Highly sensitive and multimodal sensors have recently emerged for a wide range of applications, including epidermal electronics, robotics, health‐monitoring devices and human–machine interfaces. However, cross‐sensitivity prevents accurate measurements of the target input signals when a multiple of them are simultaneously present. Therefore, the selection of the multifunctional materials and the design of the sensor structures play a significant role in multimodal sensors with decoupled sensing mechanisms. Hence, this review article introduces varying methods to decouple different input signals for realizing truly multimodal sensors. Early efforts explore different outputs to distinguish the corresponding input signals applied to the sensor in sequence. Next, this study discusses the methods for the suppression of the interference, signal correction, and various decoupling strategies based on different outputs to simultaneously detect multiple inputs. The recent insights into the materials' properties, structure effects, and sensing mechanisms in recognition of different input signals are highlighted. The presence of the various decoupling methods also helps avoid the use of complicated signal processing steps and allows multimodal sensors with high accuracy for applications in bioelectronics, robotics, and human–machine interfaces. Finally, current challenges and potential opportunities are discussed in order to motivate future technological breakthroughs.

The transition between a novel oil-in-dispersion emulsion and an oil-in-water (O/W) Pickering emulsion triggered by pH was achieved using alumina nanoparticles in combination with a cationic surfactant. In acidic and neutral aqueous media, positively charged particles and the surfactant both at very low concentrations costabilize an oil-in-dispersion emulsion with the surfactant adsorbed at droplet interfaces and particles dispersed in the aqueous phase between the droplets. In alkaline media, however, particles become negatively charged and are hydrophobized in situ by adsorption of the surfactant to become surface-active and stabilize an O/W Pickering emulsion. The transition between the two is also possible by lowering the pH. The transformation can be achieved several times in a mixture of 0.1 wt % nanoparticles and 0.01 mM surfactant. This transition is significant, since particles can be made to either adsorb at the oil–water interface, which is beneficial for applications like biphasic catalysis, or remain dispersed in the aqueous phase, which is favorable for their recovery and reuse.

A novel charge-reversible surfactant, (CH 3 ) 2 N-(CH 2 ) 10 COONa, was designed and synthesized, which together with silica nanoparticles can stabilize a smart n-octane-inwater emulsion responsive to pH. At high pH (9.3) the surfactant is anionic carboxylate, which together with the negatively charged silica nanoparticles co-stabilize flowable oil-in-dispersion emulsions, whereas at low pH (4.1) it is turned to cationic form by forming amine salt which can hydrophobize in situ the negatively charged silica nanoparticles to stabilize viscous oil-in-water (O/W) Pickering emulsions. At neutral pH (7.5), however, this surfactant is converted to zwitterionic form, which only weakly hydrophobises the silica particles to stabilize O/W Pickering emulsions of large droplet size. Moreover, demulsification can be achieved rapidly triggered by pH. With this strategy particles can be controlled either dispersed in water or adsorbed at the oil-water interface endowing emulsions with the capacity for intelligent and precise control of stability as well as viscosity and droplet size. Scheme 1. Chemical structure of 11-(N,N-dimethylamino) sodium undecanoate (DMUa, left) and charge variation with pH.

Parkinson's disease (PD) is pathologically characterized by selective loss of dopaminergic neurons in the midbrain and the existence of intracellular protein inclusions termed Lewy bodies, largely composed of α-synuclein. Genetic studies have revealed that rare point mutations in the gene encoding α-synuclein including A30P, A53T, and E46K are associated with familial forms of PD, indicating a pathological role for mutant α-synuclein in PD etiology. However, the mechanisms underlying the neuronal toxicity of mutant α-synuclein are still to be elucidated. Growing evidence has suggested a deleterious effect of mutant α-synuclein on the autophagy-lysosome pathway. In this study, we discovered that overexpression of human E46K mutant α-synuclein impaired macroautophagy in mammalian cells. Our data showed that overexpression of E46K mutant α-synuclein impaired autophagy at an early stage of autophagosome formation via the c-Jun N-terminal kinase 1 (JNK1)-Bcl-2 but not the mammalian target of rapamycin (mTOR) pathway. Overexpressed E46K mutant α-synuclein inhibited JNK1 activation, leading to a reduced Bcl-2 phosphorylation and increased association between Bcl-2 and Beclin1, further disrupting the formation of Beclin1/hVps34 complex, which is essential for autophagy initiation. Furthermore, overexpression of E46K mutant α-synuclein increased the vulnerability of differentiated PC12 cells to rotenone treatment, which would be partly due to its inhibitory effects on autophagy. Our findings may shed light on the potential roles of mutant α-synuclein in the pathogenesis of PD.