Room temperature emission at 1.6 µm from InGaAs quantum dots capped with GaAsSb

Room temperature photoluminescence at 1.6 µm is demonstrated from InGaAs quantum dots capped with an 8 nm GaAsSb quantum well. Results obtained from various sample structures are compared, including samples capped with GaAs. The observed redshift in GaAsSb capped samples is attributed to a type II band alignment and to a beneficial modification of growth kinetics during capping due to the presence of Sb. The sample structure is discussed on the basis of transmission electron microscopy results.This work was supported by the Spanish MCyT under NANOSELF project TIC2002-04096, by CAM project GR/MAT/0726/2004, by the SANDiE Network of excellence (Contract No. NMP4-CT-2004-500101) and the Junta de Andalucía (Group Tep-0120). J.M.R. acknowledges support through a Ramón y Cajal grant. TEM measurements were carried out at DME-SCCYT, UCA.Peer reviewe

Continuous and correlated nucleation during nonstandard island growth at Ag/Si(111)-7x7 heteroepitaxy

We present a combined experimental and theoretical study of submonolayer heteroepitaxial growth of Ag on Si(111)-7x7 at temperatures from 420 K to 550 K when Ag atoms can easily diffuse on the surface and the reconstruction 7x7 remains stable. STM measurements for coverages from 0.05 ML to 0.6 ML show that there is an excess of smallest islands (each of them fills up just one half-unit cell - HUC) in all stages of growth. Formation of 2D wetting layer proceeds by continuous nucleation of the smallest islands in the proximity of larger 2D islands (extended over several HUCs) and following coalescence with them. Such a growth scenario is verified by kinetic Monte Carlo simulation which uses a coarse-grained model based on a limited capacity of HUC and a mechanism which increases nucleation probability in a neighbourhood of already saturated HUCs (correlated nucleation). The model provides a good fit for experimental dependences of the relative number of Ag-occupied HUCs and the preference in occupation of faulted HUCs on temperature and amount of deposited Ag. Parameters obtained for the hopping of Ag adatoms between HUCs agree with those reported earlier for initial stages of growth. The model provides two new parameters - maximum number of Ag atoms inside HUC, and on HUC boundary.Comment: LaTeX2e, BibTeX, 9 pages, 7 images, accepted to Phys. Rev.

Quantum-well states in ultrathin Ag(111) films deposited onto H-passivated Si(111)-(1x1) surfaces

Ag(111) films were deposited at room temperature onto H-passivated Si(111)-(1x1) substrates, and subsequently annealed at 300 C. An abrupt non-reactive Ag/Si interface is formed, and very uniform non-strained Ag(111) films of 6-12 monolayers have been grown. Angle resolved photoemission spectroscopy has been used to study the valence band electronic properties of these films. Well-defined Ag sp quantum-well states (QWS) have been observed at discrete energies between 0.5-2eV below the Fermi level, and their dispersions have been measured along the GammaK, GammaMM'and GammaL symmetry directions. QWS show a parabolic bidimensional dispersion, with in-plane effective mass of 0.38-0.50mo, along the GammaK and GammaMM' directions, whereas no dispersion has been found along the GammaL direction, indicating the low-dimensional electronic character of these states. The binding energy dependence of the QWS as a function of Ag film thickness has been analyzed in the framework of the phase accumulation model. According to this model, a reflectivity of 70% has been estimated for the Ag-sp states at the Ag/H/Si(111)-(1x1) interface.Comment: 6 pages, 6 figures, submitted to Phys. Rev.

Two-domains bulklike Fermi surface of Ag films deposited onto Si(111)-(7x7)

Thick metallic silver films have been deposited onto Si(111)-(7x7) substrates at room temperature. Their electronic properties have been studied by using angle resolved photoelectron spectroscopy (ARPES). In addition to the electronic band dispersion along the high-symmetry directions, the Fermi surface topology of the grown films has been investigated. Using ARPES, the spectral weight distribution at the Fermi level throughout large portions of the reciprocal space has been determined at particular perpendicular electron-momentum values. Systematically, the contours of the Fermi surface of these films reflected a sixfold symmetry instead of the threefold symmetry of Ag single crystal. This loss of symmetry has been attributed to the fact that these films appear to be composed by two sets of domains rotated 60$^o$ from each other. Extra, photoemission features at the Fermi level were also detected, which have been attributed to the presence of surface states and \textit{sp}-quantum states. The dimensionality of the Fermi surface of these films has been analyzed studying the dependence of the Fermi surface contours with the incident photon energy. The behavior of these contours measured at particular points along the Ag $\Gamma$L high-symmetry direction puts forward the three-dimensional character of the electronic structure of the films investigated.Comment: 10 pages, 12 figures, submitted to Physical Review

