The Relationship between physical activity, nutritional status, and sarcopenia in community- dwelling older adults with type 2 diabetes: a cross-sectional study.

AIM: This study was conducted in Urumqi, Xinjiang, to assess the prevalence of sarcopenia and to determine the relationship between physical activity, nutritional status, and sarcopenia among community-dwelling patients with type 2 diabetes mellitus. METHODS: Four hundred eight cases of older people patients with type 2 diabetes mellitus in the community in Urumqi, Xinjiang, from May to August 2022 were selected for a cross-sectional on-site survey, and general information questionnaires, clinical information surveys, physical function measurements, and criteria developed by the Asian sarcopenia working group in 2019 were selected for diagnosis of sarcopenia, and unifactorial and multifactorial binary Logistic regression were applied to analyze the influencing factors of T2DM combined with sarcopenia in patients with sarcopenia. RESULTS: Among the 408 patients, 84 (20.6%) had sarcopenia, with a prevalence of 12.6%, 32.1%, and 51.9% in those aged 60-70, 71- 80, and 81 or older respectively. The prevalence increased significantly with age. Adjusting for variables, the study found that FFM of the Left Leg (OR: 0.710, 95% CI: 0.612-0.804, P = 0.024), FFM of the Right Arm (OR: 0.710, 95% CI: 0.612-0.804, P < 0.001), Age (OR: 1.246, 95% CI: 1.031-1.505, P = 0.023), Fasting Blood Glucose (OR: 1.649, 95% CI: 1.066-2.550, P = 0.025), and Post-Prandial Blood Glucose (OR: 1.455, 95% CI: 0.999-2.118, P = 0.025) were independent associated factors. An increase in MNA score (OR: 0.398, 95% CI: 0.244-0.6500, P < 0.001), ASMI (OR: 0.000, 95% CI: 0.00-0.01, P < 0.001) walking energy expenditure (MET-min) (OR: 0.998, 95% CI: 0.996-0.999, P = 0.001) reduced the prevalence of sarcopenia. CONCLUSION: This study shows that increased age, increased skeletal muscle mass index, decreased right arm FFM, increased postprandial glucose, increased MNA scores, and increased walking energy expenditure (MET-min) were associated with type 2 diabetes with sarcopenia.

Dietary energy restriction in neurological diseases: what's new?

Energy-restricted diet is a specific dietary regimen, including the continuous energy-restricted diet and the intermittent energy-restricted diet. It has been proven effective not only to reduce weight and extend the lifespan in animal models, but also to regulate the development and progression of various neurological diseases such as epilepsy, cerebrovascular diseases (stroke), neurodegenerative disorders (Alzheimer's disease and Parkinson's disease) and autoimmune diseases (multiple sclerosis). However, the mechanism in this field is still not clear and a systematic neurological summary is still missing. In this review, we first give a brief summary of the definition and mainstream strategies of energy restrictions. We then review evidence about the effects of energy-restricted diet from both animal models and human trials, and update the current understanding of mechanisms underlying the biological role of energy-restricted diet in the fight against neurological diseases. Our review thus contributes to the modification of dietary regimen and the search for special diet mimics.

DNAH14 variants are associated with neurodevelopmental disorders.

Neurodevelopmental disorders (NDD) are complex and multifaceted diseases involving genetic and environmental sciences. Rapid developments in sequencing techniques have made it possible to identify new disease-causing genes. Our study aimed to identify novel genes associated with NDDs. Trio whole-exome sequencing was performed to evaluate potential NDD variants. We identified three unrelated patients with compound heterozygous DNAH14 variants. The detailed clinical information and genetic results of the recruited patients were obtained and systematically reviewed. Three compound heterozygous DNAH14 variants were identified as follows: c.6100C > T(p.Arg2034Ter) and c.5167A > G(p.Arg1723Gly), c.12640_12641delAA(p.Lys4214Valfs*7) and c.4811T > A(p.Leu1604Gln), andc.7615C > A(p.Pro2539Thr) and c.11578G > A(p.Gly3860Ser), including one nonsense, one frameshift, and four missense variants, which were not existent or with low minor allele frequencies based on the gnomAD database. The missense variants were assumed to be damaging or probably damaging by using multiple bioinformatics tools. Four of these variants were located in the AAA+ ATPase domain, while two were located in the C-terminal domain. Most affected amino acids were highly conserved in various species. A spectrum of neurological and developmental phenotypes was observed, including seizures, global developmental delay, microcephaly, and hypotonia. Thus, our findings indicate that variants of DNAH14 could lead to previously unrecognized NDDs.

