Objective To evaluate the therapeutic efficacy of atomoxetine hydrochloride for attention deficit hyperactivity disorder (ADHID) combined with Tourette syndrome (TS).Methods Twenty-six cases of children with ADHD combined with TS were firstly diagnosed American Psychiatric Association Diagnostic and Statistical Manual of Mental Disorders fourth edition (DSM-Ⅳ) of ADHD and TS were treated with atomoxetine.The symptoms were improved and conditions were assessed based on the fourth version of ADHD parent rating scale and the severity of Yale comprehensive pumping quantity during pre-treatment,the 2nd,4th,6th and the 8 week of therapeutic courses,respectively.The adverse reaction was observed.Results 1.Compared with pre-treatment,attention deficit scores after treatment were statistically different (t =8.41,9.97,all P ＜ 0.05) in the 6th,8th week of therapeutic courses;hyperactivity /imnpulsivity scores were statistically different (Z =-4.39,-4.47,-4.46,all P ＜0.05) in the 4th,6th,8th week; Motor tics scores were statistically different (t =18.30,18.67,20.32,all P ＜ 0.05) in the 4th,6th,8th week; The vocal tic score:the second weeks already had statistically different(t =5.45,P ＜ 0.05); And the impaired function score were statistical significance (Z =-3.95,-3.94,all P ＜ 0.05) at the 6th and 8th week.2.The effective rate of ADHD and TS was 7.69％ and 15.38％,respectively in the 2td week.The curative effect had no statistical significance (x2 =0.188,P ＞0.05).But at the tourth week of assessment,and the rates of curative effect were respectively 19.23％ and 46.15 ％.It had statistical significance (x2 =3.923,P ＜ 0.05).In the 6th,8th weeks,there was no significant difference between the 2 efficiency (x2 =0.083,0.103,all P ＞0.05).3.During the treatment,no severe adverse reaction had appeared.Conclusions Atomoxetine in ADHD comorbid TS had exact curative effect and no obvious adverse reactions.In the treatment of ADHD,hyperactivity / impulsivity effect is better than the attention deficit.In the treatment of TS,vocal tics onset is better than the motor tics.In comparison of ADHD with TS,TS symptoms improve faster than ADHD in the onset,but the final effect is quite.

ObjectiveTo investigate the diagnostic value of interferon gamma release assays (IGRAs) in children with tuberculous meningitis.MethodsThe prospective case-control study was applied. From January 2012 to March 2013, 32 children diagnosed with tuberculous meningitis (TBM group) and 30 children diagnosed with non-tuberculous meningitis (non-TBM group) were recruited. The positive rates of the interferon gamma release assays (IGRAs), tuberculin skin test (TST), mycobacterium tuberculosis antibody test (TB-IgG), cerebrospinal lfuid of mycobacterium tuberculosis DNA test (TB-DNA), and the sensitivity, speciifcity, negative and positive predictive value of all these tests were compared between TBM group and non-TBM group.Results The positive rate of IGRAs, TST, TB-IgG, and TB-DNA was 87.50%, 56.25%, 46.88% and 34.38%respectively in TBM group, and 6.67%, 23.33%, 20% and 0% respectively in non-TBM group. The differences were statistically signiifcant (P<0.05). The sensitivity of IGRAs, TST, TB-IgG, and TB-DNA was 87.5%, 56.25%, 6.88% and 34.38% respectively. The speciifcity of IGRAs, TST, TB-IgG, and TB-DNA was 93.33%, 76.67%, 80.00% and 100% respectively. The differences of sensitivity and speciifcity were statistically signiifcant (P<0.05). The sensitivity of IGRAs was higher than that of other tests (P<0.017). The positive predictive value of IGRAs, TST, TB-IgG, and TB-DNA was 93.33%, 72%, 71.43% and 100% respec-tively. The negative predictive value was 87.50%, 62.16%, 58.54% and 58.82% respectively.Conclusions IGRAs, TST, TB-IgG, and TB-DNA are valuable in the diagnosis of tuberculous meningitis. IGRAs has a relatively higher sensitivity and speciifcity.

