[Related factors of acute symptomatic seizures and epilepsy in children with myelin oligodendrocyte glycoprotein antibody-associated disease].

Objective: To investigate the risk factors of acute symptomatic seizures (ASS) and epilepsy in children with myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD). Methods: A ambispective cohort study was used including 74 children with MOGAD who were admitted to the Department of Pediatrics of Peking University First Hospital from January 2013 to June 2023 and were followed up. Demographic information, clinical information, treatment status, ASS and epilepsy status were collected. The clinical phenotypes were classified. According to the presence or absence of ASS in the course of disease, the children and the course of disease were divided into groups with and without ASS. Chi-square test, Fisher exact test and Mann Whitney U test were used to analyze the correlation between symptoms and auxiliary examination characteristics and the occurrence of ASS in the two groups of children. Multivariate Logistic regression analysis was used for multivariate analysis. Results: The onset age of the 74 children with MOGAD was 6.58 (3.80, 9.67) years, including 38 females (51.4%) and 36 males (48.6%). The duration of the final follow-up was 2.67 (1.10, 4.12) years, with a total of 239 times acute clinical episodes. ASS occurred in 39.2% (29/74) children during the course of disease and in 29.3% (70/239) of attacks. The common phenotypes were ADEM (67 times (28.0%)), optic neuritis (37 times (15.4%)) and cerebral cortical encephalitis (31 times (13.0%)) in 239 times acute clinical episodes. The incidence of ASS in ADEM and cerebral cortical encephalitis phenotype was 28.4%(19/67) and 100.0% (31/31), respectively. Multivariate analysis showed that cortical involvement on magnetic resonance imaging during clinical attacks was an independent risk factor for ASS (ß=-1.49, OR=0.23) after excluding attacks involving only optic nerve or spinal cord (49 episodes). During the follow-up, 5 children (6.8%) had epilepsy, and all children with epilepsy had multiple clinical attacks of MOGAD and previous ASS. Conclusions: Cortical involvement on magnetic resonance imaging during clinical episodes is an independent risk factor for ASS in children with MOGAD. All MOGAD children with epilepsy had ASS and multiple MOGAD clinical episodes in the past.

[Clinical follow-up study of myelin oligodendrocyte glycoprotein antibody-associated disease in children].

Objective: To summarize the clinical characteristics of myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) and compare the differences in efficacy of different disease-modifying drugs. Methods: An ambispective cohort study was conducted in 42 children diagnosed with MOGAD at Department of Pediatrics, Peking University First Hospital from January 2012 to March 2021 and conducted long-term follow-up to analyze clinical phenotypes and compare the efficacy of different disease-modifying drugs such as rituximab, mycophenolate mofetil and azathioprine. Kruskal-Wallis H test was used to compare the annual relapse rate of disease-modifying drugs at different times, expanded disability status scale (EDSS) score at the last follow-up, and Wilcoxon rank test was used to compare the annual relapse rate before and after modified disease therapy. The Log-rank (Mantel-Cox) survival curve was used to compare the relapse rate of different disease-modifying drugs. Results: Of the 42 cases, 22 were male and 20 were female, with the age at disease onset of 5.96 (2.33-12.90) years. The disease duration was 4.46 (1.25-13.00) years at the last follow-up with 161 clinical acute attacks. Acute disseminated encephalomyelitis (ADEM) was the most common phenotype of first attack and all attacks during disease course ((60% (25/42) for first attack, 38% (61/161) for all attacks). The most common clinical syndrome was neuromyelitis optica spectrum disorders (NMOSD) (50%, 21/42). Of the 42 children, 5 (12%) showed encephalitis and 6 (14%) combined with anti-N-methyl-D-aspartate receptor (NMDAR) antibody overlap syndrome. The most commonly involved areas of brain magnetic resonance imaging (MRI) were subcortical white matter (71%, 88/124), cortex (26%, 32/124) and periventricular white matter (25%, 32/124). Spinal cord MRI was most frequently involved in cervical (70%, 16/23) and thoracic (61%, 14/23) medulla, and 43% (10/23) longitudinally extensive transeverse myelitis. Disease-modifying drugs were used in 34 patients. The annual relapse rate after treatment with rituximab, mycophenolate mofetil and azathioprine decreased (all P<0.05) and there was no statistically significant difference in the annual relapse proportion among the groups (P=0.307). Conclusions: The most common clinical attack of first and all of MOGAD in children is ADEM, and the most common clinical syndrome is NMOSD. Rituximab, mycophenolate mofetil and azathioprine can reduce the annual relapse rate, but it is not clear effect of which treatment is better.

