Dynamic profiles of lncRNAs reveal a functional natural antisense RNA that regulates the development of Schistosoma japonicum.

Schistosomes are flatworm parasites that undergo a complex life cycle involving two hosts. The regulation of the parasite's developmental processes relies on both coding RNAs and non-coding RNAs. However, the roles of non-coding RNAs, including long non-coding RNAs (lncRNAs) in schistosomes remain largely unexplored. Here we conduct advanced RNA sequencing on male and female S. japonicum during their pairing and reproductive development, resulting in the identification of nearly 8,000 lncRNAs. This extensive dataset enables us to construct a comprehensive co-expression network of lncRNAs and mRNAs, shedding light on their interactions during the crucial reproductive stages within the mammalian host. Importantly, we have also revealed a specific lncRNA, LNC3385, which appears to play a critical role in the survival and reproduction of the parasite. These findings not only enhance our understanding of the dynamic nature of lncRNAs during the reproductive phase of schistosomes but also highlight LNC3385 as a potential therapeutic target for combating schistosomiasis.

WTAP-induced N6-methyladenosine of PD-L1 blocked T-cell-mediated antitumor activity under hypoxia in colorectal cancer.

N6-Methyladenosine (m6A) is a important process regulating gene expression post-transcriptionally. Programmed death ligand 1 (PD-L1) is a major immune inhibitive checkpoint that facilitates immune evasion and is expressed in tumor cells. In this research we discovered that Wilms' tumor 1-associated protein (WTAP) degradation caused by ubiquitin-mediated cleavage in cancer cells (colorectal cancer, CRC) under hypoxia was inhibited by Pumilio homolog 1 (PUM1) directly bound to WTAP. WTAP enhanced PD-L1 expression in a way that was m6A-dependent. m6A "reader," Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) identified methylated PD-L1 transcripts and subsequently fixed its mRNA. Additionally, we found that T-cell proliferation and its cancer cell-killing effects were prevented by overexpression of WTAP in vitro and in vivo. Overexpression prevented T cells from proliferating and killing CRC by maintaining the expression of PD-L1. Further evidence supporting the WTAP-PD-L1 regulatory axis was found in human CRC and organoid tissues. Tumors with high WTAP levels appeared more responsive to anti-PD1 immunotherapy, when analyzing samples from patients undergoing treatment. Overall, our findings demonstrated a novel PD-L1 regulatory mechanism by WTAP-induced mRNA epigenetic regulation and the possible application of targeting WTAP as immunotherapy for tumor hypoxia.

Transverse endoplasmic reticulum expansion in hereditary spastic paraplegia corticospinal axons.

Hereditary spastic paraplegias (HSPs) comprise a large group of inherited neurologic disorders affecting the longest corticospinal axons (SPG1-86 plus others), with shared manifestations of lower extremity spasticity and gait impairment. Common autosomal dominant HSPs are caused by mutations in genes encoding the microtubule-severing ATPase spastin (SPAST; SPG4), the membrane-bound GTPase atlastin-1 (ATL1; SPG3A) and the reticulon-like, microtubule-binding protein REEP1 (REEP1; SPG31). These proteins bind one another and function in shaping the tubular endoplasmic reticulum (ER) network. Typically, mouse models of HSPs have mild, later onset phenotypes, possibly reflecting far shorter lengths of their corticospinal axons relative to humans. Here, we have generated a robust, double mutant mouse model of HSP in which atlastin-1 is genetically modified with a K80A knock-in (KI) missense change that abolishes its GTPase activity, whereas its binding partner Reep1 is knocked out. Atl1KI/KI/Reep1-/- mice exhibit early onset and rapidly progressive declines in several motor function tests. Also, ER in mutant corticospinal axons dramatically expands transversely and periodically in a mutation dosage-dependent manner to create a ladder-like appearance, on the basis of reconstructions of focused ion beam-scanning electron microscopy datasets using machine learning-based auto-segmentation. In lockstep with changes in ER morphology, axonal mitochondria are fragmented and proportions of hypophosphorylated neurofilament H and M subunits are dramatically increased in Atl1KI/KI/Reep1-/- spinal cord. Co-occurrence of these findings links ER morphology changes to alterations in mitochondrial morphology and cytoskeletal organization. Atl1KI/KI/Reep1-/- mice represent an early onset rodent HSP model with robust behavioral and cellular readouts for testing novel therapies.

