Autoimmune encephalitis antibody profiles and clinical characteristics of children with suspected autoimmune encephalitis.

AIM: To identify the spectrum of autoimmune encephalitis antibody biomarkers (AE-Abs) in children with suspected autoimmune encephalitis and explore the clinical features indicating AE-Abs presence. METHOD: We included children with suspected autoimmune encephalitis who underwent AE-Abs tests at the Children's Hospital of Chongqing Medical University between June 2020 and June 2022. Clinical features suggestive of AE-Abs were analysed based on AE-Abs test results. RESULTS: A total of 392 children were tested for AE-Abs with suspected autoimmune encephalitis. Of these, 49.5% were male, with a median age of 7 years 11 months (6 months-17 years 11 months); 93.6% (367/392) of all patients had both serum and cerebrospinal fluid (CSF) tests performed. The antibody-positive rate in the cohort was 23.7% (93/392), the serum antibody-positive rate was 21.9% (84/384), and the CSF antibody-positive rate was 20.8% (78/375). Eleven different AE-Abs were detected. Serum analysis revealed that N-methyl-D-aspartate receptor immunoglobulin-G (NMDAR-IgG) (15.1%) was greater than myelin oligodendrocyte glycoprotein (MOG)-IgG (14.6%) and glial fibrillary acidic protein (GFAP)-IgG (3.3%). CSF analysis revealed that NMDAR-IgG (16.3%) was greater than MOG-IgG (13.8%) and GFAP-IgG (3.3%). Compared with antibody-negative patients, antibody-positive patients were more often female (odds ratio [OR] 1.86, p = 0.03), with memory impairment (OR 2.91, p = 0.01) and sleep disorders (OR 2.08, p = 0.02). INTERPRETATION: In children, the most frequent AE-Abs detected were NMDAR-IgG and MOG-IgG. Female sex, memory impairment, and sleep disorders predict a higher likelihood of AE-Abs.

Computational study of the photophysical properties and electronic structure of iridium(III) photosensitizer complexes with electron-withdrawing groups.

A series of novel [Ir(tpy)(btp)Cl]+ complexes (Ir1-Ir4) have been reported to show excellent performance as photosensitizers. The introduction of electron-withdrawing groups increases visible light absorption and the lifetime of triplet states. To improve the photophysical properties, we theoretically design Ir5-Ir9 with electron-withdrawing groups (Cl, F, COOH, CN and NO2). Surprisingly, our findings indicate that the photosensitizer performance does not strictly increase with the electron-withdrawing ability of the substituents. In this work, the geometric and electronic structures, transition features, and photophysical properties of Ir1-Ir9 are investigated. The natural transition orbital (NTO) analysis indicates that the T1 and T2 states play a role in the photochemical pathways. Ultraviolet-visible (UV-vis) absorption spectra and charge-transfer spectra (CTS) have been investigated to show that the introduction of electron-withdrawing groups not only improves the visible light absorbing ability, but also changes the nature of electron excitation, providing a future molecular design strategy for similar series of photosensitizers. The rates of (reverse) intersystem crossing and the Huang-Rhys factors are evaluated to interpret the experimental results within the framework of Marcus theory. For complexes Ir1-Ir7, the introduction of electron-withdrawing groups leads to a lower efficiency of reverse intersystem crossing and a strong non-radiative process T2 → T1, resulting in a long triplet lifetime and excellent performance as a photosensitizer. Furthermore, some newly designed complexes (Ir7-Ir9) show great potential as thermally activated delayed fluorescence emitters, contrary to our initial expectations.

Self-prediction of relations in GO facilitates its quality auditing.

