(0.05)).And there were no side effects in two groups. CONCLUSION: The Yinqiao Tablet is effective and safety in treating wind-type common cold.

Objective:In order to explore the anti inflammatory mechanisms of ? melanocyte stimulating hormone (? MSH), the effects of ? MSH on the production of NO and proinflammatory cytokines in astrocytes induced by LPS were investigated Methods:Rat brain astrocytes cultured in vitro were stimulated with LPS or given ? MSH with LPS stimulation NO produced in astrocytes was tested with Griess reagent IL 1, IL 6 and TNF ? secreted from astrocytes were examined by MTT assay The expression of macrophage migration inhibitory factor (MIF) mRNA was examined with semiquantitative RT PCR analysis Results:The production of NO, IL 1, IL 6, TNF ? and the expression of MIF mRNA were significantly increased in astrocytes stimulated with LPS If giving ? MSH with LPS stimulation, the production of NO, IL 1, IL 6, TNF ? and the expression of MIF mRNA were markedly decreased Conclusion:[WT5”,6BZ]It is suggested that the inhibitory actions of ? MSH on the production of NO and proinflammatory cytokines in astrocytes are related to the inhibitory effects of ? MSH on inflammation in central nervous system

Objective To detect the expression of VEGF in NHL and analyze the relation of the expression levels with malignant aggressiveness,treatment response,and prognosis.Methods The expression of VEGF in lymph nodes taken from 39 NHL patients Wag measured by immunohistochemical-staining method.9 patients with benign lymphadenopathy were acted as control.Results The expression of VEGF in NHL(79.5%)was higher than that in the contrel(44.4%)(P=0.048＜0.05).In NHL,the VEGF level was higher in aggressive lympboma than that in indolent lymphoma(x2=5.284,P=0.044＜0.05).The patients had the higher-level expression as the Ann Arbor stage Wag higher,and the patients who had the higher-level expression of VEGF had higher serum LDH level,lower chemotherapy remission,unfavorable prognosis and lower 3-year survival (P＜0.05).Conclusion The expression of VEGF in NHL was increased.It was correlated with histopathological grade,Ann Arbor stage,chemotherapy response and prognosis.

Objective To investigate the effect of membrane-bound prostaglandin E2 synthase 1 (mPGES-1) inhibitor MK886 on cell cycle of the human acute myeloid leukemia HL-60/A cells.Methods Flow cytometry,Western blot and ELISA were used to measure the difference of cell cycle,expression of cyclin D1, mPGES-1 among HL-60/A cells,MNC and HL-60 cells.The effect of MK886 on cell cycle,cyclin D1,mPGES-1,PGE2,P-Akt and c-myc of HL-60/A cells were observed.Results Compared with MNC and HL-60 cells,the expression of cyclin D1 and mPGES-1 were higher in HL-60/A cells,the percentage of G0-G1 phase was decreased [MNC (62.63±6.58) ％,HL-60 (38.86±2.25) ％,HL-60/A (30.53±2.15) ％]and S phase increased[MNC (12.18±4.43) ％,HL-60 (47.70±1.88）％,HL-60/A (57.56±1.54) ％](all P＜ 0.05).After treated with MK886,cell cycle was arrested in G0-G1 phase.The expression of mPGES-1,cyclin D1,P-Akt and c-myc and synthesis of PGE2 were decreased.Conclusion MK886 can arrest HL-60/A cell cycles in G0-G1 phase,which possibly through down-regulation of mPGES-1/PGE2,reduction cyclin D1,P-Akt and c-myc expression.

Objectiye To investigate the effect of selective COX-2 inhibitor, nimesulide, on inhibiting proliferation of the human acute myeloid leukemia HL-60 cells. Methods HL-60 cells were treated with different concentration of nimesulide. HL-60 cell proliferation was examined by CCK-8 method. Flow cytometry, Western blotting and ELISA were used to measure the effect of nimesulide on apoptosis, cell cycle,COX-2, PGE2, bax, bcl-2 and c-myc. Results Nimesulide inhibited HL-60 cells proliferation in a dose and time dependence manner. Nimesulide induced cell apoptosis and arrested cell cycle in G0-G1 phase. The expression of COX-2 protein declined after treated with nimesulide 48 h, the total apoptosis in 100, 200,400 μmol/L nimesulide-treated group and control group were (24.97 ± 6.36) %, (34.22 ± 5.76) %, (44.59 ±6.69) % and (4.11 ± 1.26) %, there were significant differences (P ＜ 0.05). Nimesulide inhibited the synthesis of PGE2, the expressions of bcl-2 and c-myc protein and upregulated the expression of bax protein simultaneity.Conclusion Nimesulide significantly inhibited the proliferation of HL-60 cells and induced cell apoptosis,which may be associated with the downregulation of COX-2 expression, reduction of PGE2 synthesis, arrest of cell cycle and regulation bcl-2, c-myc and bax protein expression.

