Seebeck Effect in Magnetic Tunnel Junctions

Creating temperature gradients in magnetic nanostructures has resulted in a new research direction, i.e., the combination of magneto- and thermoelectric effects. Here, we demonstrate the observation of one important effect of this class: the magneto-Seebeck effect. It is observed when a magnetic configuration changes the charge based Seebeck coefficient. In particular, the Seebeck coefficient changes during the transition from a parallel to an antiparallel magnetic configuration in a tunnel junction. In that respect, it is the analog to the tunneling magnetoresistance. The Seebeck coefficients in parallel and antiparallel configuration are in the order of the voltages known from the charge-Seebeck effect. The size and sign of the effect can be controlled by the composition of the electrodes' atomic layers adjacent to the barrier and the temperature. Experimentally, we realized 8.8 % magneto-Seebeck effect, which results from a voltage change of about -8.7 {\mu}V/K from the antiparallel to the parallel direction close to the predicted value of -12.1 {\mu}V/K.Comment: 16 pages, 7 figures, 2 table

New Insights into Properties of Large-N Holographic Thermal QCD at Finite Gauge Coupling at (the Non-Conformal/Next-to) Leading Order in N

In the context of [1]'s string theoretic dual of large-N thermal QCD-like theories at finite gauge/string coupling (as part of the `MQGP' limit of [2]), we discuss the following. First, up to LO in N, using the results of [3], we show that the local T^3 of [2] is the T^2-invariant sLag of [3] in a resolved conifold. This, together with the results of [4], shows that for a (predominantly resolved or deformed) resolved warped deformed conifold, the local T^3 of [2] in the MQGP limit, is the T^2-invariant sLag of [3] justifying the construction of the delocalized SYZ type IIA mirror of the type IIB background of [1]. Then, using the prescription of [5], we obtain the temperature dependence of the thermal (and electrical) conductivity working up to leading order in N (the number of D3-branes), and upon comparison with [6] show that the results mimic a 1+1-dimensional Luttinger liquid with impurities. Further, including sub-leading non-conformal terms in the metric determined by M (the number of fractional D-branes = the number of colors = 3 in the IR after the end of a Seiberg duality cascade), by looking at respectively the scalar, vector and tensor modes of metric perturbations and using [7]'s prescription of constructing appropriate gauge-invariant perturbations, we obtain respectively the speed of sound, the diffusion constant and the shear viscosity \eta (and \eta/s) including the non-conformal O((g_s M^2) (g_s N_f)/N<<1)-corrections, N_f being the number of flavor D7-branes.Comment: 1+75 pages, LaTeX; Some corrections in Tc-related calculations, results unchange

Temperature- and thickness-dependent elastic moduli of polymer thin films

The mechanical properties of polymer ultrathin films are usually different from those of their counterparts in bulk. Understanding the effect of thickness on the mechanical properties of these films is crucial for their applications. However, it is a great challenge to measure their elastic modulus experimentally with in situ heating. In this study, a thermodynamic model for temperature- (T) and thickness (h)-dependent elastic moduli of polymer thin films Ef(T,h) is developed with verification by the reported experimental data on polystyrene (PS) thin films. For the PS thin films on a passivated substrate, Ef(T,h) decreases with the decreasing film thickness, when h is less than 60 nm at ambient temperature. However, the onset thickness (h*), at which thickness Ef(T,h) deviates from the bulk value, can be modulated by T. h* becomes larger at higher T because of the depression of the quenching depth, which determines the thickness of the surface layer δ

BosR (BB0647) Controls the RpoN-RpoS Regulatory Pathway and Virulence Expression in Borrelia burgdorferi by a Novel DNA-Binding Mechanism

In Borrelia burgdorferi (Bb), the Lyme disease spirochete, the alternative σ factor σ54 (RpoN) directly activates transcription of another alternative σ factor, σS (RpoS) which, in turn, controls the expression of virulence-associated membrane lipoproteins. As is customary in σ54-dependent gene control, a putative NtrC-like enhancer-binding protein, Rrp2, is required to activate the RpoN-RpoS pathway. However, recently it was found that rpoS transcription in Bb also requires another regulator, BosR, which was previously designated as a Fur or PerR homolog. Given this unexpected requirement for a second activator to promote σ54-dependent gene transcription, and the fact that regulatory mechanisms among similar species of pathogenic bacteria can be strain-specific, we sought to confirm the regulatory role of BosR in a second virulent strain (strain 297) of Bb. Indeed, BosR displayed the same influence over lipoprotein expression and mammalian infectivity for strain Bb 297 that were previously noted for Bb strain B31. We subsequently found that recombinant BosR (rBosR) bound to the rpoS gene at three distinct sites, and that binding occurred despite the absence of consensus Fur or Per boxes. This led to the identification of a novel direct repeat sequence (TAAATTAAAT) critical for rBosR binding in vitro. Mutations in the repeat sequence markedly inhibited or abolished rBosR binding. Taken together, our studies provide new mechanistic insights into how BosR likely acts directly on rpoS as a positive transcriptional activator. Additional novelty is engendered by the facts that, although BosR is a Fur or PerR homolog and it contains zinc (like Fur and PerR), it has other unique features that clearly set it apart from these other regulators. Our findings also have broader implications regarding a previously unappreciated layer of control that can be involved in σ54–dependent gene regulation in bacteria

