T2 Relaxation Time in Extraocular Muscles of Patients with Mild Thyroid- Associated Ophthalmopathy: Comparing T2 Mapping With and Without Fat Suppression Using Different Measurement Methods.

OBJECTIVE: This study aimed to compare the parametric value of T2 with and without fat suppression (FS) on T2 mapping for the evaluation of extraocular muscles (EOMs) in mild thyroid-associated ophthalmopathy (TAO). METHODS: We prospectively recruited 44 consecutive patients with mild TAO seen between May 2020 and October 2022 and 26 healthy controls with no history of eye- or thyroid-related or other autoimmune diseases. Patients with mild TAO were subdivided into active and inactive groups based on their clinical activity scores. The T2 of each EOM was measured over a large and small area of interest on T2-mapping images with and without FS. Receiver operating characteristic (ROC) curves were used to evaluate the diagnostic efficacy of T2 for detecting TAO activity. RESULTS: The T2 was significantly and heterogeneously higher in the active group than in the inactive and control groups (P < 0.05). FS-T2-mapping images had better signal display within and at the edges of the EOMs than those without FS. It was possible to observe high-signal aggregation visible in the periphery of some EOMs, and the central part showed relatively low signals. The maximum T2 measured in small or large areas with and without FS had good diagnostic efficacy for TAO activity, with that of no-FS being better (the area under the ROC curve of the maximum T2 measured in a small area and a large area without FS was 1.0 and 1.0 and P values of < 0.001 and < 0.001, respectively). CONCLUSION: Maximal T2 with or without FS can facilitate the early clinical detection of mild TAO activity. The maximum T2 in a small area can facilitate active staging of patients with mild TAO.

Genome-wide identification, evolution of DNA methyltransferases and their expression under salinity stress in Larimichthys crocea.

DNA methyltransferases (Dnmts) are responsible for DNA methylation which influences patterns of gene expression and plays a crucial role in response to environmental changes. In this study, 7 LcDnmt genes were identified in the genome of large yellow croaker (Larimichthys crocea). The comprehensive analysis was conducted on gene structure, protein and location site of LcDnmts. LcDnmt proteins belonged to three groups (Dnmt1, Dnmt2, and Dnmt3) according to their conserved domains and phylogenetic analysis. Although Dnmt3 can be further divided into three sub groups (Dnmt3a, Dnmt3b, and Dnmt3l), there is no Dnmnt3l member in the large yellow croaker. Phylogenetic analysis revealed that the Dnmt family was highly conserved in teleosts. Expression patterns derived from the RNA-seq, qRT-PCR and Western blot analysis revealed that 2 LcDnmt genes (LcDnmt1 and LcDnmt3a2) significantly regulated under salinity stress in the liver, which was found to be dominantly expressed in the intestine and brain, respectively. These two genes may play an important role in the salinity stress of large yellow croaker and represent candidates for future functional analysis. Our results revealed the conservation of Dnmts during evolution and indicated a potential role of Dnmts in epigenetic regulation of response to salinity stress.

Neuroimaging features in a patient with non-ketotic hyperglycaemic seizures: A case report.

BACKGROUND: Non-ketotic hyperglycaemic (NKH) seizures are a rare neurological complication of diabetes caused by hyperglycaemia in non-ketotic and non-hyperosmotic states. The clinical characteristics of NKH seizures are atypical and lack unified diagnostic criteria, leading to potential misdiagnoses in the early stages of the disease. CASE SUMMARY: This report presents a rare case of NKH seizures in a 52-year-old male patient with a history of type 2 diabetes mellitus. We performed comprehensive magnetic resonance imaging (MRI) studies at admission, 12 d post-admission, and 20 d post-discharge. The imaging techniques included contrast-enhanced head MRI, T2-weighted imaging (T2WI), fluid-attenuated inversion recovery (FLAIR), diffusion-weighted imaging, susceptibility-weighted imaging, magnetic resonance spectroscopy (MRS), and magnetic resonance venography. At the time of admission, T2WI and FLAIR of the cranial MRI showed that the left parieto-occipital cortex had gyrus-like swelling and high signal, and subcortical stripes had low signal. MRS showed a reduced N-acetylaspartate peak and increased creatine and choline peaks in the affected areas. A follow-up MRI 20 d later showed that the swelling and high signal of the left parieto-occipital cortex had disappeared, and the low signal of the subcortex had disappeared. CONCLUSION: This case study provides valuable insights into the potential pathogenesis, diagnosis, and treatment of NKH seizures. The comprehensive MRI findings highlight the potential utility of various MRI sequences in diagnosing and characterizing NKH seizures.