SMAD3 interacts with vitamin D receptor and affects vitamin D-mediated oxidative stress to ameliorate cerebral ischaemia-reperfusion injury.

Cerebral ischaemia/reperfusion (I/R) injury is caused by blood flow restoration after an ischaemic insult, and effective treatments targeting I/R injury are still insufficient. Oxidative stress plays a critical role in the pathogenesis of cerebral I/R injury. This study investigated whether vitamin D receptor (VDR) could inhibit oxidative stress caused by cerebral I/R injury and explored the detailed mechanism. VDR was highly expressed in brain tissues of mice with cerebral I/R injury. Pretreatment with the active vitamin D calcitriol and synthetic vitamin D analogue paricalcitol (PC) reduced autophagy and apoptosis, improved neurological deficits and decreased infarct size in mice after cerebral I/R. Calcitriol or PC upregulated VDR expression to prevent cerebral I/R injury by affecting oxidative stress. Silencing of VDR reversed the protective effects of calcitriol or PC on brain tissues in mice with cerebral I/R. The bioinformatics analysis revealed that VDR interacted with SMAD family member 3 (SMAD3). It was validated through the chromatin immunoprecipitation assay that SMAD3 can bind to the VDR promoter and VDR can bind to the SMAD3 promoter. Collectively, these findings provide evidence that reciprocal activation between SMAD3 and VDR transcription factors defines vitamin D-mediated oxidative stress to prevent cerebral I/R injury.

Defects in syntabulin-mediated synaptic cargo transport associate with autism-like synaptic dysfunction and social behavioral traits.

The formation and maintenance of synapses require long-distance delivery of newly synthesized synaptic proteins from the soma to distal synapses, raising the fundamental question of whether impaired transport is associated with neurodevelopmental disorders such as autism. We previously revealed that syntabulin acts as a motor adapter linking kinesin-1 motor and presynaptic cargos. Here, we report that defects in syntabulin-mediated transport and thus reduced formation and maturation of synapses are one of core synaptic mechanisms underlying autism-like synaptic dysfunction and social behavioral abnormalities. Syntabulin expression in the mouse brain peaks during the first 2 weeks of postnatal development and progressively declines during brain maturation. Neurons from conditional syntabulin-/- mice (stb cKO) display impaired transport of presynaptic cargos, reduced synapse density and active zones, and altered synaptic transmission and long-term plasticity. Intriguingly, stb cKO mice exhibit core autism-like traits, including defective social recognition and communication, increased stereotypic behavior, and impaired spatial learning and memory. These phenotypes establish a new mechanistic link between reduced transport of synaptic cargos and impaired maintenance of synaptic transmission and plasticity, contributing to autism-associated behavioral abnormalities. This notion is further confirmed by the human missense variant STB-R178Q, which is found in an autism patient and loses its adapter capacity for binding kinesin-1 motors. Expressing STB-R178Q fails to rescue reduced synapse formation and impaired synaptic transmission and plasticity in stb cKO neurons. Altogether, our study suggests that defects in syntabulin-mediated transport mechanisms underlie the synaptic dysfunction and behavioral abnormalities that bear similarities to autism.

Comparative Transcriptome Analyses of Drug-sensitive and Drug-resistant Strains of Eimeria tenella by RNA-sequencing.

