Transcendental singularities for a meromorphic function with logarithmic derivative of finite lower order

It is shown that two key results on transcendental singularities for meromorphic functions of finite lower order have refinements which hold under the weaker hypothesis that the logarithmic derivative has finite lower order

Bank-Laine functions, the Liouville transformation and the Eremenko-Lyubich class

The Bank-Laine conjecture concerning the oscillation of solutions of second order homogeneous linear differential equations has recently been disproved by Bergweiler and Ere-menko. It is shown here, however, that the conjecture is true if the set of finite critical and asymptotic values of the coefficient function is bounded. It is also shown that if E is a Bank-Laine function of finite order with infinitely many zeros, all real and positive, then its zeros must have exponent of convergence at least 3/2, and an example is constructed via quasiconformal surgery to demonstrate that this result is sharp. MSC 2000: 30D35

On solutions of linear differential equations with entire coefficients

AbstractThe first result of the paper concerns the effect of perturbation of the entire coefficients of certain linear differential equations on the oscillation of the solutions. Subsequent results involve the separation of the zeros of a Bank–Laine function

Linear differential polynomials in zero-free meromorphic functions

The paper determines all meromorphic functions f in C such that f and F have finitely many zeros, where F = f (k) + ak?1f(k?1)+ ... + a0f with k ? 3 and the aj rational functions. MSC 2010:30D35

Linear differential polynomials in zero-free meromorphic functions

The paper determines all meromorphic functions f in C such that f and F have finitely many zeros, where F = f (k) + ak−1f(k−1)+ ... + a0f with k ≥ 3 and the aj rational functions. MSC 2010:30D35

Entire functions with Julia sets of positive measure

Let f be a transcendental entire function for which the set of critical and asymptotic values is bounded. The Denjoy-Carleman-Ahlfors theorem implies that if the set of all z for which |f(z)|>R has N components for some R>0, then the order of f is at least N/2. More precisely, we have log log M(r,f) > (N/2) log r - O(1), where M(r,f) denotes the maximum modulus of f. We show that if f does not grow much faster than this, then the escaping set and the Julia set of f have positive Lebesgue measure. However, as soon as the order of f exceeds N/2, this need not be true. The proof requires a sharpened form of an estimate of Tsuji related to the Denjoy-Carleman-Ahlfors theorem.Comment: 17 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

Dimethyl fumarate in patients admitted to hospital with COVID-19 (RECOVERY): a randomised, controlled, open-label, platform trial

Dimethyl fumarate (DMF) inhibits inflammasome-mediated inflammation and has been proposed as a treatment for patients hospitalised with COVID-19. This randomised, controlled, open-label platform trial (Randomised Evaluation of COVID-19 Therapy [RECOVERY]), is assessing multiple treatments in patients hospitalised for COVID-19 (NCT04381936, ISRCTN50189673). In this assessment of DMF performed at 27 UK hospitals, adults were randomly allocated (1:1) to either usual standard of care alone or usual standard of care plus DMF. The primary outcome was clinical status on day 5 measured on a seven-point ordinal scale. Secondary outcomes were time to sustained improvement in clinical status, time to discharge, day 5 peripheral blood oxygenation, day 5 C-reactive protein, and improvement in day 10 clinical status. Between 2 March 2021 and 18 November 2021, 713 patients were enroled in the DMF evaluation, of whom 356 were randomly allocated to receive usual care plus DMF, and 357 to usual care alone. 95% of patients received corticosteroids as part of routine care. There was no evidence of a beneficial effect of DMF on clinical status at day 5 (common odds ratio of unfavourable outcome 1.12; 95% CI 0.86-1.47; p = 0.40). There was no significant effect of DMF on any secondary outcome