Targeted therapy improves cellular dysfunction, ataxia, and seizure susceptibility in a model of a progressive myoclonus epilepsy.

The recurrent variant KCNC1-p.Arg320His causes progressive myoclonus epilepsy (EPM) type 7, defined by progressive myoclonus, epilepsy, and ataxia, and is without effective treatment. KCNC1 encodes the voltage-gated potassium channel subunit Kv3.1, specifically expressed in high-frequency-firing neurons. Variant subunits act via loss of function; hence, EPM7 pathogenesis may involve impaired excitability of Kv3.1-expressing neurons, while enhancing Kv3 activity could represent a viable therapeutic strategy. We generate a mouse model, Kcnc1-p.Arg320His/+, which recapitulates the core features of EPM7, including progressive ataxia and seizure susceptibility. Kv3.1-expressing cerebellar granule cells and neocortical parvalbumin-positive GABAergic interneurons exhibit abnormalities consistent with Kv3 channel dysfunction. A Kv3-specific positive modulator (AUT00206) selectively enhances the firing frequency of Kv3.1-expressing neurons and improves motor function and seizure susceptibility in Kcnc1-Arg320His/+ mice. This work identifies a cellular and circuit basis of dysfunction in EPM7 and demonstrates that Kv3 positive modulators such as AUT00206 have therapeutic potential for the treatment of EPM7.

Effects of salinity stress on methylation of the liver genome and complement gene in large yellow croaker (Larimichthys crocea).

Salinity is an important environmental factor that affects the yield and quality of large yellow croaker (Larimichthys crocea) during aquaculture. Here, whole-genome bisulfite sequencing (WGBS), RNA-seq, bisulfite sequencing PCR (BSP), quantitative real-time PCR (qPCR), and dual luciferase reporter gene detection technologies were used to analyze the DNA methylation characteristics and patterns of the liver genome, the expression and methylation levels of important immune genes in large yellow croaker in response to salinity stress. The results of WGBS showed that the cytosine methylation of CG type was dominant, CpGIsland and repeat regions were important regions where DNA methylation occurred, and the DNA methylation in upstream 2k (2000bp upstream of the promoter) and repeat regions had different changes in the liver tissue of large yellow croaker in the response to the 12‰, 24‰, 36‰ salinity stress of 4 w (weeks). In the combined analysis of WGBS and transcriptome, the complement and coagulation cascade pathways were significantly enriched, in which the complement-related genes C7, C3, C5, C4, C1R, MASP1, and CD59 were mainly changed in response to salinity stress. In the studied area of MASP1 gene promoter, the methylation levels of many CpG sites as well as total cytosine were strongly negatively correlated with mRNA expression level. Methylation function analysis of MASP1 promoter further proved that DNA methylation could inhibit the activity of MASP1 promoter, indicating that salinity may affect the expressions of complement-related genes by DNA methylation of gene promoter region.

Corticohippocampal circuit dysfunction in a mouse model of Dravet syndrome.

