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In order to solve the problem of increased system weight and cost of current wireless power transfer (WPT) systems with ferrite, a Halbach-type coupler WPT system with flux-shielding function for linear motor has been proposed in this article. It is characterized by high transmitting efficiency, better shielding ability, and antioffset ability. First, the topology and working mechanism of the proposed coupler have been analyzed. Second, considering the coupling ability and magnetic flux density, the parameters of the proposed Halbach-type coupler have been optimized. Third, the prototype of the proposed system has been built and tested, compared with the current DD-type coupler WPT system. Fourth, the magnetic field shielding ability and antioffset ability of the proposed Halbach-type coupler and DD-type coupler have been analyzed, respectively. The experimental results have verified that the WPT system based on the Halbach-type coupler has more promising magnetic field shielding ability and better resistance to the $z$ -axis offset, compared with the WPT system based on the DD-type coupler. The efficiency of the WPT system based on the proposed Halbach coupler can achieve 80.5% and the maximum output power reaches 69.5 W at 11 mm.

Programmed cell death (PCD) plays an essential role in plant development and response to environmental stimuli. However, the underlying molecular regulatory mechanisms are largely unknown. In this study, we investigated the roles of the SMS1 gene to dissect its molecular mechanisms in rice PCD. The SMS1 gene was characterized by map-based cloning. Functional prediction and verification of the SMS1 gene were further conducted through complementation tests, subcellular localization assays, tissue-specific gene expression using GUS staining, and overexpression analysis using real-time quantitative RT-PCR. The sms1 mutant showed constitutive PCD, defective cell wall structure, and reduced pollen sterility. SMS1 encodes a uridine diphosphate glucose pyrophosphorylase (UGPase). SMS1 is ubiquitously expressed in rice, and the SMS1 protein localizes to both the cytoplasm and nucleus, implying a fundamental and crucial role in various rice tissues. Taken together, we demonstrate that by modulating UDP-glucose metabolism, SMS1 contributes to the maintenance of cell wall organization and cell viability in rice, providing, for the first time, evidence that sugar homeostasis regulates plant PCD.

Parkinson's disease (PD) is the second most prevalent central nervous system (CNS) degenerative disease. Oxidative stress is one of key contributors to PD. Nuclear factor erythroid‐2‐related factor 2 (Nrf2) is considered to be a master regulator of many genes involved in anti‐oxidant stress to attenuate cell death. Therefore, activation of Nrf2 signalling provides an effective avenue to treat PD. Ellagic acid (EA), a natural polyphenolic contained in fruits and nuts, possesses amounts of pharmacological activities, such as anti‐oxidant stress and anti‐inflammation. Recent studies have confirmed EA could be used as a neuroprotective agent in neurodegenerative diseases. Here, mice subcutaneous injection of rotenone (ROT)‐induced DA neuronal damage was performed to investigate EA‐mediated neuroprotection. In addition, adult Nrf2 knockout mice and different cell cultures including MN9D‐enciched, MN9D‐BV‐2 and MN9D‐C6 cell co‐cultures were applied to explore the underlying mechanisms. Results demonstrated EA conferred neuroprotection against ROT‐induced DA neurotoxicity. Activation of Nrf2 signalling was involved in EA‐mediated DA neuroprotection, as evidenced by the following observations. First, EA activated Nrf2 signalling in ROT‐induced DA neuronal damage. Second, EA generated neuroprotection with the presence of astroglia and silence of Nrf2 in astroglia abolished EA‐mediated neuroprotection. Third, EA failed to produce DA neuroprotection in Nrf2 knockout mice. In conclusion, this study identified EA protected against DA neuronal loss via an Nrf2‐dependent manner.