Avian coccidiosis is a widespread and economically significant disease in poultry. At present, treatment of coccidiosis mainly relies on drugs. Anticoccidial drugs can be divided into two categories: ionophorous compounds and synthetic drugs. However, the emergence of drug-resistant strains has become a challenge for coccidiosis control with anticoccidial drugs. To gain insights into the molecular mechanism governing the drug resistance of Eimeria tenella, two drug-resistant strains of E. tenella, one maduramicin-resistant (MRR) strain and one diclazuril-resistant (DZR) strain, were generated. We carried out comparative transcriptome analyses of a drug-sensitive strain (DS) and two drug-resistant MRR and DZR strains of E. tenella using RNA-sequencing. A total of 1,070 differentially expressed genes (DEGs), 672 upregulated and 398 downregulated, were identified in MRR vs. DS, and 379 DEGs, 330 upregulated and 49 downregulated, were detected in DZR vs. DS. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses were performed to better understand the functions of these DEGs. In the comparison of DZR vs. DS, some DEGs were involved in peroxisome, biosynthesis of unsaturated fatty acids, and fatty acid metabolism. In the comparison of MRR vs. DS, some DEGs were involved in glycolysis/gluconeogenesis, regulation of actin cytoskeleton, and DNA replication. In addition, some DEGs coded for surface antigens that were downregulated in two drug-resistant strains involved invasion, pathogenesis, and host-parasite interactions. These results provided suggestions for further research toward unraveling the molecular mechanisms of drug resistance in Eimeria species and contribute to developing rapid molecular methods to detect resistance to these drugs in Eimeria species in poultry.

Robust Cylindrical Panorama Stitching for Low-Texture Scenes Based on Image Alignment Using Deep Learning and Iterative Optimization.

Cylindrical panorama stitching is able to generate high resolution images of a scene with a wide field-of-view (FOV), making it a useful scene representation for applications like environmental sensing and robot localization. Traditional image stitching methods based on hand-crafted features are effective for constructing a cylindrical panorama from a sequence of images in the case when there are sufficient reliable features in the scene. However, these methods are unable to handle low-texture environments where no reliable feature correspondence can be established. This paper proposes a novel two-step image alignment method based on deep learning and iterative optimization to address the above issue. In particular, a light-weight end-to-end trainable convolutional neural network (CNN) architecture called ShiftNet is proposed to estimate the initial shifts between images, which is further optimized in a sub-pixel refinement procedure based on a specified camera motion model. Extensive experiments on a synthetic dataset, rendered photo-realistic images, and real images were carried out to evaluate the performance of our proposed method. Both qualitative and quantitative experimental results demonstrate that cylindrical panorama stitching based on our proposed image alignment method leads to significant improvements over traditional feature based methods and recent deep learning based methods for challenging low-texture environments.

Risk prediction to inform surveillance of chronic kidney disease in the US Healthcare Safety Net: a cohort study.

BACKGROUND: The capacity of electronic health record (EHR) data to guide targeted surveillance in chronic kidney disease (CKD) is unclear. We sought to leverage EHR data for predicting risk of progressing from CKD to end-stage renal disease (ESRD) to help inform surveillance of CKD among vulnerable patients from the healthcare safety-net. METHODS: We conducted a retrospective cohort study of adults (n = 28,779) with CKD who received care within 2 regional safety-net health systems during 1996-2009 in the Western United States. The primary outcomes were progression to ESRD and death as ascertained by linkage with United States Renal Data System and Social Security Administration Death Master files, respectively, through September 29, 2011. We evaluated the performance of 3 models which included demographic, comorbidity and laboratory data to predict progression of CKD to ESRD in conditions commonly targeted for disease management (hypertension, diabetes, chronic viral diseases and severe CKD) using traditional discriminatory criteria (AUC) and recent criteria intended to guide population health management strategies. RESULTS: Overall, 1730 persons progressed to end-stage renal disease and 7628 died during median follow-up of 6.6 years. Performance of risk models incorporating common EHR variables was highest in hypertension, intermediate in diabetes and chronic viral diseases, and lowest in severe CKD. Surveillance of persons who were in the highest quintile of ESRD risk yielded 83-94 %, 74-95 %, and 75-82 % of cases who progressed to ESRD among patients with hypertension, diabetes and chronic viral diseases, respectively. Similar surveillance yielded 42-71 % of ESRD cases among those with severe CKD. Discrimination in all conditions was universally high (AUC ≥0.80) when evaluated using traditional criteria. CONCLUSIONS: Recently proposed discriminatory criteria account for varying risk distribution and when applied to common clinical conditions may help to inform surveillance of CKD in diverse populations.

Midbrain-derived neurotrophins support survival of immature striatal projection neurons.