As applications of the gene ontology (GO) increase rapidly in the biomedical field, quality auditing of it is becoming more and more important. Existing auditing methods are mostly based on rules, observed patterns or hypotheses. In this study, we propose a machine-learning-based framework for GO to audit itself: we first predict the IS-A relations among concepts in GO, then use differences between predicted results and existing relations to uncover potential errors. Specifically, we transfer the taxonomy of GO 2020 January release into a dataset with concept pairs as items and relations between them as labels(pairs with no direct IS-A relation are labeled as ndrs). To fully obtain the representation of each pair, we integrate the embeddings for the concept name, concept definition, as well as concept node in a substring-based topological graph. We divide the dataset into 10 parts, and rotate over all the parts by choosing one part as the testing set and the remaining as the training set each time. After 10 rotations, the prediction model predicted 4,640 existing IS-A pairs as ndrs. In the GO 2022 March release, 340 of these predictions were validated, demonstrating significance with a p-value of 1.60e-46 when compared to the results of randomly selected pairs. On the other hand, the model predicted 2,840 out of 17,079 selected ndrs in GO to be IS-A's relations. After deleting those that caused redundancies and circles, 924 predicted IS-A's relations remained. Among 200 pairs randomly selected, 30 were validated as missing IS-A's by domain experts. In conclusion, this study investigates a novel way of auditing biomedical ontologies by predicting the relations in it, which was shown to be useful for discovering potential errors.

ATP1A3-related phenotypes in Chinese children: AHC, CAPOS, and RECA.

The aim of this research is to study the phenotype, genotype, treatment strategies, and short-term prognosis of Chinese children with ATP1A3 (Na+/K+-ATPase alpha 3 gene)-related disorders in Southwest China. Patients with pathogenic ATP1A3 variants identified using next-generation sequencing were registered at the Children's Hospital of Chongqing Medical University from December 2015 to May 2019. We followed them as a cohort and analyzed their clinical data. Eleven patients were identified with de novo pathogenic ATP1A3 heterozygous variants. One (c.2542 + 1G > T, splicing) has not been reported. Eight patients with alternating hemiplegia of childhood (AHC), one with cerebellar ataxia, areflexia, pes cavus, optic atrophy, and sensorineural hearing loss (CAPOS), and two with relapsing encephalopathy with cerebellar ataxia (RECA) were included. The initial manifestations of AHC included hemiplegia, oculomotor abnormalities, and seizures, and the most common trigger was an upper respiratory tract infection without fever. All patients had paroxysmal hemiplegic attacks during their disease course. The brain MRI showed no abnormalities. Six out of eight AHC cases reached a stable disease state after treatment. The initial symptom of the patient with CAPOS was ataxia followed by developmental regression, seizures, deafness, visual impairment, and dysarthria, and the brain MRI indicated mild cerebellar atrophy. No fluctuation was noted after using Acetazolamide. The initial manifestations of the two RECA cases were dystonia and encephalopathy, respectively. One manifested a rapid-onset course of dystonia triggered by a fever followed by dysarthria and action tremors, and independent walking was impossible. The brain MRI image was normal. The other one presented with disturbance of consciousness, seizures, sleep disturbance, tremor, and dyskinesias. The EEG revealed a slow background (δ activity), and the brain MRI result was normal. No response to Flunarizine was noted for them, and it took 61 and 60 months for them to reach a stable disease state, respectively. CONCLUSION: Pathogenic ATP1A3 variants play an essential role in the pathogenesis of Sodium-Potassium pump disorders, and AHC is the most common phenotype. The treatment strategies and prognosis depend on the phenotype categories caused by different variation sites and types. The correlation between the genotype and phenotype requires further exploration. WHAT IS KNOWN: • Pathogenic heterozygous ATP1A3 variants cause a spectrum of neurological phenotypes, and ATP1A3-disorders are viewed as a phenotypic continuum presenting with atypical and overlapping features. • The genotype-phenotype correlation of ATP1A3-disorders remains unclear. WHAT IS NEW: • In this study, the genotypes and phenotypes of ATP1A3-related disorders from Southwest of China were described. The splice-site variation c.2542+1G>T was detected for the first time in ATP1A3-related disorders. • The prognosis of twins with AHC p. Gly947Arg was more serious than AHC cases with other variants, which was inconsistent with previous reports. The phenomenon indicated the diversity of the correlation between the genotype and phenotype.

The dysfunctionality of hippocampal synapses may be directly related to PM-induced impairments in spatial learning and memory in juvenile rats.

