Electromagnetic field angular momentum in condensed matter systems

Various electromagnetic systems can carry an angular momentum in their {\bf E} and {\bf B} fields. The electromagnetic field angular momentum (EMAM) of these systems can combine with the spin angular momentum to give composite fermions or composite bosons. In this paper we examine the possiblity that an EMAM could provide an explanation of the fractional quantum Hall effect (FQHE) which is complimentary to the Chern-Simons explanation. We also examine a toy model of a non-BCS superconductor (e.g. high $T_c$ superconductors) in terms of an EMAM. The models presented give a common, simple picture of these two systems in terms of an EMAM. The presence of an EMAM in these systems might be tested through the observation of the decay modes of a charged, spin zero unstable particle inside one of these systems.Comment: 17 pages, no figures, to be published in Phys. Rev.

Super-Luminal Effects for Finsler Branes as a Way to Preserve the Paradigm of Relativity Theories

Using Finsler brane solutions [see details and methods in: S. Vacaru, Class. Quant. Grav. 28 (2011) 215001], we show that neutrinos may surpass the speed of light in vacuum which can be explained by trapping effects from gravity theories on eight dimensional (co) tangent bundles on Lorentzian manifolds to spacetimes in general and special relativity. In nonholonomic variables, the bulk gravity is described by Finsler modifications depending on velocity/ momentum coordinates. Possible super-luminal phenomena are determined by the width of locally anisotropic brane (spacetime) and induced by generating functions and integration functions and constants in coefficients of metrics and nonlinear connections. We conclude that Finsler brane gravity trapping mechanism may explain neutrino super-luminal effects and almost preserve the paradigm of Einstein relativity as the standard one for particle physics and gravity.Comment: latex2e, 15 pages, v3, accepted to: Foundations of Physics 43 (2013

Risk profiles and one-year outcomes of patients with newly diagnosed atrial fibrillation in India: Insights from the GARFIELD-AF Registry.

BACKGROUND: The Global Anticoagulant Registry in the FIELD-Atrial Fibrillation (GARFIELD-AF) is an ongoing prospective noninterventional registry, which is providing important information on the baseline characteristics, treatment patterns, and 1-year outcomes in patients with newly diagnosed non-valvular atrial fibrillation (NVAF). This report describes data from Indian patients recruited in this registry. METHODS AND RESULTS: A total of 52,014 patients with newly diagnosed AF were enrolled globally; of these, 1388 patients were recruited from 26 sites within India (2012-2016). In India, the mean age was 65.8 years at diagnosis of NVAF. Hypertension was the most prevalent risk factor for AF, present in 68.5% of patients from India and in 76.3% of patients globally (P < 0.001). Diabetes and coronary artery disease (CAD) were prevalent in 36.2% and 28.1% of patients as compared with global prevalence of 22.2% and 21.6%, respectively (P < 0.001 for both). Antiplatelet therapy was the most common antithrombotic treatment in India. With increasing stroke risk, however, patients were more likely to receive oral anticoagulant therapy [mainly vitamin K antagonist (VKA)], but average international normalized ratio (INR) was lower among Indian patients [median INR value 1.6 (interquartile range {IQR}: 1.3-2.3) versus 2.3 (IQR 1.8-2.8) (P < 0.001)]. Compared with other countries, patients from India had markedly higher rates of all-cause mortality [7.68 per 100 person-years (95% confidence interval 6.32-9.35) vs 4.34 (4.16-4.53), P < 0.0001], while rates of stroke/systemic embolism and major bleeding were lower after 1 year of follow-up. CONCLUSION: Compared to previously published registries from India, the GARFIELD-AF registry describes clinical profiles and outcomes in Indian patients with AF of a different etiology. The registry data show that compared to the rest of the world, Indian AF patients are younger in age and have more diabetes and CAD. Patients with a higher stroke risk are more likely to receive anticoagulation therapy with VKA but are underdosed compared with the global average in the GARFIELD-AF. CLINICAL TRIAL REGISTRATION-URL: http://www.clinicaltrials.gov. Unique identifier: NCT01090362

Frontotemporal dementia and its subtypes: a genome-wide association study

Background: Frontotemporal dementia (FTD) is a complex disorder characterised by a broad range of clinical manifestations, differential pathological signatures, and genetic variability. Mutations in three genes-MAPT, GRN, and C9orf72-have been associated with FTD. We sought to identify novel genetic risk loci associated with the disorder. Methods: We did a two-stage genome-wide association study on clinical FTD, analysing samples from 3526 patients with FTD and 9402 healthy controls. To reduce genetic heterogeneity, all participants were of European ancestry. In the discovery phase (samples from 2154 patients with FTD and 4308 controls), we did separate association analyses for each FTD subtype (behavioural variant FTD, semantic dementia, progressive non-fluent aphasia, and FTD overlapping with motor neuron disease [FTD-MND]), followed by a meta-analysis of the entire dataset. We carried forward replication of the novel suggestive loci in an independent sample series (samples from 1372 patients and 5094 controls) and then did joint phase and brain expression and methylation quantitative trait loci analyses for the associated (p<5 7 10-8) single-nucleotide polymorphisms. Findings: We identified novel associations exceeding the genome-wide significance threshold (p<5 7 10-8). Combined (joint) analyses of discovery and replication phases showed genome-wide significant association at 6p21.3, HLA locus (immune system), for rs9268877 (p=1\ub705 7 10-8; odds ratio=1\ub7204 [95% CI 1\ub711-1\ub730]), rs9268856 (p=5\ub751 7 10-9; 0\ub7809 [0\ub776-0\ub786]) and rs1980493 (p value=1\ub757 7 10-8, 0\ub7775 [0\ub769-0\ub786]) in the entire cohort. We also identified a potential novel locus at 11q14, encompassing RAB38/CTSC (the transcripts of which are related to lysosomal biology), for the behavioural FTD subtype for which joint analyses showed suggestive association for rs302668 (p=2\ub744 7 10-7; 0\ub7814 [0\ub771-0\ub792]). Analysis of expression and methylation quantitative trait loci data suggested that these loci might affect expression and methylation in cis. Interpretation: Our findings suggest that immune system processes (link to 6p21.3) and possibly lysosomal and autophagy pathways (link to 11q14) are potentially involved in FTD. Our findings need to be replicated to better define the association of the newly identified loci with disease and to shed light on the pathomechanisms contributing to FTD

