The development of the neurocritical care specialty in China based on the analysis of neurocritical care unit volume and quality.

PURPOSE: Through three neurocritical care unit (NCCU) surveys in China, we tried to understand the development status of neurocritical care and clarify its future development. METHODS: Using a cross-sectional survey method and self-report questionnaires, the number and quality of NCCUs were investigated through three steps: administering the questionnaire, sorting the survey data, and analyzing the survey data. RESULTS: At the second and third surveys, the number of NCCUs (76/112/206) increased by 47% and 84%, respectively. The NCCUs were located in tertiary grade A hospitals or teaching hospitals (65/100/181) in most provinces (24/28/29). The numbers of full-time doctors (359/668/1337) and full-time nurses (904/1623/207) in the NCCUs increased, but the doctor-bed ratio and nurse-bed ratio were still insufficient (0.4:1 and 1.3:1). CONCLUSION: In the past 20 years, the growth rate of NCCUs in China has accelerated, while the allocation of medical staff has been insufficient. Although most NCCU hospital bed facilities and instruments and equipment tend to be adequate, there are obvious defects in some aspects of NCCUs.

Peripheral nerve injury associated with JEV infection in high endemic regions, 2016-2020: a multicenter retrospective study in China.

Previously, we reported a cohort of Japanese encephalitis (JE) patients with Guillain-Barré syndrome. However, the evidence linking Japanese encephalitis virus (JEV) infection and peripheral nerve injury (PNI) remains limited, especially the epidemiology, clinical presentation, diagnosis, treatment, and outcome significantly differ from traditional JE. We performed a retrospective and multicenter study of 1626 patients with JE recorded in the surveillance system of the Chinese Center for Disease Control and Prevention, spanning the years 2016-2020. Cases were classified into type 1 and type 2 JE based on whether the JE was combined with PNI or not. A comparative analysis was conducted on demographic characteristics, clinical manifestations, imaging findings, electromyography data, laboratory results, and treatment outcomes. Among 1626 laboratory confirmed JE patients, 230 (14%) were type 2 mainly located along the Yellow River in northwest China. In addition to fever, headache, and disturbance of consciousness, type 2 patients experienced acute flaccid paralysis of the limbs, as well as severe respiratory muscle paralysis. These patients presented a greater mean length of stay in hospital (children, 22 years [range, 1-34]; adults, 25 years [range, 0-183]) and intensive care unit (children, 16 years [range, 1-30]; adults, 17 years [range, 0-102]). The mortality rate was higher in type 2 patients (36/230 [16%]) compared to type 1 (67/1396 [5%]). The clinical classification of the diagnosis of JE may play a crucial role in developing a rational treatment strategy, thereby mitigating the severity of the disease and potentially reducing disability and mortality rates among patients.

Intravenous immunoglobulin alleviates Japanese encephalitis virus-induced peripheral neuropathy by inhibiting the ASM/ceramide pathway.

Japanese encephalitis virus (JEV) infection is considered a global public health emergency. Severe peripheral neuropathy caused by JEV infection has increased disability and mortality rates in recent years. Because there are very few therapeutic options for JEV infection, prompt investigations of the ability of clinically safe, efficacious and globally available drugs to inhibit JEV infection and ameliorate peripheral neuropathy are urgently needed. In this study, we found that high doses of intravenous immunoglobulin, a function inhibitor of acid sphingomyelinase (FIASMA), inhibited acid sphingomyelinase (ASM) and ceramide activity in the serum and sciatic nerve of JEV-infected rats, reduced disease severity, reversed electrophysiological and histological abnormalities, significantly reduced circulating proinflammatory cytokine levels, inhibited Th1 and Th17 cell proliferation, and suppressed the infiltration of inflammatory CD4 + cells into the sciatic nerve. It also maintained the peripheral nerve-blood barrier without causing severe clinical side effects. In terms of the potential mechanisms, ASM was found to participate in immune cell differentiation and to activate immune cells, thereby exerting proinflammatory effects. Therefore, immunoglobulin is a FIASMA that reduces abnormal immune responses and thus targets the ASM/ceramide system to treat peripheral neuropathy caused by JEV infection.