Objective: To evaluate the effects and partly mechanism of Qileng decoction(QLD,芪棱汤) resisting focal cerebral ischemia/reperfusion(I/R) injury in rats by apoptosis and signal transduction pathway.Methods: The rats were randomly divided into three groups including sham operation group,normal saline(NS) control group and QLD group.The model of focal cerebral I/R injury was induced by using modified thread embolizing in rats.Rats were evaluated by neurologic function score at 2 hours after ischemia and 2,4,6,12,24 and 48 hours after cerebral reperfusion,and the pathological changes of nerve cells and mitochondria ultrastructure at pallium and hippocampus CA1 region were observed at 24 hours after reperfusion.Immunohistochemical method was performed to examine the expression of cytochrome C(cyt C) and caspase-9 at different time points after reperfusion.Apoptosis of nerve cells in ischemic penumbra(IP) was also characterized by terminal deoxynucleotidyl-transferase mediated dUTP-biotin nick end labeling(TUNEL) method.Results: Compared with NS control group,neurologic function scores at different reperfusion time points were improved and the pathological changes were ameliorated at 24 hours after cerebral I/R in QLD group.Mitochondria hydropsia was alleviated,mitochondrial cristae fragmentation and granulum basale shedding were diminished,and mitochondrial basical morphology was retained.Meanwhile,apoptosis index(AI) was decreased and the expressions of cyt C and caspase-9 were reduced in IP in QLD group.Conclusion: QLD intervenes in mitochondria mediated and caspase-9 dependent apoptopic pathway.QLD lowers AI and plays a role of protecting nerve by maintaining mitochondrial basical form,stabilizing mitochondrial membrane and inhibiting the release of cyt C and activation of caspase-9.The above actions are possibly some parts of mechanisms of QLD resisting focal cerebral I/R injury.

Objective:To screen the ectodysplasin A (EDA)gene mutation in the patients with non-syndromic tooth agenesis and ectodermal dysplasia,and to analyze the phenotype of missing teeth pattern in these two groups of patients.Methods:In the study,174 patients with tooth agenesis (143:non-syn-dromic,31:ectodermal dysplasia)and 451 health control volunteers were enrolled from the clinic,and the genome DNA was extracted from either peripheral blood or oral mucosal swab.The coding region of EDA gene was then amplified by PCR,sequenced and blasted to online NCBI database.The missing teeth were recorded for all patients,and the missing teeth from patients with EDA mutation were com-pared among the different dentition sites.Results:33 patients were identified with EDA mutation.In the non-syndromic patients,13 /143(9.09%)were identified with EDA mutation,while in patients with ec-todermal dysplasia,20 /31 (64.52%)were found with EDA mutation.Ten novel EDA mutations were identified (c.769G >C[p.G257R],c.936C >G[p.I312M],c.223G >A[p.E75K],c.1166C >T[p. P389L],c.133G >C[p.G45R],c.1109G >A[p.E370K],c.914G >T[p.S305I],c.916C >T[p. Q306X],c.602G >T[p.G201V],c.88 -89insG[p.A30GfsX69]).For each dentition site there was no statistic difference in the number of missing teeth between the left and right sides,so the number from both sides were combined later in the analysis.In the patients with EDA mutation,the non-syndromic pa-tients had fewer missing teeth (15.9 ±6.4 missing teeth for each,207 /364 in total)than the patients with ectodermal dysplasia (23.9 ±4.3,478 /560).In the non-syndromic patients with EDA mutation, the maxillay central incisors and first molars were less affected,with the same missing rate as 19.2% (5 /26).While the mandibular central incisors (with a missing rate of 76.9%,20 /26),the maxillary late-ral incisors (the missing rate:88.5%,23 /26 ),the mandibular lateral incisors (the missing rate:80.8%,21 /26),and the maxillary first premolars (the missing rate:80.8%,21 /26)were more likely to be missing.In the ectodermal dysplasia patients with EDA mutation,only maxillary central incisors (the missing rate:60%,24 /40),maxillary canines (the missing rate:70%,28 /40),mandibular ca-nines (the missing rate:67.5%,27 /40),maxillary first molars (the missing rate:65%,26 /40)and mandibular first molars (the missing rate:72.5%,29 /40)had higher possibility of persistence.Teeth at other dentition sites were more likely to be affected (the minimum missing rate:87.5%,35 /40). Conclusion:The findings would help to reveal the EDA gene and its function in ectodermal organogene-sis.

Objectlve To investigate the inhibition of Coxsackievirus B3(CVB3)infection in cardiac myocytes cultured by small interfering RNA(siRNA)-mediated RNA interference and to evaluate the feasibility of siRNA as the prophylaxis and therapy for CVB3 infection.Methods Cardiac myocytes were prepared in vitro and infected with CVB3,and transfected with siRNA by lipofectamin and electroporation.The numbers of beating cardiac myocytes were counted under the microscope.Neutral red staining was used to evaluate the mortality of cardiac myocytes.Antiviral activities of these siRNAs were estimated by observing cytopathic effect(CPE),plaque reduction assay,Western blot assay and RT-PCR.Results siRNA-3753,which aimed at sequence in 2B section of CVB3 genome,displayed a stronger inhibition of CVB3 infection through screening in HeLa cells,siRNA-3753,chosen to transfect cultured neonatal mice cardiac myocytes,Wag observed to keep a good states of growing and beating at 24 h after CVB3 infection.Whereas the cytopathic signature of controlled cells became stopping beating,round and finally the cell fell off the culture plate.The results showed that siRNA-3753 could protect cells significantly,98.1%inhibition of CVB3 replication with electroporation transfection and 78.2%inhibition of CVB3 with liposome transfection.Transfection efficiencies were 56.0 3%and 9.0%by electroporation and lipofectamin,respectively.Conclusion siRNA,which aims at sequence in 2B section of CVB3 genome,can inhibit CVB3 infection in cultured cardiac myocytes.

