A Radio Determination of the Time of the New Moon

The detection of the New Moon at sunset is of importance to communities based on the lunar calendar. This is traditionally undertaken with visual observations. We propose a radio method which allows a higher visibility of the Moon relative to the Sun and consequently gives us the ability to detect the Moon much closer to the Sun than is the case of visual observation. We first compare the relative brightness of the Moon and Sun over a range of possible frequencies and find the range 5--100\,GHz to be suitable. The next consideration is the atmospheric absorption/emission due to water vapour and oxygen as a function of frequency. This is particularly important since the relevant observations are near the horizon. We show that a frequency of $\sim 10$ GHz is optimal for this programme. We have designed and constructed a telescope with a FWHM resolution of 0$^\circ{}\!\!$.6 and low sidelobes to demonstrate the potential of this approach. At the time of the 21 May 2012 New Moon the Sun/Moon brightness temperature ratio was $72.7 \pm 2.2$ in agreement with predictions from the literature when combined with the observed sunspot numbers for the day. The Moon would have been readily detectable at $\sim 2^{\circ}$ from the Sun. Our observations at 16\,hr\,36\,min UT indicated that the Moon would have been at closest approach to the Sun 16\,hr\,25\,min earlier; this was the annular solar eclipse of 00\,hr\,00\,min\,UT on 21 May 2012.Comment: 11 pages, 15 figures, accepted for publication in MNRA

Optimal scanning protocols of 64-slice CT angiography in coronary artery stents: An in vitro phantom study

Purpose: The purpose of the studywas to investigate the optimal scanning protocol of 64-slice CT angiographyfor assessment of coronary artery stents based on a phantom study.Materials and methods: Coronary stents with a diameter of 2.5mm was implanted in thin plastic tubeswith an inner diameter of 3.0mm to simulate a coronary artery. The tubes were filled with iodinatedcontrast medium diluted to 178HU, closed at both ends and positioned in a plastic container filled withvegetable oil (-70 to -100 HU). A series of scans were performed with a 64-slice CT scanner with thefollowing protocols: section thickness: 0.67mm, 1.0mm, 1.5mm, 2.0mm, pitch value: 0.2, 0.3, 0.5 andreconstruction interval of 50% overlap of the section thickness. 2D axial and multiplanar reformattedimageswere generated to assess the visibility of stent lumen, while virtual intravascular endoscopy (VIE)was reconstructed to evaluate the artery wall and stent surface.Results: Our results showed that a scanning protocol of 1.0mmslice thickness with a pitch of 0.3 producedacceptable images with best demonstration of the intrastent lumen and stent surface with minimal imagenoise or artifacts. In contrast, submillimeter scans with 0.67mm resulted in moderate artifacts whichaffected visualization of the coronary lumen, in addition to the increased noise. When the section thicknessincreased to 1.5mmand 2.0mm, visualization of the arterywall and stent surfacewas compromised,although the intrastent lumen was still visible.Conclusion: Our in vitro study suggested that a scanning protocol of 1.0mm section thickness with pitchof 0.3 is the optimal protocol for evaluation of coronary artery stents as it allows generation of acceptableimages with better visualization of stent lumen, stent surface and coronary artery wall

Prevalence of coronary artery disease and its risk factors in Majmaah City, Kingdom of Saudi Arabia

ObjectiveThis study was carried out with an aim to outline the prevalence of coronary artery diseases, its risk of one region of the Saudi Arabia.MethodsA retrospective observational study conducted across five secondary medical centers located in the city of Majmaah. Hospital medical records and ministry of health records were screened over a 6-month period for data on patients admitted for Coronary artery disease (CAD). Data collected included sociodemographic characteristics, medical profile, and laboratory findings.ResultsA total of 327 participants were included in this study with a median age of 64 and the majority being male participants (59.8%). The majority were married, held a primary school degree and earned a salary for living. A large number (82.9%) were hypertensive and diabetic (66.7%) and one-fourth had a previous MI (25.1%). A large number (73.7%) had heart failure with a mean ejection fraction of 44% (SD = 13). The causes of heart failure were mainly ischemic (56.3%) and hypertensive (28.1%). Readmission rates at 30 and 90 days then at 6 and 12 months were 22, 53.8, 68.8, and 75.8%, respectively. The mortality rates at the same time intervals were 5.5, 8.9, 14.1, and 22.9%, respectively. Predictors of readmission are age, CCI, and NYHA class.ConclusionCoronary artery disease is the leading cause of heart failure. End stage CAD can have similar results in terms of readmission and mortality as heart failure. Future research should target patients in different stages of the condition and monitor their comorbidities which may impact the study findings

Genetic and phenotypic characterization of NKX6‐2‐related spastic ataxia and hypomyelination