Association of SHANK Family with Neuropsychiatric Disorders: An Update on Genetic and Animal Model Discoveries.

The Shank family proteins are enriched at the postsynaptic density (PSD) of excitatory glutamatergic synapses. They serve as synaptic scaffolding proteins and appear to play a critical role in the formation, maintenance and functioning of synapse. Increasing evidence from genetic association and animal model studies indicates a connection of SHANK genes defects with the development of neuropsychiatric disorders. In this review, we first update the current understanding of the SHANK family genes and their encoded protein products. We then denote the literature relating their alterations to the risk of neuropsychiatric diseases. We further review evidence from animal models that provided molecular insights into the biological as well as pathogenic roles of Shank proteins in synapses, and the potential relationship to the development of abnormal neurobehavioral phenotypes.

Integrating 16S RRNA gene sequencing and metabolomics to evaluate the association between gut microbiota and serum metabolites in patients with myositis.

AIMS: Gut microbiota and metabolites have a profound impact on the maintenance of body health. In this study, we assessed the association between gut microbiota and serum metabolite changes in myositis using 16S rRNA gene sequencing and metabolomics to provide new ideas for screening and treating myositis. METHODS AND RESULTS: Blood and faecal samples were collected from 20 myositis patients and 20 healthy control subjects. Then, 16S rRNA gene sequencing, enzyme-linked immunosorbent assays and untargeted metabolomics study were performed to evaluate the relationship between gut microbiota and serum metabolites in patients with myositis. Compared to healthy control subjects, the blood samples from the patients with myositis had elevated levels of interleukin-4 (IL-4), tumour necrosis factor-α (TNF-α), and malondialdehyde (MDA) and decreased superoxide dismutase (SOD) levels. The increase in Bacteroidota (including Bacteroides and Parabacteroides, but not Prevotella) and the decrease in Firmicutes in the patients were accompanied by functional changes in amino acid and lipid metabolism. The gut microbiota (Bacteroides and Parabacteroides) were negatively correlated with the differential serum metabolites (glutamate and taurine). The differential serum metabolites (glutamate, pyrrolidonecarboxylic acid, and taurine) were also correlated with inflammatory factors (IL-4 and TNF-α) and oxidative stress indexes (MDA and SOD). CONCLUSION: Dysbiosis of gut microbiota in patients with myositis was accompanied by changes in inflammatory factors, oxidative stress indexes, and small molecule metabolites in serum. SIGNIFICANCE AND IMPACT OF STUDY: Blood and faecal biomarkers could be used for screening myositis.

Characteristics of myasthenia gravis in elderly patients: a retrospective study.

BACKGROUND: The incidence of myasthenia gravis (MG) is increasing, and its characteristics in elderly patients are believed to differ from those in younger patients. However, only a few studies have focused on elderly patients with MG. OBJECTIVE: To review the characteristics of MG in elderly patients and evaluate whether older age is an independent factor associated with achieving minimal manifestation status (MMS). METHODS: This retrospective cohort study included 367 patients (319 non-elderly and 48 elderly patients) with MG enrolled at Xiangya Hospital from September 1, 2016, to December 31, 2018. We collected demographic data and information regarding comorbidities, antibody status, Myasthenia Gravis Foundation of America classification, affected muscle groups, thymoma, and treatment. MMS was defined as the primary outcome. RESULTS: Comorbidities were more common in elderly than in younger patients with MG. Anti-acetylcholine receptor antibody was the dominant subtype, whereas anti-muscle-specific tyrosine kinase antibody was rare and detected only in non-elderly patients. Elderly patients were more likely than younger patients to have generalized MG, but the frequency of thymoma was lower (28.5% vs. 10.4%, p = 0.0078). MMS or better was achieved in 154 (48.3%) and 13 (27.1%) non-elderly and elderly patients, respectively. Older age did not appear to be an independent factor associated with MMS (hazard ratio = 0.625; 95% confidence interval, 0.345-1.131). CONCLUSIONS: Older age was not an independent factor for a worse prognosis in patients with MG. The treatment of elderly patients with MG should be individually tailored.