Epidemiological studies have demonstrated that exposure to air particulate matter (PM) increases the incidence of cardiovascular and respiratory diseases and exerts a significant neurotoxic effect on the nervous system, especially on the immature nervous system. Here, we selected PND28 rats to simulate the immature nervous system of young children and used neurobehavioral methods to examine how exposure to PM affected spatial learning and memory, as well as electrophysiology, molecular biology, and bioinformatics to study the morphology of hippocampus and the function of hippocampal synapses. We discovered that spatial learning and memory were impaired in rats exposed to PM. The morphology and structure of the hippocampus were altered in the PM group. In addition, after exposure to PM, the relative expression of synaptophysin (SYP) and postsynaptic density 95 (PSD95) proteins decreased dramatically in rats. Furthermore, PM exposure impaired long-term potentiation (LTP) in the hippocampal Schaffer-CA1 pathway. Interestingly, RNA sequencing and bioinformatics analysis revealed that the differentially expressed genes (DEGs) were rich in terms associated with synaptic function. Five hub genes (Agt, Camk2a, Grin2a, Snca, and Syngap1) that may play a significant role in the dysfunctionality of hippocampal synapses were identified. Our findings implied that exposure to PM impaired spatial learning and memory via exerting impacts on the dysfunctionality of hippocampal synapses in juvenile rats and that Agt, Camk2a, Grin2a, Snca, and Syngap1 may drive PM-caused synaptic dysfunction.

Design of p-p heterojunctions based on CuO decorated WS2nanosheets for sensitive NH3gas sensing at room temperature.

Tungsten disulfide (WS2) nanosheets (NSs) have become a promising room-temperature gas sensor candidate due to their inherent high surface-to-volume ratio, tunable electrical properties, and high on-state current density. For further practical applications of WS2-based gas sensors, it is still necessary to overcome the insensitive response and incomplete recovery at room temperature. In this work, we controllably synthesized high-performance ammonia (NH3) gas sensor based on CuO decorated WS2NSs. The optimized p-p WS2/CuO heterojunctions improve the surface catalytic effect, thereby enhancing the gas-sensing performance. The pure WS2NSs-based gas sensors showed a low response and an incomplete recovery in the case of NH3sensing. After the functionalization of CuO nanoparticles, the WS2/CuO heterostructure-based gas sensor exhibits an improved response value of 40.5% to 5  ppm NH3and full recoverability without any external assistance. Density functional theory calculations illustrate that the adsorption of CuO for NH3is much superior to WS2. The p-p heterojunctions strategy demonstrated in this work has great potential in the design of sensitive materials for gas sensors, and provides useful guidance for enhancing the room-temperature sensitivity and recoverability.

Risk factors for mechanical ventilation in children with Guillain-Barré syndrome.

BACKGROUND: We assessed clinical predictors of mechanical ventilation in children with Guillain-Barré syndrome (GBS) to help identify patients who require mechanical ventilation. METHODS: We retrospectively collected the clinical, laboratory, and electrophysiological data of 103 children with GBS. Patients were categorized into two groups based on the requirement for mechanical ventilation. Variables that were significantly different between the two groups in univariate analysis were analyzed by multivariate logistic regression models. RESULTS: Time from symptom onset to admission (P = .002), facial or bulbar weakness (P = .001), and axonal type (P = .005) were associated with mechanical ventilation in univariate analysis. In multivariate analysis, facial or bulbar weakness (odds ratio [OR], 7.936; P = .013) and axonal type (OR, 4.582; P = .022) were independent predictors for mechanical ventilation. CONCLUSIONS: Facial or bulbar weakness and axonal type were associated with increased risk for mechanical ventilation in children with GBS.

Effects of minocycline on dendrites, dendritic spines, and microglia in immature mouse brains after kainic acid-induced status epilepticus.

