Objective:To investigate the differences in electroencephalographic (EEG) microstate characteristics between children with autism spectrum disorder (ASD) and typically developing (TD) children, and to explore the correlation between irritability and EEG microstate features in ASD children.Methods:A total of 104 children with ASD [ASD group, 83 boys, 21 girls; aged 4-13 years, mean age (9.47±1.74)years] from the Autism Cohort of Nanjing Medical University and 60 TD children [TD group; 50 boys, 10 girls; aged 5-13 years, mean age(9.86±1.78) years ]from the IEEE Dataport database were enrolled. Irritability severity was assessed using the Affective Reactivity Index-Parent (ARI-P). Resting-state EEG data with eyes closed were recorded using a 24-channel dry-electrode EEG cap. Group-level EEG microstate topographic maps and microstate parameters, including mean duration, frequency, and time coverage, were extracted and compared between groups using nonparametric tests. In the ASD group, Spearman correlation analysis was used to examine the associations between microstate features and ARI-P in ASD children. Multiple linear regression was used to identify predictors of irritability.Results:Four group-level microstates (A, B, C, D) were identified in both groups. Compared to TD children, ASD children exhibited significantly longer mean duration for all microstates, in microstates A[ M(Q1, Q3)]: 0.060 (0.054,0.070) vs 0.091 (0.0530, 0.155) s, microstate B: 0.059 (0.050, 0.066) vs 0.087 (0.057,0.149) s, microstate C: 0.059 (0.050, 0.066) vs 0.095 (0.056, 0.183) s and microstate D: 0.055 (0.049,0.075) vs 0.095 (0.053,0.162) s ( Z=-3.51, -4.89, -4.71, -4.21; all P<0.001); However, microstate occurrence frequencies were significantly lower in the ASD group: A: 5.423 (3.640,21.024) vs 1.834 (1.327,3.395) Hz, microstate B: 4.949 (3.439,20.038) vs 2.146 (1.314,3.834) Hz, microstate C: 5.888 (3.998,22.078) vs 2.234 (1.441,3.768) Hz and microstate D: 5.371 (3.170,15.208) vs 2.074 (1.147,3.582) Hz ( Z=-7.72, -6.41, -7.85, -6.60; all P<0.001). In the ASD group, ARI-P scores were positively correlated with the mean duration of microstates B, C, and D ( r=0.28, 0.26, 0.33; all P<0.05) and negatively correlated with the occurrence frequency of microstates A, C, and D ( r=-0.26, -0.27, -0.21; all P<0.05). Multiple linear regression analysis revealed that the mean duration of microstate B was a significant predictor of irritability severity ( β=0.436, 95% CI: 1.260-4.202, P<0.001). Conclusion:Resting-state EEG microstate characteristics in Children with ASD differ from those in TD children and are associated with the severity of irritability. Prolonged duration of microstate B may serve as a risk factor for increased irritability in children with ASD.

Objective:To investigate the differences in electroencephalographic (EEG) microstate characteristics between children with autism spectrum disorder (ASD) and typically developing (TD) children, and to explore the correlation between irritability and EEG microstate features in ASD children.Methods:A total of 104 children with ASD [ASD group, 83 boys, 21 girls; aged 4-13 years, mean age (9.47±1.74)years] from the Autism Cohort of Nanjing Medical University and 60 TD children [TD group; 50 boys, 10 girls; aged 5-13 years, mean age(9.86±1.78) years ]from the IEEE Dataport database were enrolled. Irritability severity was assessed using the Affective Reactivity Index-Parent (ARI-P). Resting-state EEG data with eyes closed were recorded using a 24-channel dry-electrode EEG cap. Group-level EEG microstate topographic maps and microstate parameters, including mean duration, frequency, and time coverage, were extracted and compared between groups using nonparametric tests. In the ASD group, Spearman correlation analysis was used to examine the associations between microstate features and ARI-P in ASD children. Multiple linear regression was used to identify predictors of irritability.Results:Four group-level microstates (A, B, C, D) were identified in both groups. Compared to TD children, ASD children exhibited significantly longer mean duration for all microstates, in microstates A[ M(Q1, Q3)]: 0.060 (0.054,0.070) vs 0.091 (0.0530, 0.155) s, microstate B: 0.059 (0.050, 0.066) vs 0.087 (0.057,0.149) s, microstate C: 0.059 (0.050, 0.066) vs 0.095 (0.056, 0.183) s and microstate D: 0.055 (0.049,0.075) vs 0.095 (0.053,0.162) s ( Z=-3.51, -4.89, -4.71, -4.21; all P<0.001); However, microstate occurrence frequencies were significantly lower in the ASD group: A: 5.423 (3.640,21.024) vs 1.834 (1.327,3.395) Hz, microstate B: 4.949 (3.439,20.038) vs 2.146 (1.314,3.834) Hz, microstate C: 5.888 (3.998,22.078) vs 2.234 (1.441,3.768) Hz and microstate D: 5.371 (3.170,15.208) vs 2.074 (1.147,3.582) Hz ( Z=-7.72, -6.41, -7.85, -6.60; all P<0.001). In the ASD group, ARI-P scores were positively correlated with the mean duration of microstates B, C, and D ( r=0.28, 0.26, 0.33; all P<0.05) and negatively correlated with the occurrence frequency of microstates A, C, and D ( r=-0.26, -0.27, -0.21; all P<0.05). Multiple linear regression analysis revealed that the mean duration of microstate B was a significant predictor of irritability severity ( β=0.436, 95% CI: 1.260-4.202, P<0.001). Conclusion:Resting-state EEG microstate characteristics in Children with ASD differ from those in TD children and are associated with the severity of irritability. Prolonged duration of microstate B may serve as a risk factor for increased irritability in children with ASD.