Psychological mechanisms of English academic stress and academic burnout: the mediating role of rumination and moderating effect of neuroticism.

Introduction: Academic stress is a significant and prevalent phenomenon among college students. According to the Demands-Resources Model, when individuals are unable to cope with stress that exceeds their capacity, burnout may occur. Although English courses hold a significant position in university education, there has been limited research on the mechanisms linking English academic stress to English academic burnout. Methods: This study recruited 1,130 undergraduate students taking English courses. Participants completed online questionnaires assessing English academic stress, rumination, English academic burnout, and neuroticism traits. A moderated mediation model was constructed to examine the relationship among these variables. Results: The results indicate that (1) Rumination serves as a mediator in the relationship between English academic stress and burnout; (2) neuroticism significantly moderates the pathway between English academic stress and rumination. Specifically, students with high neuroticism tendencies are more prone to developing rumination when faced with high levels of English academic stress. Conclusion: These findings offer valuable insights into the psychological mechanisms underlying the association between English learning stress and academic burnout. They emphasize the importance of addressing rumination as a mediator and considering individuals' levels of neuroticism in interventions aimed at preventing and alleviating academic burnout among university students.

Understanding the subtypes of non-suicidal self-injury: A new conceptual framework based on a systematic review.

Non-suicidal self-injury (NSSI) is a significant public health problem, but there is no consistent evidence of its risk factors. One possibility is that there are subtypes NSSI that have different risk factors and clinical symptoms. In this review we evaluated the evidence of subtypes to determine if there were consistent subtypes of NSSI that emerged across studies. Four databases (Medline; Embase; PsycINFO; Web of Science) were searched to identify studies that used data-driven approaches and were published before November 9, 2022. There were 21 studies with 23 unique samples for review. Most of the included studies used NSSI symptoms or personal characteristics as the subtyping indicators, revealing 2-5 subtypes of NSSI. Variations in subtyping indicators, sample characteristics, and statistical methods may have contributed to the inconsistent number and characteristics of subtypes across studies. A new conceptual framework is proposed to integrate these diverse findings, highlighting the important roles of NSSI function and psychological pain in differentiating NSSI subtypes. This framework sheds light on the differences among self-injurers and offers insights for future endeavors to address the complexities of NSSI.

Quantifying the Importance of Non-Suicidal Self-Injury Characteristics in Predicting Different Clinical Outcomes: Using Random Forest Model.

Existing research on non-suicidal self-injury (NSSI) among adolescents has primarily concentrated on general risk factors, leaving a significant gap in understanding the specific NSSI characteristics that predict diverse psychopathological outcomes. This study aims to address this gap by using Random Forests to discern the significant predictors of different clinical outcomes. The study tracked 348 adolescents (64.7% girls; mean age = 13.31, SD = 0.91) over 6 months. Initially, 46 characteristics of NSSI were evaluated for their potential to predict the repetition of NSSI, as well as depression, anxiety, and suicidal risks at a follow-up (T2). The findings revealed distinct predictors for each psychopathology. Specifically, psychological pain was identified as a significant predictor for depression, anxiety, and suicidal risks, while the perceived effectiveness of NSSI was crucial in forecasting its repetition. These findings imply that it is feasible to identify high-risk individuals by assessing key NSSI characteristics, and also highlight the importance of considering diverse NSSI characteristics when working with self-injurers.

Engineered PDGFA-ligand-modified exosomes delivery T3 for demyelinating disease targeted therapy.

