This study assessed the feasibility to restore finger-specific sensory feedback in transradial amputees with electrical stimulation of evoked tactile sensation (ETS). Methods: Here we investigated primary somatosensory cortical (SI) responses of ETS using Magnetoencephalography. Results: SI activations revealed a causal correlation with peripheral stimulation of projected finger regions on the stump skin. Peak latency was accountable to neural transmission from periphery to SI. Peak intensity of SI response was proportional to the strength of peripheral stimulation, manifesting a direct neural pathway from skin receptors to SI neurons. Active regions in SI at the amputated side were consistent to the finger/hand map of homunculus, forming a mirror imaging to that of the contralateral hand. With sensory feedback, amputees can recognize a pressure at prosthetic fingers as that at the homonymous lost fingers. Conclusions: Results confirmed that the direct neural pathway from periphery to SI allows effective communication of finger-specific sensory information to these amputees. INDEX TERMS Evoked tactile sensation (ETS), magnetoencephalography (MEG), prosthetic hand, sensory feedback, transcutaneous electrical nerve stimulation (TENS). IMPACT STATEMENT This study substantiated the neural basis and feasibility that electrically evoked tactile sensation can afford a non-invasive neural interface capable of restoring finger-specific sensory ability to transradial amputees.

Objective: Evoked tactile sensation (ETS) elicited by transcutaneous electrical nerve stimulation (TENS) is promising to convey digit-specific sensory information to amputees naturally and non-invasively. Fitting ETS-based sensory feedback to amputees entails customizing coding of multiple sensory information for each stimulation site. This study was to elucidate the consistency of percepts and qualities by TENS at multiple stimulation sites in amputees retaining ETS. Approach: Five transradial amputees with ETS and fourteen able-bodied subjects participated in this study. Surface electrodes with small size (10 mm in diameter) were adopted to fit the restricted projected finger map on the forearm stump of amputees. Effects of stimulus frequency on sensory types were assessed, and the map of perceptual threshold for each sensation was characterized. Sensitivity for vibration and buzz sensations was measured using distinguishable difference in stimulus pulse width. Rapid assessments for modulation ranges of pulse width at fixed amplitude and frequency were developed for coding sensory information. Buzz sensation was demonstrated for location discrimination relating to prosthetic fingers. Main results: Vibration and buzz sensations were consistently evoked at 20 Hz and 50 Hz as dominant sensation types in all amputees and able-bodied subjects. Perceptual thresholds of different sensations followed a similar strength-duration curve relating stimulus amplitude to pulse width. The averaged distinguishable difference in pulse width was 12.84 ± 7.23 μs for vibration and 15.21 ± 6.47 μs for buzz in able-bodied subjects, and 14.91 ± 10.54 μs for vibration and 11.30 ± 3.42 μs for buzz in amputees. Buzz coding strategy enabled five amputees to discriminate contact of individual fingers with an overall accuracy of 77.85%. Significance: The consistency in perceptual qualities of dominant sensations can be exploited for coding multi-modality sensory feedback. A fast protocol of sensory coding is possible for fitting ETS-based, non-invasive sensory feedback to amputees.

Mitochondrial abnormalities play critical roles in diabetic tubular injury progression. Dipeptidyl peptidase‐4 (DPP4) inhibitors are widely used antihyperglycemic agents that exert renal protective and positive effects against mitochondrial dysfunction in diabetic kidney disease (DKD). However, their underlying mechanism remains unclear. In this study, DPP4 upregulation, mitochondrial fragmentation, and altered mitochondrial dynamics‐associated protein expression were observed in the tubules of DBA2/J (D2) diabetic mice with unilateral nephrectomy and in albumin‐stimulated tubular cells. The inhibition of DPP4 by sitagliptin (Sita) ameliorated these mitochondrial perturbations both in vivo and in vitro, whereas DPP4 overexpression aggravated mitochondrial fusion‐fission disorder and tubular cell injury in albumin‐treated HK‐2 cells. Downstream of DPP4, the SDF‐1α/CXCR4 pathway was significantly suppressed in diabetic tubules. After Sita treatment, this signaling pathway was restored, and the mitochondrial dynamics was improved. Furthermore, a direct interaction between STAT3 and OPA1 was found in the mitochondria of tubular cells, and this effect was weakened by overloading albumin and by CXCR4 siRNA treatment, suggesting a possible link between DPP4‐mediated SDF‐1α/CXCR4/STAT3 signaling and mitochondrial dysfunction in diabetic tubular cells. The results suggest that a novel mechanism links the DPP4 enzyme to impaired mitochondrial dynamics homeostasis during tubular injury in DKD and highlight that the SDF‐1α/CXCR4/STAT3 signaling pathway could become a potential target for managing DKD.

Reactive Turing machines extend classical Turing machines with a facility to model observable interactive behaviour. We call a behaviour executable if, and only if, it is behaviourally equivalent to the behaviour of a reactive Turing machine. In this paper, we study the relationship between executable behaviour and behaviour that can be specified in the π-calculus. We establish that all executable behaviour can be specified in the π-calculus up to divergence-preserving branching bisimilarity. The converse, however, is not true due to (intended) limitations of the model of reactive Turing machines. That is, the π-calculus allows the specification of behaviour that is not executable up to divergencepreserving branching bisimilarity. Motivated by an intuitive understanding of executability, we then consider a restriction on the operational semantics of the π-calculus that does associate with every π-term executable behaviour, at least up to the version of branching bisimilarity that does not require the preservation of divergence. * This author is sponsored by the China Scholarship Council (CSC).