Global variation in diabetes diagnosis and prevalence based on fasting glucose and hemoglobin A1c

Fasting plasma glucose (FPG) and hemoglobin A1c (HbA1c) are both used to diagnose diabetes, but these measurements can identify different people as having diabetes. We used data from 117 population-based studies and quantified, in different world regions, the prevalence of diagnosed diabetes, and whether those who were previously undiagnosed and detected as having diabetes in survey screening, had elevated FPG, HbA1c or both. We developed prediction equations for estimating the probability that a person without previously diagnosed diabetes, and at a specific level of FPG, had elevated HbA1c, and vice versa. The age-standardized proportion of diabetes that was previously undiagnosed and detected in survey screening ranged from 30% in the high-income western region to 66% in south Asia. Among those with screen-detected diabetes with either test, the age-standardized proportion who had elevated levels of both FPG and HbA1c was 29–39% across regions; the remainder had discordant elevation of FPG or HbA1c. In most low- and middle-income regions, isolated elevated HbA1c was more common than isolated elevated FPG. In these regions, the use of FPG alone may delay diabetes diagnosis and underestimate diabetes prevalence. Our prediction equations help allocate finite resources for measuring HbA1c to reduce the global shortfall in diabetes diagnosis and surveillance

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

Molecular characterization of Cryptosporidium spp. from wild rats and mice from rural communities in the Philippines

In order to examine the prevalence of Cryptosporidium in wild rodents in the Philippines and understand the role wild rodents play in the transmission of this parasite to humans and livestock, 194 fecal samples from wild rats and mice from Luzon and Mindoro islands were examined. Molecular screening at the 18S and actin gene loci identified an overall prevalence of 25.8% (95%CI: 19.8, 32.5). Sequence and phylogenetic analysis of both loci identified C. parvum, C. muris, C. scrofarum, rat genotypes I-IV and a C. suis-like genotype in the rat-derived isolates and is the first report of C. suis-like and C. scrofarum in rats. Mixed infections were identified in 24% of the Cryptosporidium positive isolates. Rat genotypes II, III and IV showed high intragenotypic variation at the 18S gene locus compared to the actin locus

Models to assess the potential of capillaria hepatica to control population outbreaks of house mice

Population outbreaks of house mice (Mus domesticus) occur periodically in the wheatlands of southeastern Australia. This paper uses mathematical models to assist in the evaluation of the potential of a nematode, Capillaria hepatica, as a biological control agent to reduce the severity of these ‘plagues’. C. hepatica is unique amongst helminths of mammals in that its eggs are released only upon the death of an infected host. The major goal of the modelling in this paper is to determine the impact of this feature on the population dynamics of the host—parasite interaction. Simple differential equation models are used to examine the general properties of the system and determine which population parameters are most crucial to the outcome of the interaction. These models are supplemented by age-structured models which investigate the initial behaviour of the system after introduction of the parasite. The necessity of host death for transmission is a strongly destabilizing factor, suggesting that C. hepatica cannot regulate most populations stably in the absence of strong resource limitation, although it has the potential to depress mouse populations below infection-free levels. Although C. hepatica influences mouse fecundity at lower burdens than it affects mortality, the age-structured models show that parasite-induced host death cannot be neglected. Because transmission requires host death, the parasite life-cycle operates on a time-scale similar to that of the hosts, and introduction of the parasite as early as possible in the development period of an outbreak will therefore be necessary to achieve substantial reductions in plague intensity

Self-regulation within outbreak populations of feral house mice: a test of alternative models

1. Outbreaks of feral house mice, Mus domesticus, in Australia represent a fundamental failure of the behavioural control mechanisms of population density, as proposed in the hypothesis of self-regulation. 2. Mice have the potential to keep numbers in check via a suite of spacing behaviours; however, the self-regulation hypothesis implies that some social change occurs that permits the population to erupt. It also suggests that at different phases of an outbreak, distinct patterns of social activity are evident. 3. We compare predictions from two models encapsulating the self-regulation hypothesis as applied to feral house mice in south-eastern Australia. Each model may be distinguished by the timing of aggressiveness between mice that leads to a closed social system. We compare individual turnover, residency and territoriality in each sex and age cohort during the increase, peak and low phases of a population outbreak that peaked in 2001. 4. The activity of 438 mice was monitored via intensive mark-recapture trapping and an automated event recording system that detected the activity of 300 marked individuals at burrow entrances. 5. Our findings support the second model, which suggests that mice switch from an almost asocial structure at low densities to a territorial system as abundance increases. Adult females appear more likely than males or juveniles to make the significant social shift. The trigger for this change remains unclear and several alternative mechanisms are proposed