Demyelination is a proper syndrome in plenty of central nervous system (CNS) diseases, which is the main obstacle to recovery and still lacks an effective treatment. To overcome the limitations of the brain-blood barrier on drug permeability, we modified an exosome secreted by neural stem cells (NSCs), which had transfected with lentivirus armed with platelet-derived growth factors A (PDGFA)-ligand. Through the in vivo and in vitro exosomes targeting test, the migration ability to the lesion areas and OPCs significantly improved after ligand modification. Furthermore, the targeted exosomes loaded with 3,5, 30-L-triiodothyronine (T3) have a critical myelination ability in CNS development, administrated to the cuprizone animal model treatment. The data shows that the novel drug vector loaded with T3 significantly promotes remyelination compared with T3 alone. At the same time, it improved the CNS microenvironment by reducing astrogliosis, inhibiting pro-inflammatory microglia, and alleviating axon damage. This investigation provides a straightforward strategy to produce a targeting exosome and indicates a possible therapeutic manner for demyelinating disease.

Microglia-derived exosomes modulate myelin regeneration via miR-615-5p/MYRF axis.

Demyelination and failure of remyelination in the central nervous system (CNS) characterize a number of neurological disorders. Spontaneous remyelination in demyelinating diseases is limited, as oligodendrocyte precursor cells (OPCs), which are often present in demyelinated lesions in abundance, mostly fail to differentiate into oligodendrocytes, the myelinating cells in the CNS. In addition to OPCs, the lesions are assembled numbers of activated resident microglia/infiltrated macrophages; however, the mechanisms and potential role of interactions between the microglia/macrophages and OPCs are poorly understood. Here, we generated a transcriptional profile of exosomes from activated microglia, and found that miR-615-5p was elevated. miR-615-5p bound to 3'UTR of myelin regulator factor (MYRF), a crucial myelination transcription factor expressed in oligodendrocyte lineage cells. Mechanistically, exosomes from activated microglia transferred miR-615-5p to OPCs, which directly bound to MYRF and inhibited OPC maturation. Furthermore, an effect of AAV expressing miR-615-5p sponge in microglia was tested in experimental autoimmune encephalomyelitis (EAE) and cuprizone (CPZ)-induced demyelination model, the classical mouse models of multiple sclerosis. miR-615-5p sponge effectively alleviated disease progression and promoted remyelination. This study identifies miR-615-5p/MYRF as a new target for the therapy of demyelinating diseases.

Autoimmune receptor encephalitis in ApoE­/­ mice induced by active immunization with NMDA1.

Subacute progressive neuropsychiatric symptoms with cognitive and motor impairment and autoimmune seizures are some of the typical symptoms of anti­N­methyl­D­aspartate receptor (anti­NMDAR) encephalitis. The mechanisms underlying this disease are yet to be elucidated, which could be partly attributed to the lack of appropriate animal models. The present study aimed to establish an active immune mouse model of anti­NMDAR encephalitis. Mice were immunized with the extracellular segment of the NMDA1 protein, then subjected to open­field and novel object recognition experiments. Plasma was collected after euthanasia on day 30 after immunization and anti­NMDA1 antibodies were detected using ELISA. Furthermore, brain slices were analyzed to measure postsynaptic density protein 95 (PSD­95) and NMDA1 expression. Western blot analysis of NMDA1 and PSD­95 protein expression levels in the hippocampus was also performed. In addition, protein expression levels of PSD­95 and NMDA1 in mouse neuronal HT­22 cells were evaluated. Compared with controls, mice immunized with NMDA1 exhibited anxiety, depression and memory impairment. Moreover, high anti­NMDA1 antibody titers were detected with ELISA and the levels of anti­NMDA1 antibody reduced postsynaptic NMDA1 protein density in the mouse hippocampus. These findings demonstrated the successful construction of a novel mouse model of anti­NMDAR encephalitis by actively immunizing the mice with the extracellular segment of the NMDA1 protein. This model may be useful for studying the pathogenesis and drug treatment of anti­NMDAR encephalitis in the future.

SIGMAR1 variants in ALS-PD complex cases: a case report of a novel mutation and literature review.

