1.Retrobulbar injection with triamcinolone acetonide for macular edema caused by retinal vein occlusion
Ming AN ; You WANG ; Liang YING
Ophthalmology in China 2009;18(4):254-256
Objective To evaluate the therapeutic efficacy of retrobulbar injection with triamcinolone acetonide (TA) for macular edema caused by retinal vein occlusion (RVO). Design Retrospective case series. Participants 21 eyes of 21 patients with macular edema caused by RVO. Methods Retrobulbar injection with TA 40 mg was performed on 21 eyes. The visual acuity, intraocular pres-sure, fundus fluorescein angiography (FFA) and macular central thickness under the optical coherence tomography (OCT) were recorded and analyzed before and after treatment. The follow-up duration was 6-11 months. Main Outcome Measures The visual acuity and the macular central thickness of OCT. Result Visual acuity was improved at the end of follow-up in 16 eyes (76.2%) and unchanged in 5 eyes (23.8%). Macular central thickness was (287.55±121.70) μm at the end of follow-up and (617.23±185.58) μm before treatment. The difference was statistically significant(P=0.000). After treatment, the comparison of visual acuity and macular central thickness be-tween CRVO patients and BRVO patients, as well as between ischemic RVO patients and non-ischemic RVO patients had no significant difference (P>0.05). In patients of course less than 6 months, the visual prognosis after treatment is better than that of before treatment (P=0.011, 0.01), while in patients of course more than 6 months, no difference of vision could be detected before and after treatment (P= 0.583). The result of FFA showed decrease of fluorescein leakage. During follow-up, intraocular pressure of all patients was in the nor-real range. Recurrence of macular edema was found in 8 eyes 2 to 6 months after treatment. Conclusions Retrobulbar injection with TA is a safe, effective, and easy method to treat macular edema caused by RVO. Early treatment can get better efficacy. (Ophthalmal CHN, 2009, 18: 254-256)
2.The influences of xylazine on the gastrointestinal motility in mice and on the gastrointestinal electrical rhythm in rats
Liang MING ; Guansu XU ; Yu WANG
Chinese Pharmacological Bulletin 1987;0(02):-
Yohimbine (0. 5~4mg ? kg-1, sc) and idazoxan (2~8 mg ? kg-1,sc) showed a dose related antagonistic action on the inhibitory effect of xylazine (4mg ? kg-1,sc) on the gastrointestinal propulsive motility in mice. Xylazine (2mg,4mg ? kg-1,sc),clonidine(120 ?g ? kg-1,sc) exhibited the inhibitory effect of gastrointestinal basic electrical rhythm on the stomach, duodenum, jejunum and ileum in rats.The inhibitory effects of these drugs were the strongest at 30 min after administration of Compounds. Yohimibine (4mg ? kg-1,sc) was found to antagonize the inhibitory effect of xylazine (4mg ? kg-1,sc) on the gastrointestinal basic electrical Rhythm.
3.The role of intra-aortic ballon counterpulsation in acute myocardial infarction with cardiogenic shock
Weimin WANG ; Haian WU ; Ming LIANG
Chinese Journal of Interventional Cardiology 1996;0(01):-
Objective To evaluate the application of intra-aortic balloon counterpulsation(IABP) in acute myocardial infarction(AMI) with cardiogenic shock.Methods The study enrolled 65 AMI patients with cardiogenic shock and all the patients underwent primary PCI treatment.Among them,30 patients had IABP suppont during operations.Results In all the 30 cases with IABP support,the hemodynamic parameters improved in 30 minutes and stabilized in 2-8 hours.There was no reocclusion and death during querations.The death rate of the IABP group during hospitalization was 40%.Among the other 35 patients without IABP support,6 patients died during PCI and the in hospital death rate was 74.3%.Conclusion IABP can improve hemodynamic parameters and the perfusion of coronary artery in patients with cardiogenic shock.It can increase the success rate of primaty PCI,reduce the risk of low cardiac output and reocclusion during operation.IABP support during PCI can also improve the prognosis and reduce the motality rate of AMI patients with cardiogenic shock.
