Efficient suboxide sources in oxide molecular beam epitaxy using mixed metal + oxide charges: The examples of SnO and Ga2O

Sources of suboxides, providing several advantages over metal sources for the molecular beam epitaxy (MBE) of oxides, are conventionally realized by decomposing the corresponding oxide charge at extreme temperatures. By quadrupole mass spectrometry of the direct flux from an effusion cell, we compare this conventional approach to the reaction of a mixed oxide + metal charge as a source for suboxides with the examples of SnO2 + Sn → 2 SnO and Ga2O3 + 4 Ga → 3 Ga2O. The high decomposition temperatures of the pure oxide charge were found to produce a high parasitic oxygen background. In contrast, the mixed charges reacted at significantly lower temperatures, providing high suboxide fluxes without additional parasitic oxygen. For the SnO source, we found a significant fraction of Sn2O2 in the flux from the mixed charge that was basically absent in the flux from the pure oxide charge. We demonstrate the plasma-assisted MBE growth of SnO2 using the mixed Sn + SnO2 charge to require less activated oxygen and a significantly lower source temperature than the corresponding growth from a pure Sn charge. Thus, the sublimation of mixed metal + oxide charges provides an efficient suboxide source for the growth of oxides by MBE. Thermodynamic calculations predict this advantage for further oxides as well, e.g., SiO2, GeO2, Al2O3, In2O3, La2O3, and Pr2O3

Conductance model for single-crystalline/compact metal oxide gas-sensing layers in the nondegenerate limit: Example of epitaxial SnO2(101)

Semiconducting metal oxide (SMOX)-based gas sensors are indispensable for safety and health applications, for example, explosive, toxic gas alarms, controls for intake into car cabins, and monitor for industrial processes. In the past, the sensor community has been studying polycrystalline materials as sensors where the porous and random microstructure of the SMOX does not allow a separation of the phenomena involved in the sensing process. This led to conduction models that can model and predict the behavior of the overall response, but they were not capable of giving fundamental information regarding the basic mechanisms taking place. The study of epitaxial layers is a definite improvement, allowing clarifying the different aspects and contributions of the sensing mechanisms. A detailed analytical model of the transduction function for n-A nd p-type single-crystalline/compact metal oxide gas sensors was developed that directly relates the conductance of the sample with changes in the surface electrostatic potential. Combined dc resistance and work function measurements were used in a compact SnO2(101) layer in operando conditions that allowed us to check the validity of our model in the region where Boltzmann approximation holds to determine the surface and bulk properties of the material.Fil: Simion, Cristian Eugen. Institut de Physique Des Matériaux, Bucarest-magurele; RumaniaFil: Schipani, Federico. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mar del Plata. Instituto de Investigaciones en Ciencia y Tecnología de Materiales. Universidad Nacional de Mar del Plata. Facultad de Ingeniería. Instituto de Investigaciones en Ciencia y Tecnología de Materiales; ArgentinaFil: Papadogianni, Alexandra. Paul Drude Institut Fur Festkorperelektronik; AlemaniaFil: Stanoiu, Adelina. Institut de Physique Des Matériaux, Bucarest-magurele; RumaniaFil: Budde, Melanie. Paul Drude Institut Fur Festkorperelektronik; AlemaniaFil: Oprea, Alexandru. Universität Tübingen; AlemaniaFil: Weimar, Udo. Universität Tübingen; AlemaniaFil: Bierwagen, Oliver. Paul Drude Institut Fur Festkorperelektronik; AlemaniaFil: Barsan, Nicolae. Universität Tübingen; Alemani

Protection Mechanism against Photocorrosion of GaN Photoanodes Provided by NiO Thin Layers