Amyotrophic lateral sclerosis (ALS) is a devastating neurodegenerative disease characterized by progressive degeneration of upper and lower motor neurons, with occasional involvement of the extrapyramidal system. Mutations in the sigma non-opioid intracellular receptor 1 (SIGMAR1) gene have been identified as one of the causes of ALS. Here, we present a case of a 49-year-old man diagnosed with ALS-Parkinson's disease (PD) complex. The patient exhibited bradykinesia and tremor, and whole-exome sequencing revealed homozygous mutations in the SIGMAR1 gene (c.446-2A > T). In addition, we conducted an investigation into the clinical and molecular phenotype of previously reported variants of SIGMAR1 associated with ALS. This case report aims to raise awareness among physicians regarding atypical phenotypes of amyotrophic lateral sclerosis and to encourage further research on the factors leading to SIGMAR1 mutations in patients.

KLHL11 antibody-associated autoimmune encephalomyelitis in a middle-aged female patient: a case report and literature review.

HEADINGS: Kelch-like protein 11antibody is a recently identified biomarker for paraneoplastic neurological syndromes associated with germ-cell tumors that was first described as an onconeural antibody causing autoimmune encephalitis associated with seminoma in 2019. Ataxia is the most prevalent presenting symptom, with other neurological symptoms including vertigo, double vision, hearing loss, tinnitus and dysarthria. Magnetic resonance imaging scans reveal that the lesions are mostly located in the cerebellum and brainstem, particularly in the pontine region, and may also exhibit cerebellar atrophy. AIM OF THE STUDY: In this study, we report the clinical features of Kelch-like protein 11 antibody-associated paraneoplastic neurological syndrome. MATERIALS AND METHODS: We present a middle-aged female patient who presented with vertigo, cognitive decline, ataxia and limb weakness. A cell-based assay (CBA) showed positive IgG Kelch-like protein 11 in both her serum and CSF, as well as positive oligoclonal bands in her CSF. She was diagnosed with KLHL11 antibody-associated autoimmune encephalomyelitis and received high-dose intravenous methylprednisolone pulse therapy. RESULT AND CONCLUSIONS: Clinical outcomes suggest that patients with Kelch-like protein 11 antibody mostly have poor prognoses, excepting our case. We propose that early and appropriate treatments are critical for timely diagnosis and rapid improvement.

Neuromelanin-Sensitive Magnetic Resonance Imaging as a Measure for Differential Diagnosis of Essential Tremor and Parkinson's Disease.

We sought to evaluate whether the neuromelanin-sensitive magnetic resonance imaging (NM-MRI) features of the substantia nigra (SN) have utility in the differential diagnosis of Parkinson's disease (PD) and essential tremor (ET). This study enrolled 23 patients with PD, 20 patients with ET, and 18 healthy participants. All subjects underwent clinical examination, motor and cognitive assessments, and NM-MRI scans. The area and contrast-to-noise ratio (CNR) values of SN were defined according to NM-MRI images. Then, receiver operating characteristic (ROC) analysis was conducted to characterize the diagnostic power of the SN area and CNR values of SN. Compared with ET and control groups, the PD group showed a significant reduction of the area of SN (P = 0.003, PD vs. ET; P = 0.001, PD vs. control) and in the SN to midbrain area ratio in the same layer (P = 0.006, PD vs. ET; P = 0.005, PD vs. control). The SN area had a sensitivity of 65% and a specificity of 87% for distinguishing ET from PD, with an area under the curve (AUC) of 0.7630 and a Youden index of 0.5200, whereas the ratio of the SN area to midbrain area in the same layer had a sensitivity of 60% and a specificity of 87% for distinguishing ET from PD, with an AUC of 0.7478 and a Youden index of 0.4700. Compared with the ET group, the mean CNR value of the SN and the respective CNR values of the three subregions were all weakened in the PD group, and only the CNR in the middle part was significantly different from the control group (P = 0.006). The sensitivity of the CNR value of the middle part of the SN for differentiating ET from PD was 65%, the specificity was 87%, the AUC was 0.7500, and the Youden index was 0.5200.Based on our findings, we conclude that NM-MRI can improve diagnostic accuracy in PD and can be used as a specific and sensitive potential diagnostic biomarker for PD.