Neuronal death occurs at several stages during embryogenesis and early postnatal development; however, it is unknown how the survival of immature neurons at their origin is regulated before these cells migrate to their final destination. Striatal projection neurons, known as medium-sized spiny neurons (MSNs), in both the direct and indirect pathways are generated in the lateral ganglionic eminence (LGE). Here we report that brain-derived neurotrophic factor and neurotrophin-3 are anterogradely transported from midbrain dopaminergic neurons and support the survival of immature MSNs of the indirect and direct pathways, respectively, in the developing mouse striatum and LGE. These results reveal a novel mode of neurotrophic action in the nervous system by linking neurotrophins to the survival of immature neurons at their origin, while also suggesting that innervating neurons may control the size of their targeting neuronal population in the brain.

Low-carbon scheduling of electricity consumption in wastewater treatment plant by using photovoltaic system.

Sewage treatment as a high energy consumption industry, its electricity consumption accounts for 3 % of the total electricity consumption of society. That means significant greenhouse gas emissions. In the context of China's goal of "reaching carbon peak by 2030 and achieving carbon neutrality by 2060", reducing the energy consumption of wastewater treatment systems has emerged as an important issue in recent years. In this paper, the GPS-X simulation software was employed to conduct a simulation study of a modified Anoxic-Aerobic-Oxic wastewater treatment plant (WWTP) in Wuhan, and the response surface methodology (RSM) was utilized to ascertain the interactive effects of DO, IRF, ERR, and SD on the effluent quality, thereby identifying the operational parameters that minimize energy consumption while maintaining satisfactory effluent quality. Additionally, the PVsyst software was employed to design the solar power generation system of the WWTP and analyze its power generation potential. On this basis, through the coupling of photovoltaic power, electricity load, time-of-use pricing, and the water quality simulation model, and taking the WWTP data in September as a case study, the electricity usage strategies under various illumination conditions were formulated. The aim is to maximize the use of photovoltaic power to reduce the cost and carbon emissions of the WWTP. The results show that the optimal combination of operational parameters, including an external reflux ratio of 0.3, the internal recycle flow of 50,000 m3/d, and the sludge discharge of 448 m3/d, resulted in a reduction in power of 208.5 kW, and after the combination optimization of operational parameters and electricity utilization, the operation cost of the WWTP in September was reduced by 40 % âˆ¼ 60 %, and the carbon emission attributable to electricity was reduced by 30 % âˆ¼ 50 %.

Constructing the Polymer Molecules to Regulate the Electrode/Electrolyte Interface to Enhance Lithium-Metal Battery Performance.

Lithium-ion batteries, with high energy density and long cycle life, have become the battery of choice for most vehicles and portable electronic devices; however, energy density, safety and cycle life require further improvements. Single-functional group electrolyte additives are very limited in practical applications, a ternary polymer bifunctional electrolyte additive copolymer (acrylonitrile-butyl hexafluoro methacrylate- poly (ethylene glycol) methacrylate- methyl ether) (PMANHF) was synthesized by free radical polymerization of acrylonitrile, 2, 2, 3, 4, 4, 4-hexafluorobutyl methacrylate and poly (ethylene glycol) methyl ether methacrylate. A series of characterizations show that in Li metal anodes, the preferential reduction of PMANHF is conducive to the formation of a uniform and stable solid electrolyte interphase layer, and Li deposition is uniform and dense. At the NCM811 cathode, a film composed of LiF- and Li3N-rich is formed at the cathode-electrolyte interface, mitigating the side reaction at the interface. At 1.0 mA cm-2, the Li/Li cell can be stabilized for 1000 cycles. In addition, the Li/NCM811 cell can stabilize 200 cycles with a cathode capacity of 153.7 mAh g-1, with the capacity retention of 89.93 %, at a negative/positive capacity ratio of 2.5. This study brings to light essential ideas for the fabrication of additives for lithium-metal batteries.

Dendritic BDNF synthesis is required for late-phase spine maturation and recovery of cortical responses following sensory deprivation.

