Objective To investigate the effects of arsenic trioxide (ATO) on the expression of autoan-tibody and interleukin (IL)-10 IL-12 in MRL/lpr mice. Methods MRL/lpr mice wereseparated into 3 different groups. The 3 groups received arsenic trioxide (ATO, 0.4 mg·kg~(-1)·d~(-1)), cyclophosphamide (CTX,50 mg/kg) and sodium chloride (NS, volume weight-determined) abdominal injection respee-tively. The treatment stopped 2 months later. Afterwards, the rates of CD3~+(T) cells, CD3~+CD4~+(Th) cells and the CD3~+CD4~+cells which produced IL-10 and IL-12 were detected using single-cell measurement of intr-acellular eytokines by flow cytometry after polyclonal stimulation with PMA and ionomycin for 4 hours in 5% CO_(2.)Serum levels of IL 10 and IL-12 were assessed using the Mouse cytokines ELISA Kit. One-way ANOVA LSD test and paires t test were used for statistical analysis.Results ①The level of anti-dsDNA antibody after treatment was 0.92±0.06, while it was 1.14±0.58 before treatment. So the ds-DNA antibody level was significantly decreased in ATO group (P<0.01), while it was dramatically increased in the NS groups (P<0.05) after the treatment;②ATO group had significantly less CD3~+ cells and CD3~+CD4~+ cells[(44±4)% and (20±4)%]compared withNS group [(59±5)%and(30±3)%](P<0.01).③The serum level of IL-12 in the ATO group was (84±12) pg/ml,while it was (103±13)pg/ml in the NS group (P=0.018).④The intracellular levels of IL-10 and IL-12 produced by CD3~+CD4~+ (Th) cells in the ATO group were ( 1.5±0.4)% and (2.43±0.42)%, which was significantly lower than those in the NS group respectively (2.5±0.5)% and (3.24±0.40)%(P<0.01). Conclusion Arsenic trioxide can reduce the production of anti-dsDNA antibody,inhibit the activation and proliferation of both T cells and Th subsets in the MRLApr mice, and hence decrease the serum levels of IL-12 and the levels of IL-10, IL-12 produced by Th cells.

To investigate the effects of gensenoside Rg1 on expressions of phosphorylated tau protein (P-tau), protein phosphatase 2A (PP2A) and tau protein in Alzheimer's disease-like tau phosphorylation rat brain slices, and to explore the mechanisms of gensenoside Rg1 in inhibiting tau phosphorylation.

10.3969/j.issn.2095-4344.2013.25.019

To investigate the effects of Naoerkang (NEK), a compound traditional Chinese herbal medicine, on the expressions of beta-amyloid peptide 1-42 (Abeta(1-42)) and neprilysin (NEP) in hippocampal tissues in a rat model of Alzheimer's disease (AD).

Objective To explore the relationship between methylenetetra hydrofolate reduetase (MTHFR) C677T genotypo and unstable angina pectoris(UA) in Chinese population. Methods The study consisted of 90 UA cases (UA group), and an age- and sex- matched healthy control cases (control group, n = 90). PC R-RFLP was used to analyze polymorphism of the MTHFR C677T genotypo. The relationship between MTHFR C677T genotype and UA was observed. Results MTHFR 677C→T mutation was found in 30 of 90 patients with unstable angina pectoris (33.33%) and in 15 of 90 control subjects (16.67%). This difference was statistically significant (P<0.05). Conclusion MTHFR 677C→T mutation is closely related to the unstable angina poctoris.

Objective To explore the expression of the CENP-W in gliomas and investigate the effects of its invasion. Methods The expression level of the CENP-W in gliomas with varied pathologic grade were detected by immunohistochemical analysis,RealTime PCR,and Western Blotting. U251 cells were transfected with the specific siRNA to repress the CENP-W expression level. The invasion ability of U251 cells were examined by Transwell Chamber assay ,while RAS mRNA and protein levels were detected at the same time. Results The expression levels of the CENP-W in glioma tissues were significantly high and the CENP-W gene could enhance the invasion of U251 cells . The expression of RAS was down-regulated when the expression of CENP-W was repressed. Conclusion The CENP-W has an oncogenic role in human brain gliomas and may regulate the invasion of gliomas by adjusting the RAS signaling pathways.

