OBJECTIVE:To explore the effectiveness and safety of probucol combined with rosuvastatin in the treatment of vascu-lar dementia(VD). METHODS:In retrospective study,clinical information of 88 VD patients selected from neurology department of our hospital during May 2013-Feb. 2015 were divided into observation group and control group according to therapy plan,with 44 cas-es in each group. Both groups received conventional treatments such as controlling blood pressure and blood glucose,anticoagulation. Control group was additionally given Rosuvastatin calcium tablets orally 20 mg,at bedtime;observation group was additionally given Probucol tablet 0.5 g,bid,after meal,on the basis of control group. Both groups received treatment for consecutive 3 months. MMSE and ADL score were compared between 2 groups before and after treatment as well as the levels of TC,TG,LDL-C,HDL-C,CRP, TNF-α,IL-6,IL-1β,SOD and MDA. The occurrence of ADR was also observed. RESULTS:Before treatment,there was no statisti-cal significance in above indexes between 2 groups(P>0.05). Compared to before treatment,MMSE and ALD score,serum SOD lev-el of 2 groups were increased significantly,while serum levels of TC,TG,LDL-C,CRP,TNF-α,IL-6,IL-1βand MDA were de-creased significantly after treatment,with statistical significance(P<0.05). Above indexes of observation group were significantly bet-ter than those of control group,with statistical significance(P<0.05). There was no statistical significance in HDL-C level between 2 groups before and after treatment (P>0.05). There was no statistical significance in the incidence of ADR between 2 groups(P>0.05).CONCLUSIONS:Probucol combined with rosuvastatin is better than rosuvastatin alone in reducing blood lipid,serum inflamma-tory factors and oxidant stress indexes levels,improving cognitive function and quality of life with good safety.

Adolescent ; Biopsy, Fine-Needle ; Chromosomes, Human, Pair 18 ; Female ; Humans ; In Situ Hybridization, Fluorescence ; Oncogene Proteins, Fusion ; genetics ; Proto-Oncogene Proteins c-bcl-2 ; metabolism ; Sarcoma, Synovial ; genetics ; metabolism ; pathology ; Soft Tissue Neoplasms ; genetics ; metabolism ; pathology ; Translocation, Genetic ; Vimentin ; metabolism

Cardiomyopathies ; congenital ; Heart Ventricles ; pathology ; Humans ; Infant, Newborn ; Male ; Myocardium ; pathology

Adolescent ; Child ; Child, Preschool ; Female ; Humans ; Infant ; Isocitrate Dehydrogenase ; genetics ; Leukemia, Myeloid, Acute ; genetics ; Male ; Mutation ; Nuclear Proteins ; genetics ; Prognosis ; Treatment Outcome

Objective To study the influence of quedcetin on the collagen synthesis of cultured fibroblasts and to explore the mechanism.Methods The inhibitory effect of quercetin and radiation on fibroblast proliferation was assayed using MTT assay.Collagen synthesis was detected by hydroxyproline colorimetric analysis.Immunocytochemical staining method was used to investigate the expression of collagen Ⅰ and Ⅲ.The mRNA expression of typeⅠ,type Ⅲ collagens and TGF?-1 were assayed by reverse transcriptionpolymerase chain reaction(RT-PCR) and real-time PCR technique.Results Keloid fibroblast cell proliferation and collagen synthesis of fibroblasts were inhibited by quercetin in a dose-dependent manner.Significant inhibition was observed by the treatment with quercetin and radiation together.Immunocytochemical staining indicated the IOD of type I and Ⅲ collagen protein was down-regulated by quercetin and radiation.Both collagen Ⅰ and collagen Ⅲ gene in the quercetin groups showed a significantly decreased mRNA expression compared with that in the untreated group,especially in the group treated with both quercetin and X-ray.Procollagen gene expression was inhibited and then decreased type Ⅰ and Ⅲ protein syntheses of fibroblsts,particularly type Ⅰ procollagen gene(P

Objective To investigate the mechanism of PBEF in pulmonary vascular endothelial permeability increasing after car-diopulmonory bypass ,in order to provide the basis for a better lung protective measures during cardiopulmonary bypass .Methods Animal models were established ,group A :the rats were transfected with the lentiviral AD-PBEFshRNA ;group B :the rats were took 30 min deep hypothermic circulatory arrest ;group C :the rats were took 30 min deep hypothermic circulatory arrest ,then trans-fected with the lentiviral AD-PBEFshRNA ;control group :the rats were anesthetized and established CPB tube ,without CPB by-pass .Lung tissue was detected with Western blotting and ELISA .Results PBEF ,phosphorylation of P38MAPK ,ERK ,MLC ,VE-cadherin ,FAK in group C had significant difference with group A ,B and the control group(P<0 .05) .VEGF ,MMP2 ,MMP9 ,W/D in group C had significant difference with group A ,B and the control group(P<0 .05) .The pathological results showed that rat lung tissue of the control group was normal ,while in group C ,it had severe pathological damage ,the pathological damage degree in group A ,B reduced compared to group C .Conclusion PBEF can through MAPK/PI3K-Akt/VEGF signaling pathway ,increase pulmonary vascular endothelial permeability .