LRRC4 functions as a neuron-protective role in experimental autoimmune encephalomyelitis.

BACKGROUND: Leucine rich repeat containing 4 (LRRC4), also known as netrin-G ligand-2 (NGL-2), belongs to the superfamily of LRR proteins and serves as a receptor for netrin-G2. LRRC4 regulates the formation of excitatory synapses and promotes axon differentiation. Mutations in LRRC4 occur in Autism Spectrum Disorder (ASD) and intellectual disability. Multiple sclerosis (MS) is a chronic neuroinflammatory disease with spinal cords demyelination and neurodegeneration. Here, we sought to investigate whether LRRC4 is involved in spinal cords neuron-associated diseases. METHODS: LRRC4 was detected in the CNS of experimental autoimmune encephalomyelitis (EAE) mice by the use of real-time PCR and western blotting. LRRC4-/- mice were created and immunized with myelin oligodendrocyte glycoprotein peptide (MOG)35-55. Pathological changes in spinal cords of LRRC4-/- and WT mice 15 days after immunization were examined by using hematoxylin and eosin (H&E), Luxol Fast Blue (LFB) staining and immunohistochemistry. The number of Th1/Th2/Th17/Treg cells in spleens and blood were measured with flow cytometry. Differential gene expression in the spinal cords from WT and LRRC4-/- mice was analyzed by using RNA sequencing (RNA-seq). Adeno-associated virus (AAV) vectors were used to overexpress LRRC4 (AAV-LRRC4) and were injected into EAE mice to assess the therapeutic effect of AAV-LRRC4 ectopic expression on EAE. RESULTS: We report that LRRC4 is mainly expressed in neuron of spinal cords, and is decreased in the spinal cords of the EAE mice. Knockout of LRRC4 have a disease progression quickened and exacerbated with more severe myelin degeneration and infiltration of leukocytes into the spinal cords. We also first found that Rab7b is high expressed in EAE mice, and the deficiency of LRRC4 induces the elevated NF-κB p65 by up-regulating Rab7b, and up-regulation of IL-6, IFN-γ and down-regulation of TNF-α, results in more severe Th1 immune response in LRRC4-/- mice. Ectopic expression of LRRC4 alleviates the clinical symptoms of EAE mice and protects the neurons from immune damages. CONCLUSIONS: We identified a neuroprotective role of LRRC4 in the progression of EAE, which may be used as a potential target for auxiliary support therapeutic treatment of MS.

Reproduction-Associated Hormones and Adult Hippocampal Neurogenesis.

The levels of reproduction-associated hormones in females, such as estrogen, progesterone, prolactin, and oxytocin, change dramatically during pregnancy and postpartum. Reproduction-associated hormones can affect adult hippocampal neurogenesis (AHN), thereby regulating mothers' behavior after delivery. In this review, we first briefly introduce the overall functional significance of AHN and the methods commonly used to explore this front. Then, we attempt to reconcile the changes of reproduction-associated hormones during pregnancy. We further update the findings on how reproduction-related hormones influence adult hippocampal neurogenesis. This review is aimed at emphasizing a potential role of AHN in reproduction-related brain plasticity and its neurobiological relevance to motherhood behavior.

Silencing miR-20a-5p inhibits axonal growth and neuronal branching and prevents epileptogenesis through RGMa-RhoA-mediated synaptic plasticity.

