Development of thin-film nickel hydroxide electrochromic materials using in situ microfocus XAFS and XRD techniques

The use of nickel hydroxide as a colour switching material in electrochromic devices such as smart windows is yet to be fully exploited. Stabilisation of the highly electroactive α nickel hydroxide / γ nickel oxyhydroxide redox couple through co-deposition of other metal ions could lead to devices with improved performance in terms of response time and cycle lifetime. This thesis presents the current understanding of nickel hydroxide phases and their relationship to one another, various ways to form nickel hydroxide materials and the effect of doping nickel hydroxide materials with cobalt, cadmium, zinc, manganese, iron, aluminium ions. In addition, this thesis describes the basic components of an in situ electrochemical cell and compares in situ cell designs used to study electrochemically active thin films under potential control with synchrotron light sources. The thesis follows with a description of the synthesis of various phases of nickel hydroxide via chemical precipitation to form powder and the electrochemical deposition method to deposit thin films and demonstrates the development of a novel in situ electrochemical flow cell, designed for in situ XAFS analysis of nickel hydroxide thin films under potential control. The thesis also highlights that this is the first time a transparent conductive oxide coated polymer film is used as both a working electrode and x-ray window material for an in situ electrochemical cell

A First Search for coincident Gravitational Waves and High Energy Neutrinos using LIGO, Virgo and ANTARES data from 2007

We present the results of the first search for gravitational wave bursts associated with high energy neutrinos. Together, these messengers could reveal new, hidden sources that are not observed by conventional photon astronomy, particularly at high energy. Our search uses neutrinos detected by the underwater neutrino telescope ANTARES in its 5 line configuration during the period January - September 2007, which coincided with the fifth and first science runs of LIGO and Virgo, respectively. The LIGO-Virgo data were analysed for candidate gravitational-wave signals coincident in time and direction with the neutrino events. No significant coincident events were observed. We place limits on the density of joint high energy neutrino - gravitational wave emission events in the local universe, and compare them with densities of merger and core-collapse events.Comment: 19 pages, 8 figures, science summary page at http://www.ligo.org/science/Publication-S5LV_ANTARES/index.php. Public access area to figures, tables at https://dcc.ligo.org/cgi-bin/DocDB/ShowDocument?docid=p120000

Multi-ancestry GWAS of the electrocardiographic PR interval identifies 202 loci underlying cardiac conduction

The electrocardiographic PR interval reflects atrioventricular conduction, and is associated with conduction abnormalities, pacemaker implantation, atrial fibrillation (AF), and cardiovascular mortality. Here we report a multi-ancestry (N = 293,051) genome-wide association meta-analysis for the PR interval, discovering 202 loci of which 141 have not previously been reported. Variants at identified loci increase the percentage of heritability explained, from 33.5% to 62.6%. We observe enrichment for cardiac muscle developmental/contractile and cytoskeletal genes, highlighting key regulation processes for atrioventricular conduction. Additionally, 8 loci not previously reported harbor genes underlying inherited arrhythmic syndromes and/or cardiomyopathies suggesting a role for these genes in cardiovascular pathology in the general population. We show that polygenic predisposition to PR interval duration is an endophenotype for cardiovascular disease, including distal conduction disease, AF, and atrioventricular pre-excitation. These findings advance our understanding of the polygenic basis of cardiac conduction, and the genetic relationship between PR interval duration and cardiovascular disease

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 hospitalization2,3,4 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

Intragastric acidification reduces the occurrence of false-negative urea breath test results in patients taking a proton pump inhibitor

The aim of this study was to investigate whether reducing intragastric pH, at the time of urea ingestion, decreases the likelihood of false-negative (FN) urea breath test (UBT) results in patients taking a proton pump inhibitor (PPI). Methods : Patients with active Helicobacter pylori infection underwent a baseline 14 C-UBT (UBT-1) followed by treatment with lansoprazole 30 mg/day for 14 to 16 days. On day 13, patients returned for a repeat standard UBT (UBT-2). Between days 14 to 16, patients underwent a modified UBT (UBT-3), which included consuming 200 ml of 0.1 N citrate solution 30 min before and at the time of 14 C-urea administration. Breath samples were collected 10 and 15 min after 14 C-urea ingestion. Mean 14 CO 2 excretion and the number of FN and equivocal UBT results were compared for the three UBTs. Results : A total of 20 patients completed the study. Lansoprazole caused a significant decrease in mean breath 14 CO 2 excretion (disintegrations per minute) between UBT-1 (2.96 ± 0.23) and UBT-2 (2.08 ± 0.52, p < 0.05 ). Lansoprazole caused six (30%) FN and eight (40%) equivocal UBT-2 results. Mean breath 14 CO 2 excretion for UBT-3 (677 ± 514) was greater than for UBT-2 (234 ± 327, p = 0.001 ). UBT-3 caused only two (10%) FN and three (15%) equivocal results. The 15-min breath sample caused fewer FN and equivocal results than the 10-min sample for both UBT-2 and UBT-3. Conclusions : Giving citrate before and at the time of 14 C-urea administration increases mean breath 14 CO 2 excretion and decreases FN and equivocal UBT results in patients taking a PPI. These observations suggest that it may be possible to design a UBT protocol that will remain accurate in the face of PPI therapy.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/71971/1/j.1572-0241.2001.03687.x.pd