Calcium Sulfate and Platelet-Rich Plasma make a novel osteoinductive biomaterial for bone regeneration

BACKGROUND: With the present study we introduce a novel and simple biomaterial able to induce regeneration of bone. We theorized that nourishing a bone defect with calcium and with a large amount of activated platelets may initiate a series of biological processes that culminate in bone regeneration. Thus, we engineered CS-Platelet, a biomaterial based on the combination of Calcium Sulfate and Platelet-Rich Plasma in which Calcium Sulfate also acts as an activator of the platelets, therefore avoiding the need to activate the platelets with an agonist. METHODS: First, we tested CS-Platelet in heterotopic (muscle) and orthotopic (bone) bone regeneration bioassays. We then utilized CS-Platelet in a variety of dental and craniofacial clinical cases, where regeneration of bone was needed. RESULTS: The heterotopic bioassay showed formation of bone within the muscular tissue at the site of the implantation of CS-Platelet. Results of a quantitative orthotopic bioassay based on the rat calvaria critical size defect showed that only CS-Platelet and recombinant human BMP2 were able to induce a significant regeneration of bone. A non-human primate orthotopic bioassay also showed that CS-Platelet is completely resorbable. In all human clinical cases where CS-Platelet was used, a complete bone repair was achieved. CONCLUSION: This study showed that CS-Platelet is a novel biomaterial able to induce formation of bone in heterotopic and orthotopic sites, in orthotopic critical size bone defects, and in various clinical situations. The discovery of CS-Platelet may represent a cost-effective breakthrough in bone regenerative therapy and an alternative or an adjuvant to the current treatments

A nocturnal atmospheric loss of CH2I2 in the remote marine boundary layer.

Ocean emissions of inorganic and organic iodine compounds drive the biogeochemical cycle of iodine and produce reactive ozone-destroying iodine radicals that influence the oxidizing capacity of the atmosphere. Di-iodomethane (CH2I2) and chloro-iodomethane (CH2ICl) are the two most important organic iodine precursors in the marine boundary layer. Ship-borne measurements made during the TORERO (Tropical Ocean tRoposphere Exchange of Reactive halogens and Oxygenated VOC) field campaign in the east tropical Pacific Ocean in January/February 2012 revealed strong diurnal cycles of CH2I2 and CH2ICl in air and of CH2I2 in seawater. Both compounds are known to undergo rapid photolysis during the day, but models assume no night-time atmospheric losses. Surprisingly, the diurnal cycle of CH2I2 was lower in amplitude than that of CH2ICl, despite its faster photolysis rate. We speculate that night-time loss of CH2I2 occurs due to reaction with NO3 radicals. Indirect results from a laboratory study under ambient atmospheric boundary layer conditions indicate a k CH2I2+NO3 of ≤4 × 10-13 cm3 molecule-1 s-1; a previous kinetic study carried out at ≤100 Torr found k CH2I2+NO3 of 4 × 10-13 cm3 molecule-1 s-1. Using the 1-dimensional atmospheric THAMO model driven by sea-air fluxes calculated from the seawater and air measurements (averaging 1.8 +/- 0.8 nmol m-2 d-1 for CH2I2 and 3.7 +/- 0.8 nmol m-2 d-1 for CH2ICl), we show that the model overestimates night-time CH2I2 by >60 % but reaches good agreement with the measurements when the CH2I2 + NO3 reaction is included at 2-4 × 10-13 cm3 molecule-1 s-1. We conclude that the reaction has a significant effect on CH2I2 and helps reconcile observed and modeled concentrations. We recommend further direct measurements of this reaction under atmospheric conditions, including of product branching ratios.LJC acknowledges NERC (NE/J00619X/1) and the National Centre for Atmospheric Science (NCAS) for funding. The laboratory work was supported by the NERC React-SCI (NE/K005448/1) and RONOCO (NE/F005466/1) grants.This is the final version of the article. It was first available from Springer via http://dx.doi.org/10.1007/s10874-015-9320-

Association of anthropometric measures across the life-course with refractive error and ocular biometry at age 15 years

