The emergence of wearable electronics and optoelectronics requires the development of devices that are not only highly flexible but can also be woven into textiles to offer a truly integrated solution. Here, we report a colour-tunable, weavable fibre-shaped polymer light-emitting electrochemical cell (PLEC). The fibre-shaped PLEC is fabricated using all-solutionbased processes that can be scaled up for practical applications. The design has a coaxial structure comprising a modified metal wire cathode and a conducting aligned carbon nanotube sheet anode, with an electroluminescent polymer layer sandwiched between them. The fibre shape offers unique and promising advantages. For example, the luminance is independent of viewing angle, the fibre-shaped PLEC can provide a variety of different and tunable colours, it is lightweight, flexible and wearable, and it can potentially be woven into light-emitting clothes for the creation of smart fabrics. L ight-emitting electrochemical cells 1-6 , in particular polymer light-emitting electrochemical cells (PLECs), have been widely studied for various applications, including flexible flat panel displays, signage and lighting 4-6 . Like organic light-emitting diodes (OLEDs) and polymer light-emitting diodes (PLEDs), PLECs have a structure that is usually composed of two metal electrodes connected to an organic semiconductor. However, PLECs differ in that mobile ions are incorporated into the organic semiconductor, thereby offering promising advantages such as low operating voltage, high electron/photon conversion efficiency and high power efficiency compared with OLEDs 7-18 . More importantly, PLECs do not require the use of low-workfunction cathodes composed of calcium or magnesium (which are sensitive in air). In contrast, PLEDs require a low-workfunction cathode and high-workfunction anode to realize efficient charge injection 19-21 . In a typical PLEC, the electroluminescent polymer layer forms an in situ light-emitting p-i-n junction for the injection of both electrons and holes from the electrodes 4,5,22 . This means that PLECs can be effectively operated with relatively rougher surfaces than is generally possible with OLEDs and PLEDs, which is advantageous when scaling them up for practical applications with low cost and high efficiency 23-25 .Based on these described advantages, the PLEC is particularly promising for use in portable and wearable electronics, which are being developed for a wide range of applications, from microelectronics to biomedicine, transport and areospace 26-32 . Conventional planar light-emitting devices, including both rigid and flexible films, cannot satisfy the basic requirements for such an application, including softness, light weight and weavability 33,34 . To this end, advances in the textile industry have suggested a useful direction in which to pursue a solution: if a PLEC is made into a continuous fibre using a melting or all-solution-based process, it can be woven into various flexible textiles or integrated into soft substrates for u...

A fiber-shaped supercapacitor that can be stretched over 400% is developed by using two aligned carbon nanotube/polyaniline composite sheets as electrodes. A high specific capacitance of approximately 79.4 F g(-1) is well maintained after stretching at a strain of 300% for 5000 cycles or 100.8 F g(-1) after bending for 5000 cycles at a current density of 1 A g(-1). In particular, the high specific capacitance is maintained by 95.8% at a stretching speed as high as 30 mm s(-1).

Oxidative stress contributes to neurodegeneration in Huntington's disease (HD). However, the origins of oxidative stress in HD remain unclear. Studies in HD transgenic models suggest involvement of mitochondrial dysfunction, which would lead to overproduction of reactive oxygen species (ROS). Impaired mitochondria complexes occur in late stages of HD but not in presymptomatic or early-stage HD patients. Thus, other mechanisms may account for the earliest source of oxidative stress caused by endogenous mutant huntingtin. Here, we report that decreased levels of a major intracellular antioxidant glutathione coincide with accumulation of ROS in primary HD neurons prepared from embryos of HD knock-in mice (HD 140Q/140Q ), which have human huntingtin exon 1 with 140 CAG repeats inserted into the endogenous mouse huntingtin gene. Uptake of extracellular cysteine through the glutamate/cysteine transporter EAAC1 is required for de novo synthesis of glutathione in neurons. We found that, compared with wild-type neurons, HD neurons had lower cell surface levels of EAAC1 and were deficient in taking up cysteine. Constitutive trafficking of EAAC1 from recycling endosomes relies on Rab11 activity, which is defective in the brain of HD 140Q/140Q mice. Enhancement of Rab11 activity by expression of a dominant-active Rab11 mutant in primary HD neurons ameliorated the deficit in cysteine uptake, increased levels of intracellular glutathione, normalized clearance of ROS, and improved neuronal survival. Our data support a novel mechanism for oxidative stress in HD: Rab11 dysfunction slows trafficking of EAAC1 to the cell surface and impairs cysteine uptake, thereby leading to deficient synthesis of glutathione.

