The influence of Lent on marriages and conceptions explored through a new methodology

What is the influence of religion on the actual behavior of people? The present paper introduces a methodology which permits a quantitative assessment. [1] have elsewhere analyzed the impact of Lent (prior to Easter) and Advent (prior to Christmas) on births in Romania. Here we broaden the analysis (i) by studying the effect of Lent on marriages as well as births (ii) by analyzing a number of other countries which allows a comparison with non-Orthodox countries. We also introduce a new methodology (that we call the “overlap probe”) which treats the data in a way that avoids any bias related to seasonal patterns. The comparison between the effects on marriages and conceptions appears of particular interest for it permits to assess the respective weights of social pressure on one hand and personal behavior on the other hand. Our analysis reveals a strong effect of Lent on marriages with a reduction by 80% in Eastern Orthodox countries and 40% in West European Catholic and Protestant countries. Since the influence of Lent on conceptions is independent of any form of direct social control one expects this effect to be much smaller. This is born out by our results which show that the birth effect is about 10 times smaller than the marriage effect. The overlap methodology is so accurate that it allows us to determine the average length of pregnancy (from intercourse to birth) with a precision of 2 or 3 days. This methodology is also used to investigate the impact of the month of Ramadan on birth and suicide rates

Dilogarithm Identities in Conformal Field Theory and Group Homology

Recently, Rogers' dilogarithm identities have attracted much attention in the setting of conformal field theory as well as lattice model calculations. One of the connecting threads is an identity of Richmond-Szekeres that appeared in the computation of central charges in conformal field theory. We show that the Richmond-Szekeres identity and its extension by Kirillov-Reshetikhin can be interpreted as a lift of a generator of the third integral homology of a finite cyclic subgroup sitting inside the projective special linear group of all $2 \times 2$ real matrices viewed as a {\it discrete} group. This connection allows us to clarify a few of the assertions and conjectures stated in the work of Nahm-Recknagel-Terhoven concerning the role of algebraic $K$-theory and Thurston's program on hyperbolic 3-manifolds. Specifically, it is not related to hyperbolic 3-manifolds as suggested but is more appropriately related to the group manifold of the universal covering group of the projective special linear group of all $2 \times 2$ real matrices viewed as a topological group. This also resolves the weaker version of the conjecture as formulated by Kirillov. We end with the summary of a number of open conjectures on the mathematical side.Comment: 20 pages, 2 figures not include

Fermionic Quasi-Particle Representations for Characters of {(G^{(1)})_1 \times (G^{(1)})_1 \o (G^{(1)})_2}

We present fermionic quasi-particle sum representations for some of the characters (or branching functions) of ~{(G^{(1)})_1 \times (G^{(1)})_1 \o (G^{(1)})_2} ~for all simply-laced Lie algebras $G$. For given $G$ the characters are written as the partition function of a set of rank~$G$ types of massless quasi-particles in certain charge sectors, with nontrivial lower bounds on the one-particle momenta. We discuss the non-uniqueness of the representations for the identity character of the critical Ising model, which arises in both the $A_1$ and $E_8$ cases.Comment: 14/9 pages in harvmac, ITP-SB-92-64/RU-92-51. References adde

Variants associated withHHIP expression have sex-differential effects on lung function

Background: Lung function is highly heritable and differs between the sexes throughout life. However, little is known about sex-differential genetic effects on lung function. We aimed to conduct the first genome-wide genotype-by-sex interaction study on lung function to identify genetic effects that differ between males and females. Methods: We tested for interactions between 7,745,864 variants and sex on spirometry-based measures of lung function in UK Biobank (N=303,612), and sought replication in 75,696 independent individuals from the SpiroMeta consortium. Results: Five independent single-nucleotide polymorphisms (SNPs) showed genome-wide significant (P</p

Genetic architecture of spatial electrical biomarkers for cardiac arrhythmia and relationship with cardiovascular disease

The 3-dimensional spatial and 2-dimensional frontal QRS-T angles are measures derived from the vectorcardiogram. They are independent risk predictors for arrhythmia, but the underlying biology is unknown. Using multi-ancestry genome-wide association studies we identify 61 (58 previously unreported) loci for the spatial QRS-T angle (N = 118,780) and 11 for the frontal QRS-T angle (N = 159,715). Seven out of the 61 spatial QRS-T angle loci have not been reported for other electrocardiographic measures. Enrichments are observed in pathways related to cardiac and vascular development, muscle contraction, and hypertrophy. Pairwise genome-wide association studies with classical ECG traits identify shared genetic influences with PR interval and QRS duration. Phenome-wide scanning indicate associations with atrial fibrillation, atrioventricular block and arterial embolism and genetically determined QRS-T angle measures are associated with fascicular and bundle branch block (and also atrioventricular block for the frontal QRS-T angle). We identify potential biology involved in the QRS-T angle and their genetic relationships with cardiovascular traits and diseases, may inform future research and risk prediction

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