron g-2

We argue that the anomalous magnetic moment of the electron (a_e) can be used to probe new physics. We show that the present bound on new-physics contributions to a_e is 8*10^-13, but the sensitivity can be improved by about an order of magnitude with new measurements of a_e and more refined determinations of alpha in atomic-physics experiments. Tests on new-physics effects in a_e can play a crucial role in the interpretation of the observed discrepancy in the anomalous magnetic moment of the muon (a_mu). In a large class of models, new contributions to magnetic moments scale with the square of lepton masses and thus the anomaly in a_mu suggests a new-physics effect in a_e of (0.7 +- 0.2)*10^-13. We also present examples of new-physics theories in which this scaling is violated and larger effects in a_e are expected. In such models the value of a_e is correlated with specific predictions for processes with violation of lepton number or lepton universality, and with the electric dipole moment of the electron.Comment: 34 pages, 7 figures. Minor changes and references adde

Risk of Myocardial Infarction in Parents of HIV-infected Individuals: a population-based Cohort Study

<p>Abstract</p> <p>Background</p> <p>Previous studies have indicated an increased risk of myocardial infarction (MI) in HIV infected individuals especially after start of highly active antiretroviral therapy (HAART). It is however controversial whether the increased risk of atherosclerotic disease is exclusively associated with the HIV disease and HAART or whether life-style related or genetic factors also increase the risk in this population. To establish whether the increased risk of myocardial infarction in HIV patients partly reflects an increased risk of MI in their families, we estimated the relative risk of MI in parents of HIV-infected individuals.</p> <p>Methods</p> <p>From the Danish HIV Cohort Study and the Danish Civil Registration System we identified the parents of all HIV-infected patients born in Denmark after 1952 in whom a Danish born mother was identifiable. For each HIV patient, 4 matched population controls and their parents were identified. Cumulative incidence functions were constructed to illustrate time to first MI of the parents as registered in the Danish National Hospital Registry. Incidence rate ratios (IRR) were estimated by Cox's regression analyses. Due to the confidential type of the analysed data the study was approved by the Danish Data Protection Agency.</p> <p>Results</p> <p>2,269 mothers and 2,022 fathers of HIV patients as well as 9,076 mothers and 8,460 fathers of control subjects were identified. We observed an increased risk of MI in mothers of HIV patients (adjusted IRR, 1.31; 95% CI: 1.08-1.60). The strongest association was seen in case the offspring was infected heterosexually (adjusted IRR, 1.59; 95% CI: 1.07-2.35) or by IV drug abuse (IVD) (adjusted IRR, 1.63; 95% CI: 1.02-2.60). In fathers of HIV patients the risk of MI was only increased if the offspring was infected by IVD (adjusted IRR, 1.42; 95% CI: 1.01-2.00).</p> <p>Conclusion</p> <p>Mothers of HIV-infected patients have an increased risk of MI. We presume that this stems from family related life style risk factors, some of which may also influence the risk of MI in HIV-infected patients.</p

Surplus Photosynthetic Antennae Complexes Underlie Diagnostics of Iron Limitation in a Cyanobacterium

Chlorophyll fluorescence from phytoplankton provides a tool to assess iron limitation in the oceans, but the physiological mechanism underlying the fluorescence response is not understood. We examined fluorescence properties of the model cyanobacterium Synechocystis PCC6803 and a ΔisiA knock-out mutant of the same species grown under three culture conditions which simulate nutrient conditions found in the open ocean: (1) nitrate and iron replete, (2) limiting-iron and high-nitrate, representative of natural high-nitrate, low-chlorophyll regions, and (3) iron and nitrogen co-limiting. We show that low variable fluorescence, a key diagnostic of iron limitation, results from synthesis of antennae complexes far in excess of what can be accommodated by the iron-restricted pool of photosynthetic reaction centers. Under iron and nitrogen co-limiting conditions, there are no excess antennae complexes and variable fluorescence is high. These results help to explain the well-established fluorescence characteristics of phytoplankton in high-nutrient, low-chlorophyll ocean regions, while also accounting for the lack of these properties in low-iron, low-nitrogen regions. Importantly, our results complete the link between unique molecular consequences of iron stress in phytoplankton and global detection of iron stress in natural populations from space