Extensive cytokine biomarker analysis in serum of Guillain-Barré syndrome patients.

Guillain-Barré syndrome (GBS) is an acute idiopathic polyneuropathy which is related to infection and immune mechanism. The exact pathogenesis of the disease is unknown and treatment is limited. Thus, the purpose of the study is to identify biomarkers of GBS serum and elucidate their involvement in the underlying pathogenesis of GBS that could help to treat GBS more accurately. Antibody array technology was used to detect the expression levels of 440 proteins in serum of 5 GBS group and 5 healthy control group. Sixty-seven differentially expressed proteins (DEPs) were identified by antibody array, among which FoLR1, Legumain, ErbB4, IL-1α, MIP-1α and IGF-2 were down-regulated, while 61 proteins were up-regulated. Bioinformatics analysis indicated that most DEPs were associated with leukocytes, among which IL-1α, SDF-1b, B7-1, CD40, CTLA4, IL-9, MIP-1α and CD40L were in the center of protein-protein interaction (PPI) network. Subsequently, the ability of these DEPs to distinguish GBS from healthy control was further evaluated. CD23 was identified by means of Random Forests Analysis (RFA) and verified by enzyme-linked immunosorbent assay (ELISA). The ROC curve result of CD23 respectively displayed that its sensitivity, specificity and AUC were 0.818, 0.800 and 0.824. We speculate that activation of leukocyte proliferation and migration in circulating blood might be associated with inflammatory recruitment of peripheral nerves, leading to the occurrence and development of GBS, but this conclusion still requires deeper confirmation. More importantly, central proteins may play a pivotal role in the pathogenesis of GBS. In addition, we detected IL-1α, IL-9, and CD23 in the serum of GBS patients for the first time, which may be promising biomarkers for the treatment of GBS.

Peripheral Nerve Injury Induced by Japanese Encephalitis Virus in C57BL/6 Mouse.

Japanese encephalitis virus (JEV), with neurotoxic and neuroinvasive properties, is the major cause of human viral encephalitis in Asia. Although Guillain-Barré syndrome caused by JEV infections is not frequent, a few cases have been reported in recent years. To date, no existing animal model for JEV-induced peripheral nerve injury (PNI) has been established, and thus the pathogenic mechanism is not clarified. Therefore, an animal model is urgently required to clarify the correlation between JEV infection and PNI. In the present study, we used JEV GIb strain of NX1889 to establish a mouse model of JEV infection. The general neurological signs emerged on day 3 of modeling. The motor function continued to deteriorate, reaching a maximum at 8 to 13 days postinfection (dpi) and gradually recovered after 16 dpi. The injuries of 105 PFU and 106 PFU groups were the most severe. Transmission electron microscopy and immunofluorescence staining showed varying degrees of demyelination and axonal degeneration in the sciatic nerves. The electrophysiological recordings demonstrated the presence of demyelinating peripheral neuropathy with reduced nerve conduction velocity. The decreased amplitudes and the prolonged end latency revealed axonal-type motor neuropathy. Demyelination is predominant in the early stage, followed by axonal injury. The expression level of JEV-E protein and viral RNA was elevated in the injured sciatic nerves, suggesting that it may cause PNI at the early stage. Inflammatory cell infiltration and increased inflammatory cytokines indicated that neuroinflammation is involved in JEV-induced PNI. IMPORTANCE JEV is a neurotropic flavivirus belonging to the Flaviviridae family and causes high mortality and disability rates. It invades the central nervous system and induces acute inflammatory injury and neuronal death. Thus, JEV infection is a major global public health concern. Previously, motor dysfunction was mainly attributed to central nervous system damage. Our knowledge regarding JEV-induced PNI is vague and neglected. Therefore, a laboratory animal model is essential. Herein, we showed that C57BL/6 mice can be used to study JEV-induced PNI through multiple approaches. We also demonstrated that viral loads might be positively correlated with lesion severity. Therefore, inflammation and direct virus infection may be the putative mechanisms underlying JEV-induced PNI. The results of this study laid the foundation for further elucidation of the pathogenesis mechanisms of PNI caused by JEV.