Dravet syndrome (DS) is a neurodevelopmental disorder due to pathogenic variants in SCN1A encoding the Nav1.1 sodium channel subunit, characterized by treatment-resistant epilepsy, temperature-sensitive seizures, developmental delay/intellectual disability with features of autism spectrum disorder, and increased risk of sudden death. Convergent data suggest hippocampal dentate gyrus (DG) pathology in DS (Scn1a+/-) mice. We performed two-photon calcium imaging in brain slice to uncover a profound dysfunction of filtering of perforant path input by DG in young adult Scn1a+/- mice. This was not due to dysfunction of DG parvalbumin inhibitory interneurons (PV-INs), which were only mildly impaired at this timepoint; however, we identified enhanced excitatory input to granule cells, suggesting that circuit dysfunction is due to excessive excitation rather than impaired inhibition. We confirmed that both optogenetic stimulation of entorhinal cortex and selective chemogenetic inhibition of DG PV-INs lowered seizure threshold in vivo in young adult Scn1a+/- mice. Optogenetic activation of PV-INs, on the other hand, normalized evoked responses in granule cells in vitro. These results establish the corticohippocampal circuit as a key locus of pathology in Scn1a+/- mice and suggest that PV-INs retain powerful inhibitory function and may be harnessed as a potential therapeutic approach toward seizure modulation.

Mice with monoallelic GNAO1 loss exhibit reduced inhibitory synaptic input to cerebellar Purkinje cells.

GNAO1 encodes Gαo, a heterotrimeric G protein α subunit in the Gi/o family. In this report, we used a Gnao1 mouse model "G203R" previously described as a "gain-of-function" Gnao1 mutant with movement abnormalities and enhanced seizure susceptibility. Here, we report an unexpected second mutation resulting in a loss-of-function Gαo protein, and describe alterations in central synaptic transmission. Whole cell patch clamp recordings from Purkinje cells (PCs) in acute cerebellar slices from Gnao1 mutant mice showed significantly lower frequencies of spontaneous and miniature inhibitory postsynaptic currents (sIPSCs and mIPSCs) compared with WT mice. There was no significant change in sEPSCs or mEPSCs. Whereas mIPSC frequency was reduced, mIPSC amplitudes were not affected, suggesting a presynaptic mechanism of action. A modest decrease in the number of molecular layer interneurons was insufficient to explain the magnitude of IPSC suppression. Paradoxically, Gi/o inhibitors (pertussis toxin) enhanced the mutant-suppressed mIPSC frequency and eliminated the difference between WT and Gnao1 mice. Although GABAB receptor regulates mIPSCs, neither agonists nor antagonists of this receptor altered function in the mutant mouse PCs. This study is an electrophysiological investigation of the role of Gi/o protein in cerebellar synaptic transmission using an animal model with a loss-of-function Gi/o protein.NEW & NOTEWORTHY This report reveals the electrophysiological mechanisms of a movement disorder animal model with monoallelic Gnao1 loss. This study illustrates the role of Gαo protein in regulating GABA release in mouse cerebellum. This study could also facilitate the discovery of new drugs or drug repurposing for GNAO1-associated disorders. Moreover, since GNAO1 shares pathways with other genes related to movement disorders, developing drugs for the treatment of GNAO1-associated movement disorders could further the pharmacological intervention for other monogenic movement disorders.

MiR-2014-5p and miR-1231-5p regulate muscle growth of Larimichthys crocea by targeting MSTN gene.

MicroRNAs (miRNAs) play an important role in regulating gene expression, and myostatin (MSTN) has been widely recognized as a key gene for muscle growth and development. Through high-throughput sequencing to study the effects of starvation on miRNA transcriptomes in Larimichthys crocea muscle tissue, we found that the expression of miR-2014, miR-1231 and miR-1470 were significantly different between fasting and normal feeding Larimichthys crocea. Bioinformatics analysis predicted that miR-2014, miR-1231 and miR-1470 target MSTN mRNA 3'UTR. To verify the accuracy of predictions, we constructed double luciferase plasmids containing MSTN 3'UTR and confirmed that miR-2014-5p and miR-1231-5p can inhibit MSTN expression by targeting MSTN 3'UTR using double luciferase experiments, while miR-1470 is not involved in regulation. Subsequent site-directed mutation experiments reflected the specificity of the target sequence. In addition, quantitative PCR experiments revealed that miR-2014-5p and miR-1231-5p may participate in the regulation of MSTN expression in fasting and refeeding period, respectively. These results implied that miRNA may take part in muscle growth regulation during starvation. It provides some insights into the molecular regulation mechanism of MSTN in response to starvation stress in fish.