PURPOSE: This study aimed to investigate whether minocycline could influence alterations of microglial subtypes, the morphology of dendrites and dendritic spines, the microstructures of synapses and synaptic proteins, or even cognition outcomes in immature male mice following status epilepticus (SE) induced by kainic acid. METHODS: Golgi staining was performed to visualize the dendrites and dendritic spines of neurons of the hippocampus. The microstructures of synapses and synaptic proteins were observed using transmission electron microscopy and western blotting analysis, respectively. Microglial reactivation and their markers were evaluated using flow cytometry. The Morris water maze (MWM) test was used to analyze spatial learning and memory ability. RESULTS: Significant partial spines increase (predominate in thin spines) was observed in the dendrites of neurons after acute SE and partial loss (mainly in thin spines) was presented by days 14 and 28 post-SE. The postsynaptic ultrastructure was impaired on the 7th and 14th days after SE. The proportion of M1 microglia increased significantly only after acute SE Similarly, the proportion of M2 microglia increased in the acute stage with high expression levels of all surface markers. In contrast, a decrease in M2 microglia and their markers was noted by day 14 post-SE. Minocycline could reverse the changes in dendrites and synaptic proteins caused by SE, and increase the levels of synaptic proteins. Meanwhile, minocycline could inhibit the reactivation of M1 microglia and the expression of their markers, except for promoting CD200R. In addition, treatment with minocycline could regulate the expression of M2 microglia and their surface markers, as well as ameliorating the impaired spatial learning and memory on the 28th day after SE. CONCLUSIONS: Dendritic spines and microglia are dynamically changed after SE. Minocycline could ameliorate the impaired cognition in the kainic acid-induced mouse model by decreasing the damage to dendrites and altering microglial reactivation.

Photosynthetic and biochemical responses of four subtropical tree seedlings to reduced dry season and increased wet season precipitation and variable N deposition.

Interspecific variations in phenotypic plasticity of trees that are affected by climate change may alter the ecosystem function of forests. Seedlings of four common tree species (Castanopsis fissa, Michelia macclurei, Dalbergia odorifera and Ormosia pinnata) in subtropical plantations of southern China were grown in the field under rainout shelters and subjected to changing precipitation (48 L of water every 4 days in the dry season, 83 L of water every 1 day in the wet season; 4 g m-2 year-1 of nitrogen (N)), low N deposition (48 L of water every 2 days in the dry season, 71 L of water every 1 day in the wet season; 8 g m-2 year-1 N), high N deposition (48 L of water every 2 days in the dry season, 71 L of water every 1 day in the wet season; 10 g m-2 year-1 N) and their interactive effects. We found that the changes in seasonal precipitation reduced the light-saturated photosynthetic rate (Asat) for C. fissa due to declining area-based foliar N concentrations (Na). However, we also found that the interactive effects of changing precipitation and N deposition enhanced Asat for C. fissa by increasing foliar Na concentrations, suggesting that N deposition could alleviate N limitations associated with changing precipitation. Altered precipitation and high N deposition reduced Asat for D. odorifera by decreasing the maximum electron transport rate for RuBP regeneration (Jmax) and maximum rate of carboxylation of Rubisco (Vcmax). Ormosia pinnata under high N deposition exhibited increasing Asat due to higher stomatal conductance and Vcmax. The growth of D. odorifera might be inhibited by changes in seasonal precipitation and N deposition, while O. pinnata may benefit from increasing N deposition in future climates. Our study provides an important insight into the selection of tree species with high capacity to tolerate changing precipitation and N deposition in subtropical plantations.

A peptide from the Japanese encephalitis virus failed to induce the production of anti-N-methyl-d-aspartate receptor antibodies via molecular mimicry in mice.

Background: The development of anti-N-methyl-d-aspartate receptor (NMDAR) encephalitis following viral encephalitis, such as Japanese encephalitis, has received increasing attention in recent years. However, the mechanism of anti-NMDAR antibody production following Japanese encephalitis has not been explored. Methods: A peptide from the Japanese encephalitis virus (JEV), which shares a similar amino acid sequence with GluN1, was identified by sequence comparison. We then explored whether active subcutaneous immunization with the JEV peptide could induce the production of anti-NMDAR antibodies and related pathophysiological and behavioral changes in mice. In addition, a published active immune model of anti-NMDAR encephalitis using a GluN1 peptide was used as the positive control. Results: A 6-amino-acid sequence with 83 % similarity between the envelope protein of the JEV (HGTVVI) and GluN1 (NGTHVI) was identified, and the sequence included the N368/G369 region. Active immunization with the JEV peptide induced a substantial and specific immune response in mice. However, anti-NMDAR antibodies were not detected in the serum of mice immunized with the JEV peptide by ELISA, CBA, and TBA. Moreover, mice immunized with the JEV peptide presented no abnormities related to anti-NMDAR antibodies according to western blotting, patch clamp, and a series of behavioral tests. In addition, active immunization with a recently reported GluN1 peptide failed to induce anti-NMDAR antibody production in mice. Conclusions: In this study, the attempt of active immunization with the JEV peptide to induce the production of anti-NMDAR antibodies via molecular mimicry failed. The pathogenesis of anti-NMDAR encephalitis following Japanese encephalitis remains to be elucidated.