Epileptogenesis is a potential process. Mossy fibre sprouting (MFS) and synaptic plasticity promote epileptogenesis. Overexpression of repulsive guidance molecule a (RGMa) prevents epileptogenesis by inhibiting MFS. However, other aspects underlying the RGMa regulatory process of epileptogenesis have not been elucidated. We studied whether RGMa could be modulated by microRNAs and regulated RhoA in epileptogenesis. Using microRNA databases, we selected four miRNAs as potential candidates. We further experimentally confirmed miR-20a-5p as a RGMa upstream regulator. Then, in vitro, by manipulating miR-20a-5p and RGMa, we investigated the regulatory relationship between miR-20a-5p, RGMa and RhoA, and the effects of this pathway on neuronal morphology. Finally, in the epilepsy animal model, we determined whether the miR-20a-5p-RGMa-RhoA pathway influenced MFS and synaptic plasticity and then modified epileptogenesis. Our results showed that miR-20a-5p regulated RGMa and that RGMa regulated RhoA in vitro. Furthermore, in primary hippocampal neurons, the miR-20a-5p-RGMa-RhoA pathway regulated axonal growth and neuronal branching; in the PTZ-induced epilepsy model, silencing miR-20a-5p prevented epileptogenesis through RGMa-RhoA-mediated synaptic plasticity but did not change MFS. Overall, we concluded that silencing miR-20a-5p inhibits axonal growth and neuronal branching and prevents epileptogenesis through RGMa-RhoA-mediated synaptic plasticity in the PTZ-induced epilepsy model, thereby providing a possible strategy to prevent epileptogenesis.

MiR-181a regulates CD4+ T cell activation and differentiation by targeting IL-2 in the pathogenesis of myasthenia gravis.

Recently, microRNAs (miRNAs) have been reported to play crucial roles in immune responses and other biological processes, but the role of miR-181a in myasthenia gravis (MG) has been relatively less studied. We found that miR-181a was downregulated in the peripheral blood mononuclear cells (PBMCs) of MG patients and was associated with QMGs and anti-AChR Ab levels. In vitro experiments indicated that miR-181a was involved in the modulation of CD4+ T cell activation and plasticity and that miR-181a decreased the expression level of the Th1-related transcription factor T-bet and the Th17-related transcription factor RORγt. In the in vivo experiment, miR-181a treatment alleviated experimental autoimmune myasthenia gravis (EAMG) symptoms and affected both CD4+ T cell differentiation and the production of anti-AChR antibodies. Moreover, in this study, we also found that IL-2 was regulated by miR-181a and that its expression level showed a strong negative correlation with miR-181a levels in MG patients. To illustrate that the expression levels of both IL-2 and miR-181a were sensitive to immunomodulatory therapy treatment in MG, we found that IL-2 and miR-181a were correlated with clinical severity. These findings demonstrate that miR-181a can contribute to the pathogenesis of MG by regulating IL-2 expression. This article is protected by copyright. All rights reserved.

Multiple genetic factors affecting the pharmacokinetic and pharmacodynamic processes of tacrolimus in Chinese myasthenia gravis patients.

PURPOSE: Tacrolimus is a novel effective immunosuppressant for myasthenia gravis (MG) patients. However, the narrow therapeutic window, and high inter- and intrapatient variation in bioavailability largely limited its clinical application. This article intended to find the SNPs influencing clinical outcome and discover the possible mechanisms. METHODS: Based on the tagSNPs genotyped by Improved Multiple Ligase Detection Reaction, Plink 1.07 was used to find the SNPs having close interaction to tacrolimus serum concentration, QMG score changes or even reasonable drug dose. Then we searched several databases to predict the possible miRNA binding rs15524 sequence. Based on the prediction, dual-luciferase reporter assay and miRNA transfection were used to discover the mechanism of how SNP rs15524 controls tacrolimus serum concentration through influencing CYP3A5 expression. RESULTS: In this article, we found multiple SNPs on CYP3A4, CYP3A5, FKBP1A, NFATC2 genes were predicted closely related to tacrolimus serum concentration, therapeutic effect which reflected by QMG score changes or even reasonable drug dose. After in silico miRNA selection, possible relationship between hsa-miR-500a and rs15524 was found. With the help of dual-luciferase reporter assay, wild-type rs15524 (T allele) was found having a stronger binding affinity for hsa-miR-500a. Higher expression of CYP3A5 may also led by lower hsa-miR-500a level. CONCLUSIONS: SNP rs15524 may control CYP3A5 expression by affecting the binding affinity between CYP3A5 3'UTR and hsa-miR-500a. Wild type (T allele) 3'UTR of CYP3A5 has stronger binding affinity to hsa-miR-500a and cause lower CYP3A5 expression and higher tacrolimus serum concentration.