Tracing the spatiotemporal phylodynamics of Japanese encephalitis virus genotype I throughout Asia and the western Pacific.

BACKGROUND: Japanese encephalitis virus (JEV; Flaviridae: Flavivirus) causes Japanese encephalitis (JE), which is the most important arboviral disease in Asia and the western Pacific. Among the five JEV genotypes (GI-V), GI has dominated traditional epidemic regions in the past 20 years. We investigated the transmission dynamics of JEV GI through genetic analyses. METHODS: We generated 18 JEV GI near full length sequences by using multiple sequencing approaches from mosquitoes collected in natural settings or from viral isolates obtained through cell culture. We performed phylogenetic and molecular clock analyses to reconstruct the evolutionary history by integrating our data with 113 publicly available JEV GI sequences. RESULTS: We identified two subtypes of JEV GI (GIa and GIb), with a rate of 5.94 × 10-4 substitutions per site per year (s/s/y). At present, GIa still circulates within a limited region, exhibited no significant growth, the newest strain was discovered in China (Yunnan) in 2017, whereas most JEV strains circulating belong to the GIb clade. During the past 30 years, two large GIb clades have triggered epidemics in eastern Asia: one epidemic occurred in 1992 [95% highest posterior density (HPD) = 1989-1995] and the causative strain circulates mainly in southern China (Yunnan, Shanghai, Guangdong, and Taiwan) (Clade 1); the other epidemic occurred in 1997 (95% HPD = 1994-1999) and the causative strain has increased in circulation in northern and southern China during the past 5 years (Clade 2). An emerging variant of Clade 2 contains two new amino acid markers (NS2a-151V, NS4b-20K) that emerged around 2005; this variant has demonstrated exponential growth in northern China. CONCLUSION: JEV GI stain circulating in Asia have shifted during the past 30 years, spatiotemporal differences were observed among JEV GI subclade. GIa is still circulating within a limited range, exhibite no significant growth. Two large GIb clades have triggered epidemics in eastern Asia, all JEV sequences identified in northern China during the past 5 years were of the new emerging variant of G1b-clade 2.

The development of neurocritical care in China from the perspective of evaluation and treatment of critical neurological diseases.

Objective: To understand the varieties, evaluation, treatment, and prognosis of severe neurological diseases using the third NCU survey in China. Design: A cross-sectional questionnaire study. The study was completed in three main steps: filling in the questionnaire, sorting out the survey data, and analyzing the survey data. Results: Of 206 NCUs, 165 (80%) provided relatively complete information. It was estimated that 96,201 patients with severe neurological diseases were diagnosed and treated throughout the year, with an average fatality rate of 4.1%. The most prevalent severe neurological disease was cerebrovascular disease (55.2%). The most prevalent comorbidity was hypertension (56.7%). The most prevalent complication was hypoproteinemia (24.2%). The most common nosocomial infection was hospital-acquired pneumonia (10.6%). The GCS, APACHE II, EEG, and TCD were the most commonly used (62.4-95.2%). The implementation rate of the five nursing evaluation techniques reached 55.8-90.9%. Routinely raising the head of the bed by 30°, endotracheal intubation and central venous catheterization were the mostprevalent treatment strategies (97.6, 94.5, and 90.3%, respectively). Traditional tracheotomy, invasive mechanical ventilation and nasogastric tube feeding (75.8, 95.8, and 95.8%, respectively) were more common than percutaneous tracheotomy, non-invasive mechanical ventilation and nasogastric tube insertion (57.6, 57.6, and 66.7%, respectively). Body surface hypothermia brain protection technology was more commonly used than intravascular hypothermia technology (67.3 > 6.1%). The rates of minimally invasive hematoma removal and ventricular puncture were only 40.0 and 45.5%, respectively. Conclusion: In addition to traditional recognized basic life assessment and support technology, it is necessary to the use of promote specialized technology for neurological diseases, according to the characteristics of critical neurological diseases.