Ambient particulate matter exposure induces ferroptosis in hippocampal cells through the GSK3B/Nrf2/GPX4 pathway.

Epidemiological studies have established a robust correlation between exposure to ambient particulate matter (PM) and various neurological disorders, with dysregulation of intracellular redox processes and cell death being key mechanisms involved. Ferroptosis, a cell death form characterized by iron-dependent lipid peroxidation and disruption of antioxidant defenses, may be involved in the neurotoxic effects of PM exposure. However, the relationship between PM-induced neurotoxicity and ferroptosis in nerve cells remains to be elucidated. In this study, we utilized a rat model (exposed to PM at a dose of 10 mg/kg body weight per day for 4 weeks) and an HT-22 cell model (exposed to PM at concentrations of 50, 100, and 200 µg/mL for 24 h) to investigate the potential induction of ferroptosis by PM exposure. Furthermore, RNA sequencing analysis was employed to identify hub genes that potentially contribute to the process of ferroptosis, which was subsequently validated through in vivo and in vitro experiments. The results revealed that PM exposure increased MDA content and Fe2+ levels, and decreased SOD activity and GSH/GSSG ratio in rat hippocampal and HT-22 cells. Through RNA sequencing analysis, bioinformatics analysis, and RT-qPCR experiments, we identified GSK3B as a possible hub gene involved in ferroptosis. Subsequent investigations demonstrated that PM exposure increased GSK3B levels and decreased Nrf2, and GPX4 levels in vivo and in vitro. Furthermore, treatment with LY2090314, a specific inhibitor of GSK3B, was found to mitigate the PM-induced elevation of MDA and ROS and restore SOD activity and GSH/GSSG ratio. The LY2090314 treatment promoted the upregulation of Nrf2 and GPX4 and facilitated the nuclear translocation of Nrf2 in HT-22 cells. Moreover, treatment with LY2090314 resulted in the upregulation of Nrf2 and GPX4, along with the facilitation of nuclear translocation of Nrf2. This study suggested that PM-induced ferroptosis in hippocampal cells may be via the GSK3B/Nrf2/GPX4 pathway.

Autophagy alleviates hippocampal neuroinflammation by inhibiting the NLRP3 inflammasome in a juvenile rat model exposed particulate matter.

Ambient fine particulate matter (PM) is a global public and environmental problem. PM is closely associated with several neurological diseases, which typically involve neuroinflammation. We investigated the impact of PM exposure on neuroinflammation using both in vivo (in a juvenile rat model with PM exposure concentrations of 1, 2, and 10 mg/kg for 28 days) and in vitro (in BV-2 and HT-22 cell models with PM concentrations of 50-200 µg/ml for 24 h). We observed that PM exposure induced the activation of the NLRP3 inflammasome, leading to the production of IL-1ß and IL-18 in the rat hippocampus and BV-2 cells. Furthermore, inhibition of the NLRP3 inflammasome with MCC950 effectively reduced neuroinflammation and ameliorated hippocampal damage. In addition, autophagy activation was observed in the hippocampus of PM-exposed rats, and the promotion of autophagy by rapamycin (Rapa) effectively attenuated the NLRP3-mediated neuroinflammation induced by PM exposure. However, autophagic flow was blocked in BV-2 cells exposed to PM, and Rapa failed to ameliorate NLRP3 inflammasome activation. We found that autophagy was activated in HT-22 cells exposed to PM and that treatment with Rapa reduced the release of reactive oxygen species (ROS) and malondialdehyde (MDA), as well as cell apoptosis. In a subsequent coculture model of BV-2 and HT-22 cells, we observed the activation of the NLRP3 inflammasome in BV-2 cells when the HT-22 cells were exposed to PM, and this activation was alleviated when PM-exposed HT-22 cells were pretreated with Rapa. Overall, our study revealed that PM exposure triggered hippocampal neuroinflammation by activating the NLRP3 inflammasome. Notably, autophagy mitigated NLRP3 inflammasome activation, potentially by reducing neuronal ROS and apoptosis. This research emphasized the importance of reducing PM exposure and provided valuable insight into its neurotoxicity.