The Expression Pattern and Regulatory Mechanism of the G0/G1 Switch Gene 2 (G0S2) in the Pathogenesis and Treatment of AChR Myasthenia Gravis (MG).

This study is aimed at exploring the expression pattern and methylation level of G0S2 in the peripheral blood mononuclear cells (PBMCs) of myasthenia gravis (MG) patients with positive acetylcholine receptor (AChR) autoantibodies and revealing the relationship between the G0S2 methylation pattern and MG. The relationship between the NFAT family members and G0S2 was explored to reveal the regulatory mechanism of G0S2 in the pathogenesis and treatment of AChR MG. Moreover, we attempted to demonstrate the potential therapeutic mechanism of tacrolimus in AChR MG. The relative G0S2 expression level in the PBMCs of healthy people was compared with that in the PBMCs of AChR MG patients with quantitative real-time PCR (qRT-PCR). The methylation frequency of the G0S2 promoter was detected by bisulfite sequencing PCR (BSP) and pyrosequencing. A dual-luciferase reporter system was used to reveal the relationship between the G0S2 promoter and nuclear factor of activated T cells 5 (NFAT5). The qRT-PCR results showed that G0S2 expression was significantly upregulated in the B cells and CD8+ T cells of AChR MG patients but not in the CD4+ T cells, and these expression differences were significantly associated with a decrease in G0S2 methylation. NFAT5, which was speculated to bind to island 1 (p1) in the G0S2 promoter, may regulate the lymphocyte balance by regulating G0S2 gene expression but failed to affect the methylation of the G0S2 promoter. Tacrolimus therapy-induced methylation and overexpression of NFAT5 could significantly reduce the expression of G0S2 in AChR MG patients. The G0S2 gene was remarkably upregulated in the PBMCs of MG patients. NFAT5 may affect transcription initiation and downregulate G0S2 expression through p1 in the promoter, thus controlling G0S2 gene expression and regulating the lymphocyte balance. Therefore, G0S2 could be an immune regulatory factor in both AChR MG occurrence and treatment with tacrolimus.

Correction to: miR-18a reactivates the Epstein-Barr virus through defective DNA damage response and promotes genomic instability in EBV-associated lymphomas.

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Expression of Nav1.5 in the pathogenesis of temporal lobe epilepsy.

To investigate the expressions of Nav1.5 mRNA at different time points in a rat model of temporal lobe epilepsy (TLE), and to assess the potential contribution of Nav1.5 to epileptogenesis. Male Sprague-Dawley rats (72) weighing 230 to 250 g were used for this study. They were randomly assigned to six groups (12 rats/group): control and five TLE groups. The TLE groups were day 1 (acute period), days 7 and 14 (latent period), and days 30 and 60 (chronic period). With the exception of control, epilepsy was induced in the rats with an intraperitoneal (i.p.) injection of aqueous solution of lithium chloride 18 h prior to pilocarpine injection (i.p.) at a dose of 125 mg/kg body weight (b.wt). Rats in the control group were injected i.p. with 0.9 % sodium chloride (125 mg/kg b.wt.) in place of pilocarpine. A total of 84 out of 112 rats developed status epilepticus (SE). The expression of Nav1.5 in the brains of rats was assessed using quantitative real-time polymerase chain reaction (qRT-PCR), immunohistochemistry and Western blot analysis. The expressions of Scn5a mRNA in the hippocampus during the latent and chronic periods were significantly higher than in the control group (p < 0.05), but there were no significant differences in the corresponding expressions between the two different time points in the latent and chronic period groups (p > 0.05). The expression peaked 30 days post-SE, and was sustained for 60 days. There was no significant difference in the expression of Scn5a mRNA in the acute group, when compared to control. Immunohistochemical staining showed that expression levels of Nav1.5 in the CA3 region during latent and chronic periods were significantly higher than those in control group (p < 0.05), and the expressions peaked at day 30. However, there was no significant difference in the expression of Nav1.5 in the latent group, relative to the chronic period group. These results show that Nav1.5 might be involved in the pathogenesis of TLE.

