Surface composition of BaTiO3/SrTiO3(001) films grown by atomic oxygen plasma assisted molecular beam epitaxy

We have investigated the growth of BaTiO3 thin films deposited on pure and 1% Nb-doped SrTiO3(001) single crystals using atomic oxygen assisted molecular beam epitaxy (AO-MBE) and dedicated Ba and Ti Knudsen cells. Thicknesses up to 30 nm were investigated for various layer compositions. We demonstrate 2D growth and epitaxial single crystalline BaTiO3 layers up to 10 nm before additional 3D features appear; lattice parameter relaxation occurs during the first few nanometers and is completed at {\guillemotright}10 nm. The presence of a Ba oxide rich top layer that probably favors 2D growth is evidenced for well crystallized layers. We show that the Ba oxide rich top layer can be removed by chemical etching. The present work stresses the importance of stoichiometry and surface composition of BaTiO3 layers, especially in view of their integration in devices.Comment: In press in J. Appl. Phy

Vulnerability of CMOS image sensors in megajoule class laser harsh environment

CMOS image sensors (CIS) are promising candidates as part of optical imagers for the plasma diagnostics devoted to the study of fusion by inertial confinement. However, the harsh radiative environment of Megajoule Class Lasers threatens the performances of these optical sensors. In this paper, the vulnerability of CIS to the transient and mixed pulsed radiation environment associated with such facilities is investigated during an experiment at the OMEGA facility at the Laboratory for Laser Energetics (LLE), Rochester, NY, USA. The transient and permanent effects of the 14 MeV neutron pulse on CIS are presented. The behavior of the tested CIS shows that active pixel sensors (APS) exhibit a better hardness to this harsh environment than a CCD. A first order extrapolation of the reported results to the higher level of radiation expected for Megajoule Class Laser facilities (Laser Megajoule in France or National Ignition Facility in the USA) shows that temporarily saturated pixels due to transient neutron-induced single event effects will be the major issue for the development of radiation-tolerant plasma diagnostic instruments whereas the permanent degradation of the CIS related to displacement damage or total ionizing dose effects could be reduced by applying well known mitigation techniques

Convolutional LSTM Networks for Subcellular Localization of Proteins

Machine learning is widely used to analyze biological sequence data. Non-sequential models such as SVMs or feed-forward neural networks are often used although they have no natural way of handling sequences of varying length. Recurrent neural networks such as the long short term memory (LSTM) model on the other hand are designed to handle sequences. In this study we demonstrate that LSTM networks predict the subcellular location of proteins given only the protein sequence with high accuracy (0.902) outperforming current state of the art algorithms. We further improve the performance by introducing convolutional filters and experiment with an attention mechanism which lets the LSTM focus on specific parts of the protein. Lastly we introduce new visualizations of both the convolutional filters and the attention mechanisms and show how they can be used to extract biological relevant knowledge from the LSTM networks

Crystallographic structure of ultrathin Fe films on Cu(100)

We report bcc-like crystal structures in 2-4 ML Fe films grown on fcc Cu(100) using scanning tunneling microscopy. The local bcc structure provides a straightforward explanation for their frequently reported outstanding magnetic properties, i.e., ferromagnetic ordering in all layers with a Curie temperature above 300 K. The non-pseudomorphic structure, which becomes pseudomorphic above 4 ML film thickness is unexpected in terms of conventional rules of thin film growth and stresses the importance of finite thickness effects in ferromagnetic ultrathin films.Comment: 4 pages, 3 figures, RevTeX/LaTeX2.0

Between tinkering and transformation: A contemporary appraisal of climate change adaptation research on the world's islands

