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ABSTRACT: BACKGROUND: This study explored the prevalence and severity of post-traumatic stress disorder (PTSD) in college students who lived in earthquake center one year after the Wenchuan earthquake on May 12, 2008, the factors affecting the prevalence of PTSD was also investigated. METHODS: 2987 students studying at the senior normal school in Tibetan autonomous region which was one of the most devastated regions were selected for this study. The PTSD Checklist-Civilian Version (PCL-C) was used as a screening instrument. RESULTS: A total of 420 cases (14.1%) were diagnosed with PTSD, among which mild, moderate, severe and extreme symptoms were reported in 122, 185, 106 and 7 cases, respectively. The PTSD prevalence in college students lived in the severely affected area was significantly higher than that in the less severe area (P < 0.001). According to the multivariate logistic regression analysis, the students who were injured in the earthquake, those lost their first degree relative, and those confronted with dead bodies were more likely to express PTSD. Male students were more prone than female students to develop PTSD. However, the students who received psychological tutorship were less prone to express PTSD. CONCLUSIONS: At one year after the earthquake, the PTSD rate in college students in the severely affected area was high. The social support, psychological help and rehabilitation project should be strengthened to improve their ability to cope with the trauma.
Child and Adolescent Psychiatry and Mental Health 01/2013; 7(1):1.
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ABSTRACT: We previously show the expression of transient receptor potential vanilloid 1 (TRPV1) in primary synoviocytes from collagen-induced arthritis (CIA) rats. Capsaicin and lowered extracellular pH from 7.4 to 5.5 induce cell death through TRPV1-mediated Ca(2+) entry and reactive oxygen species (ROS) production. However, under the pathological condition in rheumatoid arthritis, the synovial fluid is acidified to a moderate level (about pH 6.8). In the present study, we examined the effects of pH 6.8 on the TRPV1-mediated cell death. Our finding is different or even opposite from what was observed at pH 5.5. We found that the moderate extracellular acidification (from pH 7.4 to 6.8) inhibited the capsaicin-induced Ca(2+) entry through attenuating the activity of TRPV1. In the mean time, it triggered a phospholipse C (PLC)-related Ca(2+) release from intracellular stores. The nuclear translocation of NF-κB was found at pH 6.8, and this also depends on PLC activation. Moreover, the capsaicin-evoked massive ROS production and cell death were depressed at pH 6.8, both of which are dependent on the activation of PLC and NF-κB. Taken together, these results suggested that the moderate extracellular acidification inhibited the capsaicin-induced synoviocyte death through regulating Ca(2+) mobilization, activating NF-κB nuclear translocation and depressing ROS production.
Biochemical and Biophysical Research Communications 06/2012; 424(1):196-200. · 2.48 Impact Factor
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ABSTRACT: A murine model of skin injury from vinorelbine extravasation was established to evaluate the treatment efficacy of basic fibroblast growth factor (bFGF) and recombinant human granulocyte-macrophage colony-stimulating factor (rhGM-CSF).
Experimental models were divided into bFGF, rhGM-CSF, and control (saline) groups, with 40 mice in each group. Edema and ulceration were measured on Days 1, 3, 5, 7, 10, 14, and 18 after the onset of extravasation; injuries were examined pathomorphologically in three mice/group/time point.
Edema reached maximum size on Day 3 in the bFGF and rhGM-CSF groups and Day 5 in the control group. The difference between the two experimental groups was not significant; differences between the control group and the experimental groups were statistically significant at all time points. Edema and ulceration began to improve on Day 10 in the bFGF and rhGM-CSF groups and Day 18 in the control group. Healing duration was 14-18 days in the experimental groups, with a (not significantly) shorter duration in the bFGF group. Healing was completed by Day 27.5 in the control group. Pathomorphological evaluation showed regular re-epithelization and newly formed granulation tissue in the bFGF and rhGM-CSF groups on Day 13. In the control group, wounds were partially healed, edema and shallow ulcers existed, and epithelization was fragile and disorganized on Day 18.
bFGF and rhGM-CSF are useful for the treatment of skin injury due to vinorelbine extravasation, but bFGF may be slightly more effective in decreasing time and improving quality of healing.
Biological Research for Nursing 01/2011; 13(1):32-7. · 1.28 Impact Factor
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ABSTRACT: Emodin (1,3,8-trihydroxy-6-methylanthraquinone), an anthraquinone derivative from Rheum officinale Baill, exhibits anti-inflammatory and immunosuppressive activities, however, the underlying mechanisms are not fully understood. This study examined the effects of emodin on ATP-evoked responses in rat peritoneal macrophages and in human embryonic kidney 293 cells (HEK293) heterologously expressing the cloned rat P2X7 receptor. Emodin reduced macrophage death induced by millimolar ATP in a concentration-dependent manner with the half of maximal inhibition values (IC50) of 0.2 microM. It also strongly inhibited ATP-induced dye uptake or pore formation, a hallmark property associated with P2X7 receptor activation, and 2',3'-O-(benzoyl-4-benzoyl)-ATP (BzATP) induced increases in intracellular Ca2+ concentrations in macrophages with an IC50 of 0.5 microM. Furthermore, emodin significantly suppressed BzATP-evoked currents in P2X7 receptor expressing HEK293 cells with an IC50 of 3.4 microM. Taken together, these results provide compelling evidence for a novel action of emodin as a P2X7 receptor antagonist, which may underlie its anti-inflammatory and immunosuppressive activities.