miR-18a reactivates the Epstein-Barr virus through defective DNA damage response and promotes genomic instability in EBV-associated lymphomas.

BACKGROUND: The Epstein-Barr virus (EBV) is closely associated with several types of malignancies. EBV is normally present in the latent state in the peripheral blood B cell compartment. The EBV latent-to-lytic switch is required for virus spread and virus-induced carinogenesis. Immunosuppression or DNA damage can induce the reactivation of EBV replication. EBV alone is rarely sufficient to cause cancer. In this study, we investigated the roles of host microRNAs and environmental factors, such as DNA-damage agents, in EBV reactivation and its association with lymphomagenesis. METHODS: We first analyzed the publicly available microRNA array data containing 45 diffuse large B-cell lymphoma patients and 10 control lymph nodes or B cells with or without EBV infection. In situ hybridization for miR-18a and immunohistochemitry were performed to evaluate the correlation between the expression of miR-18a and nuclear EBV protein EBNA1 in lymphoid neoplasm. The proliferative effects of miR-18a were investigated in EBV-positive or -negative lymphoid neoplasm cell lines. EBV viral load was measured by a quantitative real-time EBV PCR and FISH assay. The genomic instability was evaluated by CGH-array. RESULTS: In this study, we analyzed the publicly available microRNA array data and observed that the expression of the miR-17-92 cluster was associated with EBV status. In situ hybridization for miR-18a, which is a member of the miR-17-92 cluster, showed a significant upregulation in lymphoma samples. miR-18a, which shares the homolog sequence with EBV-encoded BART-5, promoted the proliferation of lymphoma cells in an EBV status-dependent manner. The DNA-damaging agent UV or hypoxia stress induced EBV activation, and miR-18a contributed to DNA damaging-induced EBV reactivation. In contrast to the promoting effect of ATM on the lytic EBV reactivation in normoxia, ATM inhibited lytic EBV gene expression and decreased the EBV viral load in the prescence of hypoxia-induced DNA damage. miR-18a reactivated EBV through inhibiting the ATM-mediated DNA damage response (DDR) and caused genomic instability. CONCLUSIONS: Taken together, these results indicate that DNA-damaging agents and host microRNAs play roles in EBV reactivation. Our study supported the interplay between host cell DDR, environmental genotoxic stress and EBV.

The origin of high hydrocarbon groundwater in shallow Triassic aquifer in Northwest Guizhou, China.

Original high hydrocarbon groundwater represents a kind of groundwater in which hydrocarbon concentration exceeds 0.05 mg/L. The original high hydrocarbon will significantly reduce the environment capacity of hydrocarbon and lead environmental problems. For the past 5 years, we have carried out for a long-term monitoring of groundwater in shallow Triassic aquifer in Northwest Guizhou, China. We found the concentration of petroleum hydrocarbon was always above 0.05 mg/L. The low-level anthropogenic contamination cannot produce high hydrocarbon groundwater in the area. By using hydrocarbon potential, geochemistry and biomarker characteristic in rocks and shallow groundwater, we carried out a comprehensive study in Dalongjing (DLJ) groundwater system to determine the hydrocarbon source. We found a simplex hydrogeology setting, high-level water-rock-hydrocarbon interaction and obviously original hydrocarbon groundwater in DLJ system. The concentration of petroleum hydrocarbon in shallow aquifer was found to increase with the strong water-rock interaction. Higher hydrocarbon potential was found in the upper of Guanling formation (T2g3) and upper of Yongningzhen formation (T1yn4). Heavily saturated carbon was observed from shallow groundwater, which presented similar distribution to those from rocks, especially from the deeper groundwater. These results indicated that the high concentrations of original hydrocarbon in groundwater could be due to the hydrocarbon release from corrosion and extraction out of strata over time.