Objective To find out the cerebral blood flow velocity and its relationship with attention and execu?tion function in patients with major depressive episode. Methods A total of 70 patients with major depressive episode and 65 healthy controls were included. The 24 items Hamilton depression scale (HAMD-24) was adopted for patients' depressive symptoms assessment. The Cancellation Test (CT) and Wisconsin Card Sorting Test (WCST) were adopted for cognitive function assessment. And the blood flow velocity of cerebral arteries were detected by transcranial Doppler ul?trasonography (TCD). Results Compared with the controls, the patients showed significantly slower average blood flow ve?locity in basilar artery, left middle cerebral artery, right middle cerebral artery, left anterior cerebral artery and right ante?rior cerebral artery (P<0.05). Compared with those in the controls, the net score of each stage and the total net score of CT were significantly lower in the patients, while the total number of responses, response errors, perseverative errors and the necessary response number to complete the first category of WCST were significantly higher (P<0.01). The blood flow velocity in the cerebral basilar artery (r=0.25), left middle cerebral artery (r=0.46), right middle cerebral artery (r=0.25) and right posterior cerebral artery (r=0.26) showed positive correlations with total net score of CT (P<0.05), and the cere?bral artery average blood flow velocity showed negative correlations with the total number of responses, response errors and perseverative errors of WCST in the patients (P<0.05). Conclusions Compared with healthy controls, patients with major depressive episode suffer from lower average cerebral artery blood flow velocity, bad attention and executive func?tion. The change of average cerebral artery blood flow velocity may be responsible for impaired cognitive function in epi?sode major depression patients.

Objective Our preliminary study demonstrates that quercetin can inhibit the proliferation of HL-60 cells. This sudy aimed to find some drugs which could have synergistic effects with quercetin on apoptosis of HL-60 cells. Methods HL-60 cells were cultured with bortezomib at different concentrations (1, 2, 4, 8, 16, and 32μmol/L) alone or combined with quercetin at different concentrations for 48 h. HL-60 cells were cultured with lenalidomide at different concentrations (5, 10, 20, 40, 80, 160, and 320 μmol/L) alone or in combination with quercetin at different concentrations for 48 h. The CCK-8 assay was used to determine the effects on proliferation of HL-60 cells. Results Bortezomib significantly inhibited the proliferation of HL-60 cells (P<0.01). IC50 of quercetin was 49.24μmol/L after cells treated by quercetin combined with bortezomib, which was 13.44μmol/L lower than that treated by quercetin alone. Isobolographic analysis revealed the two drugs had synergistic effect. The results of cell viability of HL-60 cells treated by lenalidomide at lower concentrations (5, 10, 20, 40, and 80μmol/L)were not different from those of the control group (P > 0.05). The results of cell viability of HL-60 cells treated by lenalidomide at higher concentrations (160 and 320μmol/L) were lower than those of the control group (P<0.05). IC50 of quercetin after cells treated by quercetin combined with bortezomib was not different from that treated by quercetin alone. Isobolographic analysis revealed the two drugs had no synergistic effect. Conclusions Bortezomib can inhibit the proliferation of HL-60 cells and it has a synergistic effect with quercetin on HL-60 cells. Lenalidomide has a weaker role in inhibition of the proliferation of HL-60 cells, and it has no synergistic effect with quercetin on HL-60 cells.

Objective To explore the correlation of atheroselerosis progression and the expression of platelet derived endothelial nitric oxide synthase (eNOS) in rabbits. Methods A total of 24 male New Zealand white rabbits were used in this study. Six of the animals were fed with normal food (control group). Eighteen rabbits were fed with cholesterol-rich food (1 g/d) for 12 weeks to establish the atherosclerosis model. Among 18 models, 6 rabbits were executed immediately and their aorta and platelet samples were collected for further analysis (model group), 6 rabbits were orally administered with pravastatin (10 rag/d) for additional 12 weeks (treated group), and the remaining 6 rabbits were left untreated until the end of the study (untreated group). The control, treated and untreated animals were then killed, and the aorta and platelet samples were collected for eNOS expression analysis (RT-PCR). Results The aorta samples in model and untreated group exhibited rough intima and a lot of longitudinal fatty streaks, which indicated that atherosclerosis models were established successfully. While in treated group, the degree of atherosclerosis was decreased. The average percent of thickness of fatty streaks or atheroselerotic plaques relative to the whole thickness of vessel walls was 0. 04±0. 02, 0. 82±0. 16, 0. 33±0. 18,0. 77±0. 14 in control, model, treated and untreated group, respectively. The thickness of fatty streaks or atherosclerotic plaques was significantly increased in the model and untreated groups and decreased in treated group compared with the control group (both P<0. 05). The expressions of platelet derived eNOS/mRNA were 1. 02± 0. 28, 0. 41± 0. 27, 1.00 ± 0. 77, 0. 40±0. 29 in control, model, treated and untreated group, respectively. The expression of eNOS/mRNA was markedly decreased in model group and untreated group compared with the control group, but was increased in treated group compared with untreated and model groups (F=3. 544, P = 0. 024). Conclusions There is a negative correlation between eNOS expression and atherosclerosis development, which suggests that the reversal effect of pravastatin on atheroselerosis progression and plaque formation may relate to the expression of platelet derived eNOS.

