1.Preparation of Lysozyme-loaded PLGA Microspheres by SPG Membrane Emulsification
Mengqi YANG ; Yongming ZHANG ; De CHEN ; Wanhua ZHU ; Fan YANG
China Pharmacist 2015;(3):376-380
Objective:To develop a new preparation process of PLGA microparticles for protein drugs by SPG membrane emulsifi-cation combined with W/O/W double emulsion-solvent technique. Methods:Lysozyme was used as the model drug to prepare the mi-croparticles. The influence of formula factors on the properties of the microparticles was studied, and the physicochemical properties, in vivo compatibility and degradation of the microparticles were investigated as well. Results:The drug loading of lysozyme-loaded mi-croparticles was 35%, the entrapment efficiency was 72. 43% and the average size was 63. 89 μm with PDI of 0. 675. DSC and FTIR showed that lysozyme was entrapped in the microparticles. The microspheres had promising biocompatibility and sustained degradation in vivo. Conclusion:The paper describes a new satisfactory preparation process of PLGA microparticles for protein drugs with good in vitro and in vivo properties.
2.Fifty-six cases of Hunt facial paralysis treated by syndrome differentiation acupuncture combined with buccal mucosal bleeding.
Yi YANG ; Guang-Tao ZHOU ; De-Qing ZHANG
Chinese Acupuncture & Moxibustion 2012;32(2):111-112
Acupuncture Therapy
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Adolescent
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Adult
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Aged
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Bloodletting
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Combined Modality Therapy
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Facial Paralysis
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therapy
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Female
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Humans
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Male
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Middle Aged
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Mouth Mucosa
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blood supply
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Young Adult
3.Effect of Vertebral Plate Resection and Disc Excision from Posterior Approach Combined with Lumbar Interbody Fusion for Treatment of Lumbar Disc Herniation Associated with Lumbar Instability
Xiaobing JIANG ; Zhidong YANG ; Shuncong ZHANG ; De LIANG
Journal of Guangzhou University of Traditional Chinese Medicine 2004;0(05):-
【Objective】To assess the indications and therapeutic effect of surgical treatment for lumbar disc herniation(LDH) associated with lumbar degenerative instability(LDI).【Methods】Fifty-eight LDH associated with LDI patients,which were ineffective after strictly conservative treatment or simple decompression with disc excision,received lumbar vertebral plate resection and disc excision from posterior approach,and transpedicular screw fixation combined with posterior lumbar interbody fusion.【Results】A averaged 13-month follow-up was carried out in 54 patients.The therapeutic effect assessed by Japanese Orthopaedics Association(JOA) was as follows: excellent in 37 patients,good in 13,ordinary in 4,and the excellent +good rate was 92.59%.The results of X radiography 3 months after the operation showed that lumbar interbody fusion was successful in 52 patients,the infusion rating being 96.30%.【Conclusion】Lumbar vertebral plate resection and disc excision from posterior approach,and transpedicular screw fixation combined with posterior lumbar interbody fusion are effective for the treatment of LDH associated with LDI.
6.Optimization of Expression by Response Surface Methodology and Purification of Recombinant Human Cardiac Troponin-I(cTnI) in Escherichia coli
Lei YANG ; Chun-Ming ZHANG ; De-Zhi WANG ;
China Biotechnology 2006;0(10):-
To optimize the growth condition for the established gene engineer bacteria express cardiac troponin-I(cTnI) and to obtain purified cTnI as an antigen to produce clinical assay kits used in acute myocardial injury(AMI) diagnosis.Plackett Burman Design(PBD) was applied to select the factors which effect the expression of cTnI in Escherichial coli(E.coli) mostly.Induction time,pH and KCl were proved influenced expression of cTnI notably.Afterward,Response Surface Methodology(RSM) as second step to optimize the selected three factors,an equation was deduced to predict the percent of cTnI.In the most optimized condition,the percent of cTnI can reach to 26% of total cell protein.The procedures of purification included ammonium sulfate deposition and DEAE Cellulose ion exchange chromatography.SDS-PAGE shows that purified cTnI contain one band.cTnI could be used to immune animals as an antigen to produce monoclonal antibodies with high affinity and specificity.It maybe as calibrators to harmony the difference assays of cTnI measurement in clinical.
8.Time-series analysis on effect of air pollution on stroke mortality in Tianjin, China.
De-zheng WANG ; Qing GU ; Guo-hong JIANG ; De-yi YANG ; Hui ZHANG ; Gui-de SONG ; Ying ZHANG
Chinese Journal of Industrial Hygiene and Occupational Diseases 2012;30(12):902-907
OBJECTIVETo investigate the effect of air pollution on stroke mortality in Tianjin, China, and to provide basis for stroke control and prevention.
METHODSTotal data of mortality surveillance were collected by Tianjin Centers for Disease Control and Prevention. Meteorological data and atmospheric pollution data were from Tianjin Meteorological Bureau and Tianjin Environmental Monitoring Center, respectively. Generalized additive Poisson regression model was used in time-series analysis on the relationship between air pollution and stroke mortality in Tianjin. Single-pollutant analysis and multi-pollutant analysis were performed after adjustment for confounding factors such as meteorological factors, long-term trend of death, "days of the week" effect and population.
