Lyapunov exponents for products of complex Gaussian random matrices

The exact value of the Lyapunov exponents for the random matrix product $P_N = A_N A_{N-1}...A_1$ with each $A_i = \Sigma^{1/2} G_i^{\rm c}$, where $\Sigma$ is a fixed $d \times d$ positive definite matrix and $G_i^{\rm c}$ a $d \times d$ complex Gaussian matrix with entries standard complex normals, are calculated. Also obtained is an exact expression for the sum of the Lyapunov exponents in both the complex and real cases, and the Lyapunov exponents for diffusing complex matrices.Comment: 15 page

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

Inhibitory neuromuscular transmission to ileal longitudinal muscle predominates in neonatal guinea pigs

BACKGROUND: Inhibitory neurotransmission to the longitudinal muscle is more prominent in the neonatal than in the adult guinea pig small intestine. METHODS: Inhibitory neuromuscular transmission was investigated using in vitro ileal longitudinal muscle myenteric plexus (LMMP) preparations made from neonatal (≤ 48 h postnatal) and adult (~ 4 weeks postnatal) guinea pigs. KEY RESULTS: Amperometric measurements of nicotine induced nitric oxide release (measured as an oxidation current) from myenteric ganglia revealed larger currents in neonatal (379 ± 24 pA) vs. adult (119 ± 39 pA, P < 0.05) tissues. Nicotine-induced oxidation currents were blocked by the nitric oxide synthase (NOS) inhibitor, nitro-L-arginine (NLA, 100 µM). Nicotine-induced, NLA-sensitive oxidation currents could be detected in the tertiary plexus of neonatal but not adult tissues. Immunohistochemistry demonstrated stronger NOS immunoreactivity in neonatal compared to adult myenteric ganglia. Western blot studies revealed higher levels of NOS in neonatal compared to adult LMMP. Cell counts revealed that the total number of myenteric neurons in the small intestine was greater in adults than in neonatal guinea pigs, however the ratio of NOS:Calbindin neurons was significantly higher in neonatal compared to adult tissues. CONCLUSIONS: NO signaling to the longitudinal muscle is stronger in neonatal compared to adult guinea pig ileum. NOS-containing neurons are diluted postnatally by cholinergic and other, as yet unidentified neuronal subtypes

Converging Divergence: How Competitive Advantages Condition Institutional Change under EMU

Recognizing that the institutional design of EMU leads to the co-ordination of national wage-bargaining structures, this article asks why bargaining systems in some EMU Member States have become co-ordinated and centralized, whereas others have become co-ordinated and decentralized. In contrast to neoliberal theory, it is argued that different bargaining levels are best explained by a country's competitive advantage: whilst countries with a competitive advantage in high-quality manufacturing favour a centralized bargaining system which supports a high-skill strategy, countries with a competitive advantage in low-cost production prefer decentralized bargaining structures which accommodate high wage differentials within the various employment categories of an industry. Thus, even though EMU asserts unilateral pressure for institutional change, it does not lead to the convergence of national institutions. Copyright Blackwell Publishing Ltd 2005.