Epilepsy is one of the most common chronic neurological diseases, which results from diverse etiologies, and its mechanism is very complicated.Ion channel gene mutation is a common genetic cause of epilepsy.Voltage-gated chloride channels (ClCs) can change the chloride ion concentration and electric potential difference across the plasma membrane, and thereby regulate the electrical excitability of neurons.CLCN-1, CLCN-2, CLCN-3, CLCN-4 and CLCN-6 are reported to be associated with epilepsy, which could increase susceptibility to epilepsy or cause seizures.This review is focused on recent advances in ClCs and epilepsy.

Objective K93T point mutation exists in the quinoid dihydropteridine reductase ( QDPR) of OLEFT rats which catalyzes QDPR into tetrahydrobinopterin(BH4), while dihydrofolate reductase(DHFR) can reduce QDPR to BH4, which implies crosstalk between hydrobiopterin and folate metabolism.By investigating the influence of QDPR expression on DHFR expression of NRK-52E cells, the article aimed to find out the possible underlying mechanism of QDPR gene in diabetic nephropathy ( DN). Methods Western blot was performed to identify the expression level in NRK-52E cell under high glucose ambience and DHFR pro-tein expression of OLETF rats.NRK-52E cells were transfected by the lentivirus to establish no-load overexpression, overexpressed QDPR and knockdown QDPR models.Each group was given 5.4 mmol/L normal sugar medium and 30mmol/L in high glucose ambi-ence for 72 hours'cell cultivation to simulate DN model.Observation was made on the influence of QDPR gene expression levels on DHFR in high glucose ambience. Results The western blot analysis revealed that DHFR protein decreased in NHG group( [0.33 ± 0.16] vs [0.64 ±0.5], P<0.05) and OLETF rats cortex ([0.56 ±0.16] vs [1.03 ±0.12], P<0.01).In high glucose ambi-ence, compared with LV-OCON-HG group, the protein expression of DHFR was significantly decreased in LV-QDPR-HG group ([0.12 ±0.09] vs [0.63 ±0.08], P<0.01).No difference was found in the comparison of DHFR expression levels between LV-SHQDPR-HG and LV-SHCON-HG group. Conclusion DHFR protein expression decreases in NRK-52E cells of high glucose and LOLETF rat model, which suggests that DHFR protein plays an important role in the development of DN.QDPR overexpression leads to the decreased expression of DHFR, which implies that overexpressed QDPR influences the occurrence and process of DN by down-regulating DHFR expression level.

OBJECTIVETo study the effect of chronic intermittent hypoxia-induced inflammatory cytokines and reoxygenation on glucose transporter 4 (GLUT-4) expression in rat skeletal muscles.

METHODSTwenty-four male Sprague-Dawley rats were randomly assigned to blank control group, chronic intermittent hypoxia (CIH) group, and reoxygenation group. At the end of the experiment, fasting blood glucose (FBG), fasting blood insulin (FINS) and serum inflammatory cytokine levels were measured with glucose oxidase-peroxidase, insulin radioimmunoassay and ELISA, respectively. Homeostasis model assessment (IRI) was used to evaluate insulin resistance in the rats, and GLUT-4 protein expression in the skeletal muscles was measured with Western blotting.

RESULTSCompared with the blank control group, CIH resulted in significantly increased fasting blood glucose, blood insulin levels and insulin resistance index (IRI) (P<0.05); fasting blood glucose was significantly elevated in reoxygenation group (P<0.05). Inflammatory cytokines levels (IL-6 and TNF-α) were significantly higher in CIH group than in the blank control and reoxygenation groups (P<0.05), and were higher in reoxygenation group than in the blank control group. GLUT-4 expression in the skeletal muscles was significantly reduced after CIH (P<0.05) but increased after subsequent reoxygenation (P<0.05).

CONCLUSIONCIH can cause increased release of inflammatory cytokines to lower GLUT-4 protein expression in the skeletal muscles, which contributes to insulin resistance in adult rats.