Circulating and tumor-infiltrating arginase 1-expressing cells in gastric adenocarcinoma patients were mainly immature and monocytic Myeloid-derived suppressor cells.

Myeloid-derived suppressor cells (MDSCs) are a group of heterogeneous cells derived from immature myeloid cells (IMCs). MDSCs are known to play important roles in tumor immune evasion. While we know that there are a large number of circulating and tumor-infiltrating MDSCs existing in gastric cancer (GC) patients, the phenotypic characteristics and arginase 1 (ARG1) expression levels of these MDSCs remain very unclear. In our study, flow cytometric analysis of circulating MDSCs from 20 gastric adenocarcinoma (GAC) patients found that ≥80% ARG1-expressing MDSCs were mainly early-stage MDSCs (HLA-DR-CD33+CD14-CD15-MDSCs). In addition, our investigation showed that tumor-infiltrating MDSCs from 6 GAC patients consisted of >35% ARG1-expressing naïve MDSCs (HLA-DR-CD33-CD11b-CD14-CD15-MDSCs), >15% early-stage MDSCs and >40% monocytic MDSCs (HLA-DR-CD14+MDSCs). This preliminary study describes the phenotypic characteristics and ARG1 expression levels of MDSCs from GAC patients and shows that circulating and tumor-infiltrating ARG1-expressing cells were mainly immature and monocytic MDSCs, which provides information to better understand the mechanisms that allow gastric cancer cells to evade the immune system.

Mice with GNAO1 R209H Movement Disorder Variant Display Hyperlocomotion Alleviated by Risperidone.

Neurodevelopmental disorder with involuntary movements (Online Mendelian Inheritance in Man: 617493) is a severe, early onset neurologic condition characterized by a delay in psychomotor development, hypotonia, and hyperkinetic involuntary movements. Heterozygous de novo mutations in the GNAO1 gene cause neurodevelopmental disorder with involuntary movements. Gα o, the gene product of GNAO1, is the alpha subunit of Go, a member of the heterotrimeric Gi/o family of G proteins. Go is found abundantly throughout the brain, but the pathophysiological mechanisms linking Gα o functions to clinical manifestations of GNAO1-related disorders are still poorly understood. One of the most common mutant alleles among the GNAO1 encephalopathies is the c.626G>A or p.Arg209His (R209H) mutation. We developed heterozygous knock-in Gnao1 +/R209H mutant mice using CRISPR/Cas9 methodology to assess whether a mouse model could replicate aspects of the neurodevelopmental disorder with involuntary movements clinical pattern. Mice carrying the R209H mutation exhibited increased locomotor activity and a modest gait abnormality at 8-12 weeks. In contrast to mice carrying other mutations in Gnao1, the Gnao1 +/R209H mice did not show enhanced seizure susceptibility. Levels of protein expression in multiple brain regions were unchanged from wild-type (WT) mice, but the nucleotide exchange rate of mutant R209H Gα o was 6.2× faster than WT. The atypical neuroleptic risperidone has shown efficacy in a patient with the R209H mutation. It also alleviated the hyperlocomotion phenotype observed in our mouse model but suppressed locomotion in WT mice as well. In this study, we show that Gnao1 +/R209H mice mirror elements of the patient phenotype and respond to an approved pharmacological agent. SIGNIFICANCE STATEMENT: Children with de novo mutations in the GNAO1 gene may present with movement disorders with limited effective therapeutic options. The most common mutant variant seen in children with GNAO1-associated movement disorder is R209H. Here we show, using a novel Gnao1 +/R209H mouse, that there is a clear behavioral phenotype that is suppressed by risperidone. However, risperidone also affects wild-type mouse activity, so its effects are not selective for the GNAO1-associated movement disorder.

Exosomal miRNA-107 induces myeloid-derived suppressor cell expansion in gastric cancer.