4.Correlation between frustration tolerance and personality of college students and its promotion strategies
Ming GUO ; Baojia CHEN ; Yao WANG ; Liang ZHAO
Chinese Journal of Medical Education Research 2013;(5):527-530
Objective To investigate the correlation between the frustration tolerance and personality of medical college students and to discuss its promoting strategies.Methods Totally 460 college students were selected randomly.Questionnaire of frustration tolerance and scale of Eysenck personality inventory(EPQ) were used and the measurement data were compared with correlation analysis and regression analysis of SPSS 13.0.Results Correlation was significant between frustration tolerance (total score and 6 inducing factors) and personality (EPQ factors) of college students ; personality (EPQ factors)of students could predict their frustration tolerance and corresponding t value was -4.85,P < 0.01 (psychoticism),6.93,P < 0.01 (extraversion),-11.15,P < 0.01 (neuroticism).Conclusions Personality of college students are greatly influenced by their frustration tolerance.Targeted anti-frustration ability training should be conducted according to the different personality characteristics.
5.Effects of extract of astragalus on hippocampal delayed neuronal death in rats
Weizu LI ; Liang MING ; Ting HE ; Shaobin WANG ; Weiping LI
Chinese Pharmacological Bulletin 1986;0(05):-
Aim To study the effects of extract of astragalus on hippocampal delayed neuronal death of totalcerebral ischemia and 7 days reperfusion in rats.Methods Global ischemia was made by four-vessel occlusion. Electron microscope was used to observe the ultramicrostructure of dorsal hippocampal neurons.Light microscope was used to survey the structure of hippocampal neurons and to count the number of normal neurons in CA1 sector. Glial fibrillary acidic protein(GFAP) was detected by immune histochemistry.Results Compared with ischemia and reperfusion group(I/R),EA improved the ultrastructure of hippocampal neurons, suppressed the decrease of normal neurons in CA1 and degraded the expression of GFAP .The number of normal neurons in I/R group was 38?11.5,and in EA(20,40 mg?kg -1) groups,63?12.8(P
6.Effect of extract of astragalus on inflammatory factor and apoptosis after focal cerebral ischemia/reperfusion injury in rats
Yanyan YIN ; Weiping LI ; Shaobin WANG ; Ting HE ; Liang MING
Chinese Pharmacological Bulletin 2003;0(12):-
Aim To study the mechanisms of protective effects of extract of astragalus against focal cerebral ischemia/reperfusion injury in rats. Methods Focal cerebral ischemia was induced by intraluminal thread occlusion of middle cerebral artery. Immunohistochemistry was used to determine expression of TNF-?,IL-1? was measured by radioimmunity, and the apoptosis was observed by TUNEL. Results EA(20、40、80 mg?kg -1,ig)could decrease the expression of TNF-? and the level of IL-1? and reduce cell apoptosis. Conclusion EA has inhibitory action on the increase in the expression of TNF-?,the level of IL-1? and the apoptosis of neurons induced by focal cerebral ischemia/reperfusion.
7.Effect of sapindoside on primary hypertension rat
Hai BIAN ; Zijiang LONG ; Ming CHEN ; Liang WANG
Chinese Traditional Patent Medicine 1992;0(03):-
AIM: To observe the effects of sapindoside on blood pressure,AngⅡ,Ald,ET in the blood plasma and NO in the serum in primary hypertension rat. METHODS: The primary hypertension rats were divided into 5 groups(high,middle and low sapindoside group,control group and captopril group,10 each) in a random fashion and drugs had been given by ig.for 32 days.The blood pressure was messured in the 1,3,7,32 day after administration.At the end of the 32 nd days,AngⅡ,Ald,ET in the blood plasma and NO in the serum were measured. RESULTS: Sapindoside could significantly lower the blood pressure,increase the levels of NO in serum,reduce the concentration of AngⅡ,Ald,ET in the blood plasma. CONCLUSION: Sapindoside plays an important role in decreasing the blood pressure of primary hypertension rat.
8.Expression of CXCL12-CXCR4 and its association with angiogenesis in pancreatic cancer.