Tuning the translational freedom of DNA for high speed AFM

Direct observation is arguably the preferred way to investigate the interactions between two molecular complexes. With the development of high speed atomic force microscopy it is becoming possible to observe directly DNA protein interactions with relevant spatial and temporal resolutions. These interactions are of central importance to biology, bio-nanotechnology but also functional biologically inspired materials. Critically, sample preparation plays a central role in all microscopy studies and minimal perturbation of the sample is desired. Here, we demonstrate the ability to tune the interactions of DNA molecules with the surface such that an association strong enough to enable high resolution AFM imaging while providing sufficient translational freedom to allow the relevant protein DNA interactions to take place, can be maintained. Furthermore, we describe a quantitative method for measuring the DNA mobility, which also allows the dissection of the different contributions to the overall movement of the DNA molecules. We find that for weak surface association, a significant contribution to the movement arises from the interaction of the AFM tip with the DNA. In combination, these methods enable the tuning of the surface translational freedom of DNA molecules to allow the direct study of a wide range of nucleo-protein interactions by high speed atomic force microscopy

Loss of Myotubularin Function Results in T-Tubule Disorganization in Zebrafish and Human Myotubular Myopathy

Myotubularin is a lipid phosphatase implicated in endosomal trafficking in vitro, but with an unknown function in vivo. Mutations in myotubularin cause myotubular myopathy, a devastating congenital myopathy with unclear pathogenesis and no current therapies. Myotubular myopathy was the first described of a growing list of conditions caused by mutations in proteins implicated in membrane trafficking. To advance the understanding of myotubularin function and disease pathogenesis, we have created a zebrafish model of myotubular myopathy using morpholino antisense technology. Zebrafish with reduced levels of myotubularin have significantly impaired motor function and obvious histopathologic changes in their muscle. These changes include abnormally shaped and positioned nuclei and myofiber hypotrophy. These findings are consistent with those observed in the human disease. We demonstrate for the first time that myotubularin functions to regulate PI3P levels in a vertebrate in vivo, and that homologous myotubularin-related proteins can functionally compensate for the loss of myotubularin. Finally, we identify abnormalities in the tubulo-reticular network in muscle from myotubularin zebrafish morphants and correlate these changes with abnormalities in T-tubule organization in biopsies from patients with myotubular myopathy. In all, we have generated a new model of myotubular myopathy and employed this model to uncover a novel function for myotubularin and a new pathomechanism for the human disease that may explain the weakness associated with the condition (defective excitation–contraction coupling). In addition, our findings of tubuloreticular abnormalities and defective excitation-contraction coupling mechanistically link myotubular myopathy with several other inherited muscle diseases, most notably those due to ryanodine receptor mutations. Based on our findings, we speculate that congenital myopathies, usually considered entities with similar clinical features but very disparate pathomechanisms, may at their root be disorders of calcium homeostasis

Influence of alternating current electrokinetic forces and torque on the elongation of immobilized DNA

The authors investigate the elongation and orientation of different-sized deoxyribose nucleic acid (DNA) molecules, tethered onto gold electrodes via a terminal thiol, under the influence of high frequency ac electric fields. The DNA molecules are elongated from a random coil into an extended conformation and orientated along the electric field lines as a result of the forces acting on the molecules during the application of the ac electric fields. Elongation was observed in the frequency range 100 kHz-1 MHz, with field strengths of 0.06-1.0 MV/m. Maximum elongation for all DNA fragments tested, irrespective of size, was found for frequencies between 200 and 300 kHz. The torque acting on the induced dipole in the DNA molecules, complemented by a directional bias force, opposite in direction to the dielectrophoretic force, provides the main contribution to the elongation process. The length of elongation is limited to either half the distance between opposing electrodes or to the contour length of the DNA, whichever is shorter. Further, the authors show that the normalized length of the elongated DNA molecules is independent of the contour length of the DNA. (C) 2005 American Institute of Physics

Disrupted autophagy undermines skeletal muscle adaptation and integrity

This review assesses the importance of proteostasis in skeletal muscle maintenance with a specific emphasis on autophagy. Skeletal muscle appears to be particularly vulnerable to genetic defects in basal and induced autophagy, indicating that autophagy is co-substantial to skeletal muscle maintenance and adaptation. We discuss emerging evidence that tension-induced protein unfolding may act as a direct link between mechanical stress and autophagic pathways. Mechanistic links between protein damage, autophagy and muscle hypertrophy, which is also induced by mechanical stress, are still poorly understood. However, some mouse models of muscle disease show ameliorated symptoms upon effective targeting of basal autophagy. These findings highlight the importance of autophagy as therapeutic target and suggest that elucidating connections between protein unfolding and mTOR-dependent or mTOR-independent hypertrophic responses is likely to reveal specific therapeutic windows for the treatment of muscle wasting disorders

3 years of liraglutide versus placebo for type 2 diabetes risk reduction and weight management in individuals with prediabetes: a randomised, double-blind trial