Animals ; Blood Glucose ; Glucose Transporter Type 4 ; metabolism ; Hypoxia ; Insulin ; blood ; Insulin Resistance ; Interleukin-6 ; Male ; Muscle, Skeletal ; metabolism ; Rats ; Rats, Sprague-Dawley ; Tumor Necrosis Factor-alpha ; blood

Objective To discuss the expression and clinical significance of microRNA(miR)- 766 in chil-dren with polyarticular juvenile idiopathic arthritis (poly - JIA). Methods A total of 23 children with poly - JIA who received treatment at the Department of Rheumatology,the Affiliated Children′s Hospital of Capital Institute of Pediat-rics,from November 2014 to September 2016,were enrolled as research group,and 24 healthy children at the same age were selected as healthy control group,while 24 children with oligoarticular juvenile idiopathic arthritis (oligo - JIA) and 19 children with juvenile ankylosing spondylitis (JAS)were selected as case - control groups. The expression lev-els of miR - 766 in plasmas were detected by real - time quantitative polymerase chain reaction (qPCR). The clinical diagnostic values were analyzed by operating characteristic curve (ROC). Correlations between the expression levels of miR - 766 and clinical,laboratory results were analyzed by conducting Pearson correlation coefficient analysis. Results Compared with the healthy control group and case - control group,the expression levels of miR - 766 in poly - JIA group decreased,and the differences were statistically significant (t = 6. 897,6. 446,6. 218,all P < 0. 001). There was no statistical difference of miR - 766 levels in plasma between case - control groups and healthy control group (P >0. 05). Compared with the healthy control group,the area under ROC curve of miR - 766 was 0. 938 (95％ CI:0. 872 -1. 000),and when the cutoff value of miR - 766 was 6. 083 pmol/ L,the sensitivity was 87. 0％ and the specificity was 91. 7％ . Compared with oligo - JIA and JAS,the area under ROC curves of miR - 766 was 0. 908 (95％ CI:0. 819 -0. 996)and 0. 927 (95％ CI:0. 865 - 1. 000),respectively. Correlation analysis indicated that the level of miR - 766 in plasma of poly - JIA children was positively associated with hemoglobin (r = 0. 651,P < 0. 001),but negatively asso-ciated with the 28 - joint Disease Activity Score (DAS28)and the percentage of type 1 helper T cells(Th1％)(r =- 0. 434,P = 0. 038;r = - 0. 417,P = 0. 008). Conclusions The expression levels of plasma miR - 766 in poly - JIA are significantly decreasing. miR -766 may serve as an evaluation indicator for the diagnosis and prognosis of poly - JIA.

Objective:To investigate the proportion of helper T lymphocytes 22(Th22) and levels of interleukin(IL)-22 in peripheral blood of children with juvenile idiopathic arthritis (JIA), and analyze their relevance with JIA-related inflammatory cytokines.Methods:A total of 30 children with JIA who received treatment at the Department of Rheumatology, the Affiliated Children′s of Capital Institute of Pediatrics from November 2018 to December 2019 were enrolled as JIA group, and 12 healthy children at the same age were selected as healthy control group.The percen-tage of Th22 cells in peripheral blood was detected using flow cytometry.Concentrations of IL-22, IL-6, tumor necrosis factor(TNF-α), IL-17 and IL-10 were measured by enzyme-linked immunosorbent assay.Statistical analysis of the relevance of Th22 cells, IL-22 levels and inflammatory cytokines levels of IL-6, TNF-α, IL-17 and IL-10 in JIA were performed by Pearson test. Results:The proportion of Th22 cells in peripheral blood of patients in JIA group[(0.94±0.26)%] was higher than that of the healthy control group [(0.46±0.29)%], and the difference was statistically significant ( t=2.227, P<0.05). Plasma level of IL-22 of patients in JIA group[(185.2±11.93) ng/L] was significantly higher than that of healthy control group[(114.7±6.29) ng/L], and the difference was statistically significant ( t=3.632, P<0.001). The proportion of Th22 cells and the levels of plasma IL-22 in JIA patients were positively correlated with plasma levels of IL-6 (Th22: r=0.501, IL-22: r=0.573, all P<0.01), IL-17 (Th22: r=0.686, P<0.001; IL-22: r=0.445, P<0.01) and IL-10 (Th22: r=0.609, IL-22: r=0.284, all P<0.001). There was no relationship for Th22 cells and plasma levels of IL-22 with TNF-α. Conclusions:The proportion of Th22 cells and plasma levels of IL-22 significantly increase in peripheral blood of JIA patients and correlated with JIA-related inflammatory cytokines, which may play a potential role in the pathogenesis of JIA disease.