AIM:To establish an assay of oxymatrine and matrine in Compound Shiwei Tablets(Folium Pyrrosiae, Radix Sophorae Flavescentis, Radix Astragali, Herba Polygoni Avicularis, etc.) and Radix Sophorae Flavescentis by HPLC. METHODS: Diamonsil C 18 (10 ?m,250 mm?4.6 mm) analytical column was used.The mobile phase consisted of methanol-0.2% phosphoric acid solution (45∶55). The detection wavelength was 220nm. RESULTS : The average recoveries of oxymatrine and matrine in Compound Shiwei Tablets were 100.3% and 100.6% , respectively and in Radix Sophorae Flavescentis were 101.0% and 101.2%, respectlively. CONCLUSION: This method could be used for the quality evaluation of Compound Shiwei Tablets and Radix Sophorae Flavescentis.

AIM: To study the effects of (-)-epigallocatechin-3-gallate (EGCG), a tea extract, on the invasion and metastasis of breast cancer cell line MDA-MB-231 and the possible mechanisms in vitro. METHODS: The expression of MUC1 in breast cancer cells treated with or without EGCG was detected by immunohistochemistry. The effect of EGCG on invasion of MDA-MB-231 cells was evaluated using Transwell chambers attached with polycarbonate filters and reconstituted basement membrane (Matrigel). Gelatin zymography was performed to detect the secretion of collagenase-Ⅳ. RESULTS: EGCG reduced the expression of MUC1, significantly suppressed the invasion of tumor cells to basement membrane and reduced the secretion of collagenase-Ⅳ. CONCLUSION: In vitro, EGCG may suppress invasion, metastasis, and collagenase-Ⅳ secretion in MDA-MB-231 cells by inhibiting the production of MUC1.

The traditional denoising algorithm for ultrasound images would lost a lot of details and weak edge information when suppressing speckle noise. A new denoising algorithm of adaptive threshold based on curvelet transform is proposed in this paper. The algorithm utilizes differences of coefficients' local variance between texture and smooth region in each layer of ultrasound image to define fuzzy regions and membership functions. In the end, using the adaptive threshold that determine by the membership function to denoise the ultrasound image. The experimental text shows that the algorithm can reduce the speckle noise effectively and retain the detail information of original image at the same time, thus it can greatly enhance the performance of B ultrasound instrument.
Algorithms ; Diagnostic Imaging ; Image Processing, Computer-Assisted ; Ultrasonics

Objective To investigate the effects of ischemic postconditioning on apoptosis, structural and functional changes of mitochondria induced by myocardial isehemia/reperfusion (I/R) injury of rabbits and potential mechanism. Methods Eighty healthy rabbits were divided randomly into five groups: sham operation group ( Group Sham) , ischemic reperfusion group (Group IR) , ischemic preconditioning group (Group IP) , ischemic postconditioning group (Group PC) and 5-HD plus ischemic postconditioning group (Group PC +5-HD). All rabbits in the five groups were killed 4 h after reperfusion. The hearts were quickly collected for microscopy by TUNEL. We observed ultrastructural changes of myocardium under electron microscope and examined mitochondrial membrane potential and Ca~(2+) concentration, MDA content and SOD activity of myocardial mitochondria. Results Compared with group IR, the damage of mitoehondrial ultrastrueture was milder, the apoptosis rate decreased and Ca concentration and MDA content were much lower in group IP and group PC ( P < 0. 05 ). Mitochondrial membrane potential and SOD activity of myocardial mitochondria in group IP and group PC was significantly higher than that in group IR(P<0.05). The protective effect of PC against I/R injury was partially counteracted by 5-HD .Conclusion Ischemic posteonditioning can protect the heart from I/R injury, this is supported by improvement mitochondrial ultrastructure and by decreasing apoptosis, increasing mitochondrial membrane potential and SOD activity, alleviating Ca~(2+) overload and decreasing MDA content in myocardial mitochondria. The cardio protective effects may be explained by mitochondrial ATP sensitive potassium channel.