Background Liraglutide 3\ub70 mg was shown to reduce bodyweight and improve glucose metabolism after the 56-week period of this trial, one of four trials in the SCALE programme. In the 3-year assessment of the SCALE Obesity and Prediabetes trial we aimed to evaluate the proportion of individuals with prediabetes who were diagnosed with type 2 diabetes. Methods In this randomised, double-blind, placebo-controlled trial, adults with prediabetes and a body-mass index of at least 30 kg/m2, or at least 27 kg/m2 with comorbidities, were randomised 2:1, using a telephone or web-based system, to once-daily subcutaneous liraglutide 3\ub70 mg or matched placebo, as an adjunct to a reduced-calorie diet and increased physical activity. Time to diabetes onset by 160 weeks was the primary outcome, evaluated in all randomised treated individuals with at least one post-baseline assessment. The trial was conducted at 191 clinical research sites in 27 countries and is registered with ClinicalTrials.gov, number NCT01272219. Findings The study ran between June 1, 2011, and March 2, 2015. We randomly assigned 2254 patients to receive liraglutide (n=1505) or placebo (n=749). 1128 (50%) participants completed the study up to week 160, after withdrawal of 714 (47%) participants in the liraglutide group and 412 (55%) participants in the placebo group. By week 160, 26 (2%) of 1472 individuals in the liraglutide group versus 46 (6%) of 738 in the placebo group were diagnosed with diabetes while on treatment. The mean time from randomisation to diagnosis was 99 (SD 47) weeks for the 26 individuals in the liraglutide group versus 87 (47) weeks for the 46 individuals in the placebo group. Taking the different diagnosis frequencies between the treatment groups into account, the time to onset of diabetes over 160 weeks among all randomised individuals was 2\ub77 times longer with liraglutide than with placebo (95% CI 1\ub79 to 3\ub79, p<0\ub70001), corresponding with a hazard ratio of 0\ub721 (95% CI 0\ub713\u20130\ub734). Liraglutide induced greater weight loss than placebo at week 160 (\u20136\ub71 [SD 7\ub73] vs 121\ub79% [6\ub73]; estimated treatment difference 124\ub73%, 95% CI 124\ub79 to 123\ub77, p<0\ub70001). Serious adverse events were reported by 227 (15%) of 1501 randomised treated individuals in the liraglutide group versus 96 (13%) of 747 individuals in the placebo group. Interpretation In this trial, we provide results for 3 years of treatment, with the limitation that withdrawn individuals were not followed up after discontinuation. Liraglutide 3\ub70 mg might provide health benefits in terms of reduced risk of diabetes in individuals with obesity and prediabetes. Funding Novo Nordisk, Denmark

A randomized, controlled trial of 3.0 mg of liraglutide in weight management

BACKGROUND Obesity is a chronic disease with serious health consequences, but weight loss is difficult to maintain through lifestyle intervention alone. Liraglutide, a glucagonlike peptide-1 analogue, has been shown to have potential benefit for weight management at a once-daily dose of 3.0 mg, injected subcutaneously. METHODS We conducted a 56-week, double-blind trial involving 3731 patients who did not have type 2 diabetes and who had a body-mass index (BMI; the weight in kilograms divided by the square of the height in meters) of at least 30 or a BMI of at least 27 if they had treated or untreated dyslipidemia or hypertension. We randomly assigned patients in a 2:1 ratio to receive once-daily subcutaneous injections of liraglutide at a dose of 3.0 mg (2487 patients) or placebo (1244 patients); both groups received counseling on lifestyle modification. The coprimary end points were the change in body weight and the proportions of patients losing at least 5% and more than 10% of their initial body weight. RESULTS At baseline, the mean (±SD) age of the patients was 45.1±12.0 years, the mean weight was 106.2±21.4 kg, and the mean BMI was 38.3±6.4; a total of 78.5% of the patients were women and 61.2% had prediabetes. At week 56, patients in the liraglutide group had lost a mean of 8.4±7.3 kg of body weight, and those in the placebo group had lost a mean of 2.8±6.5 kg (a difference of -5.6 kg; 95% confidence interval, -6.0 to -5.1; P&lt;0.001, with last-observation-carried-forward imputation). A total of 63.2% of the patients in the liraglutide group as compared with 27.1% in the placebo group lost at least 5% of their body weight (P&lt;0.001), and 33.1% and 10.6%, respectively, lost more than 10% of their body weight (P&lt;0.001). The most frequently reported adverse events with liraglutide were mild or moderate nausea and diarrhea. Serious events occurred in 6.2% of the patients in the liraglutide group and in 5.0% of the patients in the placebo group. CONCLUSIONS In this study, 3.0 mg of liraglutide, as an adjunct to diet and exercise, was associated with reduced body weight and improved metabolic control. (Funded by Novo Nordisk; SCALE Obesity and Prediabetes NN8022-1839 ClinicalTrials.gov number, NCT01272219.)