A Continuous Dilution Calibration Technique for Flame Atomic-Absorption Spectrophotometry

Calibration in atomic-absorption spectrometry is achieved by means of a concentration-­gradient chamber using a single concentrated standard solution. Calibration is rapid and extends over the entire working concentration range of the analyte, irrespective of the shape of the conventionally obtained calibration curve. No curve-fitting approximations are involved. With well-designed apparatus, deviations are less than 1%

A Variable Dispersion Flow Injection Manifold for Calibration and Sample Dilution in Flame Atomic Absorption Spectrometry

A flow injection (FI) introduction system for flame atomic absorption spectrometry (FAAS) has been constructed for single-standard calibration and sample dilution. Dilution factors ranging from 5.93 to 38.8 in six discrete stages were produced by replicate injection of 12.5-pl volumes into an aqueous carrier stream flowing down lines of different lengths. The dilution factors were measured for five different solutions for each line. No dependence on concentration was found and the relative standard deviations ranged from 0.75 to 3.1%. The manifold was evaluated by the analysis of solutions of magnesium (6,12.5 and 35 p.p.m.), nickel (180 p.p.m.), calcium (75 p.p.m.) and chromium (180 p.p.m.). Recoveries ranging from 95.3 to 106.8% were obtained with no over-all evidence of bias. The uncertainty in the over-all method, including a contribution from the curve-fitting procedure, was estimated to be 5%

Performance of distributed PV in the UK: a statistical analysis of over 7000 systems

In June 2015, the UK fleet of solar photovoltaic (PV) systems reached 7.8 GWp of capacity, but there are wide gaps in our understanding of the performance of these systems, which has lead to the conservative limit of 10 GWp being imposed on UK PV capacity by the Department of Energy and Climate Change. Here we present the results of a statistical analysis of real world UK PV systems which donate data to the Microgen Database, of which there are over 7000. The mean yearly-integrated Performance Ratio (PR) of domestic scale UK PV is 83% with a standard deviation of 7%. By considering yearly-integrated PR, we have shown that 4.1 % of systems suffered long-term underperformance relative to their nominal efficiencies during 2013. The mean degradation rate for crystalline Siliconbased PV systems in the UK is -0.8 ± 0.1% per year. The state-of-the-art of UK PV, in terms of technology, manufacturing, and installation-standards, is found to have increased by 1% per year between 2002 and 2013

Detection and diversity of a putative novel heterogeneous polymorphic proline-glycine repeat (Pgr) protein in the footrot pathogen Dichelobacter nodosus

Dichelobacter nodosus, a Gram-negative anaerobic bacterium, is the essential causative agent of footrot in sheep. Currently, depending on the clinical presentation in the field, footrot is described as benign or virulent; D. nodosus strains have also been classified as benign or virulent, but this designation is not always consistent with clinical disease. The aim of this study was to determine the diversity of the pgr gene, which encodes a putative proline-glycine repeat protein (Pgr). The pgr gene was present in all 100 isolates of D. nodosus that were examined and, based on sequence analysis had two variants, pgrA and pgrB. In pgrA, there were two coding tandem repeat regions, R1 and R2: different strains had variable numbers of repeats within these regions. The R1 and R2 were absent from pgrB. Both variants were present in strains from Australia, Sweden and the UK, however, only pgrB was detected in isolates from Western Australia. The pgrA gene was detected in D. nodosus from tissue samples from two flocks in the UK with virulent footrot and only pgrB from a flock with no virulent or benign footrot for >10 years. Bioinformatic analysis of the putative PgrA protein indicated that it contained a collagen-like cell surface anchor motif. These results suggest that the pgr gene may be a useful molecular marker for epidemiological studies

Photoluminescence and raman scattering of GaAs1-xBix alloy

Photoluminescence (PL) and Raman spectra of GaAs1-xBix samples grown at different rates (0.09 to 0.5 µm/h) were investigated. The PL peak wavelength initially redshifted with the increase of growth rate and reached the longest wavelength (1158 nm) for sample grown at 0.23 µm/h. This is followed by PL peak wavelength blueshift for higher growth rates. The Raman data show peaks at 162, 228, 270, and 295 cm-1 which can be attributed to GaAs like phonons. GaBi like vibrational modes were also observed at 183 and 213 cm-1. However, the intensity of Bi induced phonons is significantly weaker compared to GaAs due to low concentration of Bi compared to As and thin GaAs1-xBix epilayer. The PL data and GaAs transverse optical (TO) to longitudinal optical (LO) phonons intensity ratio indicate that Bi concentration is highly dependent on the growth rate and the highest Bi concentration was obtained by sample grown at 0.23 µm/h. It is found that the full-width-at-half-maximum (FWHM) of GaAs LO mode increases significantly for samples grown at high growth rates suggesting crystal quality degradation due to lack of surfactant effects

Von Hippel-Lindau mutations disrupt vascular patterning and maturation via Notch

Von Hippel-Lindau (VHL) gene mutations induce neural tissue hemangioblastomas, as well as highly vascularized clear cell renal cell carcinomas (ccRCCs). Pathological vessel remodeling arises from misregulation of HIFs and VEGF, among other genes. Variation in disease penetrance has long been recognized in relation to genotype. We show Vhl mutations also disrupt Notch signaling, causing mutation-specific vascular abnormalities, e.g., type 1 (null) vs. type 2B (murine G518A representing human R167Q). In conditional mutation retina vasculature, Vhl-null mutation (i.e., UBCCreER/+Vhlfl/fl) had little effect on initial vessel branching, but it severely reduced arterial and venous branching at later stages. Interestingly, this mutation accelerated arterial maturation, as observed in retina vessel morphology and aberrant α-smooth muscle actin localization, particularly in vascular pericytes. RNA sequencing analysis identified gene expression changes within several key pathways, including Notch and smooth muscle cell contractility. Notch inhibition failed to reverse later-stage branching defects but rescued the accelerated arterialization. Retinal vessels harboring the type 2B Vhl mutation (i.e., UBCCreER/+Vhlfl/2B) displayed stage-specific changes in vessel branching and an advanced progression toward an arterial phenotype. Disrupting Notch signaling in type 2B mutants increased both artery and vein branching and restored arterial maturation toward nonmutant levels. By revealing differential effects of the null and type 2B Vhl mutations on vessel branching and maturation, these data may provide insight into the variability of VHL-associated vascular changes - particularly the heterogeneity and aggressiveness in ccRCC vessel growth - and also suggest Notch pathway targets for treating VHL syndrome

The polycystic kidney disease 1 gene encodes a 14 kb transcript and lies within a duplicated region on chromosome 16

Autosomal dominant polycystic kidney disease (ADPKD) is a common genetic disorder that frequently results in renal fallure due to progressive cyst development. The major locus, PKD1, maps to 16p13.3. We identified a chromosome translocation associated with ADPKD that disrupts a gene (PBP) encoding a 14 kb transcript in the PKD1 candidate region. Further mutations of the PBP gene were found in PKD1 patients, two deletions (one a de novo event) and a splicing defect, confirming that PBP is the PKD1 gene. This gene is located adjacent to the TSC2 locus in a genomic region that is reiterated more proximally on 16p. The duplicate area encodes three transcripts substantially homologous to the PKD1 transcript. Partial sequence analysis of the PKD1 transcript shows that it encodes a novel protein whose function is at present unknown