Role of leukocyte cell-derived chemotaxin 2 as a biomarker in hepatocellular carcinoma

We sought to identify a secreted biomarker for β-catenin activation commonly seen in hepatocellular carcinoma (HCC). By examination of our previously published genearray of hepatocyte-specific β-catenin knockout (KO) livers, we identified secreted factors whose expression may be β-catenin-dependent. We verified expression and secretion of the leading factor in HCC cells transfected with mutated (Hep3BS33Y)-β- catenin. Serum levels of biomarker were next investigated in a mouse model of HCC with β-catenin gene (Ctnnb1) mutations and eventually in HCC patients. Leukocyte cell-derived chemotaxin-2 (LECT2) expression was decreased in KO livers. Hep3BS33Y expressed and secreted more LECT2 in media as compared to Hep3BWT. Mice developing HCC with Ctnnb1 mutations showed significantly higher serum LECT2 levels. However patients with CTNNB1 mutations showed LECT2 levels of 54.28±22.32 ng/mL (Mean ± SD; n = 8) that were insignificantly different from patients with non-neoplastic chronic liver disease (32.8±21.1 ng/mL; n = 15) or healthy volunteers (33.2±7.2 ng/mL; n = 11). Intriguingly, patients without β-catenin mutations showed significantly higher serum LECT2 levels (54.26 ± 22.25 ng/mL; n = 46). While β-catenin activation was evident in a subset of non-mutant β-catenin HCC group with high LECT2 expression, serum LECT2 was unequivocally similar between β-catenin-active and -normal group. Further analysis showed that LECT2 levels greater than 50 ng/ml diagnosed HCC in patients irrespective of β-catenin mutations with specificity of 96.1% and positive predictive value of 97.0%. Thus, LECT2 is regulated by β-catenin in HCC in both mice and men, but serum LECT2 reflects β-catenin activity only in mice. Serum LECT2 could be a potential biomarker of HCC in patients. © 2014 Okabe et al

Family History of Alcoholism and Childhood Adversity: Joint Effects on Alcohol Consumption and Dependence

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/65494/1/j.1530-0277.1994.tb00085.x.pd

The 5-HTTLPR polymorphism of the serotonin transporter gene and short term behavioral response to methylphenidate in children with ADHD

<p>Abstract</p> <p>Background</p> <p>Animal models of ADHD suggest that the paradoxical calming effect of methylphenidate on motor activity could be mediated through its action on serotonin transmission. In this study, we have investigated the relationship between the 5-HTTLPR polymorphism in the serotonin transporter gene (<it>SLC6A4</it>) and the response of ADHD relevant behaviors with methylphenidate treatment.</p> <p>Methods</p> <p>Patients between ages 6-12 (n = 157) were assessed with regard to their behavioral response to methylphenidate (0.5 mg/kg/day) using a 2-week prospective within-subject, placebo-controlled (crossover) trial. The children were then genotyped with regard to the triallelic 5-HTTLPR polymorphism in the <it>SLC6A4 </it>gene. Main outcome measure: Conners' Global Index for parents (CGI-Parents) and teachers (CGI-Teachers) at baseline and at the end of each week of treatment with placebo and methylphenidate. For both outcome measurements, we used a mixed model analysis of variance to determine gene, treatment and gene × treatment interaction effects.</p> <p>Results</p> <p>Mixed model analysis of variance revealed a gene × treatment interaction for CGI-Parents but not for CGI-Teachers. Children homozygous for the lower expressing alleles (<it>s+l_G= s'</it>) responded well to placebo and did not derive additional improvement with methylphenidate compared to children carrying a higher expressing allele (<it>l_A</it>). No genotype main effects on either CGI-Parents or CGI-teachers were observed.</p> <p>Conclusions</p> <p>A double blind placebo-controlled design was used to assess the behavioral effects of methylphenidate in relation to the triallelic 5-HTTLPR polymorphism of the <it>SLC6A4 </it>gene in children with ADHD. This polymorphism appears to modulate the behavioral response to methylphenidate in children with ADHD as assessed in the home environment by parents. Further investigation is needed to assess the clinical implications of this finding.</p> <p>Trial Registration</p> <p>ClinicalTrials.gov NCT00483106</p