  Background: Myeloid-derived suppressor cells (MDSCs) promote immunosuppression in the tumor microenvironment, support tumor growth and survival, and may contribute to immunotherapy resistance. Recent studies showed that tumor-derived exosomes (TDEs) can induce MDSCs accumulation and expansion, the mechanisms of which are largely unknown. Methods: The morphologies and sizes of the exosomes was observed by using a JEM-1400 transmission electron microscope. MicroRNA(miR)-107 and ARG1, DICER1, PTEN, PI3K, AKT, mTOR, and NF-kB mRNAs were quantified by quantitative reverse tanscription PCR. Dual-Luciferase Reports Assay were used to examine the expression of genes which was targeted by miR-107. The expression of proteins were analyzed by using western blot. Results: MiR-107 was not only overexpressed in gastric cancer cells but also enriched in their secreted TDEs. Also, these miR-107 enriched TDEs could be taken up by HLA-DR-CD33+MDSCs, where miR-107 was able to target and suppress expression of DICER1 and PTEN genes. Dampened DICER1 expression supported expansion of MDSCs , while decreased PTEN led to activation of the PI3K pathway, resulting in increased ARG1 expression. Furthemore, gastric cancer-derived miR-107 TDEs, when dosed intravenously into mice, were also capable of inducing expansion of CD11b+Gr1+/high MDSCs in mouse peripheral blood and altering expression of DICER1, PTEN, ARG1, and NOS2 in the MDSCs. Conclusions: Our findings demonstrate for the first time that gastric cancer-secreted exosomes are able to deliver miR-107 to the host MDSCs where they induce their expansion and activition by targeting DICER1 and PTEN genes, thereby may provide novel cancer therapeutics target for gastric cancer.

Mouse models of GNAO1-associated movement disorder: Allele- and sex-specific differences in phenotypes.

BACKGROUND: Infants and children with dominant de novo mutations in GNAO1 exhibit movement disorders, epilepsy, or both. Children with loss-of-function (LOF) mutations exhibit Epileptiform Encephalopathy 17 (EIEE17). Gain-of-function (GOF) mutations or those with normal function are found in patients with Neurodevelopmental Disorder with Involuntary Movements (NEDIM). There is no animal model with a human mutant GNAO1 allele. OBJECTIVES: Here we develop a mouse model carrying a human GNAO1 mutation (G203R) and determine whether the clinical features of patients with this GNAO1 mutation, which includes both epilepsy and movement disorder, would be evident in the mouse model. METHODS: A mouse Gnao1 knock-in GOF mutation (G203R) was created by CRISPR/Cas9 methods. The resulting offspring and littermate controls were subjected to a battery of behavioral tests. A previously reported GOF mutant mouse knock-in (Gnao1+/G184S), which has not been found in patients, was also studied for comparison. RESULTS: Gnao1+/G203R mutant mice are viable and gain weight comparably to controls. Homozygotes are non-viable. Grip strength was decreased in both males and females. Male Gnao1+/G203R mice were strongly affected in movement assays (RotaRod and DigiGait) while females were not. Male Gnao1+/G203R mice also showed enhanced seizure propensity in the pentylenetetrazole kindling test. Mice with a G184S GOF knock-in also showed movement-related behavioral phenotypes but females were more strongly affected than males. CONCLUSIONS: Gnao1+/G203R mice phenocopy children with heterozygous GNAO1 G203R mutations, showing both movement disorder and a relatively mild epilepsy pattern. This mouse model should be useful in mechanistic and preclinical studies of GNAO1-related movement disorders.

A mechanistic review on GNAO1-associated movement disorder.

Mutations in the GNAO1 gene cause a complex constellation of neurological disorders including epilepsy, developmental delay, and movement disorders. GNAO1 encodes Gαo, the α subunit of Go, a member of the Gi/o family of heterotrimeric G protein signal transducers. Go is the most abundant membrane protein in the mammalian central nervous system and plays major roles in synaptic neurotransmission and neurodevelopment. GNAO1 mutations were first reported in early infantile epileptic encephalopathy 17 (EIEE17) but are also associated with a more common syndrome termed neurodevelopmental disorder with involuntary movements (NEDIM). Here we review a mechanistic model in which loss-of-function (LOF) GNAO1 alleles cause epilepsy and gain-of-function (GOF) alleles are primarily associated with movement disorders. We also develop a signaling framework related to cyclic AMP (cAMP), synaptic vesicle release, and neural development and discuss gene mutations perturbing those mechanisms in a range of genetic movement disorders. Finally, we analyze clinical reports of patients carrying GNAO1 mutations with respect to their symptom onset and discuss pharmacological/surgical treatments in the context of our mechanistic model.