A teosinte-derived allele of ZmSC improves salt tolerance in maize.

Maize, a salt-sensitive crop, frequently suffers severe yield losses due to soil salinization. Enhancing salt tolerance in maize is crucial for maintaining yield stability. To address this, we developed an introgression line (IL76) through introgressive hybridization between maize wild relatives Zea perennis, Tripsacum dactyloides, and inbred Zheng58, utilizing the tri-species hybrid MTP as a genetic bridge. Previously, genetic variation analysis identified a polymorphic marker on Zm00001eb244520 (designated as ZmSC), which encodes a vesicle-sorting protein described as a salt-tolerant protein in the NCBI database. To characterize the identified polymorphic marker, we employed gene cloning and homologous cloning techniques. Gene cloning analysis revealed a non-synonymous mutation at the 1847th base of ZmSCIL76 , where a guanine-to-cytosine substitution resulted in the mutation of serine to threonine at the 119th amino acid sequence (using ZmSCZ58 as the reference sequence). Moreover, homologous cloning demonstrated that the variation site derived from Z. perennis. Functional analyses showed that transgenic Arabidopsis lines overexpressing ZmSCZ58 exhibited significant reductions in leaf number, root length, and pod number, alongside suppression of the expression of genes in the SOS and CDPK pathways associated with Ca2+ signaling. Similarly, fission yeast strains expressing ZmSCZ58 displayed inhibited growth. In contrast, the ZmSCIL76 allele from Z. perennis alleviated these negative effects in both Arabidopsis and yeast, with the lines overexpressing ZmSCIL76 exhibiting significantly higher abscisic acid (ABA) content compared to those overexpressing ZmSCZ58 . Our findings suggest that ZmSC negatively regulates salt tolerance in maize by suppressing downstream gene expression associated with Ca2+ signaling in the CDPK and SOS pathways. The ZmSCIL76 allele from Z. perennis, however, can mitigate this negative regulatory effect. These results provide valuable insights and genetic resources for future maize salt tolerance breeding programs.

Improving language model of human genome for DNA-protein binding prediction based on task-specific pre-training.

The DNA-protein binding plays a pivotal role in regulating gene expression and evolution, and computational identification of DNA-protein has drawn more and more attention in bioinformatics. Recently, variants of BERT are also used to capture the semantic information of DNA sequences for predicting DNA-protein bindings. In this study, we leverage a task-specific pre-training strategy on BERT using large-scale multi-source DNA-protein binding data and present TFBert. TFBert treats DNA sequences as natural sentences and k-mer nucleotides as words. It can effectively extract upstream and downstream nucleotide context information by pre-training the 690 unlabeled ChIP-seq datasets. Experiments show that the pre-trained model can achieve promising performance on every single dataset in the 690 ChIP-seq datasets after simple fine tuning, especially on small datasets. The average AUC is 94.7%, outperforming existing popular methods. In conclusion, this study provides a variant of BERT based on pre-training and achieved state-of-the-art results in predicting DNA-protein bindings. We believe that TFBert can provide insights into other biological sequence classification problems.

SENet: A deep learning framework for discriminating super- and typical enhancers by sequence information.

Super-enhancers are large domains on the genome where multiple short typical enhancers within a specific genomic distance are stitched together. Typically, they are cell type-specific and responsible for defining cell identity and regulating gene transcription. Numerous studies have demonstrated that super-enhancers are enriched for trait-associated variants, and mutations in super-enhancers are possibly related to known diseases. Recently, several machine learning-based methods have been used to distinguish super-enhancers from typical enhancers by using high-throughput data from various experimental methods. The acquisition of such experimental data is usually costly and time-consuming. In this paper, we innovatively proposed SENet, a groundbreaking method based on a deep neural network model, for discriminating between the two categories solely utilizing sequence information. SENet employs dna2vec feature embedding, convolution for local feature extraction, attention pooling for refined feature retention, and Transformer for contextual information extraction. Experiments demonstrate that SENet outperforms all current state-of-the-art computational methods and shows satisfactory performance in cross-species validation. Our method pioneers the distinction between super-enhancers and typical ones using only sequence information. The source code and datasets are stored in https://github.com/lhy0322/SENet.