YesBackground A recent Genome-wide association meta-analysis (GWAS) of refractive error reported shared genetics with anthropometric traits such as height, BMI and obesity. To explore a potential relationship with refractive error and ocular structure we performed a life-course analysis including both maternal and child characteristics using data from the Avon Longitudinal Study of Parents and Children cohort. Methods Measures collected across the life-course were analysed to explore the association of height, weight, and BMI with refractive error and ocular biometric measures at age 15 years from 1613children. The outcome measures were the mean spherical equivalent (MSE) of refractive error (dioptres), axial length (AXL; mm), and radius of corneal curvature (RCC; mm). Potential confounding variables; maternal age at conception, maternal education level, parental socio-economic status, gestational age, breast-feeding, and gender were adjusted for within each multi-variable model. Results Maternal height was positively associated with teenage AXL (0.010 mm; 95% CI: 0.003, 0.017) and RCC (0.005 mm; 95% CI: 0.003, 0.007), increased maternal weight was positively associated with AXL (0.004 mm; 95% CI: 0.0001, 0.008). Birth length was associated with an increase in teenage AXL (0.067 mm; 95% CI: 0.032, 0.10) and flatter RCC (0.023 mm; 95% CI: 0.013, 0.034) and increasing birth weight was associated with flatter RCC (0.005 mm; 95% CI: 0.0003, 0.009). An increase in teenage height was associated with a lower MSE (− 0.007 D; 95% CI: − 0.013, − 0.001), an increase in AXL (0.021 mm; 95% CI: 0.015, 0.028) and flatter RCC (0.008 mm; 95% CI: 0.006, 0.010). Weight at 15 years was associated with an increase in AXL (0.005 mm; 95% CI: 0.001, 0.009). Conclusions At each life stage (pre-natal, birth, and teenage) height and weight, but not BMI, demonstrate an association with AXL and RCC measured at age 15 years. However, the negative association between refractive error and an increase in height was only present at the teenage life stage. Further research into the growth pattern of ocular structures and the development of refractive error over the life-course is required, particularly at the time of puberty

Discontinuation of thyroid hormone treatment among children in the United States with congenital hypothyroidism: findings from health insurance claims data

<p>Abstract</p> <p>Background</p> <p>Thyroid hormone treatment in children with congenital hypothyroidism can prevent intellectual disability. Guidelines recommend that children diagnosed with congenital hypothyroidism through newborn screening remain on treatment to at least 3 years of age, after which a trial off therapy can determine which children have transient hypothyroidism. The purpose of this study was to describe the rate at which children with congenital hypothyroidism in the United States discontinue thyroid hormone treatment in early childhood.</p> <p>Methods</p> <p>Retrospective analysis of the 2002-2006 MarketScan^®Commercial Claims and Encounters research databases and the 2001-2005 MarketScan Multi-State Medicaid databases. Children were classified as having congenital hypothyroidism based on billing codes and having filled a prescription for thyroid hormone treatment. Kaplan-Meier curve analysis was used to determine discontinuation rates.</p> <p>Results</p> <p>There were a total of 412 Medicaid-enrolled children and 292 privately-insured children with presumed congenital hypothyroidism included in this study. The overall birth prevalence of congenital hypothyroidism across both datasets was about 1 per 2,300. By 36 months, the percentage who had discontinued thyroid replacement treatment was 38% (95% Confidence Interval: 32%-44%). Medicaid-enrolled children had a more rapid decline in the first 24 months of treatment compared to those with private insurance (<it>P </it>= 0.02).</p> <p>Conclusions</p> <p>More than one-third of children treated for congenital hypothyroidism discontinued treatment within 36 months, which is inconsistent with current guidelines. It is not known how many of these children required continued treatment or experience adverse effects from discontinuation. These findings emphasize the critical need for follow-up systems to monitor the outcome of newborn screening.</p

Promoter methylation correlates with reduced NDRG2 expression in advanced colon tumour

<p>Abstract</p> <p>Background</p> <p>Aberrant DNA methylation of CpG islands of cancer-related genes is among the earliest and most frequent alterations in cancerogenesis and might be of value for either diagnosing cancer or evaluating recurrent disease. This mechanism usually leads to inactivation of tumour-suppressor genes. We have designed the current study to validate our previous microarray data and to identify novel hypermethylated gene promoters.</p> <p>Methods</p> <p>The validation assay was performed in a different set of 8 patients with colorectal cancer (CRC) by means quantitative reverse-transcriptase polymerase chain reaction analysis. The differential RNA expression profiles of three CRC cell lines before and after 5-aza-2'-deoxycytidine treatment were compared to identify the hypermethylated genes. The DNA methylation status of these genes was evaluated by means of bisulphite genomic sequencing and methylation-specific polymerase chain reaction (MSP) in the 3 cell lines and in tumour tissues from 30 patients with CRC.</p> <p>Results</p> <p>Data from our previous genome search have received confirmation in the new set of 8 patients with CRC. In this validation set six genes showed a high induction after drug treatment in at least two of three CRC cell lines. Among them, the N-myc downstream-regulated gene 2 (<it>NDRG2) </it>promoter was found methylated in all CRC cell lines. <it>NDRG2 </it>hypermethylation was also detected in 8 out of 30 (27%) primary CRC tissues and was significantly associated with advanced AJCC stage IV. Normal colon tissues were not methylated.</p> <p>Conclusion</p> <p>The findings highlight the usefulness of combining gene expression patterns and epigenetic data to identify tumour biomarkers, and suggest that NDRG2 silencing might bear influence on tumour invasiveness, being associated with a more advanced stage.</p