BACKGROUND: It has been considered that Cestrum nocturnum L. (CNL) has the effects of antiarrhythmia, local anesthesia and central inhibition.OBJECTIVE: To investigate the analgesic effect of CNL extract on mice,so as to find new drugs for clinical treatment of pain.DESIGN: A randomized control observation.SETTING: Center of Modern Education and Department of Pharmacology,Gannan Medical College.MATERIALS: The experiments were carried out in the laboratory of scientific research center, Gannan Medical College between March and April in 2005. ① A total of 150 healthy adult Kunming mice were used in four independent experiments. ② Drugs: CNL extract was provided by the Department of Phytochemistry, Shenyang Pharmaceutical University (batch number: 2002080901), morphine hydrochloride injection by Shenyang No.1Pharmaceutical Factory (batch number: 000305), and naloxone hydrochloride injection by Yanqiao (Hunan) Pharmaceutical Co. Ltd., (batch number:20021109).METHODS: ① Effects of CNL extract on writhing times induced by acetic acid: Forty female mice were randomly divided into four groups with10 mice in each, and they were treated with intraperitoneal injections of 0.02 mL/g saline, 0.10 and 0.20 mg/g CNL extract and 0.10 mg/g aminophenazone respectively. The intraperineal injection of 6 g/L glacial acetic acid was given after 15 minutes. The writhing times of mice within 15 minutes were observed and recorded in each group. ② Effects of CNL extract on the pain induced by hot pla in mice: Forty female mice were randomly divided into four groups with 10 mice in each, and they were treated with intraperineal injections of 0.02 mL/g saline, 0. 10 and 0.20 mg/g CNL extract and 0.10 mg/g morphine respectively. The pain responses were detected at 15, 30 and 60 minutes after administration. ③ The antagonistic effect of naloxone on morphine and CNL extract to the pain induced by hot plate in mice: Thirty female mice were randomly divided into three groups ith 10 mice in each group, and they were given intraperitoneal injections of 0.02 mL/g saline, naloxone 0.004 mg/g +morphine 0.01 mg/g and naloxone 0.004 mg/g+CNL extract 0.01 mg/g respectively. The pain responses were detected at 15, 30 and 60 minutes after administration respectively. ④ Effects of CNL extract on electrostimulation induced pain in mice: Forty mice were randomly divided into four groups with 10 mice in ach group, and they were administrated with intraperineal injections of 0.02 mL/g saline, 0.10 and 0.20 mg/g CNL extract and 1 g/L morphine respectively. Repeated electrostimulations were given at 20, 35, 50 and 70minutes after administration, and the pain responses were detected by means of electrostimulation.MAIN OUTCOME MEASURES: ① Writhing times; ② Time for the pain response induced by hot plate; ③ Analgesic rate induced by electrostimulation.RESULTS: Totally 150 healthy adult Kunming mice were used in the four independent experiments, and all were involved in the analysis of results. ①Writhing times in the mice: 0.10 and 0.20 mg/g CNL extracts and 0.10 mg/g aminophenazone had very significant analgesic effects on writhing induced byacetic acid in mice, and the writhing times after administration were all fewer than those in the saline group (20.2±10.8, 14.5±7.6, 7.6±4.5,50.6±15.5, P ＜ 0.01), and the analgesic effects of CNL extract were dosedependently. ② Time for the pain response induced by hot plate: 0.10 and 0.20 mg/g CNL extracts had significant analgesic effects on the pain in duced by hot plate, and the time for pain sensation at 15, 30 and 60 minutes after administration were all longer than those in the saline group (P ＜ 0.05 or P ＜ 0.01), and the analgesic effect was dose-dependently. The times for pain sensation at each time point after administration in the naloxone 0.004 mg/g+CNL extract 0.01 mg/g group were all longer than those in the saline group, but those were close between the naloxone 0.004 mg/g+morphine 0.01 mg/g group and the saline group. ③ Analgesic rate induced by electrostimulation in the mice: The analgesic rates at20, 35, 50 and 70minutes after administration in the CNL extract 0.10 and 0.20 mg/g groups were all higher than those in the saline group (P ＜ 0.01).CONCLUSION: Our data suggested that CNL extract has obvious analgesic effect, and the analgesic intensity is dose-dependently. Naloxone, an opiate receptor antagonist, can antagonize the analgesic effect of morphine,but cannot antagonize that of CNL extract on mice with pain induced by hot plate, which indicates that CNL extract exert its analgesic role not through binding with opiate receptor.

