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The long-range (average) and short-range (local) structures in the Yb 2 (Ti 2- x Yb x)O 7- x /2 (x ​= ​0.00–0.67) series were studied using a combination of diffraction and spectroscopic techniques. The average structure, established from synchrotron X-ray and neutron powder diffraction data, shows the development of multiphase regions from x ​= ​0.134 and the formation of anti-site disorder from x ​= ​0.335. The local structure, established from X-ray absorption near-edge structure (XANES), shows a gradual evolution of short-range disorder. The crystal field splitting energy of the Ti4+ ions decreases from 2.15 to 1.91 ​eV with increasing Yb3+ content, reflecting the increase in coordination number from 6 to predominantly 7. Electrochemical impedance spectroscopic studies show an increase in oxygen ionic conductivity by almost a factor of 3 upon doping with small amounts of Yb3+ (x ​= ​0.067). These results imply that the disordering across the anion and cation sublattices are different and inducing small amounts of disorder into the pyrochlore structure may lead to applications in solid-oxide fuel cells. [Display omitted] • Structures of the Yb 2 (Ti 2- x Yb x)O 7- x /2 series determined using a combination of diffraction and spectroscopic techniques. • Diffraction shows the sudden development of multiphase regions and anti-site disorder. • XANES shows a gradual evolution of short-range disorder. • Inducing small amounts of disorder (x ​= ​0.067) increases the bulk oxygen ionic conductivity by a factor of 3 ​at 1000 ​°C. • The advantages of using both diffraction and spectroscopic techniques when quantifying disorder are highlighted. [ABSTRACT FROM AUTHOR]

Analyzes the construction of variance from the triangular reduction of data matrix. Presentation of procedures used in reducing data matrix; Calculation of the sums of squares, degrees of freedom and expected mean squares; Use of statistical interference on linear combinations of a linear model.

A successful attempt by Edinburgh Athletic Club on the world record for the 24-hour 10-man x 1 mile relay is reported. The effects of a variety of factors on the performances of the athletes are assessed, and some physiological changes noted. In the light of these observations recommendations are made to help the planning of future record attempts. [ABSTRACT FROM PUBLISHER]

We introduce laser cavitation rheology (LCR) as a minimally-invasive optical method to characterize mechanical properties within the interior of biological and synthetic aqueous soft materials at high strain-rates. We utilized time-resolved photography to measure cavitation bubble dynamics generated by the delivery of focused 500 ps duration laser radiation at λ = 532 nm within fibrin hydrogels at pulse energies of Ep = 12, 18 µJ and within polyethylene glycol (600) diacrylate (PEG (600) DA) hydrogels at Ep = 2, 5, 12 µJ. Elastic moduli and failure strains of fibrin and PEG (600) DA hydrogels were calculated from these measurements by determining parameter values which provide the best fit of the measured data to a theoretical model of cavitation bubble dynamics in a Neo-Hookean viscoelastic medium subject to material failure. We demonstrate the use of this method to retrieve the local, interior elastic modulus of these hydrogels and both the radial and circumferential failure strains. [ABSTRACT FROM AUTHOR]

Examines correspondence between linear restriction and inverse in linear model analysis. Integration of linear restriction and generalized inverse solution; Effect of corresponding generalized inverse existence on restriction; Comparison of treatment effects.

The case of a 32 year old female who presented with her first epileptic fit and took over 36 hours to recover is described. Investigations led to a diagnosis of hypothyroidism as the cause. Following treatment with thyroxine she has remained well with no further fits for over 2 years. Hypothyroidism should be considered as a possible underlying cause of epilepsy especially when there is a prolonged recovery time after a fit. [ABSTRACT FROM PUBLISHER]

Loss of the microvascular (MV) network results in tissue ischemia, loss of tissue function, and is a hallmark of chronic diseases. The incorporation of a functional vascular network with that of the host remains a challenge to utilizing engineered tissues in clinically relevant therapies. We showed that vascular-bed-specific endothelial cells (ECs) exhibit differing angiogenic capacities, with kidney microvascular endothelial cells (MVECs) being the most deficient, and sought to explore the underlying mechanism. Constitutive activation of the phosphatase PTEN in kidney MVECs resulted in impaired PI3K/AKT activity in response to vascular endothelial growth factor (VEGF). Suppression of PTEN in vivo resulted in microvascular regeneration, but was insufficient to improve tissue function. Promoter analysis of the differentially regulated genes in KMVECs suggests that the transcription factor FOXO1 is highly active and RNAseq analysis revealed that hyperactive FOXO1 inhibits VEGF-Notch-dependent tip-cell formation by direct and indirect inhibition of DLL4 expression in response to VEGF. Inhibition of FOXO1 enhanced angiogenesis in human bio-engineered capillaries, and resulted in microvascular regeneration and improved function in mouse models of injury-repair. [ABSTRACT FROM AUTHOR]

The intestinal epithelium comprises diverse cell types and executes many specialized functions as the primary interface between luminal contents and internal organs. A key function provided by the epithelium is maintenance of a barrier that protects the individual from pathogens, irritating luminal contents, and the microbiota. Disruption of this barrier can lead to inflammatory disease within the intestinal mucosa, and, in more severe cases, to sepsis. Animal models to study intestinal permeability are costly and not entirely predictive of human biology. Here we present a model of human colon barrier function that integrates primary human colon stem cells into Draper's PREDICT96 microfluidic organ-on-chip platform to yield a high-throughput system appropriate to predict damage and healing of the human colon epithelial barrier. We have demonstrated pharmacologically induced barrier damage measured by both a high throughput molecular permeability assay and transepithelial resistance. Using these assays, we developed an Inflammatory Bowel Disease-relevant model through cytokine induced damage that can support studies of disease mechanisms and putative therapeutics. [ABSTRACT FROM AUTHOR]

Fibrotic disease is associated with matrix deposition that results in the loss of organ function. Pericytes, the precursors of myofibroblasts, are a source of pathological matrix collagens and may be promising targets for treating fibrogenesis. Here, we have shown that pericytes activate a TLR2/4- and MyD88-dependent proinflammatory program in response to tissue injury. Similarly to classic immune cells, pericytes activate the NLRP3 inflammasome, leading to IL-1β and IL-18 secretion. Released IL-1β signals through pericyte MyD88 to amplify this response. Unexpectedly, we found that MyD88 and its downstream effector kinase IRAK4 intrinsically control pericyte migration and conversion to myofibroblasts. Specific ablation of MyD88 in pericytes or pharmacological inhibition of MyD88 signaling by an IRAK4 inhibitor in vivo protected against kidney injury by profoundly attenuating tissue injury, activation, and differentiation of myofibroblasts. Our data show that in pericytes, MyD88 and IRAK4 are key regulators of 2 major injury responses: inflammatory and fibrogenic. Moreover, these findings suggest that disruption of this MyD88-dependent pathway in pericytes might be a potential therapeutic approach to inhibit fibrogenesis and promote regeneration. [ABSTRACT FROM AUTHOR]