OBJECTIVETo analyze the phenotypes and proline-rich transmenbrane protein 2 (PRRT2) gene mutations in patients of infantile convulsions with paroxysmal choreoathetosis (ICCA).

METHODSClinical data were collected from ICCA patients and their family members. Genomic DNA was extracted from peripheral blood samples with standard protocol. Mutations of PRRT2 were screened using PCR amplification and Sanger sequencing.

RESULTSEleven families and one sporadic case with ICCA were recruited in this study. In 11 ICCA families, 49 family members were affected, of which 15 individuals had benign infantile convulsions (BIC) alone, 18 individuals had only paroxysmal kinesigenic dyskinesia(PKD), and 16 individuals had BIC followed by PKD. The seizure onset age of infantile convulsions was between 3 and 12 months. The onset age of PKD was ranging from 5 to 17 years old. Four affected members in two ICCA families had PKD or ICCA co-existing with migraine. The one sporadic ICCA case had afebrile seizures between 3.5 and 4 months, and developed paroxysmal twists of limbs after 3 years and 9 months of age. He had good response to treatment with oxcarbazepine at the age of 4 years and 10 months. PRRT2 mutations were identified in all 11 ICCA families. The most common mutation, c.649_650insC (p.R217PfsX8), was detected in 6 of the 11 families (54.5%). PRRT2 mutation (c.649_650insC) was also found in the sporadic ICCA case, and was identified as de novo mutation.

CONCLUSIONThe phenotype of PKD in ICCA families occurred in childhood or adolescence. Few affected members in some ICCA families may have migraine. PRRT2 is the causative gene of ICCA and the mutation c.649_650insC was the hotspot of PRRT2 mutations. PRRT2 mutation was also found in sporadic case with ICCA.

Adolescent ; Adult ; Age of Onset ; Aged ; Aged, 80 and over ; Base Sequence ; Child ; Child, Preschool ; Dyskinesias ; genetics ; Epilepsy, Benign Neonatal ; genetics ; Female ; Humans ; Infant ; Male ; Membrane Proteins ; genetics ; Middle Aged ; Molecular Sequence Data ; Nerve Tissue Proteins ; genetics ; Pedigree ; Phenotype ; Point Mutation ; Seizures ; genetics ; Young Adult

OBJECTIVETo study the phenotypes and proline-rich transmembrane protein 2 (PRRT2) mutations in families with benign familial infantile epilepsy (BFIE).

METHODData of all BFIE probands and their family members were collected from Peking University First Hospital between September 2006 and August 2013. Clinical phenotypes of affected members were analyzed. Genomic DNA was extracted from peripheral blood samples with standard protocol. Mutations in PRRT2 were screened using PCR amplification and Sanger sequencing.

RESULTTwenty-nine BFIE families were recruited in this study. In total, 110 family members were affected. The age of seizure onset of these affected members was between 2 and 12 months (median: 4.5 months). All probands presented with clusters of seizures. Two probands had one seizure induced by diarrhea respectively at 25 months and 31 months. In four BFIE families, four family members had a history of febrile seizures. PRRT2 mutations were found in 17 of the 29 (58.6%) BFIE families. Mutation c.649_650insC was detected in 12 of the 17 families with PRRT2 mutations. Mutation c.649delC (p.R217EfsX12) was identified in three families. Mutation c.323_324delCA (p. T108SfsX25) and c.904_ 905insG (p. D302GfsX39) were detected in one family, respectively.

CONCLUSIONThe minimum seizure onset age of affected members in BFIE families was 2 months of age. The seizures often occur in clusters. PRRT2 is the major causative gene of BFIE in Chinese families. Mutation c.649_650insC is the hotspot mutation of PRRT2. A novel mutation c.323_324delCA was first reported in BFIE family. Few affected members with PRRT2 mutation presented with febrile seizures phenotype.

Age of Onset ; Asian Continental Ancestry Group ; genetics ; DNA Mutational Analysis ; Epilepsy, Benign Neonatal ; genetics ; Humans ; Infant ; Membrane Proteins ; genetics ; Mutation ; genetics ; Nerve Tissue Proteins ; genetics ; Phenotype ; Seizures ; Seizures, Febrile