AIM: To investigate the effects of heptanol preconditioning on the changes of structure, function and connexin 43 (Cx43) content in mitochondria in a rabbit model of myocardial isehemia-reperfusion (IR) injury. METHODS: In anesthetized open-chest rabbits, the left anterior descending artery (LAD) was occluded for 30 min and reperfused for 4 h. Sixty-four rabbits were randomly divided into 4 groups (n=16 in each group): sham operation group (sham group), ischemia-reperfusion group (IR group), ischemic preconditioning group (IP group) and heptanol preconditioning group (HT group). All rabbits in the 4 groups were killed 4 h after reperfusion. Myocardial infarct size was determined at the end of the experiment. Mitochondria was isolated by centrifugations. The ultrastructural changes of the mitochondria were observed under electronic microscope. The mitochondrial membrane potential, Ca~(2+) concentration, MDA content and SOD activity of myocardial mitochondria were also examined. The content of mitochondria Cx43 was detected by Western blotting. RESULTS: Compared to IR group, the myocardial infarct size was significantly reduced in IP (18.97%±2.80%) and HT (19.97%±3.80%) groups, the damage of mitoehondrial ultrastructure was milder (P<0.05), mitochondrial membrane potential was significantly higher and Ca~(2+) concentration was much lower (P<0.01) in IP group and HT group. No significant difference of MDA content and SOD activity in myocardial mitochondria between IR group and HT group was found. However, MDA content were much lower and SOD activity was significantly higher in IP group as compared to IR group (P<0.01). Compared to sham group, the mitochondria Cx43 expression was distinctly decreased compared to IR group (P<0.05) and no significant difference was found between IP group and HT group (P>0.05). CONCLUSION: Heptanol preconditioning protects myocardium from ischemia-reperfusion injury. The mechanism may be related to increasing in mitochondrial membrane potential, alleviating Ca~(2+) overload in myocardial mitochondria and attenuating the decrease in mitochondria Cx43 expression induced by isehemia-reperfusion.

Aim To investigate the roles of Cx43 in mitochondria and mitochondrial ATP sensitive potassium channe1(mitoK_(ATP)~+)participating in the protection for heptanol preconditioning on myocardial ischemia/reperfusion injury of rabbits.Methods In anesthetized open-chest rabbits,the left anterior descending artery(LAD)was occluded for 30 min and reperfused for 4 hrs.All rabbits were randomly divided into five groups(n=16 in each group):sham operation group(Group Sham),ischemic reperfusion group(Group IR),ischemic preconditioning group(Group IP),heptanol preconditioning group(Group HT)and 5-HD plus heptanol preconditioning group(Group HT+5-HD),All rabbits in the five groups were killed 4h after reperfusion.Myocardial infarct size was determined at the end of the experiment.The heart rate and the mean arterial pressure(MAP)were recorded and plasma CK-MB and cTnI activity were measured at baseline,the end of ischemia,and after 2 hrs and 4 hrs of reperfusion respectively.Mitochondria was isolated with different centrifugations.Ultrastructural changes of mitochondria were observed under electron microscope.The content of the mitochondria Cx43 was detected with Western blot.Results The plasma CK-MB,cTnI activity and myocardial infarct size were significantly reduced in IP(18.97±2.8)% and HT(19.97±3.8)% groups as compared to IR groups (35.67±5.8)%,(P<0.01).Compared to group IR,the damage of mitochondria in group IP and group HT were milder(P<0.01).No significant difference was found between Group IP and Group HT.Compared to sham group, the mitochondria Cx43 expression was distinctly decreased in group IR and group HT+5-HD(P<0.01)and no significant difference was found between Group IP and Group HT.Conclusions Heptanol preconditioning can protect the heart from I/R injury by improving mitochondrial ultrastructure and by attenuating the decrease of mitochondria Cx43 expression induced by I/R.The mitochondrial Cx43 expression may be concerned with depending on mito K_(ATP)~+.

Objective To explore the effects of celecoxib combined with arsenic trioxide (As2O3) on the mRNA expression,protein expression and protein tyrosine kinase (PTK) activity of bcr-abl fusion gene and its downstream signal transduction in chronic myeloid leukemia (CML) primary cells.Methods The cells were incubated with celecoxib (40 μmol/L) or As2O3 (2 μmol/L) alone and celecoxib (40 μmol/L) combined with As2O3 (2 μmol/L) for 36 hours.The changes of mRNA expression,p210 expression and PTK activity of bcr-abl fusion gene in each group were examined respectively by real time quantitative reverse transcriptase polymerase chain reaction (RQ-RT-PCR),Western blot and PTK activity analysis.The important proteins STAT1,STAT5 and their phosphorylatic proteins p-STAT1 and p-STAT5 and inhibitor of DNA binding 1 (ID1)a common downstream target of oncogenic tyrosine kinase were also analyzed by Western blot.Results The mRNA expressions in control group,celecoxib group,As203 group and celecoxib combined with As2O3 group were (5.97±0.53) ％,(5.74±0.46) ％,(5.94±0.57) ％ and (3.06±0.41) ％ respectively,and the statistical difference was found only between celecoxib combined with As2O3 group and control group (t =28.35,P =0.00).The similar statistic difference was only observed between the two groups from PTK activity tests (t =4.38,P =0.04).Western blot also showed that p210,STAT1,STAT5,p-STAT1,p-STAT5 and ID1 were more extraordinaryly downregulated by celecoxib combined with As2O3 than others treatments.Conclusion Celecoxib combined with As2O3 can downregulate mRNA,p210 expression,PTK activity of bcr-abl fusion gene and inhibit STAT and ID1 signal transduction pathways in a synergistic way.

