Properties of a general quaternion-valued gradient operator and its applications to signal processing

The gradients of a quaternion-valued function are often required for quaternionic signal processing algorithms. The HR gradient operator provides a viable framework and has found a number of applications. However, the applications so far have been limited to mainly real-valued quaternion functions and linear quaternionvalued functions. To generalize the operator to nonlinear quaternion functions, we define a restricted version of the HR operator, which comes in two versions, the left and the right ones. We then present a detailed analysis of the properties of the operators, including several different product rules and chain rules. Using the new rules, we derive explicit expressions for the derivatives of a class of regular nonlinear quaternion-valued functions, and prove that the restricted HR gradients are consistent with the gradients in the real domain. As an application, the derivation of the least mean square algorithm and a nonlinear adaptive algorithm is provided. Simulation results based on vector sensor arrays are presented as an example to demonstrate the effectiveness of the quaternion-valued signal model and the derived signal processing algorithm

Filtering and Tracking with Trinion-Valued Adaptive Algorithms

A new model for three-dimensional processes based on the trinion algebra is introduced for the first time. Compared with the pure quaternion model, the trinion model is more compact and computationally more efficient, while having similar or comparable performance in terms of adaptive linear filtering. Moreover, the trinion model can effectively represent the general relationship of state evolution in Kalman filtering, where the pure quaternion model fails. Simulations on real-world wind recordings and synthetic data sets are provided to demonstrate the potentials of this new modeling method

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