Pediatric anti-NMDAR encephalitis with demyelination on brain MRI: A single center study.

OBJECTIVE: To explore the clinical characteristics, immunotherapy response, and prognosis of pediatric anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis associated with demyelination on brain magnetic resonance (MRI). METHODS: We retrospectively reviewed the medical records of children diagnosed with anti-NMDAR encephalitis in our hospital between January 2016 and December 2021. All children with evidence of demyelination on brain MRI were included. RESULTS: A total of 183 anti-NMDAR encephalitis children were included; 8.7 % (16/183) of them had demyelination on brain MRI. Nine were positive for myelin oligodendrocyte glycoprotein (MOG)-IgG, while two were positive for both MOG-IgG and glial fibrillary acidic protein (GFAP)-IgG. Four patients had a history of acquired demyelinating syndromes and encephalitis, respectively, while nine (56.3 %) had atypical symptoms of anti-NMDAR encephalitis. All children had supratentorial demyelination on brain MRI; four of them had additional infratentorial lesions. All children received first-line immunotherapy; four were administered repeated first-line immunotherapy and/or rituximab because of poor initial response. During the follow-up, 37.5 % (6/16) of the children relapsed, but all responded well to immunotherapy. There were no significant differences in mRS score before immunotherapy, response to first-line immunotherapy, and long-term prognosis between anti-NMDAR encephalitis children with and without demyelination. However, patients with demyelination were more likely to have a history of acquired demyelinating syndromes or unexplained cortical encephalitis and to relapse. CONCLUSION: Pediatric anti-NMDAR encephalitis can co-occur with demyelination and has a high rate of MOG-IgG positivity. A history of acquired demyelinating syndromes or unexplained cortical encephalitis and atypical symptoms may indicate demyelination in children with anti-NMDAR encephalitis. Pediatric anti-NMDAR encephalitis with demyelination is more likely to relapse and needs a closer follow-up. However, it remains unknown whether more intensive immunotherapy is required in these patients.

Fully Flexible MXene-based Gas Sensor on Paper for Highly Sensitive Room-Temperature Nitrogen Dioxide Detection.

Flexible chemiresistive gas sensors have attracted growing interest due to their capability in real-time and rapid detection of gas. However, the performance of gas sensors has long been hindered by the poor charge transfer ability between the conventional metal electrode and gas sensing semiconductors. Herein, for the first time, a fully flexible paper-based gas sensor integrated with the Ti3C2Tx-MXene nonmetallic electrode and the Ti3C2Tx/WS2 gas sensing film was designed to form Ohmic contact and Schottky heterojunction in a single gas sensing channel. Ti3C2Tx/WS2 has outstanding physical and chemical properties for both Ti3C2Tx and WS2 nanoflakes, showing high conductivity, effective charge transfer, and abundant active sites for gas sensing. The response of the gas sensor to NO2 (1 ppm) at room temperature is 15.2%, which is about 3.2 and 76.0 times as high as that of the Au interdigital electrode integrated with the Ti3C2Tx/WS2 sensor (4.8%) and the MXene electrode integrated with the Ti3C2Tx sensor (0.2%), respectively. Besides, this design performed at a limit of detection with 11.0 ppb NO2 gas and displayed excellent stability under high humidities. Based on first-principles density functional theory calculation results, the improvement of the gas sensing performance can be mainly attributed to the heterojunction regulation effect, work function matching, and suppressing metal-induced gap states. This work provides a new approach for the design of flexible gas sensors on paper with MXene-based conductive electrodes and gas sensing materials.

Associations between urinary heavy metals and anxiety among adults in the National Health and Nutrition Examination Survey (NHANES), 2007-2012.