Sensory experience in early postnatal life shapes neuronal connections in the brain. Here we report that the local synthesis of brain-derived neurotrophic factor (BDNF) in dendrites plays an important role in this process. We found that dendritic spines of layer 2/3 pyramidal neurons of the visual cortex in mutant mice lacking dendritic Bdnf mRNA and thus local BDNF synthesis were normal at 3 weeks of age, but thinner, longer, and more closely spaced (morphological features of immaturity) at 4 months of age than in wild-type (WT) littermates. Layer 2/3 of the visual cortex in these mutant animals also had fewer GABAergic presynaptic terminals at both ages. The overall size and shape of dendritic arbors were, however, similar in mutant and WT mice at both ages. By using optical imaging of intrinsic signals and single-unit recordings, we found that mutant animals failed to recover cortical responsiveness following monocular deprivation (MD) during the critical period, although they displayed normally the competitive loss of responsiveness to an eye briefly deprived of vision. Furthermore, MD still induced a loss of responsiveness to the closed eye in adult mutant mice, but not in adult WT mice. These results indicate that dendritic BDNF synthesis is required for spine pruning, late-phase spine maturation, and recovery of cortical responsiveness following sensory deprivation. They also suggest that maturation of dendritic spines is required for the maintenance of cortical responsiveness following sensory deprivation in adulthood.

TNFRSF10B is involved in motor dysfunction in Parkinson's disease by regulating exosomal α-synuclein secretion from microglia.

A-synuclein (α-syn) is a protein associated with the pathogenesis of Parkinson's disease (PD), a neurodegenerative disease with no effective treatment. Therefore, there has been a strong drive to clarify the pathology of PD associated with α-syn. Several mechanisms have been proposed to unravel the pathological cascade of this disease, and most of them share a particular similarity: cell-to-cell communication through exosomes (EXO). Here, we show that tumor necrosis factor receptor superfamily member 10B (TNFRSF10B) promotes the secretion of α-syn-containing EXO by microglia, resulting in motor dysfunction in PD. Upregulation of TNFRSF10B predicted severer condition in PD patients. In response to α-syn preformed fibrils (PFF), the expression of TNFRSF10B was increased in microglia. PFF-treated microglia exhibited a pro-inflammatory phenotype and caused neuronal damage by secreting α-syn-containing EXO. TNFRSF10B downregulation in microglia inhibited the secretion of α-syn-containing EXO and the release of pro-inflammatory factors, and ameliorated neuronal injury. PFF induced motor dysfunction in mice, which was ameliorated by inhibiting TNFRSF10B to suppress microglia-mediated α-syn communication or by directly depleting microglia. Taken together, these results indicate that TNFRSF10B promotes neuronal injury and motor dysfunction by delivery of α-syn-containing EXO and highlight the TNFRSF10B knockdown as a potential therapeutic target in PD.

Lightweight ZnO/Carbonated Cotton Fiber Nanocomposites for Electromagnetic Interference Applications: Preparation and Properties.

Electromagnetic wave pollution has become a significant harm posed to human health and precision instruments. To shelter such instruments from electromagnetic radiation, high-frequency electromagnetic interference (EMI) shielding materials are extremely desirable. The focus of this research is lightweight, high-absorption EMI shielding composites. Simple aqueous dispersion and drying procedures were used to prepare cotton fiber (CF)-based sheets combined with various zinc oxide (ZnO) contents. These composites were carbonated in a high-temperature furnace at 800 °C for two hours. The obtained CF/ZnO samples have densities of 1.02-1.08 g/cm3. The EMI shielding effectiveness of CF-30% ZnO, CF-50% ZnO, and CF-70% ZnO reached 32.06, 38.08, and 34.69 dB, respectively, to which more than 80% of absorption is attributed. The synergetic effects of carbon networks and surface structures are responsible for the high EMI shielding performance; various reflections inside the interconnected networks may also help in improving their EMI shielding performance.

Surface modification using heptafluorobutyric acid to produce highly stable Li metal anodes.