Background and purpose Hypomyelinating leukodystrophies are a heterogeneous group of genetic disorders with a wide spectrum of phenotypes and a high rate of genetically unsolved cases. Bi‐allelic mutations in NKX6‐2 were recently linked to spastic ataxia 8 with hypomyelinating leukodystrophy. Methods Using a combination of homozygosity mapping, exome sequencing, and detailed clinical and neuroimaging assessment a series of new NKX6‐2 mutations in a multicentre setting is described. Then, all reported NKX6‐2 mutations and those identified in this study were combined and an in‐depth analysis of NKX6‐2‐related disease spectrum was provided. Results Eleven new cases from eight families of different ethnic backgrounds carrying compound heterozygous and homozygous pathogenic variants in NKX6‐2 were identified, evidencing a high NKX6‐2 mutation burden in the hypomyelinating leukodystrophy disease spectrum. Our data reveal a phenotype spectrum with neonatal onset, global psychomotor delay and worse prognosis at the severe end and a childhood onset with mainly motor phenotype at the milder end. The phenotypic and neuroimaging expression in NKX6‐2 is described and it is shown that phenotypes with epilepsy in the absence of overt hypomyelination and diffuse hypomyelination without seizures can occur. Conclusions NKX6‐2 mutations should be considered in patients with autosomal recessive, very early onset of nystagmus, cerebellar ataxia with hypotonia that rapidly progresses to spasticity, particularly when associated with neuroimaging signs of hypomyelination. Therefore, it is recommended that NXK6‐2 should be included in hypomyelinating leukodystrophy and spastic ataxia diagnostic panels

Controlled depolymerisation, as assessed by analytical ultracentrifugation, of low molecular weight chitosan for potential use in archaeological conservation

The heterogeneity and molecular weight of a chitosan of low molecular weight (molar mass) and low degree of acetylation (0.1), for potential use as a consolidant for decayed archaeological wood, has been examined by sedimentation velocity and sedimentation equilibriumin the analytical ultracentrifuge before and after depolymerisation. Sedimentation velocity before polymerisation revealed a uniform distribution of sedimentation coefficient with little concentration dependence. SEDFIT-MSTAR analysis revealed a weight average molecular weight Mw of (14.2 + 1.2) kDa, and polydispersity index of ~ 1.2. Further analysis using MULTISIG revealed a distribution of material between 2-20 kDa and consistent with the weight average Mw. Controlled depolymerisation using hydrogen peroxide and UV in an acetic acid medium reduced this to (4.9 + 0.7) kDa, with a similar polydispersity. The depolymerised material appears to be within the range that has been predicted to fully penetrate into archaeological wood. The consequences for this and the use of the analytical ultracentrifuge in wood conservation strategies is considered

SPARC 2018 Internationalisation and collaboration : Salford postgraduate annual research conference book of abstracts

Welcome to the Book of Abstracts for the 2018 SPARC conference. This year we not only celebrate the work of our PGRs but also the launch of our Doctoral School, which makes this year’s conference extra special. Once again we have received a tremendous contribution from our postgraduate research community; with over 100 presenters, the conference truly showcases a vibrant PGR community at Salford. These abstracts provide a taster of the research strengths of their works, and provide delegates with a reference point for networking and initiating critical debate. With such wide-ranging topics being showcased, we encourage you to take up this great opportunity to engage with researchers working in different subject areas from your own. To meet global challenges, high impact research inevitably requires interdisciplinary collaboration. This is recognised by all major research funders. Therefore engaging with the work of others and forging collaborations across subject areas is an essential skill for the next generation of researchers

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2–4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

Erratum to: 36th International Symposium on Intensive Care and Emergency Medicine

[This corrects the article DOI: 10.1186/s13054-016-1208-6.]

SARS-CoV-2 susceptibility and COVID-19 disease severity are associated with genetic variants affecting gene expression in a variety of tissues

Variability in SARS-CoV-2 susceptibility and COVID-19 disease severity between individuals is partly due to genetic factors. Here, we identify 4 genomic loci with suggestive associations for SARS-CoV-2 susceptibility and 19 for COVID-19 disease severity. Four of these 23 loci likely have an ethnicity-specific component. Genome-wide association study (GWAS) signals in 11 loci colocalize with expression quantitative trait loci (eQTLs) associated with the expression of 20 genes in 62 tissues/cell types (range: 1:43 tissues/gene), including lung, brain, heart, muscle, and skin as well as the digestive system and immune system. We perform genetic fine mapping to compute 99% credible SNP sets, which identify 10 GWAS loci that have eight or fewer SNPs in the credible set, including three loci with one single likely causal SNP. Our study suggests that the diverse symptoms and disease severity of COVID-19 observed between individuals is associated with variants across the genome, affecting gene expression levels in a wide variety of tissue types