Huntingtin (Htt) localizes to endosomes, but its role in the endocytic pathway is not established. Recently, we found that Htt is important for the activation of Rab11, a GTPase involved in endosomal recycling. Here we studied fibroblasts of healthy individuals and patients with Huntington's disease (HD), which is a movement disorder caused by polyglutamine expansion in Htt. The formation of endocytic vesicles containing transferrin at plasma membranes was the same in control and HD patient fibroblasts. However, HD fibroblasts were delayed in recycling biotin-transferrin back to the plasma membrane. Membranes of HD fibroblasts supported less nucleotide exchange on Rab11 than did control membranes. Rab11-positive vesicular and tubular structures in HD fibroblasts were abnormally large, suggesting that they were impaired in forming vesicles. We used total internal reflection fluorescence imaging of living fibroblasts to monitor fluorescence-labeled transferrin-carrying transport intermediates that emerged from recycling endosomes. HD fibroblasts had fewer small vesicles and more large vesicles and long tubules than did control fibroblasts. Dominant active Rab11 expressed in HD fibroblasts normalized the recycling of biotin-transferrin. We propose a novel mechanism for cellular dysfunction by the HD mutation arising from the inhibition of Rab11 activity and a deficit in vesicle formation at recycling endosomes.Polyglutamine expansion in huntingtin (Htt) causes Huntington's disease (HD). Htt localizes to the cytoplasm and associates with vesicles (12) and subcellular organelles (51), including endosomes. Cells with mutant Htt have deficits in the transport of different cargo-carrying vesicles and subcellular organelles including mitochondria and early endosomes (15,21,29,36,44,45). The molecular basis for these deficits is thought to involve aberrant interactions of mutant Htt with HAP1 and the motor proteins dynactin and kinesin (14,31,35). Htt interacts with components of the molecular machinery for clathrin-coated vesicles, leading to speculation that Htt might also be involved in the formation of clathrin-coated vesicles. However, the endocytosis of transferrin, a process that involves the packaging of transferrin and its receptor into clathrin-coated vesicles at the plasma membrane, is unaffected by the presence of mutant Htt (46). A recent study reported that mutant Htt does not affect the formation of clathrincoated vesicles at the trans-Golgi network (11).Endocytic recycling is a process whereby internalized receptors and other molecules are returned to the cell surface for reuse. This process is required for the maintenance of the plasma membrane and cellular homeostasis. The critical organelles in endocytic recycling are the sorting endosomes (short-loop recycling) and the recycling endosomes (long-loop recycling). Rab4 regulates the recycling events at sorting endosomes, whereas Rab11 acts at recycling endosomes by regulating vesicle formation (19,34,43,47,55). Recently, we found that the absence of wild-...

Huntingtin has an expanded polyglutamine tract in patients with Huntington’s disease. Huntingtin localizes to intracellular and plasma membranes but the function of huntingtin at membranes is unknown. Previously we reported that exogenously expressed huntingtin bound pure phospholipids using protein‐lipid overlays. Here we show that endogenous huntingtin from normal (Hdh7Q/7Q) mouse brain and mutant huntingtin from Huntington’s disease (Hdh140Q/140Q) mouse brain bound to large unilamellar vesicles containing phosphoinositol (PI) PI 3,4‐bisphosphate, PI 3,5‐bisphosphate, and PI 3,4,5‐triphosphate [PI(3,4,5)P3]. Huntingtin interactions with multivalent phospholipids were similar to those of dynamin. Mutant huntingtin associated more with phosphatidylethanolamine and PI(3,4,5)P3 than did wild‐type huntingtin, and associated with other phospholipids not recognized by wild‐type huntingtin. Wild‐type and mutant huntingtin also bound to large unilamellar vesicles containing cardiolipin, a phospholipid specific to mitochondrial membranes. Maximal huntingtin‐phospholipid association required inclusion of huntingtin amino acids 171–287. Endogenous huntingtin recruited to the plasma membrane in cells that incorporated exogenous PI 3,4‐bisphosphate and PI(3,4,5)P3 or were stimulated by platelet‐derived growth factor or insulin growth factor 1, which both activate PI 3‐kinase. These data suggest that huntingtin interacts with membranes through specific phospholipid associations and that mutant huntingtin may disrupt membrane trafficking and signaling at membranes.