The Li metal is an ideal anode material owing to its high theoretical specific capacity and low electrode potential. However, its high reactivity and dendritic growth in carbonate-based electrolytes limit its application. To address these issues, we propose a novel surface modification technique using heptafluorobutyric acid. In-situ spontaneous reaction between Li and the organic acid generates a lithiophilic interface of lithium heptafluorobutyrate for dendrite-free uniform Li deposition, which significantly improves the cycle stability (Li/Li symmetric cells >1200 h at 1.0 mA cm-2) and Coulombic efficiency (>99.3%) in conventional carbonate-based electrolytes. This lithiophilic interface also enables full batteries to achieve 83.2% capacity retention over 300 cycles under realistic testing condition. Lithium heptafluorobutyrate interface acts as an electrical bridge for uniform lithium-ion flux between Li anode and plating Li, which minimizes the occurrence of tortuous lithium dendrites and lowers interface impedance.

An Ultra-Low Power Reconfigurable Biomedical AI Processor With Adaptive Learning for Versatile Wearable Intelligent Health Monitoring.

Wearable intelligent health monitoring devices with on-device biomedical AI processor can be used to detect the abnormity in users' biomedical signals (e.g., ECG arrythmia classification, EEG-based seizure detection). This requires ultra-low power and reconfigurable biomedical AI processor to support battery-supplied wearable devices and versatile intelligent health monitoring applications while achieving high classification accuracy. However, existing designs have issues in meeting one or more of the above requirements. In this work, a reconfigurable biomedical AI processor (named BioAIP) is proposed, mainly featuring: 1) a reconfigurable biomedical AI processing architecture to support versatile biomedical AI processing. 2) an event-driven biomedical AI processing architecture with approximate data compression to reduce the power consumption. 3) an AI-based adaptive-learning architecture to address patient-to-patient variation and improve the classification accuracy. The design has been implemented and fabricated using a 65nm CMOS process technology. It has been demonstrated with three typical biomedical AI applications, including ECG arrythmia classification, EEG-based seizure detection and EMG-based hand gesture recognition. Compared with the state-of-the-art designs optimized for single biomedical AI tasks, the BioAIP achieves the lowest energy per classification among the designs with similar accuracy, while supporting various biomedical AI tasks.

Up-regulation of PUM1 by miR-218-5p promotes colorectal tumor-initiating cell properties and tumorigenesis by regulating the PI3K/AKT axis.

Background: Colorectal cancer (CRC) is the third most common cancer and the fourth most common cause of cancer-related death worldwide. Advanced stage CRC, during the recent past, had a dismal prognosis and only a few available treatments. Pumilio homologous protein 1 (PUM1) is reportedly aberrant in human malignancies, including CRC. However, the role of PUM1 in the regulation of tumor-initiating cells (T-ICs) remains unknown. Methods: The levels of messenger RNAs (mRNAs) were determined by quantitative reverse transcription polymerase chain reaction (qRT-PCR) and immunoblot analyses. Statistical analyses were performed to determine the associations between the levels of PUM1 and tumor features and patient outcomes. Whether PUM1 is a downstream target of miR-218-5p was verified by bioinformatics target gene prediction and qRT-PCR. Results: Herein, it was found that T-ICs, chemoresistance, and recurrent CRC samples all manifest increased PUM1 expression. Functional investigations have shown that PUM1 increased the self-renewal, tumorigenicity, malignant proliferation, and chemoresistance of colorectal cells. PUM1 activates the phosphatidylinositol-3-kinase (PI3K)/protein kinase B (AKT) signaling pathway biochemically. Furthermore, it was discovered that miR-218-5p specifically targets T-ICs' PUM1 3'-untranslated region (3'-UTR). More importantly, the PUM1/PI3K/AKT axis regulates CRC cells' responses to treatment with cetuximab, and PUM1 overexpression increased cetuximab resistance. More evidence points to the possibility that low PUM1 may predict cetuximab benefits in CRC patients after analysis of the patient cohort, patient-derived tumor organoids, and patient-derived xenografts (PDXs). Conclusions: Taken together, the result of this work points to the critical function of the miR-218-5p/PUM1/PI3K/AKT regulatory circuit in regulating T-ICs characteristics and thus suggests possible therapeutic targets for CRC.

Solid Electrolyte Interphase Structure Regulated by Functional Electrolyte Additive for Enhancing Li Metal Anode Performance.