RESULTSThe crude death rates of stroke in Tianjin were from 136.67 in 2001 to 160.01/100000 in 2009, with an escalating trend (P = 0.000), while the standardized mortality ratios of stroke in Tianjin were from 138.36 to 99.14/100000, with a declining trend (P = 0.000). An increase of 10 µg/m³ in daily average concentrations of atmospheric SO₂, NO₂ and PM₁₀ led to 1.0105 (95%CI: 1.0060 ∼ 1.0153), 1.0197 (95%CI: 1.0149 ∼ 1.0246) and 1.0064 (95%CI: 1.0052 ∼ 1.0077), respectively, in relative risks of stroke mortality. SO₂ effect peaked after 1-day exposure, while NO₂ and PM₁₀ effects did within 1 day.
CONCLUSIONAir pollution in Tianjin may increase the risk of stroke mortality in the population and induce acute onset of stroke. It is necessary to carry out air pollution control and allocate health resources rationally to reduce the hazard of stroke mortality.
Air Pollutants ; analysis ; Air Pollution ; analysis ; China ; epidemiology ; Environmental Monitoring ; Humans ; Models, Theoretical ; Particulate Matter ; analysis ; Poisson Distribution ; Stroke ; epidemiology ; mortality ; Survival Rate ; Time Factors
9.Effect of Peroxisome Proliferator-activated Receptor δ Activation on the Expression of Tenascin-C in Infarcted Myocardium
Dachun YANG ; Shuangtao MA ; Xiaohua SU ; Xiuchuan LI ; Jihong ZHANG ; Bing TANG ; De LI ; Yongjian YANG
Journal of China Medical University 2010;(9):730-732
Objective The purpose of the present study was to investigate the effect of peroxisome proliferator-activated receptors δ(PPAR δ)activation with dietary GW610742X on the expression of tenascin-C in the infarcted and remodeling myocardium.Methods Sixty male Wistar rats were divided into four groups,including control group,sham group,myocardial infarction(MI) group,and MI+GW610742X(GW)group.The left coronary artery was ligated to establish the MI model.PPAR δ activator GW610742X(100mg/kg/d)was administrated into the rats of GW group.At 3 months after procedure,the expression and distribution of tenascin-C in left ventricular free wall from each group were examined by Western blotting and immunofluorescence,respectively.Results After 3 months following procedure,there were obvious necrosis and fibrosis in left ventricular free wall from MI group.The expression of tenascin-C in MI and GW group was significantly higher than those in control and sham group(P 〈 0.01).Moreover,tenascin-C expression in GW group was remarkably decreased compared to MI group(P 〈 0.05).Additionally,tenascin-C expression in sham group was similar to that in control group(P 〉 0.05).Conclusion The tenascin-C is upregulated in infarcted myocardium during the remodeling process,which can be significantly attenuated by PPAR δ activation.
10.Stretch-induced Expression of CYR61 Increases the Secretion of IL-8 in A549 Cells via the NF-κβ/Iκβ Pathway
Yan ZHANG ; Ping GUI ; Shang-Long YAO ; Dong YANG ; Yang LV ; De-Fang DING
Journal of Huazhong University of Science and Technology (Medical Sciences) 2018;38(4):672-678
Mechanical ventilation (MV) with large tidal volumes can increase lung alveolar permeability and initiate inflammatory responses,resulting in ventilator-induced lung injury (VILI).The mechanisms of the injurious effects of MV and the genetic susceptibility remain unclear.VILI-related genes such as cysteine-rich angiogenic inducer 61 (Cyr61)have been demonstrated to play a detrimental role in the aggressive ventilation strategies.In the present study,we investigated the involvement of Cyr61 in the VIM and the underlying mechanism.A549 cells were exposed to cyclic stretch of varying durations and then the mRNA and protein levels of Cyr61 were measured by real-time PCR and Western blotting,respectively.Additionally,after exposure ofA549 cells to cyclic stretch for 5 min to 1 h,the expression levels of nuclear factor kappaB (NF-κB) and IL-8 were detected by ELISA and Western blotting.Thereafter,Cyr61 expression was depressed in A549 cells with the siRNA pGenesill.1-Cyr61-3 before the cyclic stretch,and IL-8 secretion and the activation of NF-κB pathways were probed by ELISA and Western blotting,respectively.Moreover,a NF-κB inhibitor (PDTC) and an activator (TNF) were used before mechanical stretch.Realtime PCR and ELISA were performed to detect the mRNA and protein of IL-8,respectively.The results showed that the mechanical cyclic stretch led to increased Cyr61 expression at mRNA and protein levels in A549 cells.Additionally,cyclic stretch also mobilized NF-κB from the cytoplasm to the nucleus and increased IL-8 secretion in A549 cells.The inhibition of Cyr61 blocked the NF-κB activation and IL-8 secretion in response to cyclic stretch.Inhibition of NF-κB attenuated the mRNA and protein expression of IL-8 in A549 cells transfected with Cyr61 siRNA.It was suggested that Cyr61/NF-κB signaling pathway mediates the upregulation of IL-8 in response to cyclic stretch in A594 cells.These findings support the hypothesis that Cyr61 plays a critical role in acute lung inflammation triggered by mechanical strain.