Neuroinflammation mediated by microglia is essential for the occurrence and development of Alzheimer’s disease (AD). Through the analysis of the GEO database, it was found that IL-27 expression decreased in both the cerebral cortex and hippocampus of AD patients. In this study, the AD cell model of BV-2 cells injured by Aβ1-42, the inflammatory cell model of BV-2 cells damaged by LPS, and the inflammatory animal model were established and the effects of IL-27 after its administration in the above models in regulating microglial phenotype and neuroinflammation were evaluated. In the animal models, the number of Iba1+ microglia in the hippocampus was detected by immunohistochemistry, the expression of pro-inflammatory factors such as TNF-α, IL-1β and IL-6 was detected by qPCR, ELISA and Western blot, and the expression of M1/M2 phenotypic markers in microglia was detected by qPCR. To further explore the action mechanism of IL-27, Western blot was used to detect the expression levels of NF-κB, p-NF-κB, IκBα and p-IκBα in microglia after administration of IL-27 and Aβ1-42. The results showed that IL-27 alleviated the abnormal activation of microglia induced by lipopolysaccharide (LPS), decreased the expression of pro-inflammatory factors such as TNF- α, IL-1β and IL-6, transformed microglia induced by LPS or Aβ1-42 from neurotoxic M1 to neuroprotective M2, and improved the abnormal phosphorylation of NF-κB and IκBα induced by Aβ1-42. The research suggested that IL-27 can regulate the M1/M2 polarization of microglia induced by Aβ1-42 or LPS, and alleviate neuroinflammation.

Objective The anti-tumor effect by sequential treatment with Newcastle disease virus (NDV) strain 7793 and 5-FU in liver-metastases mice model was evaluated and immune-active response stimulated by sequential therapy was investigated. Methods Liver metastasis mice model was established by intra-peritoneal injection. The model mice were randomly divided into 3 groups, being given PBS (0.1 mL/d,10 d), NDV7793 [512 HU/(kg·d),5 d] and NDV7793[512 HU/(kg·d),5 d] + fluorouracil [5-FU,10 mg/(kg·d),5 d]. The effect on survival time,body weight,liver weight change and the formation of liver metastasis in tumor-bearing mice model were detected after different treatments in evaluating the regression of mice liver metastasis by sequential therapy. The detection of thymus index and IFN-γ concentrations in liver tissue of tumor-bearing mice model may indicate the stimulation of immune-active response by sequential therapy. Results The mean survival time of tumor-bearing mice treated with NDV7793 and 5-Fu sequentially was 32 d , which was significantly higher than those of tumor-bearing mice treated with NDV7793(30 d) or PBS injections (17 d), respectively (P< 0.05); The metastatic foci of tumor-bearing mice treated with NDV and 5-FU sequentially (30.60 ± 9.32) which was significantly less than those of tumor-bearing mice treated with PBS injection (273.30 ± 30.73), (P <0.05), seem quite similar to those treated with NDV (24.83 ± 6.90),(P > 0.05), and the liver weight was lighter than PBS (P < 0.05); Compared with NDV treatment, the decreased thymus index and increased amount of the effector IFN γ were observed in tumor-bearing mice treated with NDV 7793 and 5-FU sequentially (P <0.05). Conclusions The sequential therapy with Newcastle disease virus 7793 strain and 5-FU was observed to co-exert a significant suppressive effect in liver metastases of colon cancer cells in tumor-bearing mice model. Compared with NDV treatment , the survival time of mice model and the induction of antitumor effector molecules were significantly improved after sequential therapy.

Objective To evaluate the clinical value of ultrasonography guided percutaneous core needle biopsy in pancreatic lesions. Methods Thirty-four patients with 36 pancreatic lesions in Shanghai First People′s Hospital Afifliated to Shanghai Jiao Tong University from February 2012 to November 2013 underwent conventional ultrasound-guided percutaneous core needle biopsy using automatic gun and 18-gauge biopsy needles. The site, size, internal and surrounding vascularity, the sampling number of the lesions, and whether the specimens′ quality was satisfied were recorded. Then specimens were sent for pathological examination, and all above observations were compared with the ifnal diagnosis. Results The number of lesions with 2, 3 and 4 samplings was 32, 2 and 2, respectively. The average number of sampling was 2.2 (mean, 2.17;standard deviation, 0.51) and the acquisition rate of satisifed specimens was 89%(32/36). The pathological results of biopsy were malignant in 31 of 36 lesions including 27 cases of ductal adenocarcinoma, 2 cases of lymphoma, 1 case of small cell neuroendocrine carcinoma and 1 case of uterine leiomyosarcoma metastasis. The other 5 lesions were non-malignant including 3 cases of benign lesion, 1 cases of atypical hyperplasia and 1 cases of granulation tissue. The 36 lesions were ifnally diagnosed as 34 cases of pancreatic malignancy, 2 cases of non-malignant neoplasm. The sensitivity, speciifcity, accuracy, positive predictive value and negative predictive value of ultrasonography guided percutaneous core needle biopsy in pancreatic lesions were 91%(31/34), 100%(2/2), 92%(33/36), 100%(31/31) and 40%(2/5), respectively. Youden index was 0.91. Two patients had mild upper abdominal pain and 1 patient had transient elevated serum amylase. No pancreatitis, pancreatic fistula, peritonitis, bleeding or dispersion of malignant cells along the penetrating channel or other serious complications occurred. Conclusion Ultrasonography guided percutaneous core needle biopsy is a simple, rapid, safe and effective diagnostic method in pancreatic lesions with high clinical value.