High-Temperature Interactions Between Titanium Alloys And Strontium Zirconate Refractories

We investigated interactions between Ti6Al4V alloys and strontium zirconate (SrZrO3) ceramic to assess its potential as a refractory mold material in investment casting. We developed a robust yet simple procedure to examine both the liquid–solid and solid–solid interactions using pellets in drop casting and diffusion couple methods. Reaction layers were characterized using optical microscopy, scanning electron microscopy (SEM), transmission electron microscopy (TEM), and x-ray diffraction (XRD). The results were compared to alumina (Al2O3) which is still a common refractory ceramic for molds in investment casting. Our findings indicate that Ti6Al4V surfaces in contact with SrZrO3 had no apparent changes in surface chemistry nor microstructure. On the other hand, Ti6Al4V surfaces in contact with Al2O3 developed γ-TiAl and α 2-Ti3Al intermetallics with thicknesses of ~ 100 μm in diffusion couples and ~ 10 μm in drop-casting experiments. Nanoindentation results showed that the surface of Ti6Al4V in contact with Al2O3 was significantly harder compared to SrZrO3, confirming our conclusion. Given the time and costs associated with mechanical and chemical removal of reaction layers on Ti6Al4V castings, SrZrO3 can be a better choice for a mold material in the investment casting of titanium alloys

Unique Proteomic Signatures Distinguish Macrophages and Dendritic Cells

Monocytes differentiate into heterogeneous populations of tissue macrophages and dendritic cells (DCs) that regulate inflammation and immunity. Identifying specific populations of myeloid cells in vivo is problematic, however, because only a limited number of proteins have been used to assign cellular phenotype. Using mass spectrometry and bone marrow-derived cells, we provided a global view of the proteomes of M-CSF-derived macrophages, classically and alternatively activated macrophages, and GM-CSF-derived DCs. Remarkably, the expression levels of half the plasma membrane proteins differed significantly in the various populations of cells derived in vitro. Moreover, the membrane proteomes of macrophages and DCs were more distinct than those of classically and alternatively activated macrophages. Hierarchical cluster and dual statistical analyses demonstrated that each cell type exhibited a robust proteomic signature that was unique. To interrogate the phenotype of myeloid cells in vivo, we subjected elicited peritoneal macrophages harvested from wild-type and GM-CSF-deficient mice to mass spectrometric and functional analysis. Unexpectedly, we found that peritoneal macrophages exhibited many features of the DCs generated in vitro. These findings demonstrate that global analysis of the membrane proteome can help define immune cell phenotypes in vivo

Large Transverse Momenta in Statistical Models of High Energy Interactions

The creation of particles with large transverse momenta in high energy hadronic collisions is a long standing problem. The transition from small- (soft) to hard- parton scattering `high-pt' events is rather smooth. In this paper we apply the non-extensive statistical framework to calculate transverse momentum distributions of long lived hadrons created at energies from low (sqrt(s)~10 GeV) to the highest energies available in collider experiments (sqrt(s)~2000 GeV). Satisfactory agreement with the experimental data is achieved. The systematic increase of the non-extensivity parameter with energy found can be understood as phenomenological evidence for the increased role of long range correlations in the hadronization process. Predictions concerning the rise of average transverse momenta up to the highest cosmic ray energies are also given and discussed.Comment: 20 pages, 10 figure

IDH-mutant glioma specific association of rs55705857 located at 8q24.21 involves MYC deregulation

The single nucleotide polymorphism rs55705857, located in a non-coding but evolutionarily conserved region at 8q24.21, is strongly associated with IDH-mutant glioma development and was suggested to be a causal variant. However, the molecular mechanism underlying this association has remained unknown. With a case control study in 285 gliomas, 316 healthy controls, 380 systemic cancers, 31 other CNS-tumors, and 120 IDH-mutant cartilaginous tumors, we identified that the association was specific to IDH-mutant gliomas. Odds-ratios were 9.25 (5.17–16.52; 95% CI) for IDH-mutated gliomas and 12.85 (5.94–27.83; 95% CI) for IDH-mutated, 1p/19q co-deleted gliomas. Decreasing strength with increasing anaplasia implied a modulatory effect. No somatic mutations were noted at this locus in 114 blood-tumor pairs, nor was there a copy number difference between risk-allele and only-ancestral allele carriers. CCDC26 RNA-expression was rare and not different between the two groups. There were only minor subtype-specific differences in common glioma driver genes. RNA sequencing and LC-MS/MS comparisons pointed to significantly altered MYC-signaling. Baseline enhancer activity of the conserved region specifically on the MYC promoter and its further positive modulation by the SNP risk-allele was shown in vitro. Our findings implicate MYC deregulation as the underlying cause of the observed association

Relationships between serum adiponectin and soluble TNF-α receptors and glucose and lipid oxidation in lean and obese subjects