Lithium (Li) metal anodes have become an important component of the next generation of high energy density batteries. However, the Li metal anode still has problems such as Li dendrite growth and unstable solid electrolyte interface layer. Herein, we present a functional electrolyte additive (PANHF) successfully synthesized from acrylonitrile and hexafluorobutyl methacrylate via a polymerization reaction. With extensive analytical characterization, it is found that the PANHF can improve the reversibility and Coulombic efficiency of the Li deposition/dissolution reaction and prevent the growth of Li dendrites by forming a solid electrolyte interphase rich in organic matter on the outer layer and LiF on the inner layer. The results show that the cycling performance of the Li/Li cell was greatly improved in the electrolyte containing 0.5 wt % PANHF. Specifically, the cycling stability of more than 700 cycles was achieved at a current density of 1.0 mA cm-2. Moreover, the Li/NCM811 cell with 0.5 wt % PANHF has a higher capacity of 137.7 mA h g-1 at 1.0 C and a capacity retention of 83.41% after 200 cycles. This work highlights the importance of protecting the Li metal anode with functional bipolymer additives for next-generation Li metal batteries.

A novel high-energy-density lithium-free anode dual-ion battery and in situ revealing the interface structure evolution.

Lithium-free anode dual-ion batteries have attracted extensive studies due to their simple configuration, reduced cost, high safety and enhanced energy density. For the first time, a novel Li-free DIB based on a carbon paper anode (Li-free CGDIB) is reported in this paper. Carbon paper anodes usually have limited application in DIBs due to their poor electrochemical performance. Herein, by using a lithium bis(fluorosulfonyl)imide (LiFSI)-containing electrolyte, the battery shows outstanding electrochemical performance with a capacity retention of 96% after 300 cycles at 2C with a stable 98% coulombic efficiency and 89% capacity retention after 500 cycles at 5C with a stable coulombic efficiency of 98.5%. Moreover, the electrochemical properties of the CGDIB were investigated with a variety of in situ characterization techniques, such as in situ EIS, XRD and online differential electrochemical mass spectrometry (OEMS). The multifunctional effect of the LiFSI additive on the electrochemical properties of the Li-free CGDIB was also systematically analyzed, including generating a LiF-rich interfacial film, prohibiting Li dendrite growth effectively and forming a defective structure of graphite layers. This design strategy and fundamental analysis show great potential and lay a theoretical foundation for facilitating the further development of DIBs with high energy density.

A metabotropic glutamate receptor affects the growth and development of Schistosoma japonicum.

Schistosomiasis is a zoonotic parasitic disease caused by schistosome infection that severely threatens human health. Therapy relies mainly on single drug treatment with praziquantel. Therefore, there is an urgent need to develop alternative medicines. The glutamate neurotransmitter in helminths is involved in many physiological functions by interacting with various cell-surface receptors. However, the roles and detailed regulatory mechanisms of the metabotropic glutamate receptor (mGluR) in the growth and development of Schistosoma japonicum remain poorly understood. In this study, we identified two putative mGluRs in S. japonicum and named them SjGRM7 (Sjc_001309, similar to GRM7) and SjGRM (Sjc_001163, similar to mGluR). Further validation using a calcium mobilization assay showed that SjGRM7 and SjGRM are glutamate-specific. The results of in situ hybridization showed that SjGRM is mainly located in the nerves of both males and gonads of females, and SjGRM7 is principally found in the nerves and gonads of males and females. In a RNA interference experiment, the results showed that SjGRM7 knockdown by double-stranded RNA (dsRNA) in S. japonicum caused edema, chassis detachment, and separation of paired worms in vitro. Furthermore, dsRNA interference of SjGRM7 could significantly affect the development and egg production of male and female worms in vivo and alleviate the host liver granulomas and fibrosis. Finally, we examined the molecular mechanisms underlying the regulatory function of mGluR using RNA sequencing. The data suggest that SjGRM7 propagates its signals through the G protein-coupled receptor signaling pathway to promote nervous system development in S. japonicum. In conclusion, SjGRM7 is a potential target for anti-schistosomiasis. This study enables future research on the mechanisms of action of Schistosomiasis japonica drugs.