LINC01503 promotes cell proliferation, invasion and EMT process in cholangio-carcinoma.

OBJECTIVE: This work aimed to analyze the relative expression level of long intergenic non-protein coding ribonucleic acid 1503 (LINC01503) in cholangiocarcinoma tissues and cells, and to explore the effects of LINC01503 on cell proliferation, migration and invasion. PATIENTS AND METHODS: Logarithmic growth phase cholangiocarcinoma cells were selected and transfected with Lipofectamine 2000 (si-LINC01503, si-NC). The expression of LINC01503 was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The proliferation of cells was observed by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT) assay. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay was used to detect cell apoptosis. Transwell assay was used to observe the cell migration and invasion ability. RESULTS: The expression of LINC01503 was significantly increased in cholangiocarcinoma tissues compared with adjacent tissues (p<0.05), and the up-regulated expression of LINC01503 was associated with lymph node metastasis. Compared with normal bile duct cells (HIBEC), cholangiocarcinoma cells (RBE, QBC939) have higher expression of LINC01503, and si-LINC01503 transfection can effectively reduce the proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) of cholangiocarcinoma cells. CONCLUSIONS: LINC01503 is highly expressed in cholangiocarcinoma and can effectively promote the proliferation, migration, invasion and EMT process of cancer cells, and LINC01503 is expected to be a potential biomarker for cholangiocarcinoma.

Association between the CYP1A1 polymorphisms and hepatocellular carcinoma: a meta-analysis.

Numerous studies have evaluated the association between CYP1A1 gene polymorphisms and hepatocellular carcinoma (HCC) risk. However, the specific association is still controversial. The aim of our study was to clarify the effects of CYP1A1 gene polymorphisms (3801 T＞C and A2455G) on HCC risk by conducting a meta-analysis. We conducted searches of the literature published in PubMed and EMBASE databases up to April 2014. We estimated the pooled odds ratio with its 95% confidence interval to assess the association using a fixed or random-effects model. Publication bias was investigated by the Begg funnel plot. Meta-analysis was performed using the STATA package version 12.0. Meta-analysis results showed no significant association between the CYP1A1 3801 T＞C polymorphism and HCC risk. In a subgroup analysis by nationality, we found a significant association between 3801 T＞C polymorphism and HCC risk in Asians (TT vs TC: OR = 0.77, 95%CI = 0.60-0.99). As for A2455G, the meta-analysis indicated no significant association between the CYP1A1 A2455G polymorphism and HCC risk. In conclusion, the 3801 T＞C polymorphism in the CYP1A1 gene may be related to increased risk of HCC in Asians. Conclusive evidence on the effects of the variants in HCC should be addressed in further studies.

Determination of trace europium based on new fluorimetric system of europium(III) with thenoyltrifluoroacetone and N,N'-dinaphthyl-N,N'-diphenyl-3,6-dioxaoctanediamide.

In the present paper, N,N'-dinaphthyl-N,N'-diphenyl-3,6-dioxaoctanediamide acts as a specific reagent for enhancing the fluorescence intensity of Eu(III) complex with thenoyl trifluoroacetone (TTA), the spectrofluorimetric determination of trace amounts of Eu(III) based on the above system was carried out and its luminescence mechanism was studied. The excitation and emission wavelengths are 343.6 and 613.3 nm, respectively. The fluorescence intensities vary linearly with the concentration of europium(III) in the range 3.647x10(-3)-3.039 mug ml(-1) for the original fluorescence with a detection limit down to 2.279x10(-4) mug ml(-1) and the standard deviation is 0.063 mug ml(-1) for 10 times measurements, and in the range 7.598x10(-4)-0.0243 mug ml(-1) (SD=0.035 for 15 times measurements), 0.06078-0.6100 mug ml(-1) (SD=0.52 for 10 times measurements) for the first derivative fluorescence signal with a detection limit down to 8.566x10(-5) mug ml(-1). The interferences of other rare earths and some of inorganic ions are described. This method is a direct, rapid, selective and sensitive analytical method for the determination of trivalent europium in rare earth ore samples and high purity of rare earth oxides.