IFNA-AS1 regulates CD4+ T cell activation in myasthenia gravis though HLA-DRB1.

Abnormal CD4+T cell activation is known to play roles in the pathogenesis of myasthenia gravis (MG). However, little is known about the mechanisms underlying the roles of lncRNAs in regulating CD4+ T cell. In this study, we discovered that the lncRNA IFNG-AS1 is abnormally expressed in MG patients associated with quantitative myasthenia gravis (QMG) and the positive anti-AchR Ab levels patients. IFNG-AS1 influenced Th1/Treg cell proliferation and regulated the expression levels of their transcription factors in an experimental autoimmune myasthenia gravis (EAMG)model. IFNG-AS1 could reduce the expression of HLA-DRB and HLA-DOB and they had a negative correlation in MG. Furthermore IFNG-AS1 influenced the expression levels of CD40L and CD4+ T cells activation in MG patient partly depend on effecting the HLA-DRB1 expression. It suggests that IFNG-AS1 may be involved in CD4+T cell-mediated immune responses in MG.

MicroRNA in glutamate receptor-dependent neurological diseases.

Glutamate-mediated excitotoxicity is the major neuropathological process contributing to numerous neurological diseases. Recently, emerging evidence indicates that microRNAs (miRNAs) play essential roles in the pathophysiology of a wide range of neurological diseases. Notably, there have been significant developments in understanding the biogenesis of miRNAs, their regulatory mechanisms, and their potential as effective biomarkers and therapies. In the present review, we summarize the recent literature that highlights the versatile roles played by miRNAs in glutamate receptor (GluR)-dependent neurological diseases. Based on the reported studies to date, modulation of miRNAs could emerge as a promising therapeutic target for a variety of neurological diseases that were discussed in this review.

Hydrothermal Synthesis and Electrochemical Performance of Manganese Oxide (Na-OMS-2) Nanorods.

Sodium octahedral molecular sieve nanorods (Na-OMS-2) were prepared through a facile hydrothermal method. The effects of reaction temperature and duration on particle sizes of the products were investigated. The electrochemical performance of samples was studied by constant current charge­discharge tests as cathode material for Li-ion batteries (LIBs). The initial discharge capacity of Na-OMS-2 is 123.4 mAh g−1 and the capacity retention was 123.9 mAh g−1 after 100 cycles. The result demonstrates that Na-OMS-2 cathode material behaves a good cycling stability.

MiR-15a contributes abnormal immune response in myasthenia gravis by targeting CXCL10.

MiR-15a is likely to be associated with autoimmunity. Here, we aimed to examine the expression of miR-15 cluster in PBMCs from myasthenia gravis (MG) patients and investigate the potential roles of miR-15a in MG. We found that the expression of all miR-15 cluster was decreased in MG, furthermore, miR-15a levels in ocular MG (oMG) were much lower, while CXCL10 production was increased in MG. We display that CXCL10 was a functional target gene of miR-15a in MG. Increasing miR-15a expression could reduce CXCL10 expression and alleviate the abnormal T cells activation in immune response, while decreasing miR-15a expression could activate immune response abnormally. Moreover, miR-15a expression was significantly decreased after stimulation, and prednisone treatment could upregulate miR-15a expression in steroid-responsive MG patients. Take together, our data suggest that decreased miR-15a expression facilitates proinflammatory cytokines production and contributes to immune response at least in part via regulating CXCL10 expression in MG.