Dual-source computed tomography for quantitative assessment of tracheobronchial anomaly from type IIA pulmonary artery sling in pediatric patients.

PURPOSE: As an extremely rare abnormity, type IIA pulmonary artery sling (PAS) tracheobronchial anomalies should be differentiated from normal airway for therapeutic decision-making. This study aimed to investigate the quantitative characteristics of type IIA PAS tracheobronchial anomalies using dual-source computed tomography (DSCT). MATERIALS AND METHODS: From January 2009 to December 2016, there were 11 type IIA PAS patients enrolled for analysis and compared with 32 controls. The areas of the trachea, right upper lobar bronchus, left main bronchus, right intermediate bronchus [bridging bronchus (BB) in patients], and subcarinal angle [subpseudocarinal angle in patients] were measured. Measurements other than that for the angle were standardized with body surface area. RESULTS: Significant differences were found between the type IIA PAS patients and controls in terms of DSCT measurements in the trachea (0.51 ±â€¯0.32 cm2/m2 vs. 0.92 ±â€¯0.18 cm2/m2, P < 0.001); left main bronchus (0.29 ±â€¯0.14 cm2/m2 vs. 0.43 ±â€¯0.18 cm2/m2, P = 0.01); right intermediate bronchus [BB in patients] (0.36 ±â€¯0.13 cm2/m2 vs. 0.47 ±â€¯0.12 cm2/m2, P = 0.02); and subcarinal angle [subpseudocarinal angle in patients] (116.27 ±â€¯16.45° vs. 79.41 ±â€¯15.71°, P < 0.001). Receiver operating characteristic analysis further revealed that these parameters may be indicators to differentiate tracheobronchial anomalies due to type IIA PAS from controls (AUC, 0.88-0.98; sensitivity, 81.7%-100%; specificity, 91.7%-100%). CONCLUSIONS: DSCT is an alternative technique to detect tracheobronchial anomalies in pediatric patients with type IIA PAS. It can provide accurate anatomic details for surgeons to determine therapeutic strategies.

Movement disorder in GNAO1 encephalopathy associated with gain-of-function mutations.

OBJECTIVE: To define molecular mechanisms underlying the clinical spectrum of epilepsy and movement disorder in individuals with de novo mutations in the GNAO1 gene. METHODS: We identified all GNAO1 mutations reported in individuals with epilepsy (early infantile epileptiform encephalopathy 17) or movement disorders through April 2016; 15 de novo mutant alleles from 25 individuals were introduced into the Gαo subunit by site-directed mutagenesis in a mammalian expression plasmid. We assessed protein expression and function in vitro in HEK-293T cells by Western blot and determined functional Gαo-dependent cyclic adenosine monophosphate (cAMP) inhibition with a coexpressed α2A adrenergic receptor. RESULTS: Of the 15 clinical GNAO1 mutations studied, 9 show reduced expression and loss of function (LOF; <90% maximal inhibition). Six other mutations show variable levels of expression but exhibit normal or even gain-of-function (GOF) behavior, as demonstrated by significantly lower EC50 values for α2A adrenergic receptor-mediated inhibition of cAMP. The GNAO1 LOF mutations are associated with epileptic encephalopathy while GOF mutants (such as G42R, G203R, and E246K) or normally functioning mutants (R209) were found in patients with movement disorders with or without seizures. CONCLUSIONS: Both LOF and GOF mutations in Gαo (encoded by GNAO1) are associated with neurologic pathophysiology. There appears to be a strong predictive correlation between the in vitro biochemical phenotype and the clinical pattern of epilepsy vs movement disorder.

Solvothermal Synthesis of Three-Dimensional Hierarchical CuS Microspheres from a Cu-Based Ionic Liquid Precursor for High-Performance Asymmetric Supercapacitors.

