Magnetic moments of the 3/2 resonances and their quark spin structure

We discuss magnetic moments of the $J=3/2$ baryons based on an earlier model for the baryon magnetic moments, allowing for flavor symmetry breaking in the quark magnetic moments as well as a general quark spin structure. From our earlier analysis of the nucleon-hyperon magnetic moments and the measured values of the magnetic moments of $\Delta^{++}$ and $\Omega^{-}$ we predict the other magnetic moments and deduce the spin structure of the resonance particles. We find from experiment that the total spin polarization of the decuplet baryons, $\Delta\Sigma(3/2)$, is considerably smaller than the non-relativistic quark model value of 3, although the data is still not good enough to give a precise determination.Comment: 13 pages, REVTeX, 2 figures, minor clarifying change

Genome-wide association analyses identify 13 new susceptibility loci for generalized vitiligo

We previously reported a genome-wide association study (GWAS) identifying 14 susceptibility loci for generalized vitiligo. We report here a second GWAS (450 individuals with vitiligo (cases) and 3,182 controls), an independent replication study (1,440 cases and 1,316 controls) and a meta-analysis (3,187 cases and 6,723 controls) identifying 13 additional vitiligo-associated loci. These include OCA2-HERC2 (combined P = 3.80 × 10 ), MC1R (P = 1.82 × 10 ), a region near TYR (P = 1.57 × 10 ), IFIH1 (P = 4.91 × 10 ), CD80 (P = 3.78 × 10 ), CLNK (P = 1.56 × 10 ), BACH2 (P = 2.53 × 10 ), SLA (P = 1.58 × 10 ), CASP7 (P = 3.56 × 10 ), CD44 (P = 1.78 × 10 ), IKZF4 (P = 2.75 × 10 ), SH2B3 (P = 3.54 × 10 ) and TOB2 (P = 6.81 × 10 ). Most vitiligo susceptibility loci encode immunoregulatory proteins or melanocyte components that likely mediate immune targeting and the relationships among vitiligo, melanoma, and eye, skin and hair coloration

Magnetic Moments of JP=3/2+J^P=3/2^+ Heavy Baryons Using Effective Mass and Screened Charge Scheme

Magnetic moments of heavy charmed baryons with $J^P=3/2^+$ are predicted employing the concept of effective quark mass and screened charge of quark. We also extend our scheme to predict the $3/2^+ --> 1/2^+$ transition magnetic moments. A comparison of our results with the predictions obtained in recent models is presented.Comment: 19 pages, Accepted for publication in EPJ-

Use of SMS texts for facilitating access to online alcohol interventions: a feasibility study

A41 Use of SMS texts for facilitating access to online alcohol interventions: a feasibility study In: Addiction Science & Clinical Practice 2017, 12(Suppl 1): A4

A disease-associated gene desert directs macrophage inflammation through ETS2

Increasing rates of autoimmune and inflammatory disease present a burgeoning threat to human health1. This is compounded by the limited efficacy of available treatments1 and high failure rates during drug development2, highlighting an urgent need to better understand disease mechanisms. Here we show how functional genomics could address this challenge. By investigating an intergenic haplotype on chr21q22—which has been independently linked to inflammatory bowel disease, ankylosing spondylitis, primary sclerosing cholangitis and Takayasu’s arteritis3–6—we identify that the causal gene, ETS2, is a central regulator of human inflammatory macrophages and delineate the shared disease mechanism that amplifies ETS2 expression. Genes regulated by ETS2 were prominently expressed in diseased tissues and more enriched for inflammatory bowel disease GWAS hits than most previously described pathways. Overexpressing ETS2 in resting macrophages reproduced the inflammatory state observed in chr21q22-associated diseases, with upregulation of multiple drug targets, including TNF and IL-23. Using a database of cellular signatures7, we identified drugs that might modulate this pathway and validated the potent anti-inflammatory activity of one class of small molecules in vitro and ex vivo. Together, this illustrates the power of functional genomics, applied directly in primary human cells, to identify immune-mediated disease mechanisms and potential therapeutic opportunities

Adiponectin and the systemic inflammatory response in weight-losing patients with non-small cell lung cancer

The aim of the present study was to examine the relationship between adiponectin and the systemic inflammatory response in weight-losing patients with non-small cell lung cancer (NSCLC). Measurement of anthropometry, acute phase proteins, interleukin-6, leptin (total and free) and adiponectin were carried out on healthy subjects (n=13) and non-small cell lung cancer patients with weight loss (n=20). The groups were age and sex matched. Compared with the controls the cancer group had a lower BMI (p<0.01), mid-upper arm circumference (p<0.001), triceps skinfold thickness (p<0.05) and circulating concentrations of albumin (p<0.001), haemoglobin (p<0.05), free and total leptin (p<0.05) and adiponectin (p<0.01). In contrast, the cancer group had elevated circulating concentrations of interleukin-6 and C-reactive protein concentrations (p<0.001). In the cancer group circulating adiponectin concentrations were significantly inversely correlated with both free (rs=−0.675, p=0.001) and total leptin concentrations (rs=−0.690, p=0.001). However, neither weight loss, interleukin-6 or C-reactive protein concentrations were correlated with either adiponectin, free or total leptin concentrations in the cancer group. These results suggest that adipokine production is normal and is unlikely to play a major role in the abnormal fat metabolism in weight-losing cancer patients

Comparison of simple acid-ethanol precipitation with gel exclusion chromatography for measuring leptin binding in serum of normal subjects and cancer patients

<p><b>Background:</b> In humans, leptin circulates in a free form and is also bound to macromolecules. The aim of the present study was to compare a rapid acid-ethanol precipitation (AEP) method of measuring bound leptin with the more laborious gel exclusion chromatography (GEC) reference procedure. Serum samples collected from healthy subjects and cancer patients were used in this comparison.</p> <p><b>Methods:</b> AEP and GEC methods for measuring leptin binding in serum (from 14 healthy volunteers and 14 patients with advanced non-small cell lung cancer) were adapted from previously published procedures.</p> <p><b>Results:</b> Intra- and inter-assay precision of the AEP method were 6% (n = 10) and 8% (n = 10), respectively. Bland-Altman analysis of results obtained from the AEP and GEC methods indicated no significant difference in healthy controls. However, significantly higher results were obtained by the AEP method in the cancer patients.</p> <p><b>Conclusions:</b> Evaluation of the AEP method revealed that on examination of normal subjects the method was less precise than had previously been reported. Moreover, the method gave differing results in the cancer patients when compared with the GEC method. This study indicates that careful evaluation of any new method for measuring leptin binding requires comparison with a GEC method using the sample matrix of interest.</p&gt