The photoelectrochemical properties of n-type Ga-polar GaN photoelectrodes covered with NiO layers of different thicknesses in the range 0–20 nm are investigated for aqueous solution. To obtain layers of well-defined thickness and high crystal quality, NiO is grown by plasma-assisted molecular-beam epitaxy. Stability tests reveal that the NiO layers suppress photocorrosion. With increasing NiO thickness, the onset of the photocurrent is shifted to more positive voltages and the photocurrent is reduced, especially for low bias potentials, indicating that hole transfer to the electrolyte interface is hindered by thicker NiO layers. Furthermore, cathodic transient spikes are observed under intermittent illumination, which hints at surface recombination processes. These results are inconsistent with the common explanation of the protection mechanism that the band alignment of GaN/NiO enables efficient hole-injection, thus preventing hole accumulation at the GaN surface that would lead to anodic photocorrosion. Interestingly, the morphology of the etch pits as well as further experiments involving the photodeposition of Ag indicate that photocorrosion of GaN photoanodes is related to reductive processes at threading dislocations. Therefore, it is concluded that the NiO layers block the transfer of photogenerated electrons from GaN to the electrolyte interface, which prevents the cathodic photocorrosion. © 2020 The Authors. Solar RRL published by Wiley-VCH Gmb

Plasma-assisted molecular beam epitaxy of SnO(001) films: Metastability, hole transport properties, Seebeck coefficient, and effective hole mass

Transparent conducting or semiconducting oxides are important materials for (transparent) optoelectronics and power electronics applications. While most of these oxides can be doped n-type only with room-temperature electron mobilities on the order of 100cm^2/Vs p-type oxides are needed for the realization of pn-junction devices but typically suffer from exessively low (<<1cm^2/Vs) hole mobilities. Tin monoxide (SnO) is one of the few p-type oxides with a higher hole mobility, lacking a well-established understanding of its hole transport properties. Moreover, growth of SnO is complicated by its metastability with respect to SnO2 and Sn, requiring epitaxy for the realization of single crystalline material typically required for high-end applications. Here, we give a comprehensive account on the epitaxial growth of SnO, its (meta)stability, and its thermoelectric transport properties in the context of the present literature. Textured and single-crystalline, unintentionally-doped p-type SnO(001) films are grown by plasma-assisted molecular beam epitaxy. The metastability of this semiconducting oxide is addressed theoretically through an equilibrium phase diagram. Experimentally, the related SnO growth window is rapidly determined by an in-situ growth kinetics study as function of Sn-to-O-plasma flux ratio and growth temperature. The presence of secondary Sn and SnOx (1 < x <= 2) phases is comprehensively studied by different methods, indicating the presence of Sn3O4 or Sn as major secondary phases, as well as a fully oxidized SnO2 film surface. The hole transport properties, Seebeck coefficient, and density-of-states effective mass are determined and critically discussed in the context of the present literature on SnO, considering its anisotropic hole-effective mass

Noncompaction of the Ventricular Myocardium Is Associated with a De Novo Mutation in the β-Myosin Heavy Chain Gene

Noncompaction of the ventricular myocardium (NVM) is the morphological hallmark of a rare familial or sporadic unclassified heart disease of heterogeneous origin. NVM results presumably from a congenital developmental error and has been traced back to single point mutations in various genes. The objective of this study was to determine the underlying genetic defect in a large German family suffering from NVM. Twenty four family members were clinically assessed using advanced imaging techniques. For molecular characterization, a genome-wide linkage analysis was undertaken and the disease locus was mapped to chromosome 14ptel-14q12. Subsequently, two genes of the disease interval, MYH6 and MYH7 (encoding the α- and β-myosin heavy chain, respectively) were sequenced, leading to the identification of a previously unknown de novo missense mutation, c.842G>C, in the gene MYH7. The mutation affects a highly conserved amino acid in the myosin subfragment-1 (R281T). In silico simulations suggest that the mutation R281T prevents the formation of a salt bridge between residues R281 and D325, thereby destabilizing the myosin head. The mutation was exclusively present in morphologically affected family members. A few members of the family displayed NVM in combination with other heart defects, such as dislocation of the tricuspid valve (Ebstein's anomaly, EA) and atrial septal defect (ASD). A high degree of clinical variability was observed, ranging from the absence of symptoms in childhood to cardiac death in the third decade of life. The data presented in this report provide first evidence that a mutation in a sarcomeric protein can cause noncompaction of the ventricular myocardium

Cardiac Alpha-Myosin (MYH6) Is the Predominant Sarcomeric Disease Gene for Familial Atrial Septal Defects