A mutation in the huntingtin (Htt) gene produces mutant Htt and Huntington's disease (HD), a neurodegenerative disorder. HD patients have oxidative damage in the brain, but the causes are unclear. Compared with controls, we found brain levels of NADPH oxidase (NOX) activity, which produces reactive oxygen species (ROS), elevated in human HD postmortem cortex and striatum and highest in striatum of presymptomatic individuals. Synaptosome fractions from cortex and striatum of HD(140Q/140Q) mice had elevated NOX activity at 3 months of age and a further rise at 6 and 12 months compared with synaptosomes of age-matched wild-type (WT) mice. High NOX activity in primary cortical and striatal neurons of HD(140Q/140Q) mice correlated with more ROS and neurite swellings. These features and neuronal cell death were markedly reduced by treatment with NOX inhibitors such as diphenyleneiodonium (DPI), apocynin (APO) and VAS2870. The rise in ROS levels in mitochondria of HD(140Q/140Q) neurons followed the rise in NOX activity and inhibiting only mitochondrial ROS was not neuroprotective. Mutant Htt colocalized at plasma membrane lipid rafts with gp91-phox, a catalytic subunit for the NOX2 isoform. Assembly of NOX2 components at lipid rafts requires activation of Rac1 which was also elevated in HD(140Q/140Q) neurons. HD(140Q/140Q) mice bred to gp91-phox knock-out mice had lower NOX activity in the brain and in primary neurons, and neurons had normal ROS levels and significantly improved survival. These findings suggest that increased NOX2 activity at lipid rafts is an early and major source of oxidative stress and cell death in HD(140Q/140Q) neurons.

Accurate and timely prediction of remaining useful life (RUL) of a machine enables the machine to have an appropriate operation and maintenance decision. Data-driven RUL prediction methods are more attractive to researchers because they can be deployed quicker and cheaper compared to other approaches. The existing deep neural network (DNN) models proposed for the applications of RUL prediction are mostly single-path and top-down propagation. In order to improve the prognostic accuracy of the network, this paper proposes a directed acyclic graph (DAG) network that combines long short term memory (LSTM) and a convolutional neural network (CNN) to predict the RUL. Different from the existing prediction models combined with CNN and LSTM, the method proposed in this paper combines CNN and LSTM organically instead of just using CNN for feature extraction. Moreover, when a single timestamp is used as an input, padding the signals in the same training batch would affect the prediction ability of the developed model. To overcome this drawback, the proposed method generates a short-term sequence by sliding the time window (TW) with one step size. In addition, based on the degradation mechanism, the piece-wise RUL function is used instead of the traditional linear function. In the experimental test, the turbofan engine degradation simulation dataset provided by NASA is used to validate the proposed RUL prediction model. By comparing with the existing methods using the same dataset, it can be concluded that the prediction method proposed in this paper has better prediction capability. INDEX TERMS Remaining useful life prediction, long-short-term memory network, convolutional neural networks, turbofan engine.

Patients with Huntington's disease have an expanded polyglutamine tract in huntingtin and suffer severe brain atrophy and neurodegeneration. Because membrane dysfunction can occur in Huntington's disease, we addressed whether mutant huntingtin in brain and primary neurons is present in lipid rafts, which are cholesterol-enriched membrane domains that mediate growth and survival signals. Biochemical analysis of detergent-resistant membranes from brains and primary neurons of wild-type and presymptomatic Huntington's disease knock-in mice showed that wild-type and mutant huntingtin were recovered in lipid raft-enriched detergent-resistant membranes. The association with lipid rafts was stronger for mutant huntingtin than wild-type huntingtin. Lipid rafts extracted from Huntington's disease mice had normal levels of lipid raft markers (G(alphaq), Ras, and flotillin) but significantly more glycogen synthase kinase 3-beta. Increases in glycogen synthase kinase 3-beta have been associated with apoptotic cell death. Treating Huntington's disease primary neurons with inhibitors of glycogen synthase kinase 3-beta reduced neuronal death. We speculate that accumulation of mutant huntingtin and glycogen synthase kinase 3-beta in lipid rafts of presymptomatic Huntington's disease mouse neurons contributes to neurodegeneration in Huntington's disease.