Review of the techniques used in motor‐cognitive human‐robot skill transfer

Abstract A conventional robot programming method extensively limits the reusability of skills in the developmental aspect. Engineers programme a robot in a targeted manner for the realisation of predefined skills. The low reusability of general‐purpose robot skills is mainly reflected in inability in novel and complex scenarios. Skill transfer aims to transfer human skills to general‐purpose manipulators or mobile robots to replicate human‐like behaviours. Skill transfer methods that are commonly used at present, such as learning from demonstrated (LfD) or imitation learning, endow the robot with the expert's low‐level motor and high‐level decision‐making ability, so that skills can be reproduced and generalised according to perceived context. The improvement of robot cognition usually relates to an improvement in the autonomous high‐level decision‐making ability. Based on the idea of establishing a generic or specialised robot skill library, robots are expected to autonomously reason about the needs for using skills and plan compound movements according to sensory input. In recent years, in this area, many successful studies have demonstrated their effectiveness. Herein, a detailed review is provided on the transferring techniques of skills, applications, advancements, and limitations, especially in the LfD. Future research directions are also suggested

Genome-wide association and Mendelian randomisation analysis provide insights into the pathogenesis of heart failure

Heart failure (HF) is a leading cause of morbidity and mortality worldwide. A small proportion of HF cases are attributable to monogenic cardiomyopathies and existing genome-wide association studies (GWAS) have yielded only limited insights, leaving the observed heritability of HF largely unexplained. We report results from a GWAS meta-analysis of HF comprising 47,309 cases and 930,014 controls. Twelve independent variants at 11 genomic loci are associated with HF, all of which demonstrate one or more associations with coronary artery disease (CAD), atrial fibrillation, or reduced left ventricular function, suggesting shared genetic aetiology. Functional analysis of non-CAD-associated loci implicate genes involved in cardiac development (MYOZ1, SYNPO2L), protein homoeostasis (BAG3), and cellular senescence (CDKN1A). Mendelian randomisation analysis supports causal roles for several HF risk factors, and demonstrates CAD-independent effects for atrial fibrillation, body mass index, and hypertension. These findings extend our knowledge of the pathways underlying HF and may inform new therapeutic strategies.Cardiolog