European journal of pharmacology 05/2010; 640(1-3):15-9. · 2.59 Impact Factor
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ABSTRACT: Zn phytotoxicity and its possible detoxifying responses in two ecotypes of Sedum alfredii Hance, i.e. hyperaccumulating ecotype (HE) and non-hyperaccumulating ecotype (NHE) were investigated. HE grew better with high Zn concentrations of 29.11gkg(-1) DW in shoots when exposed to 500microM Zn2+. Toxicity symptoms caused by Zn in root cells of both ecotypes mainly included plasmolysis, disruption of plasma membranes and increased cell vacuolation. At high supplied Zn concentration, chloroplasts suffered from structural disorganization in both ecotypes. Zn-induced hydrogen peroxide (H2O2) and superoxide radical (O(2)-) productions in leaves were determined by a histochemical method, which revealed that Zn stress may have involved NADPH oxidase, protein phosphatases and intracellular Ca2+ to activate the reactive oxygen species production. Inhibition of glutathione synthesis may have led to increased H2O2 and O(2)- accumulations in leaves of HE. In response to higher Zn concentrations, ascorbic acid significantly increased in both ecotypes and levels of glutathione increased in both leaves and roots of HE and in roots of NHE without any change in the leaves of NHE. The enzymatic activities like those of superoxide dismutase (SOD, EC 1.15.1.1), catalase (CAT, EC 1.11.1.6), guaiacol peroxidase (GPX, EC 1.11.1.7), ascorbate peroxidase (APX, EC 1.11.1.11), dehydroascorbate reductase (DHAR, EC 1.8.5.1), and glutathione reductase (GR, EC 1.6.4.2) in leaves of HE were all enhanced at supplied Zn concentration of 500microM, which may account for its better growth.
Plant Physiology and Biochemistry 07/2008; 46(11):997-1006. · 2.84 Impact Factor
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ABSTRACT: Hydroponics experiments were conducted to study the effects of Pb on mined ecotype (ME) and non-mined ecotype (NME) of Elsholtzia argyi from Pb/Cu mining and the non-contaminated agricultural areas, respectively. The results showed that at 200 microM Pb treatment, although concentrations of Pb in leaves and stem of the ME were 2.6 and 4.5 times higher than those of the NME, these plants exhibited higher tolerance to excessive levels of Pb in the growth medium. In both the ecotypes, Pb caused inhibition of leaf growth and photosynthesis, and induced the membrane damage which was more obvious in the NME. Pb treatment decreased the activities of superoxide dismutase (SOD) and guaiacol peroxidase (G-POD) while activity of catalase (CAT) and levels of total soluble proteins (TSP), ascorbic acid (AsA) and glutathione (GSH) were significantly induced after Pb exposure, however, increase was sharp in the ME plants. Leaf ultrastructural analysis of the spongy mesophyll cells revealed that the excessive Pb concentrations caused adverse effects on chloroplast ultrastructure of both ecotypes whereby internal damage was more severe in NME. The higher tolerance to Pb displayed by ME is mainly attributed to maintenance of its leaf growth and physiology, induction of GSH and integrity of cell organelles especially chloroplast ultrastructure.
Journal of Hazardous Materials 07/2008; 154(1-3):914-26. · 4.17 Impact Factor
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ABSTRACT: Lipopolysaccharide (LPS)-activated macrophages are pivotal in innate immunity. With LPS treatment, extracellular signals are transduced into macrophages via Toll-like receptor 4 and induce inflammatory mediator production by activating signaling pathways, including the nuclear factor-kappaB (NF-kappaB) pathway and the mitogen-activated protein kinase (MAPK) pathway. However, the mechanisms by which the intracellular free Ca2+ concentration ([Ca2+]i) increases and protein kinase C (PKC) is activated remain unclear. Therefore, we investigated the signaling pathway for Ca2+- and PKC-dependent NF-kappaB activation, inducible nitric-oxide synthase expression, and tumor necrosis factor-alpha (TNF-alpha) production in LPS-stimulated rat peritoneal macrophages. The results demonstrated that the LPS-induced transient [Ca2+]i increase is due to Ca2+ release and influx. Extracellular and intracellular Ca2+ chelators inhibited phosphorylation of PKCalpha and PKCbeta. A PKCbeta-specific and a general PKC inhibitor blunted phosphorylation of serine in mitogen-activated/extracellular signal-regulated kinase kinase kinase (MEKK) 1. Moreover, a MEKK inhibitor reduced activation of inhibitorykappaB kinase and NF-kappaB. Upstream of the [Ca2+]i increase, a protein-tyrosine kinase inhibitor reduced phosphorylation of phospholipase C (PLC) gamma. Furthermore, a PLC inhibitor eliminated the transient [Ca2+]i increase and decreased the amount of activated PKC. Therefore, these results revealed the following roles of Ca2+ and PKC in the signaling pathway for NF-kappaB activation in LPS-stimulated macrophages. After LPS treatment, protein-tyrosine kinase mediates PLCgamma1/2 phosphorylation, which is followed by a [Ca2+]i increase. Several PKCs are activated, and PKCbeta regulates phosphorylation of serine in MEKK1. Moreover, MEKKs regulate inhibitory kappaB kinase activation. Sequentially, NF-kappaB is activated, and inducible nitric-oxide synthase and tumor necrosis factor-alpha production is promoted.
Journal of Biological Chemistry 11/2006; 281(42):31337-47. · 4.77 Impact Factor