BACKGROUND: Few studies have investigated the associations between heavy metals and anxiety. The purpose of this study was to examine the associations between single and combined exposure to heavy metals and anxiety. METHODS: This study employed data from the National Health and Nutrition Examination Survey (NHANES) from 2007 to 2012. Anxiety was assessed by patients self-reporting the number of anxious days per month. First, we evaluated the associations between 10 heavy metals single exposure and anxiety by multivariable logistic regression. We then selected 5 heavy metals (cadmium, antimony, cobalt, tungsten, and uranium) for further analysis by elastic net regression. Subsequently, principal component analysis (PCA), weighted quantile regression (WQS), and Bayesian kernel machine regression (BKMR) were utilized to evaluate the associations between 5 heavy metals co-exposure and anxiety. RESULTS: This study included 4512 participants, among whom 1206 participants were in an anxiety state. Urinary cadmium and antimony were separately related to an increased risk of anxiety (p for trend <0.01 and < 0.01, respectively). In PCA analysis, PC1 was associated with an increased risk of anxiety (p for trend <0.001). In WQS analysis, the positive WQS index was substantially linked with the risk of anxiety (OR (95%CI): 1.23 (1.04,1.39)). In BKMR analysis, the overall effects of co-exposure to heavy metals were positively connected with anxiety. CONCLUSION: Our study identified a positive correlation between individual exposure to cadmium and antimony and the risk of anxiety. Additionally, the co-exposure to cadmium, antimony, cobalt, tungsten, and uranium was associated with an increased risk of anxiety.

Inflammatory properties of diet mediate the effect of epilepsy on moderate to severe depression: Results from NHANES 2013-2018.

BACKGROUND: Depression is a major public health problem, and epilepsy and a high-inflammatory diet are important causes of depression. We aimed to explore the level of dietary inflammation in epileptic patients and its relationship with moderate to severe depression (MSD). METHODS: This cross-sectional study included 12,788 participants aged 20-80 years from the NHANES database from 2013 to 2018. Depressive symptoms were evaluated using the nine-item Patient Health Questionnaire (PHQ-9), and epilepsy was diagnosed based on the use of antiepileptic drugs within the previous 30 days. Dietary inflammatory index (DII) scores and energy-adjusted DII (E-DII) scores were calculated based on dietary recalls of the past 24 h, and average DII (ADII) and energy-adjusted ADII (E-ADII) were calculated based on two 24-hour dietary recalls. RESULTS: The DII, E-DII, and ADII scores and prevalence of MSD were significantly increased in epileptic patients compared with non-epilepsy subjects. The E-ADII score (P = 0.078) was weakly associated with comorbid MSD in patients with epilepsy. Mediation models showed that dietary inflammation scores mediated 2.31 % to 12.25 % of epilepsy-related MSD. In stratified analysis, an increased prevalence of MSD was present in the Quartile 2 subgroup based on DII and E-ADII scores and in the Quartile 3 subgroup of epileptic patients based on DII, E-DII, and ADII scores. CONCLUSIONS: Epileptics consume more proinflammatory foods and nutrients than control subjects. MSD in patients with epilepsy is associated with their high inflammatory diet. Suggesting an urgent need for rational dietary management in the epileptic population.

Dietary Intake of Flavonoids Associated with Sleep Problems: An Analysis of Data from the National Health and Nutrition Examination Survey, 2007-2010.

Flavonoids possess the latent ability to protect against sleep disorders. We examined the correlation between daily flavonoid intake and sleep duration, and sleep disorders. We enrolled 8216 participants aged ≥ 20 from the National Health and Nutrition Examination Survey (NHANES, 2007-2010), carrying out a cross-sectional study. Flavonoid intake was collected by dietary intake interview recalls. Logistic regression was utilized to evaluate the association between flavonoid intake sleep duration, and sleep disorders. We used subgroup and interaction analysis to explore differences between subgroups. When adjusting covariates in model 2, anthocyanidins, flavan-3-ols, flavones, flavonols, and the sum of flavonoids were considerably related to insufficient sleep duration (odds ratio (OR) (95% confidence interval (CI)); 0.83 (0.72, 0.95); 0.91 (0.83, 0.98); 0.63 (0.41, 0.98); 0.78 (0.64, 0.94); 0.85 (0.76, 0.95), respectively); the converse association was observed between flavanones, and flavones and the risk of sleep disorders (OR (95% CI); 0.85 (0.77, 0.95); 0.61 (0.41, 0.90), respectively). In relation to insufficient sleep, there were statistically significant interactions between flavonoid consumption and race/ethnicity, and education level. In relation to insufficient sleep, there were statistically significant interactions between flavonoid consumption and working status. In this study, we found that certain flavonoids were linked to increased sleep duration and a lower risk of sleep problems. Our research indicated that flavonoids might be a preventive factor for sleep disorders.