Characterizing volcanic ash density and its implications on settling dynamics

Volcanic ash clouds are carefully monitored as they present a significant hazard to humans and aircraft. The primary tool for forecasting the transport of ash from a volcano is dispersion modelling. These models make a number of assumptions about the size, sphericity and density of the ash particles. Few studies have measured the density of ash particles or explored the impact that the assumption of ash density might have on the settling dynamics of ash particles. In this paper, the raw apparent density of 23 samples taken from 15 volcanoes are measured with gas pycnometry, and a negative linear relationship is found between the density and the silica content. For the basaltic ash samples, densities were measured for different particle sizes, showing that the density is approximately constant for particles smaller than 100 µm, beyond which it decreases with size. While this supports the current dispersion model used by the London Volcanic Ash Advisory Centre (VAAC), where the density is held at a constant (2.3 g cm-3), inputting the measured densities into a numerical simulation of settling velocity reveals a primary effect from the silica content changing this constant. The VAAC density overestimates ash removal times by up to 18 %. These density variations, including those varying with size beyond 100 µm, also impact short-range particle-size distribution (PSD) measurements and satellite retrievals of ash

Integration of an On-Axis General Sun-Tracking Formula in the Algorithm of an Open-Loop Sun-Tracking System

A novel on-axis general sun-tracking formula has been integrated in the algorithm of an open-loop sun-tracking system in order to track the sun accurately and cost effectively. Sun-tracking errors due to installation defects of the 25 m2 prototype solar concentrator have been analyzed from recorded solar images with the use of a CCD camera. With the recorded data, misaligned angles from ideal azimuth-elevation axes have been determined and corrected by a straightforward changing of the parameters' values in the general formula of the tracking algorithm to improve the tracking accuracy to 2.99 mrad, which falls below the encoder resolution limit of 4.13 mrad

Comparison of performance of the Assessment of Spondyloarthritis International Society, the European Spondyloarthropathy Study Group and the modified New York criteria in a cohort of Chinese patients with spondyloarthritis

Early diagnosis of spondyloarthritis (SpA) is essential as anti-tumor necrosis factor therapy can achieve significant symptomatic relief and control of disease activity. This study aims to compare the clinical characteristics, disease activity, and functional status of a Chinese cohort of SpA patients who were re-classified into ankylosing spondylitis (AS) patients fulfilling the modified New York (MNY) criteria, those with undifferentiated SpA (USpA) fulfilling the European Spondyloarthropathy Study Group (ESSG) classification criteria only (USpA/ESSG) and those who fulfill Assessment of SpondyloArthritis International Society (ASAS) only (USpA/ASAS). Disease activity was evaluated by Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), severity of morning stiffness, patient global assessment, and C-reactive protein. Functional status was evaluated by Bath Ankylosing Spondylitis Functional Index (BASFI), modified Schober index, and dimension of chest expansion. One hundred and twenty-eight patients with disease duration of 16.3 ± 10.4 years were recruited. Patients in USpA/ESSG and USpA/ASAS were significantly younger (p = 0.01), had shorter disease duration (p < 0.01), and lower BASFI (p = 0.03) than established AS patients. All three groups have active disease with comparable BASDAI >3. BASFI correlated inversely with dimension of chest expansion and negatively modified Schober index in AS patients (p < 0.01) and modestly with BASDAI (r = 0.25, p < 0.01). BASFI correlated moderately with BASDAI in USpA/ESSG (r = 0.61, p < 0.01) but not with chest expansion or modified Schober index. Compared with established AS patients recognized by MNY criteria, patients fulfilling USpA defined by ESSG or ASAS criteria had earlier disease, as active disease and less irreversible functional deficit

Genome-Wide Association Study in Asian Populations Identifies Variants in ETS1 and WDFY4 Associated with Systemic Lupus Erythematosus