Islands are at the center of discourses on climate change. Yet despite extensive work on diverse island systems in a changing climate, we still lack an understanding of climate change-related responses amongst islands and what shifting from what might be called “tinkering” (perhaps heat warnings) to “transformational” adaptation (perhaps relocation) means for these vastly different landmasses which are often grouped together by default. Through a systematic review of the climate change adaptation scientific literature, this paper critically reflects on how considering islands as a homogenous ensemble and the use of buzzwords such as “transformational adaptation” may be problematic for diverse island realities under climate change. Our findings show that the adaptation evidence base actually provides literature on contrasting island types and cultural and political contexts, including Small Island Developing States as well as other island territories. This study finds research gaps with respect to regions (e.g., South America, Africa, and Mediterranean) and that there is overall both little evidence of and a lack of context-specific definitions of transformational adaptation in island contexts. The adaptation literature does not yet fully reflect the experiences or needs of islands regarding transitions and transformations throughout history

The zinc transporter Slc30a8/ZnT8 is required in a subpopulation of pancreatic alpha-cells for hypoglycemia-induced glucagon secretion

SLC30A8 encodes a zinc transporter ZnT8 largely restricted to pancreatic islet β- and α-cells, and responsible for zinc accumulation into secretory granules. Although common SLC30A8 variants, believed to reduce ZnT8 activity, increase type 2 diabetes risk in humans, rare inactivating mutations are protective. To investigate the role of Slc30a8 in the control of glucagon secretion, Slc30a8 was inactivated selectively in α-cells by crossing mice with alleles floxed at exon 1 to animals expressing Cre recombinase under the pre-proglucagon promoter. Further crossing to Rosa26:tdRFP mice, and sorting of RFP+: glucagon+ cells from KO mice, revealed recombination in ∼30% of α-cells, of which ∼50% were ZnT8-negative (14 ± 1.8% of all α-cells). Although glucose and insulin tolerance were normal, female αZnT8KO mice required lower glucose infusion rates during hypoglycemic clamps and displayed enhanced glucagon release (p < 0.001) versus WT mice. Correspondingly, islets isolated from αZnT8KO mice secreted more glucagon at 1 mm glucose, but not 17 mm glucose, than WT controls (n = 5; p = 0.008). Although the expression of other ZnT family members was unchanged, cytoplasmic (n = 4 mice per genotype; p < 0.0001) and granular (n = 3, p < 0.01) free Zn2+ levels were significantly lower in KO α-cells versus control cells. In response to low glucose, the amplitude and frequency of intracellular Ca2+ increases were unchanged in α-cells of αZnT8KO KO mice. ZnT8 is thus important in a subset of α-cells for normal responses to hypoglycemia and acts via Ca2+-independent mechanisms

The Constitutive Lack of α7 Nicotinic Receptor Leads to Metabolic Disorders in Mouse.

Type 2 diabetes (T2D) occurs by deterioration in pancreatic β-cell function and/or progressive loss of pancreatic β-cell mass under the context of insulin resistance. α7 nicotinic acetylcholine receptor (nAChR) may contribute to insulin sensitivity but its role in the pathogenesis of T2D remains undefined. We investigated whether the systemic lack of α7 nAChR was sufficient to impair glucose homeostasis. We used an α7 nAChR knock-out (α7 &lt;sup&gt;-/-&lt;/sup&gt; ) mouse model fed a standard chow diet. The effects of the lack of α7 nAChR on islet mass, insulin secretion, glucose and insulin tolerance, body composition, and food behaviour were assessed in vivo and ex vivo experiments. Young α7 &lt;sup&gt;-/-&lt;/sup&gt; mice display a chronic mild high glycemia combined with an impaired glucose tolerance and a marked deficit in β-cell mass. In addition to these metabolic disorders, old mice developed adipose tissue inflammation, elevated plasma free fatty acid concentrations and presented glycolytic muscle insulin resistance in old mice. Finally, α7 &lt;sup&gt;-/-&lt;/sup&gt; mice, fed a chow diet, exhibited a late-onset excessive gain in body weight through increased fat mass associated with higher food intake. Our work highlights the important role of α7 nAChR in glucose homeostasis. The constitutive lack of α7 nAChR suggests a novel pathway influencing the pathogenesis of T2D