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Objective@#To explore the quality of life and mental health status of adolescents in Zhengzhou, and to compare with HongKong and Taiwan.@*Methods@#A total of 6 401 students from 12 primary and secondary schools in Zhengzhou City. A total of 3 642 students from HongKong and 1 547 students from Taiwan were selected by cluster sampling. And Padiatric Quality of Life Inventory Version 4.0, Self-Esteem Scale, General Self-efficacy Scale, Depression Anxiety Stress Scale and self-made general situation questionnaire were used to conduct questionnaire survey.@*Results@#The total score of quality of life and the scores of each dimension in Zhengzhou were significantly higher than those in HongKong, while self-esteem and anxiety were lower than those of Taiwan adolescents（P<0.05). In addition to self-esteem, anxiety and stress, the scores of quality of life and mental health of adolescents of different grades and genders in Zhengzhou were statistically different(t=13.53，20.71，10.92，20.26，14.68，-16.03，21.26；6.16，3.81，-2.22，-0.33，8.76，4.16，2.71，P<0.01). The quality of life of adolescents in HongKong and Taiwan in different grades and genders were basically the same as those in Zhengzhou, and the differences of depression and stress scores in grades were the same as those in Zhengzhou.@*Conclusion@#The overall quality of life and mental health of adolescents in Zhengzhou is better than that in Hong Kong and Taiwan. It is necessary to explore the relationship between the quality of life and mental health of adolescents in order to improve their quality of life.
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Aim To evaluate the effects of notoginsen-oside R1 on store-operated calcium entry ( SOCE ) in pulmonary arterial smooth muscle cells ( PASMCs ) of chronic hypoxia ( CH)-and monocrotaline ( MCT)-in-duced pulmonary hypertension ( PH) rats. Methods Mn2+ quenching of Fura-2 and measurement of intra-cellular free calcium concentration ( [ Ca2+] i ) using fluo-3 were examined in PASMCs of CH-exposed and MCT-treated rats. Results ①CH-exposed and MCT-treated rats exhibited profound PH when examined 3 weeks after hypoxia exposure or MCT injection, respec-tively. ②In the presence of 3 μmol·L-1 nifedipine, 10 μmol · L-1 notoginsenoside R1 significantly re-duced cyclopiazonic acid ( CPA )-induced the percent reduction in Fura-2 fluorescence measured 500 sec af-ter application of Mn2+, the maximal rate of Mn2+quenching, the amplitude of the Ca2+ influx transient and the resting [ Ca2+] i in PASMCs of CH-exposed and MCT-treated rats. Conclusion Notoginsenoside R1 inhibits SOCE and reduces resting [ Ca2+] i in PASMCs of CH-and MCT-induced PH rats.
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Aim Tostudytheeffectsofferulicacid (FA) on doxorubicin (DOX) induced cellular injury inH9c2ratmyocardialcells.Methods H9c2cells were treated with 1μmol·L-1 DOX treated for 24 h to establish a myocardial injury model. 10, 20, 40μmol ·L-1 FA was added 2 h before DOX treatment. Cell viability was measured by cell counter kit ( CCK-8 ) . Morphological changes were observed by phase contrast microscope. LDH, CK, MDA, SOD levels were detec-ted by biochemical kits. Intracellular level of reactive oxygen species ( ROS) was examined by DCF-DA stai-ning with flow cytometry. Cellular apoptosis was detec-ted by AO-EB staining and DNA agarose gel electro-phoresis. The expression of caspase-3, Bax, Bcl-2 was evaluatedbyWesternblot.Results Exposureof H9c2 cells to DOX led to decrease in cell viability, in-crease in stress and apoptosis. FA pre-treatment im-proved cell viability in a dose-dependent manner, at-tenuated leakage of LDH and CK, and reversed mor-phological changes induced by DOX. FA suppressed DOX-induced oxidative stress as evidenced by reducing ROS and MDA generation and increasing SOD enzyme activity. FA depressed myocardial apoptosis by down-regulating pro-apoptotic protein caspase-3 and Bax, whereas up-regulating apoptosis inhibitory protein Bcl-2.Conclusions FAhasaprotectiveeffectonDOX-induced injury in H9c2 cells. This protection may re-sult from inhibition of myocardial oxidative stress and apoptosis.
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Aim To evaluate the time-course curve of expression of TRPC1 and vascular tone of pulmonary arteries(PAs)mediated by SOCE in chronic hypoxia pulmonary hyperte-nsion rats.Methods Both tension of PA rings and expression of TRPC1 were tested in CH exposure (1 0.0 % ±0.5 %partialpressure ofoxygen ) induced pulmonary hypertensive (PH)rats,and the time-course curve(detected respectively in CH 1 ,3,5, 7,1 4,21 d)was traced.Results ①CH could up-regulate the mean right ventricular pressure(mRVSP) ,which was increased significantly on 1 d,and reached the maximum on 7d;right ventricular weight index (RV-MI)began increase on 3d,and kept rising;②semi-quantitative reverse transcription polyme-rase chain reaction (RT-PCR)was performed to detect the expression of TRPC1 in PAs.The expression of TRPC1 increased significantly on 1 d,and reached the maxi-mum on 3d;③CH could up-regulate the vascular tone of PAs mediated by SOCE,which was increased signif-icantly on 3d,and reached the maximum on 7d.Con-clusions TRPC1 /SOCE increases significantly in the early days of CH,and the time-course curve of the two has correlation,which reflects the important role of the upregulation of TRPC1 /SOCE in the process of chronic hypoxia pulmonary hypertension.
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AIM: To investigate antitumor effect of allotri-tridecyl diethylamine (D-108) in vivo and in vitro. METHODS: The cytotoxic effects of D-108 on various tumor cell lines, human gingival fibroblast and marrow stromal cell cultured in vitro were determined with trypan blue dye exclusion test and MTT method. The acute toxicity of mice by administration of D-108 was evaluated by Bliss method. At a tolerable dose level, D-108 was administrated to treat transplanted solid tumor U14, and tumor weight inhibition was observed. Apoptosis morphological transformation of HL 60 cell induced by D-108 was detected by the Giemsa staining. RESULTS: The cytotoxic effects in vitro of D-108 on various tumor cell lines (IC_ 50 : 0.22 to 2.19 mg?L~ -1 ) were more powerful than both human gingival fibroblast and marrow stromal cell (IC_ 50 : 5.55 and 3.57 mg?L~ -1 ). LD_ 50 of D-108 was 36.49 mg?kg~ -1 (mice, i.g.). D-108 inhibited in vivo growth of implanted solid tumor U14 of mice effectually. The inhibition rate of tumor weight of D-108 (100 mg?kg~ -1 ?d~ -1 i.g.) was 45.27 %. HL 60 cell appearanced typical apoptosis morphological transformation induced by D-108. CONCLUSION: D-108 had obvious antitumor activity in vivo and in vitro and little toxicity. D-108 could induce the apoptosis of HL 60 cell.