AIM:To study the effect of centromere protein W ( CENP-W) down-regulation on human glioma U87 cells.METHODS:Small interfering RNA ( siRNA) was used to inhibit the expression of CENP-W in the U87 cells. The interference effect of siRNA was evaluated by RT-qPCR and Western blot .The proliferation of the cells was analyzed by MTT assay , BrdU staining and colony formation experiment .Transwell chamber assay was used to detect the invasion a-bility of the cells .The cell migration ability was measured by a scratch test .The changes of the cell cycle distribution and apoptosis were analyzed by flow cytometry .RESULTS:The results of MTT assay , colony formation experiment and BrdU staining showed that the cell proliferation and colony formation abilities in experimental group were significantly lower than those in control group and negative control group .The results of Transwell and scratch experiments showed that the migra-tion and invasion abilities in experimental group were weaker than those in blank control group and negative control group . The results of flow cytometry analysis showed that the cell cycle distribution in experimental group was arrested in G 0/G1 phase .The percentage of apoptotic cells in experimental group was higher than that in control group ( P<0.05 ) .CON-CLUSION:Down-regulation of CENP-W expression inhibits the proliferation , migration and invasion of human glioma cells and promotes the apoptosis of the cells , suggesting that CENP-W may be a potential target of gene therapy for human glioma.

Objective To investigate the metabolite changes in the preschool children with autism spectrum disorder (ASD) using MR spectroscopy (MRS) and explore the associations between image findings and clinical variables, which may provide a noninvasive brain biochemical method for the early diagnosis and prevention of autism. Methods Twenty one cases of preschool ASD children (3-6 years old) and age-and sex-matched 20 preschool healthy controls underwent single voxel short (SVS) short TE (TE=30 ms) MRS. The absolute metabolite concentrations in the anterior cingulate cortex (ACC) , anterior middle anterior cingulate cortex (aMCC) and posterior cingulate (PCC) were quantitatively analyzed using LCModel software. Two independent sample t tests were used for analysis. The relationships between metabolite concentrations and diagnostic and statistical manual of mental disorders (DSM-IV) , childhood autism rating scale (CARS) and autism behavior checklist (ABC) were analyzed by Pearson correlation analysis. Results Compared to control subjects, ASD patients had significantly lower N-acetylaspartate (NAA) values (4.35 ± 0.80, 6.34±0.82, 8.04±0.97 mmol/L respectively) in ACC, aMCC and PCC (t=2.640, P=0.012;t=2.182, P=0.035;t=3.343, P=0.002) , had significantly lower choline (Cho) 1.32±0.22 mmol/L (t=2.905, P=0.006) and glutamine and glutamate complex (Glx) 10.02 ± 0.88 mmol/L (t=2.090, P=0.043) in PCC. Cho, total creatine (tCr) , myo-Inositol (MI) and Glx levels did not differ between groups in other aforementioned regions (P>0.05). Negative correlations between the NAA ualues in the PCC and CARS (r=-0.504, P=0.020) were detected, and no significant correlation among DSM-IV, CARS, ABC and other metabolite values (P>0.05). Condnsions The biochemical changes in the preschool children with ASD in cingulate reflect the neuronal loss, structural or functional damage and cell membrane enzyme metabolic dysfunctions, may reveal the pathological basis of ASD. These results may provide noninvasive and quantitative methods for the diagnosis and prognosis evaluation of ASD child.

Gastric cancer is a malignant tumor with high morbidity and mortality, which is a serious threat to human life and health. At present, the diagnosis and course monitoring of gastric cancer mainly rely on gastroscopic biopsy and CT, but their invasiveness and delay limit their clinical value. Gastric cancer patients urgently need a real-time, accurate, non-invasive diagnosis and course monitoring method. Circulating tumor DNA(ctDNA) is single or double stranded DNA released into body fluid by tumor cells, which contains the same genetic mutations as the original tumor cells. It is also one of the newly emerged biological markers. With the emergence and development of next-generation sequencing(NGS) technology, the sensitivity and specificity of ctDNA detection continue to increase, and it is gradually becoming a new choice for tumor diagnosis and disease course monitoring. In this paper, the current application of the next-generation sequencing technology detecting ctDNA in diagnosis and treatment of gastric cancer was discussed.

Gastric cancer is a malignant tumor with high morbidity and mortality, which is a serious threat to human life and health. At present, the diagnosis and course monitoring of gastric cancer mainly rely on gastroscopic biopsy and CT, but their invasiveness and delay limit their clinical value. Gastric cancer patients urgently need a real-time, accurate, non-invasive diagnosis and course monitoring method. Circulating tumor DNA(ctDNA) is single or double stranded DNA released into body fluid by tumor cells, which contains the same genetic mutations as the original tumor cells. It is also one of the newly emerged biological markers. With the emergence and development of next-generation sequencing(NGS) technology, the sensitivity and specificity of ctDNA detection continue to increase, and it is gradually becoming a new choice for tumor diagnosis and disease course monitoring. In this paper, the current application of the next-generation sequencing technology detecting ctDNA in diagnosis and treatment of gastric cancer was discussed.