Insulin resistance might be associated with an impaired ability of insulin to stimulate glucose oxidation and inhibit lipid oxidation. Insulin action is also inversely associated with TNF-α system and positively related to adiponectin. The aim of the present study was to analyze the associations between serum adiponectin, soluble TNF-α receptors concentrations and the whole-body insulin sensitivity, lipid and glucose oxidation, non-oxidative glucose metabolism (NOGM) and metabolic flexibility in lean and obese subjects. We examined 53 subjects: 25 lean (BMI < 25 kg × m−2) and 28 with overweight or obesity (BMI > 25 kg × m−2) with normal glucose tolerance. Hyperinsulinemic euglycemic clamp and indirect calorimetry were performed. An increase in respiratory exchange ratio in response to insulin was used as a measure of metabolic flexibility. Obese subjects had lower insulin sensitivity, adiponectin and higher sTNFR1 (all P < 0.001) and sTNFR2 (P = 0.001). Insulin sensitivity was positively related to adiponectin (r = 0.49, P < 0.001) and negatively related to sTNFR1 (r = −0.40, P = 0.004) and sTNFR2 (r = −0.52, P < 0.001). Adiponectin was related to the rate of glucose (r = 0.47, P < 0.001) and lipid (r = −0.40, P = 0.003) oxidation during the clamp, NOGM (r = 0.41, P = 0.002) and metabolic flexibility (r = 0.36, P = 0.007). Serum sTNFR1 and sTNFR2 were associated with the rate of glucose (r = −0.45, P = 0.001; r = −0.51, P < 0.001, respectively) and lipid (r = 0.52, P < 0.001; r = 0.46, P = 0.001, respectively) oxidation during hyperinsulinemia, NOGM (r = −0.31, P = 0.02; r = −0.43, P = 0.002, respectively) and metabolic flexibility (r = −0.47 and r = −0.51, respectively, both P < 0.001) in an opposite manner than adiponectin. Our data suggest that soluble TNF-α receptors and adiponectin have multiple effects on glucose and lipid metabolism in obesity

A new method for chlorhexidine (CHX) determination: CHX release after application of differently concentrated CHX-containing preparations on artificial fissures

Aims of the study were (1) to establish a method for quantification of chlorhexidine (CHX) in small volumes and (2) to determine CHX release from differently concentrated CHX-containing preparations, varnishes, and a CHX gel applied on artificial fissures. CHX determination was conducted in a microplate reader using polystyrene wells. The reduced intensity of fluorescence of the microplates was used for CHX quantification. For verification of the technique, intra- and inter-assay coefficients of variation were calculated for graded series of CHX concentrations, and the lower limit of quantification (LLOQ) was determined. Additionally, artificial fissures were prepared in 50 bovine enamel samples, divided into five groups (A–E, n = 10) and stored in distilled water (7 days); A: CHX-varnish EC40; B: CHX-varnish Cervitec; C: CHX-gel Chlorhexamed; D: negative control, no CHX application; and E: CXH-diacetate standard (E1, n = 5) or CHX-digluconate (E2, n = 5) in the solution. The specimens were brushed daily, and CHX in the solution was measured. The method showed intra- and inter-assay coefficients of variation of <10 and <20%, respectively; LLOQ was 0.91–1.22 nmol/well. The cumulative CHX release (mean ± SD) during the 7 days was: EC40 (217.2 ± 41.8 nmol), CHX-gel (31.3 ± 8.5 nmol), Cervitec (18.6 ± 1.7 nmol). Groups A–C revealed a significantly higher CHX release than group D and a continuous CHX-release with the highest increase from day 0 to 7 for EC40 and the lowest for Chlorhexamed. The new method is a reliable tool to quantify CHX in small volumes. Both tested varnishes demonstrate prolonged and higher CHX release from artificial fissures than the CHX-gel tested

Postnatal Development of Numbers and Mean Sizes of Pancreatic Islets and Beta-Cells in Healthy Mice and GIPRdn Transgenic Diabetic Mice

The aim of this study was to examine postnatal islet and beta-cell expansion in healthy female control mice and its disturbances in diabetic GIPRdn transgenic mice, which exhibit an early reduction of beta-cell mass. Pancreata of female control and GIPRdn transgenic mice, aged 10, 45, 90 and 180 days were examined, using state-of-the-art quantitative-stereological methods. Total islet and beta-cell volumes, as well as their absolute numbers increased significantly until 90 days in control mice, and remained stable thereafter. The mean islet volumes of controls also increased slightly but significantly between 10 and 45 days of age, and then remained stable until 180 days. The total volume of isolated beta-cells, an indicator of islet neogenesis, and the number of proliferating (BrdU-positive) islet cells were highest in 10-day-old controls and declined significantly between 10 and 45 days. In GIPRdn transgenic mice, the numbers of islets and beta-cells were significantly reduced from 10 days of age onwards vs. controls, and no postnatal expansion of total islet and beta-cell volumes occurred due to a reduction in islet neogenesis whereas early islet-cell proliferation and apoptosis were unchanged as compared to control mice. Insulin secretion in response to pharmacological doses of GIP was preserved in GIPRdn transgenic mice, and serum insulin to pancreatic insulin content in response to GLP-1 and arginine was significantly higher in GIPRdn transgenic mice vs. controls. We could show that the increase in islet number is mainly responsible for expansion of islet and beta-cell mass in healthy control mice. GIPRdn transgenic mice show a disturbed expansion of the endocrine pancreas, due to perturbed islet neogenesis

Using an insect mushroom body circuit to encode route memory in complex natural environments

Ants, like many other animals, use visual memory to follow extended routes through complex environments, but it is unknown how their small brains implement this capability. The mushroom body neuropils have been identified as a crucial memory circuit in the insect brain, but their function has mostly been explored for simple olfactory association tasks. We show that a spiking neural model of this circuit originally developed to describe fruitfly (Drosophila melanogaster) olfactory association, can also account for the ability of desert ants (Cataglyphis velox) to rapidly learn visual routes through complex natural environments. We further demonstrate that abstracting the key computational principles of this circuit, which include one-shot learning of sparse codes, enables the theoretical storage capacity of the ant mushroom body to be estimated at hundreds of independent images