Soil salinity is a key source of abiotic stress in the cultivation of rice. In this study, two currently cultivated japonica rice species—Zhegeng 78 (salt-tolerant) and Zhegeng 99 (salt-sensitive)—with similar backgrounds were identified and used to investigate their differential responses to salt stress at the post-germination and seedling stages. Quantitative RT-PCR analysis demonstrated that the expression of OsSOS1, OsHAK1, and OsHAK5 at the post-germination stage, and the expression of OsHKT1,1, OsHTK2,1, and OsHAK1 at the seedling stage, were significantly higher in the salt-tolerant Zhegeng 78 compared with those of the salt-sensitive Zhegeng 99 under salt stress. The significantly lower Na+ net uptake rate at the post-germination and higher K+ net uptake rates at the post-germination and seedling stages were observed in the salt-tolerant Zhegeng 78 compared with those of the salt-sensitive Zhegeng 99 under salt stress. Significantly higher activity of peroxidase (POD) and the lower hydrogen peroxide (H2O2) accumulation were observed in the salt-tolerant Zhegeng 78 compared with those of salt-sensitive Zhegeng 99 under salt stress at the seeding stage. The salt-tolerant Zhegeng 78 might be valuable in future cultivation in salinity soils.

Astroglia support neuron by providing substrates for neuronal metabolism, glutamate clearance, and antioxidative protection. Nuclear factor erythroid 2-related factor 2 (Nrf2) participates in the antioxidative defense response. Also, Nrf2 signaling is recognized to activate the neurotrophic pathway to replace/protect damaged organelles. Ellagic acid (EA), an extraction component of fruits and nuts, presents many pharmacological activities such as anti-inflammation, antioxidation, and neuroprotection. However, few studies have been focused on the neurotrophic properties of EA. Our study investigated whether EA could increase neuronal survival and the target cells. Thus, primary neuron-enriched cultures and primary astroglia-enriched cultures were applied to detect whether EA-elicited neurotrophic effects were mediated by astroglia Nrf2. This study indicated that EA promoted neuronal survival. Further, astroglia Nrf2 participate in EA-elicited neuronal survival with the following scenarios. First, EA elicited astroglia proliferation, glial cell line-derived neurotrophic factor (GDNF) release, and Nrf2 activation. Second, after silencing astroglia Nrf2, EA-induced astrogliosis, GDNF release, and neuronal survival disappeared. Thus, EA-mediated astroglia Nrf2 activation is important to enhance neurotrophic effects on neurons, which might provide new insights for neurodegenerative disease.

Background Glyphosate has become the most widely used herbicide in the world. Therefore, the development of new varieties of glyphosate-tolerant crops is a research focus of seed companies and researchers. The glyphosate stress-responsive genes were used for the development of genetically modified crops, while only the EPSPS gene has been used currently in the study on glyphosate-tolerance in rice. Therefore, it is essential and crucial to intensify the exploration of glyphosate stress-responsive genes, to not only acquire other glyphosate stress-responsive genes with clean intellectual property rights but also obtain non-transgenic glyphosate-tolerant rice varieties. This study is expected to elucidate the responses of miRNAs, lncRNAs, and mRNAs to glyphosate applications and the potential regulatory mechanisms in response to glyphosate stress in rice. Results Leaves of the non-transgenic glyphosate-tolerant germplasm CA21 sprayed with 2 mg·ml− 1 glyphosate (GLY) and CA21 plants with no spray (CK) were collected for high-throughput sequencing analysis. A total of 1197 DEGs, 131 DELs, and 52 DEMs were identified in the GLY samples in relation to CK samples. Genes were significantly enriched for various biological processes involved in detoxification of plant response to stress. A total of 385 known miRNAs from 59 miRNA families and 94 novel miRNAs were identified. Degradome analysis led to the identification of 32 target genes, of which, the squamosa promoter-binding-like protein 12 (SPL12) was identified as a target of osa-miR156a_L + 1. The lncRNA-miRNA-mRNA regulatory network consisted of osa-miR156a_L + 1, two transcripts of SPL12 (LOC_Os06g49010.3 and LOC_Os06g49010.5), and 13 lncRNAs (e.g., MSTRG.244.1 and MSTRG.16577.1). Conclusion Large-scale expression changes in coding and noncoding RNA were observed in rice mainly due to its response to glyphosate. SPL12, osa-miR156, and lncRNAs (e.g., MSTRG.244.1 and MSTRG.16577.1) could be a novel ceRNA mechanism in response to glyphosate in rice by regulating transcription and metal ions binding. These findings provide a theoretical basis for breeding glyphosate-tolerant rice varieties and for further research on the biogenesis of glyphosate- tolerance in rice.

