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This study was designed to investigate the expression of short-chain acyl-CoA dehydrogenase (SCAD), a key enzyme of fatty acid β-oxidation, during rat heart development and the difference of SCAD between pathological and physiological cardiac hypertrophy. The expression of SCAD was lowest in the foetal and neonatal heart, which had time-dependent increase during normal heart development. In contrast, a significant decrease in SCAD expression was observed in different ages of spontaneously hypertensive rats (SHR). On the other hand, swim-trained rats developed physiological cardiac hypertrophy, whereas SHR developed pathological cardiac hypertrophy. The two kinds of cardiac hypertrophy exhibited divergent SCAD changes in myocardial fatty acids utilization. In addition, the expression of SCAD was significantly decreased in pathological cardiomyocyte hypertrophy, however, increased in physiological cardiomyocyte hypertrophy. SCAD siRNA treatment triggered the pathological cardiomyocyte hypertrophy, which showed that the down-regulation of SCAD expression may play an important role in pathological cardiac hypertrophy. The changes in peroxisome proliferator-activated receptor α (PPARα) was accordant with that of SCAD. Moreover, the specific PPARα ligand fenofibrate treatment increased the expression of SCAD and inhibited pathological cardiac hypertrophy. Therefore, we speculate that the down-regulated expression of SCAD in pathological cardiac hypertrophy may be responsible for ‘the recapitulation of foetal energy metabolism’. The deactivation of PPARα may result in the decrease in SCAD expression in pathological cardiac hypertrophy. Changes in SCAD are different in pathological and physiological cardiac hypertrophy, which may be used as the molecular markers of pathological and physiological cardiac hypertrophy.

Brain regions associated with creativity is a focal point in research related to the field of cognitive neuroscience. Previous studies have paid more attention to the role of activation of the left dorsolateral prefrontal cortex in creativity tasks, which are mostly abstract conceptual tasks, and less attention to real-world creativity tasks. The right dorsolateral prefrontal cortex is involved in functions such as visuospatial processing, which may have a positive impact on innovative solutions to real-world problems. In this study, tDCS technology was used to explore the effect of anodal stimulation of the right dorsolateral prefrontal cortex on design creativity performance in a real-word problem-solving task related to product design. The experimental task comprised three stages, of which the first two were idea generation stages based on divergent thinking using text and graphics, respectively, whereas the third was the creative evaluation stage based on convergent thinking. Thirty-six design students were recruited to partake in the experiment. They were randomly assigned into anodal stimulation and sham stimulation groups. The results showed that anodal stimulation of the right dorsolateral prefrontal cortex produced a significant positive effect during the creative evaluation stage, promoting the usefulness of ideas (p = 0.009); thus, improving product creativity scores. However, there was no significant impact on the idea generation stage (p > 0.05), which is dominated by divergent thinking. The results suggest that activating the right dorsolateral prefrontal cortex with tDCS can improve people’s performance in creative activities by promoting convergent thinking rather than divergent thinking. It also provides further evidence that the right hemisphere of the brain has an advantage in solving complex problems that require the participation of visuospatial information.