AIM: To investigate the differential expression profile between nasopharyngeal carcinoma cell line CNE1 and its steady EBV-LMP1-transfected cell line CNE1-LMP1, and to explore the regulatory effect of LMP1 on oncomiRs expression in CNE1 cell line. METHODS: A microRNA array that targets 132 of the most well studied oncomiRs was used to detect the expression profile of CNE1 and CNE1-LMP1. qRT-PCR assay were used to verify the expression data detected by microarray. RESULTS: Among the restricted 132 miRNAs, 30 were detectable. Among which, 30 were expressed in CNE1-LMP1, 19 in CNE1 and 11 were specifically expressed in CNE1-LMP1. Among the 19 shared miRNAs, the expression level of 6 miRNAs (hsa-miR-19b, hsa-miR-17-3p, hsa-miR-22, hsa-miR-149, hsa-miR-150 and hsa-miR-188) elevated over two folds in CNE1-LMP1. No decrease in miRNA expression more than two folds was observed. qRT-PCR confirmed the expression difference of these six miRNAs (P<0.01). Among the 11 specifically expressed miRNAs in CNE1-LMP1, hsa-miR-122a showed the highest expression level surpassing the internal control sample. CONCLUSION: Our data suggest that LMP1 may play an important role in regulating the expression of miRNAs in tumor, which may be another important pathway employed by LMP1 in the development of nasopharyngeal carcinoma.

AIM: To study the characteristic of liver X receptor alpha (LXRα), its target gene expression and cholesterol efflux in human macrophages treated with atorvastatin. METHODS: Human monocyte-derived macrophages were collected and cultured. Macrophages were treated with or without atorvastatin. Apolipoprotein A-I mediated human monocyte-derived macrophage cholesterol efflux was detected by liquid scintillation counting method. Reverse transcription-polymerase chain reaction (RT-PCR) was used to evaluate the mRNA expression of LXRα and some of its target genes ABCA1, SREBP2, CETP, PLTP, apoE, MMP-9 and MIP-1α. The protein expression of LXRα, ABCA1, MMP-9 and MIP-1α was determined by Western blotting. RESULTS: Pre-incubation of human monocyte-derived macrophages with atorvastatin dose dependently (1-2 μmol/L) stimulated cholesterol efflux mediated by apolipoprotein A-I. Atorvastatin also increased the mRNA expression of LXRα, ABCA1, SREBP2, CETP, PLTP, and protein expression of LXRα, ABCA1, but decreased the expression of MMP-9 and MIP-1α at both mRNA and protein levels. CONCLUSION: Atorvastatin enhances the cholesterol efflux, upregulates LXR and some genes associated with cholesterol metabolism and inhibits inflammatory responses in macrophages, indicating that statins may affect the formation of foam cells by activating LXR signaling pathway.

Objective: To explore influence of coping style on sleep quality and blood pressure in community male population with high normal value blood pressure. Methods: The Pittsburgh sleep quality index (PSQI) and coping style questionnaire (CSQ) were used to assess 120 men with high normal blood pressure in community. With PSQI>7 scores as criterion for judging sleep quality disorders, the subjects were divided into sleep disorder group (n=51) and normal sleep group (n=69), and sleep disorder group received psychological intervention. Results: Sleep disorders existed in 42.5% male population with high normal blood pressure. Compared with normal sleep group, there was significant increase in PSQI [（6.43±2.59）scores vs. (8.33±3.14）scores] and diastolic blood pressure [(81.00±8.91) mmHg vs. (88.00±5.69) mmHg] and significant decrease in factor scores of “problem solving” [(0.76±0.21) scores vs. (0.61±0.18) scores] and “asking for help” [(0.52±0.26) scores vs. (0.41±0.11) scores] in sleep disorder group, P<0.05 all; Compared with before intervention there were significant increase in scores of “problem solving” [(0.61±0.18) scores vs. (0.71±0.12) scores]and “asking for help” [(0.41±0.11) scores vs. ( 0.51±0.13) scores]and significant decrease in PSQI score [(8.33±3.14) scores vs. (7.41±2.37) scores] and diastolic blood pressure [(88±5.69)mmHg vs. (80± 4.17)mmHg] after psychological intervention 12 weeks in sleep disorder group, P<0.05 all. Conclusion: Psychological intervention may improve sleep quality and reduce blood pressure in community male population with high normal value blood pressure.