Background: At present, L-DOPA remained the gold standard therapy for motor symptoms of Parkinson’s disease (PD) patients. However, prolonged administration of L-DOPA led to the development of dyskinesia. Aspirin, a non-steroidal anti-inflammatory drug (NSAID), had been widely used to relieve pain and inflammation. Recent studies indicated aspirin produced neuroprotection against dopamine (DA) neuronal loss in animal model. This study aimed to explore the effects of aspirin pre-treatment and co-treatment with L-DOPA on DA neurotoxicity and L-DOPA-induced dyskinesia (LID) as well.Methods: Rats received a single 6-hydroxydopamine (6-OHDA) injection into substantia nigra to induce DA neuronal loss. For aspirin pre-treatment before L-DOPA studies: One day after 6-OHDA stimulation, rats were daily administrated with aspirin for 3 weeks followed by daily L-DOPA treatment along with aspirin for additional 3 weeks. For aspirin co-treatment with L-DOPA studies: Three weeks after 6-OHDA administration, rats were daily treated by L-DOPA together with aspirin for another 3 weeks. DA neurotoxicity was analyzed via rat PD-like behavior test and DA neuronal counting. The movement disorders of dyskinesia triggered by L-DOPA were determined by the abnormal involuntary movements (AIM) scores analysis.Results: we demonstrated both aspirin pre-treatment and co-treatment exerted anti-LID effects during L-DOPA treatment on 6-OHDA-lesioned rats. In addition, aspirin not only ameliorated DA neuronal damage, but also reduced the development of dyskinesia without affecting L-DOPA efficacy. Furtherly, inhibition of glial cells activation and the subsequent neuroinflammatory response might be involved in aspirin-attenuated dyskinesia.Conclusion: the present study suggested aspirin could have beneficial potential to attenuate LID in PD.

BackgroundParkinson’s disease (PD) is the second most prevalent central nervous system (CNS) degenerative disease. Oxidative stress is one of key contributors to the degeneration of dopamine (DA) neurons in the pathogenesis of PD. Nuclear factor erythroid-2-related factor 2 (Nrf2) is considered to be a ‘master regulator’ of many genes involved in anti-oxidant stress to attenuate cell death. Therefore, activation of Nrf2 signaling provides an effective avenue to treat PD. Ellagic acid (EA), a natural polyphenolic contained in fruits and nuts, possesses amounts of pharmacological activities, such as anti-oxidant stress and anti-inflammation. Recent studies have confirmed EA could be used as a neuroprotective agent in neurodegenerative diseases. However, the underlying mechanisms have not yet been entirely elucidated. MethodsIn this study, mice subcutaneous injection of rotenone (ROT)-induced DA neuronal damage was performed to investigate EA-mediated neuroprotection. In addition, adult Nrf2 knockout mice and different cell cultures including MN9D-enciched, MN9D-BV-2 and MN9D-C6 cell co-cultures were applied to explore the underlying mechanisms. ResultsThe present study demonstrated EA protected DA neurons against ROT-induced neurotoxicity. Furtherly, activation of astroglial Nrf2 signaling pathway participated in EA-mediated neuroprotection as evidenced by the following observations. First, EA activated Nrf2 signaling pathway in ROT-induced DA neuronal injury. Second, EA generated neuroprotection with the presence of astroglia and silence of Nrf2 in astroglia abolished EA-conferred DA neuroprotection. Third, EA failed to produce DA neuroprotection in Nrf2 knockout mice. ConclusionThis study identified EA protected against DA neuronal loss via an Nrf2-dependent manner in astroglia.