Zuo-xing NIU ; Li-ming FEI ; Chang-liang WANG
Chinese Journal of Oncology 2009;31(4):286-287
Adenocarcinoma, Papillary
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blood supply
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metabolism
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pathology
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Adult
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Aged
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Carcinoma, Pancreatic Ductal
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blood supply
;
metabolism
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pathology
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Chemokine CXCL12
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metabolism
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Female
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Gene Expression Regulation, Neoplastic
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Humans
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Lymph Nodes
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metabolism
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Lymphatic Metastasis
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Male
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Microvessels
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pathology
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Middle Aged
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Neoplasm Staging
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Neovascularization, Pathologic
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metabolism
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pathology
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Pancreas
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metabolism
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Pancreatic Neoplasms
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blood supply
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metabolism
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pathology
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Receptors, CXCR4
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metabolism
9.A comparative study of nurse work environment between military hospital and civilian hospital
Ping LIANG ; Yuan WANG ; Ming HOU ; Xiaoyu YANG
Chinese Journal of Practical Nursing 2013;29(21):7-9
Objective To investigate the current situation and the differences of nurse work environment between a military hospital and a civilian hospital.Methods By quota sampling,a questionnaire survey was conducted among a total of 1244 nurses in a military hospital and a civilian hospital in Urumqi.Results The nurse work environment in both hospitals was favorable overall.The total scores of nursing environment and subscale scores of the military hospital were lower than those of the civilian hospital.There were no statistical differences between the two hospitals on their perceptions of the collaboration with physicians as well as leadership and ability of nurse manager.Conclusions The nurse work environ-ment in the civilian hospital was a little more favorable than the military one.Both of their managers,espe-cially the military hospital,should pay more attention to manpower and resources as well as nurses'involve-ment in hospital affairs in order to further optimize nurse work environment.
10.Effect of 1, 25(OH)2D3 on the proliferative ability of and methylation levels of genomic DNA and proliferation-associated gene promoter in human HaCaT keratinocytes
Yanling JIANG ; Ming ZHAO ; Gongping LIANG ; Litao WANG ; Yuwen SU
Chinese Journal of Dermatology 2013;46(12):885-888
Objective To estimate the influence of 1,25(OH)2D3 on the proliferative ability of and methylation levels of genomic DNA and proliferation-associated gene promoter in human HaCaT keratinocytes.Methods Some cultured HaCaT cells were treated with 1,25 (OH)2D3 of 10-6,10-7 and 10-8 mol/L for 24 hours,then,methyl thiazolyl tetrazolium (MTT) assay was carried out to evaluate the proliferative activity of cells,and a global DNA methylation quantification kit was used to determine the global DNA methylation level.Real-time PCR was conducted to quantify the mRNA expression of DNA methyl transferases (DNMTs) and methyl-DNA binding domain (MBD) proteins,and methylation-specific PCR (MS-PCR) to evaluate the methylation status of promoter region in the programmed cell death 5 (PDCD5) and tissue inhibitor of metalloproteinase 2 (TIMP2) genes,in HaCaT cells after 24-hour treatment with 1,25 (OH)2D3 of 10-6 mol/L.The HaCaT cells receiving no treatment served as the control.Results Compared with the untreated HaCaT cells,those treated with 1,25(OH)2D3 of 10-6 mol/L showed significantly down-regulated proliferative activity (0.152 ± 0.027 vs.0.290 ± 0.017,P < 0.01),global DNA methylation level (0.187 ± 0.071 vs.0.316 ± 0.049,P < 0.05),DNMT3a and DNMT3b mRNA expression levels (P < 0.01 or 0.05),but markedly upregulated mRNA expression levels of MECP2,MBD2,PDCD5 and TIMP2 (P < 0.01 or 0.05).Moreover,the DNA methylation levels within the promoter region of PDCD5 and TIMP2 genes were significantly lower in HaCaT cells treated with 1,25 (OH)2D3 of 10-6 mol/L than in the control cells (0.38 ± 0.135 vs.0.72 ± 0.121,0.46 ± 0.172 vs.0.68 ± 0.133,both P< 0.05).Conclusions 1,25(OH)2D3 may down-regulate the global genomic DNA methylation level of,and modulate the expression of DNA methylationmodifying genes in,HaCaT cells.Furthermore,1,25 (OH)2D3 can decrease the promoter methylation levels but induce the overexpression of PDCD5 and TIMP2 genes,and decelerate the proliferation of HaCaT cells.