Systemic lupus erythematosus is a complex and potentially fatal autoimmune disease, characterized by autoantibody production and multi-organ damage. By a genome-wide association study (320 patients and 1,500 controls) and subsequent replication altogether involving a total of 3,300 Asian SLE patients from Hong Kong, Mainland China, and Thailand, as well as 4,200 ethnically and geographically matched controls, genetic variants in ETS1 and WDFY4 were found to be associated with SLE (ETS1: rs1128334, P = 2.33×10−11, OR = 1.29; WDFY4: rs7097397, P = 8.15×10−12, OR = 1.30). ETS1 encodes for a transcription factor known to be involved in a wide range of immune functions, including Th17 cell development and terminal differentiation of B lymphocytes. SNP rs1128334 is located in the 3′-UTR of ETS1, and allelic expression analysis from peripheral blood mononuclear cells showed significantly lower expression level from the risk allele. WDFY4 is a conserved protein with unknown function, but is predominantly expressed in primary and secondary immune tissues, and rs7097397 in WDFY4 changes an arginine residue to glutamine (R1816Q) in this protein. Our study also confirmed association of the HLA locus, STAT4, TNFSF4, BLK, BANK1, IRF5, and TNFAIP3 with SLE in Asians. These new genetic findings may help us to gain a better understanding of the disease and the functions of the genes involved

Meta-analysis Followed by Replication Identifies Loci in or near CDKN1B, TET3, CD80, DRAM1, and ARID5B as Associated with Systemic Lupus Erythematosus in Asians

Systemic lupus erythematosus (SLE) is a prototype autoimmune disease with a strong genetic involvement and ethnic differences. Susceptibility genes identified so far only explain a small portion of the genetic heritability of SLE, suggesting that many more loci are yet to be uncovered for this disease. In this study, we performed a meta-analysis of genome-wide association studies on SLE in Chinese Han populations and followed up the findings by replication in four additional Asian cohorts with a total of 5,365 cases and 10,054 corresponding controls. We identified genetic variants in or near CDKN1B, TET3, CD80, DRAM1, and ARID5B as associated with the disease. These findings point to potential roles of cell-cycle regulation, autophagy, and DNA demethylation in SLE pathogenesis. For the region involving TET3 and that involving CDKN1B, multiple independent SNPs were identified, highlighting a phenomenon that might partially explain the missing heritability of complex diseases

Genome-Wide DNA Methylation Analysis of Chinese Patients with Systemic Lupus Erythematosus Identified Hypomethylation in Genes Related to the Type I Interferon Pathway

<div><p>Background</p><p>Epigenetic variants have been shown in recent studies to be important contributors to the pathogenesis of systemic lupus erythematosus (SLE). Here, we report a 2-step study of discovery followed by replication to identify DNA methylation alterations associated with SLE in a Chinese population. Using a genome-wide DNA methylation microarray, the Illumina Infinium HumanMethylation450 BeadChip, we compared the methylation levels of CpG sites in DNA extracted from white blood cells from 12 female Chinese SLE patients and 10 healthy female controls.</p><p>Results</p><p>We identified 36 CpG sites with differential loss of DNA methylation and 8 CpG sites with differential gain of DNA methylation, representing 25 genes and 7 genes, respectively. Surprisingly, 42% of the hypomethylated CpG sites were located in CpG shores, which indicated the functional importance of the loss of DNA methylation. Microarray results were replicated in another cohort of 100 SLE patients and 100 healthy controls by performing bisulfite pyrosequencing of four hypomethylated genes, <i>MX1</i>, <i>IFI44L</i>, <i>NLRC5</i> and <i>PLSCR1</i>. In addition, loss of DNA methylation in these genes was associated with an increase in mRNA expression. Gene ontology analysis revealed that the hypomethylated genes identified in the microarray study were overrepresented in the type I interferon pathway, which has long been implicated in the pathogenesis of SLE.</p><p>Conclusion</p><p>Our epigenetic findings further support the importance of the type I interferon pathway in SLE pathogenesis. Moreover, we showed that the DNA methylation signatures of SLE can be defined in unfractionated white blood cells.</p></div

Comparison of the methylation level of four hypomethylated genes between control and SLE patients.

<p>Bisulfite pyrosequencing was carried out on four of the genes that were found to be differentially methylated in the 450k microarray and in a larger cohort of 100 SLE patients and 100 healthy controls. These genes are <i>MX1</i>, <i>IFI44L</i>, <i>NLRC5</i> and <i>PLSCR1</i>. Bisulfite pyrosequencing of all four genes confirmed the microarray findings, showing that SLE patients have a significant loss of methylation when compared to healthy controls.</p