Secundum-type atrial septal defects (ASDII) account for approximately 10% of all congenital heart defects (CHD) and are associated with a familial risk. Mutations in transcription factors represent a genetic source for ASDII. Yet, little is known about the role of mutations in sarcomeric genes in ASDII etiology. To assess the role of sarcomeric genes in patients with inherited ASDII, we analyzed 13 sarcomeric genes (MYH7, MYBPC3, TNNT2, TCAP, TNNI3, MYH6, TPM1, MYL2, CSRP3, ACTC1, MYL3, TNNC1, and TTN kinase region) in 31 patients with familial ASDII using array-based resequencing. Genotyping of family relatives and control subjects as well as structural and homology analyses were used to evaluate the pathogenic impact of novel non-synonymous gene variants. Three novel missense mutations were found in the MYH6 gene encoding alpha-myosin heavy chain (R17H, C539R, and K543R). These mutations co-segregated with CHD in the families and were absent in 370 control alleles. Interestingly, all three MYH6 mutations are located in a highly conserved region of the alpha-myosin motor domain, which is involved in myosin-actin interaction. In addition, the cardiomyopathy related MYH6-A1004S and the MYBPC3-A833T mutations were also found in one and two unrelated subjects with ASDII, respectively. No mutations were found in the 11 other sarcomeric genes analyzed. The study indicates that sarcomeric gene mutations may represent a so far underestimated genetic source for familial recurrence of ASDII. In particular, perturbations in the MYH6 head domain seem to play a major role in the genetic origin of familial ASDII

Atrasentan and renal events in patients with type 2 diabetes and chronic kidney disease (SONAR): a double-blind, randomised, placebo-controlled trial

Background: Short-term treatment for people with type 2 diabetes using a low dose of the selective endothelin A receptor antagonist atrasentan reduces albuminuria without causing significant sodium retention. We report the long-term effects of treatment with atrasentan on major renal outcomes. Methods: We did this double-blind, randomised, placebo-controlled trial at 689 sites in 41 countries. We enrolled adults aged 18–85 years with type 2 diabetes, estimated glomerular filtration rate (eGFR)25–75 mL/min per 1·73 m 2 of body surface area, and a urine albumin-to-creatinine ratio (UACR)of 300–5000 mg/g who had received maximum labelled or tolerated renin–angiotensin system inhibition for at least 4 weeks. Participants were given atrasentan 0·75 mg orally daily during an enrichment period before random group assignment. Those with a UACR decrease of at least 30% with no substantial fluid retention during the enrichment period (responders)were included in the double-blind treatment period. Responders were randomly assigned to receive either atrasentan 0·75 mg orally daily or placebo. All patients and investigators were masked to treatment assignment. The primary endpoint was a composite of doubling of serum creatinine (sustained for ≥30 days)or end-stage kidney disease (eGFR <15 mL/min per 1·73 m 2 sustained for ≥90 days, chronic dialysis for ≥90 days, kidney transplantation, or death from kidney failure)in the intention-to-treat population of all responders. Safety was assessed in all patients who received at least one dose of their assigned study treatment. The study is registered with ClinicalTrials.gov, number NCT01858532. Findings: Between May 17, 2013, and July 13, 2017, 11 087 patients were screened; 5117 entered the enrichment period, and 4711 completed the enrichment period. Of these, 2648 patients were responders and were randomly assigned to the atrasentan group (n=1325)or placebo group (n=1323). Median follow-up was 2·2 years (IQR 1·4–2·9). 79 (6·0%)of 1325 patients in the atrasentan group and 105 (7·9%)of 1323 in the placebo group had a primary composite renal endpoint event (hazard ratio [HR]0·65 [95% CI 0·49–0·88]; p=0·0047). Fluid retention and anaemia adverse events, which have been previously attributed to endothelin receptor antagonists, were more frequent in the atrasentan group than in the placebo group. Hospital admission for heart failure occurred in 47 (3·5%)of 1325 patients in the atrasentan group and 34 (2·6%)of 1323 patients in the placebo group (HR 1·33 [95% CI 0·85–2·07]; p=0·208). 58 (4·4%)patients in the atrasentan group and 52 (3·9%)in the placebo group died (HR 1·09 [95% CI 0·75–1·59]; p=0·65). Interpretation: Atrasentan reduced the risk of renal events in patients with diabetes and chronic kidney disease who were selected to optimise efficacy and safety. These data support a potential role for selective endothelin receptor antagonists in protecting renal function in patients with type 2 diabetes at high risk of developing end-stage kidney disease. Funding: AbbVie