High-voltage energy-storage devices are quite commonly needed for robots and dielectric elastomers. This paper presents a flexible high-voltage microsupercapacitor (MSC) with a planar in-series architecture for the first time based on laser-induced graphene. The high-voltage devices are capable of supplying output voltages ranging from a few to thousands of volts. The measured capacitances for the 1, 3, and 6 V MSCs were 60.5, 20.7, and 10.0 μF, respectively, under an applied current of 1.0 μA. After the 5000-cycle charge-discharge test, the 6 V MSC retained about 97.8% of the initial capacitance. It also was recorded that the all-solid-state 209 V MSC could achieve a high capacitance of 0.43 μF at a low applied current of 0.2 μA and a capacitance of 0.18 μF even at a high applied current of 5.0 μA. We further demonstrate the robust function of our flexible high-voltage MSCs by using them to power a piezoresistive microsensor (6 V) and a walking robot (>2000 V). Considering the simple, direct, and cost-effective fabrication method of our laser-fabricated flexible high-voltage MSCs, this work paves the way and lays the foundation for high-voltage energy-storage devices.

Neuroprotection offers potential as an alternative therapy for glaucoma. Pilocarpine, as a typical muscarinic receptor agonist, remains among the major intraocular pressure lowering drugs for the conventional treatment of glaucoma. However, whether pilocarpine also possesses neuroprotection against glutamate cytotoxicity in retinal neurons is still unknown. In rat primary retinal cultures, identification of neuron, cell viability, apoptosis, intracellular Ca(2+) concentration, mitochondrial membrane potential, gene expression were studied by immunofluorescence, MTT, High Content Scanning, confocal microscopy, reverse-transcription PCR, and western blot analysis, respectively. Pretreatment of pilocarpine could prevent glutamate-induced neuron death, which was blocked by the non-selective antagonist atropine and the M1-selective muscarinic receptor antagonist pirenzepine. The antiapoptotic effect of pilocarpine was associated with maintaining calcium homeostasis, recovering mitochondrial membrane potential, and regulating the expression of Bcl-2 and Caspase-3. These studies demonstrated that pilocarpine had effective protection against glutamate-induced neuronal apoptosis through M1 muscarinic receptor. The results may provide an insight into the new mechanism of glaucoma therapy that pilocarpine may potentially act as a retinal neuroprotectant.

It is believed that the intrinsic chemical sensitivity of graphene comes from the gas adsorption associated doping [4] and scattering [5] effects, which can change the carrier density, n(t), and the field effect mobility, µ(t), of graphene, respectively. On the other hand, the extrinsic defects on graphene, especially the charged impurities, [6] were also reported to affect the graphene gas sensing performance. [7][8][9] Specifically, it was predicted in theory [10,11] that the charged gas molecules (after doping) will first adsorb and compensate on the oppositely charged defects on graphene, increasing the µ(t); then adsorbs graphene intrinsically, decreasing the µ(t).However, it was difficult to validate such phenomenon experimentally as the previous methods [4,[12][13][14] in obtaining n(t) and µ(t) require sweeping the gate voltage V G across the charge neutral point (CNP) [15] to track the incremental changes of the CNP voltage, ∆V CNP (∆n = C G ∆V CNP /e c , where C G is the gate capacitance per unit area of the graphene FET, e c = 1.6 × 10 −19 C is the elementary charge, and ∆n is the change of carrier density); while the range of V G sweeping needs to be large enough to cover the linear region of the graphene FET to extract µ(t). [6] These large gate voltage sweepings inevitably cause significant disturbance of the defect states on graphene due to the fluctuation of the graphene work function [16] (a few hundred meV) and the flipping of the electric field direction at the graphene surface. [17] Here, a new method to probe n(t) and µ(t) is introduced to observe the defect-induced gas adsorption without sweeping the gate voltage as shown in Figure 1a,b. By adding a serial small AC voltage v g on the static DC gate voltage, one can analytically solve both n(t) and µ(t) from the graphene conductance g AB directly in the linear region. For simplicity, we use the hole branch of graphene as the example as most devices are naturally p-doped in air [18] after fabrication (see the Experimental Section), such that n(t) represents the density of holes. Figure 1c shows that the DC gate voltage of the FET is kept at V G = −10 V (V CNP = 20 V) and the AC gate voltage |v g | = 1 V is oscillating at 50 Hz to slightly fluctuate the work function of graphene by a few meV while keeping the work function quasistatic. The carrier density variation, n(t) − n 0 (Figure 1d), and the inverse of the field effect mobility variation, µ −1 (t) − µ 0 −1 (Figure 1e), can be extracted from the channel conductance of graphene in real time (see Note 1 in the Supporting Information for extraction method), where n 0 = 2.0 × 10 12 cm −2 is the initial carrier density and µ 0 −1 = 4.0 V s m −2 is the initial value of the inverse of field Understanding the influences of defect states on gas adsorption on graphene is at the heart of developing graphene based gas sensors for practical applications. However, it has been challenging to experimentally discriminate the gas adsorptions induced by the defects on graphene, especially the charged impurit...

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Fibrocytes of the spiral limbus are thought to play a significant role in maintaining ion homeostasis in the cochlea. The present study measured physiological and morphological changes in spiral limbus of mice in response to noise exposure. 6-week-old male C3H/HeJJcl mice were exposed to octave-band noise (120 dB SPL) for 2 h and evaluated at a series of times thereafter, up to 8 weeks. Permanent hearing loss resulted in the mice, as assessed by auditory brainstem response (ABR) recordings. The fibrocytes loss was found in the spiral limbus of the apical turn, which has been proved to be induced by apoptosis. These results suggest that noise exposure might result in apoptosis of fibrocytes in spiral limbus, which suggest a mechanism for noise-induced hearing loss.

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Hyperandrogenemia is associated with insulin resistance and type 2 diabetes in women with polycystic ovary syndrome raising the possibility that androgen receptor signaling pathway plays an important role in the development and progression of β-cell dysfunction. Testosterone is the major circulating androgen in women. In this study, we investigated the effect of testosterone on INS-1 cells to find whether excess androgen could produce endoplasmic reticulum (ER) stress thereby contributing to β-cell dysfunction. The role of testosterone in INS-1 cell apoptosis was detected by flow cytometry and electron microscopy. Expression of BIP, ATF4, and CHOP were assessed by RT-PCR and Western blot. Testosterone/AR could not only initiate cell apoptosis but also induce the activation of eukaryotic initiation factor 2 alpha (eIF2α) cascades in INS-1 cells. Treatment of ER stress inhibitor or flutamide (AR inhibitor) could inhibit testosterone-induced cell apoptosis and CHOP expression. These results suggest that testosterone/AR pathway caused INS-1 cell apoptosis was at least in part through eIF2α/CHOP cascades.

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