It is meaningful to exploit copper sulfide materials with desired structure as well as potential application due to their cheapness and low toxicity. A low-temperature and facile solvothermal method for preparing three-dimensional (3D) hierarchical covellite (CuS) microspheres from an ionic liquid precursor [Bmim]2Cu2Cl6 (Bmim = 1-butyl-3-methylimidazolium) is reported. The formation of CuS nanostructures was achieved by decomposition of intermediate complex Cu(Tu)3Cl (thiourea = Tu), which produced CuS microspheres with diameters of 2.5-4 µm assembled by nanosheets with thicknesses of 10-15 nm. The ionic liquid, as an "all-in-one" medium, played a key role for the fabrication and self-assembly of CuS nanosheets. The alkylimidazolium rings ([Bmim](+)) were found to adsorb onto the (001) facets of CuS crystals, which inhibited the crystal growth along the [001] direction, while the alkyl chain had influence on the assembly of CuS nanosheets. The CuS microspheres showed enhanced electrochemical performance and high stability for the application in supercapacitors due to intriguing structural design and large specific surface area. When this well-defined CuS electrode was assembled into an asymmetric supercapacitor (ASC) with an activated carbon (AC) electrode, the CuS//AC-ASC demonstrated good cycle performance (∼88% capacitance after 4000 cycles) and high energy density (15.06 W h kg(-1) at a power density of 392.9 W kg(-1)). This work provides new insights into the use of copper sulfide electrode materials for asymmetric supercapacitors and other electrochemical devices.

[Analysis of association between the IRF5 gene single nucleotide polymorphism and allergic rhinitis].

OBJECTIVE: To study the possible association between interferon regulatory factor 5 (IRF5) gene polymorphism and allergic rhinitis (AR). METHODS: Six independent single nucleotide polymorphism (SNP, rs729302, rs4728142, rs3807306, rs2070197, rs11770589, rs2280714) were analyzed. The genotype and allele frequencies were detected in 110 AR patients and 101 healthy controls in Singapore Chinese population by polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP). RESULTS: Rs729302 was rejected as it was not polymorphic. For others SNP, no statistically significant difference was detected in genotype between AR and healthy control group (χ(2) value were 0.21, 5.02, 0.01, 2.91, 0.37, all P > 0.05). No statistically significant difference was detected in allele frequencies between AR and healthy control group (χ(2) value were 0.00, 2.78, 0.01, 2.31, 0.00, all P > 0.05). CONCLUSION: No association is observed between IRF5 and AR in Singapore Chinese population.

[To study of the nasal mucosa remodeling of allergic rhinitis patients].

OBJECTIVE: To explore whether there was tissue remodeling in the nasal mucosa of allergic rhinitis (AR) patients and detect the protein expressions of transforming growth factor beta1 (TGF-beta1), matrix metalloproteinases 9 (MMP-9) and tissue inhibitors of matrix metalloproteinases 1 (TIMP-1) in the nasal mucosa of these patients. METHOD: Pathologic staining was used to explore the mucosa of the middle turbinate tissues from 16 patients with mild AR, from 12 patients with severe AR, and from 15 non-AR, respect. The infiltrating of eosinophils and damage of epithelium were examined by the hematoxylin-eosin staining; goblet cells were counted by the alcian blue-periodic acid-schiff staining; the percentage area of extracellular matrix was determined by the MT; the protein expressions were measured by ELISA of TGF-beta1, MMP-9 and TIMP-1 in the middle turbinate tissues. RESULT: Compared with the control group, significant eosinophil infiltration and goblet cells were observed in both AR groups (P < 0.05). Evident epithelial damage and extracellular matrix deposition were observed in severe-AR group (P < 0.05). The expressions of TGF-beta1, MMP-9 and TIMP-1 in AR tissues were significant increased (P < 0.05). CONCLUSION: The nasal mucosa remodeling was observed in AR groups. The characteristics were as follows: eosinophils infiltration, epithelial damage, goblet cells hyperplasia and extracellular matrix deposition. TGF-beta1, MMP-9, TIMP-1 may play a role in the tissue remodeling processes.