Sodium-ion capacitors can potentially combine the virtues of high power capability of conventional electrochemical capacitors and high energy density of batteries. However, the lack of high-performance electrode materials has been the major challenge of sodium-based energy storage devices. In this work, we report a microwave-assisted synthesis of single-crystal-like anatase TiO mesocages anchored on graphene as a sodium storage material. The architecture of the nanocomposite results in pseudocapacitive charge storage behavior with fast kinetics, high reversibility, and negligible degradation to the micro/nanostructure. The nanocomposite delivers a high capacity of 268 mAh g at 0.2 C, which remains 126 mAh g at 10 C for over 18 000 cycles. Coupling with a carbon-based cathode, a full cell of sodium-ion capacitor successfully demonstrates a high energy density of 64.2 Wh kg at 56.3 W kg and 25.8 Wh kg at 1357 W kg, as well as an ultralong lifespan of 10 000 cycles with over 90% of capacity retention.
Accumulation of ␣-synuclein (␣-syn) in the brain is a core feature of Parkinson disease (PD) and leads to microglial activation, production of inflammatory cytokines and chemokines, T-cell infiltration, and neurodegeneration. Here, we have used both an in vivo mouse model induced by viral overexpression of ␣-syn as well as in vitro systems to study the role of the MHCII complex in ␣-syn-induced neuroinflammation and neurodegeneration. We find that in vivo, expression of full-length human ␣-syn causes striking induction of MHCII expression by microglia, while knock-out of MHCII prevents ␣-syn-induced microglial activation, antigen presentation, IgG deposition, and the degeneration of dopaminergic neurons. In vitro, treatment of microglia with aggregated ␣-syn leads to activation of antigen processing and presentation of antigen sufficient to drive CD4 T-cell proliferation and to trigger cytokine release. These results indicate a central role for microglial MHCII in the activation of both the innate and adaptive immune responses to ␣-syn in PD and suggest that the MHCII signaling complex may be a target of neuroprotective therapies for the disease.
Little is known about the role of
specific delta GST genes in the
detoxification of lambda-cyhalothrin in the global
quarantine fruit pest codling moth, Cydia pomonella (L.). Real-time quantitative PCR shows that CpGSTd3 was ubiquitously expressed at all developmental stages and is most
abundant in the larval stage and lowest in the egg stage; the mRNA
level of CpGSTd3 is higher in the midgut and Malpighian
tubules of fourth-instar larvae and abdomens of adults than in other
tissues. Exposure of fourth-instar larvae to an LD10 dosage
of lambda-cyhalothrin significantly induced the transcript
of CpGSTd3 at 3 h, but the mRNA level was down-regulated
after 12 h of treatment. Recombinant CpGSTd3 expressed in Escherichia coli was able to catalyze the conjugation of
1-chloro-2,4-dinitrobenzene (CDNB) and with an IC50 value
of 0.65 mM for lambda-cyhalothrin. Metabolism assays
indicate that recombinant CpGSTd3 could metabolize lambda-cyhalothrin. These results suggest that CpGSTd3 is probably a lambda-cyhalothrin metabolizing GST in C. pomonella.
Accumulation of alpha-synuclein (α-syn) in the central nervous system (CNS) is a core feature of Parkinson disease (PD) that leads to activation of the innate immune system, production of inflammatory cytokines and chemokines, and subsequent neurodegeneration. Here, we used heterozygous reporter knock-in mice in which the first exons of the fractalkine receptor (CX3CR1) and of the C-C chemokine receptor type 2 (CCR2) are replaced with fluorescent reporters to study the role of resident microglia (CX3CR1+) and infiltrating peripheral monocytes (CCR2+), respectively, in the CNS. We used an α-syn mouse model induced by viral over-expression of α-syn. We find that in vivo, expression of full-length human α-syn induces robust infiltration of pro-inflammatory CCR2+ peripheral monocytes into the substantia nigra. Genetic deletion of CCR2 prevents α-syn induced monocyte entry, attenuates MHCII expression and blocks the subsequent degeneration of dopaminergic neurons. These results demonstrate that extravasation of pro-inflammatory peripheral monocytes into the CNS plays a key role in neurodegeneration in this model of PD synucleinopathy, and suggest that peripheral monocytes may be a target of neuroprotective therapies for human PD.
The layered graphene/g-C3N4 composites show high conductivity, electrocatalytic performance and visible light response and have potential applications in microelectronic devices and photocatalytic technology. In the present work, the stacking patterns and the correlations between electronic structures and related properties of graphene/g-C3N4 bilayers are investigated systematically by means of first-principles calculations. Our results indicate that the band gap of graphene/g-C3N4 bilayers can be up to 108.5 meV, which is large enough for the gap opening at room temperature. The calculated charge density difference unravels that the charge redistribution drives the interlayer charge transfer from graphene to g-C3N4. Interestingly, the investigation also shows that external electric field can tune the band gap of graphene/g-C3N4 bilayers effectively. Our research demonstrates that graphene on g-C3N4 with a tunable band gap and high carrier mobility may provide a novel way for fabricating high-performance graphene-based nanodevices.
DYT1 dystonia, a common and severe primary dystonia, is caused by a 3-bp deletion in TOR1A which encodes torsinA, a protein found in the endoplasmic reticulum. Several cellular functions are altered by the mutant protein, but at a systems level the link between these and the symptoms of the disease is unclear. The most effective known therapy for DYT1 dystonia is use of anticholinergic drugs. Previous studies have revealed that in mice, transgenic expression of human mutant torsinA under a non-selective promoter leads to abnormal function of striatal cholinergic neurons. To investigate what pathological role torsinA plays in cholinergic neurons, we created a mouse model in which the Dyt1 gene, the mouse homolog of TOR1A, is selectively deleted in cholinergic neurons (ChKO animals). These animals do not have overt dystonia, but do have subtle motor abnormalities. There is no change in the number or size of striatal cholinergic cells or striatal acetylcholine content, uptake, synthesis, or release in ChKO mice. There are, however, striking functional abnormalities of striatal cholinergic cells, with paradoxical excitation in response to D2 receptor activation and loss of muscarinic M2/M4 receptor inhibitory function. These effects are specific for cholinergic interneurons, as recordings from nigral dopaminergic neurons revealed normal responses. Amphetamine stimulated dopamine release was also unaltered. These results demonstrate a cell-autonomous effect of Dyt1 deletion on striatal cholinergic function. Therapies directed at modifying the function of cholinergic neurons may prove useful in the treatment of the human disorder.
A number of graphene-like materials have been theoretically predicted and experimentally confirmed so far. Here, based on the first-principles calculations, we predict that stable BiTeX (X = Br and I) monolayers possess intrinsic large polar electric fields along the normal direction to the plane, making them two-dimensional polar systems. Moreover, we find that these novel monolayers with thicknesses of only 3.8 Å can produce a giant Rashba spin splitting derived from their peculiarly polar atomic configurations. Furthermore, the Rashba parameters of BiTeX monolayers can be effectively modulated by applying strain, and are thus promising for wide applications in nanoelectronics.
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