Parental corporal punishment and adolescent drinking: the protective role of personal growth initiative and gender difference.

Introduction: Parenting and peer victimization (PV) are crucial for adolescent drinking. To further explore the cause of adolescent drinking, the present study investigated the role of PV and personal growth initiative (PGI) in the relationship between parental corporal punishment (PCP) and adolescent drinking. Methods: Present study build moderated mediation models to test the hypothesis, and detailed analysis of gender differences was conducted on the models. The data were collected in a cross-sectional questionnaire study with n = 1,007 adolescents (mean age = 13.16 years, 51.84% girls, n = 522). Results: Model analysis showed that: (1) PV totally mediated the relationship between PCP and adolescent girls' drinking behavior; (2) The positive association between PV and drinking was only significant for girls with low PGI. Discussion: These findings underscore the importance of the protective effect of a personality trait characterized by spontaneous self-promotion on adolescent girls' drinking.

English-learning stress and performance in Chinese college students: A serial mediation model of academic anxiety and academic burnout and the protective effect of grit.

Introduction: Having to adapt to a new environment with various other challenges while completing their studies, Chinese college students experience intense stress related to the study of the English language. However, there has been little research on the serial mediating mechanism of English-learning stress on English academic performance. Methods: Present study recruited 1130 undergraduate students to finish self-report online questionnaire to collect the information about their English-learning stress, academic anxiety and burnout, English academic performance and grit. We constructed a moderated serial mediation model to test the effect of academic anxiety and academic burnout and explored whether grit can restrict the decrease in academic performance caused by English-learning stress. Results: Results show that: (1) both academic anxiety and academic burnout mediate the relationship between English-learning stress and performance; (2) academic anxiety and academic burnout show a significant serial mediating role between academic pressure and English academic performance; and (3) grit significantly moderates the relationship between academic burnout and English academic performance. Discussion: These results lead us to believe that cultivating the grit of Chinese college students may be an effective way to improve the academic performance of those experiencing high English-learning stress.

A mouse model of peripheral nerve injury induced by Japanese encephalitis virus.

Japanese encephalitis virus (JEV) is the most important cause of acute encephalitis in Eastern/Southern Asia. Infection with this virus also induces peripheral nerve injury. However, the disease pathogenesis is still not completely understood. Reliable animal models are needed to investigate the molecular pathogenesis of this condition. We studied the effect of Japanese encephalitis virus infection in C57BL/6 mice after a subcutaneous challenge. Limb paralysis was determined in mice using behavioral tests, including a viral paralysis scale and the hanging wire test, as well as by changes in body weight. Nerve conduction velocity and electromyography testing indicated the presence of demyelinating neuropathy of the sciatic nerve. Pathological changes in neural tissues were examined by immunofluorescence and transmission electron microscopy, which confirmed that the predominant pathologic change was demyelination. Although Western blots confirmed the presence of the virus in neural tissue, additional studies demonstrated that an immune-induced inflammatory response resulted in severe never injury. Immunofluorescence confirmed the presence of Japanese encephalitis virus in the brains of infected mice, and an inflammatory reaction was observed with hematoxylin-eosin staining as well. However, these observations were inconsistent at the time of paralysis onset. In summary, our results demonstrated that Japanese encephalitis virus infection could cause inflammatory demyelination of the peripheral nervous system in C57BL/6 mice.