Diseases of the peroneal tendons and superior peroneal retinaculum (SPR) are frequently underdiagnosed causes of lateral ankle pain and instability. Common diseases include tenosynovitis, rupture, and dislocation of the peroneal tendons as well as injuries to the SPR. Many anatomic variants, such as a flat or convex retromalleolar fibular groove, hypertrophy of the peroneal tubercle, an accessory peroneus quartus muscle, a low-lying peroneus brevis muscle belly, or an os peroneum, may be associated with or predispose to lateral ankle disease. Magnetic resonance (MR) imaging is excellent for detecting soft-tissue and bone variants and abnormalities related to the lateral ankle. Knowledge of the MR imaging appearances of these entities aids radiologists in making the precise diagnosis of disorders of the peroneal tendons and SPR. Pitfalls and normal variants of the peroneal tendons, including magic angle phenomenon, pseudosubluxation of the peroneus brevis tendon, a bifurcated or mildly crescentic peroneus brevis tendon, insertion of the peroneus quartus tendon into the peroneus brevis tendon, and the presence of an os peroneum are important to recognize. It is also useful to be familiar with the MR imaging appearances of SPR injuries, which can be an overlooked but treatable cause of lateral ankle pain and instability.

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The Monty Hall problem (or three-door problem) is a famous example of a "cognitive illusion," often used to demonstrate people's resistance and deficiency in dealing with uncertainty. The authors formulated the problem using manipulations in 4 cognitive aspects, namely, natural frequencies, mental models, perspective change, and the less-is-more effect. These manipulations combined led to a significant increase in the proportion of correct answers given by novice participants, largely because of the synergy of frequency-based formulation and perspective change (Experiments 1, 2). In a raining study (Experiment 3) frequency formulation and mental models, but not Bayes's rule training, showed significant positive transfer in solving related problems.

It is well documented that N-methyl-D-aspartate and alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate receptors play a pivotal role in ischaemic brain injury. Recent studies have shown that kainate (KA) receptors are involved in neuronal cell death induced by seizure, which is mediated by the GluR6*PSD-95*MLK3 signalling module and subsequent c-Jun N-terminal kinase (JNK) activation. Here we investigate whether GluR6 mediated JNK activation is correlated with ischaemic brain injury. Our results show that cerebral ischaemia followed by reperfusion can enhance the assembly of the GluR6*PSD-95*MLK3 signalling module and JNK activation. As a result, activated JNK can not only phosphorylate the transcription factor c-Jun and up-regulate Fas L expression but can also phosphorylate 14-3-3 and promote Bax translocation to mitochondria, increase the release of cytochrome c and increase caspase-3 activation. These results indicate that GluR6 mediated JNK activation induced by ischaemia/reperfusion ultimately results in neuronal cell death via nuclear and non-nuclear pathways. Furthermore, the peptides we constructed, Tat-GluR6-9c, show a protective role against neuronal death induced by cerebral ischaemia/reperfusion through inhibiting the GluR6 mediated signal pathway. In summary, our results indicate that the KA receptor subunit GluR6 mediated JNK activation is involved in ischaemic brain injury and provides a new approach for stroke therapy.