Objective To discuss the influence of microRNA(miR)-155/miR-21 on toll-like receptor 4 (TLR4) in children with sepsis.Methods Fifty children with sepsis who were hospita-lized in Pediatric Intensive Care Unit,Shenzhen Children's Hospital,were enrolled in the study,and 15 healthy children at the same age were selected as healthy control group.Expression levels of TLR4 protein and human leukocyte antigen(HLA)-DR in CD14 + monocytes (MC) were detected by using flow cytometry,and sepsis patients were divided into 2 groups according to whether they exceeded the value of HLA-DR by 30％ or not.Expression level of programmed cell death factor 4 (PDCDM) and inositol phosphatases 1 containing SH2 (SHIP1) were detected at the same time.MC were separated by CD14 + immune magnetic bead,and expression level of miR-155,miR-21 and tumor necrosis factor-α (TNF-α),interleukin-10 (IL-10) mRNA in CD14 + MC were detected by using real-time fluorescent quantitative PCR.Results Sepsis group consisted of 27 male and 23 female,and their ages were (2.34 ± 0.79) years old,among whom 9 patients died.There were 36 patients in the HLA-DR increase group and 14 patients in the HLA-DR decrease group.Expressions ofTLR4(2.33±0.90),miR-155[(7.19±3.75) ×10 3] and TNF-α[(21.98±14.15) ×10-2 pg/L] in CD14 + MC were higher in the HLA-DR increase group than those in the HLA-DR decrease group [1.24±0.60,(4.83 ±1.17) × 10-3,(14.18±5.45) ×10-2 μg/L] and healthy control group[1.57±0.55,(3.99 ± 1.29) × 10-3,(1.61 ± 0.84) × 10 2 pg/L],and the differences were statistically significant(F =11.943,7.583,18.538,all P ＜0.05),while the expressions of miR-21 (12.10 ±5.66),IL-10[(29.74 ± 12.55) × 10-4 μg/L] in CD14 + MC were lower in the HLA-DR increase group than those in the HLA-DR decrease group[4.68 ± 2.07,(12.50 ± 5.73) × 10-4 μg/L] and healthy control group [2.39 ± 0.86,(2.04 ± 0.92) × 10-4 μg/L],and the differences were statistically significant(F =41.673,54.991,all P ＜ 0.05).The levels of SH1P1 and PDCD4 decreased in sepsis compared with healthy control group[0.70 ±0.36)vs.(1.59 ±0.48);(1.55 ±0.56) vs.(3.01 ±0.70)],and the differences were statistically significant (t =7.682,8.339,all P ＜ 0.05),but SHIP1 decreased more significantly in the HLA-DR increase group than that in the HLA-DR decrease group [(0.60 ± 0.34) vs.(0.97 ± 0.26)],and the difference was statistically significant (F =39.214,P ＜ 0.05).PDCD4 decreased more significantly in the HLA-DR decrease group than that in the HLA-DR increase group (0.94 ±0.19 vs.1.79 ±0.47),the difference was statistically significant(F =65.367,P ＜ 0.05).Conclusions Regulation imbalance of miR-155/miR-21 may be one of the reasons for abnormal expression of TLR4 in children with sepsis,and it plays a role in enlarged or inhibited expression of TLR4 in the sepsis process which results in different immune status in sepsis patients.

Objective To observe the effects of radiation on the growth and expression of cysteine-rich 61(Cyr61/CCN1) of L929 cells and investigate the relationship between CCN1 expression and radiation injury.Methods L929 cells were cultured and divided into 2 groups,cells irradiated with 4 Gy ?-irradiation as radio-group and untreated cells as control group.The cell proliferation was measured by MTT assay and plate colony formation testing.Flow cytometry was utilized to quantify the cell cycle distribution.CCN1 expression at protein and mRNA levels were determined by immunocytochemistry(ICC) and RT-PCR respectively.Results Significant inhibition of proliferation(P

Objective To establish an evaluation index system of electricity saving at general hospitals.Methods Based on civil building energy saving studies and in accordance with national regulations on hospital energy saving, the authors build an electricity saving index system for general hospitals.The indexes were reduced by the rough set theory, and their weight was determined by analytical hierarchy process and expert analysis.Results An electricity saving evaluation index system for general hospitals is so developed, consisting of six level-2 indexes and 27 level-3 indexes.Conclusions Such an evaluation index system can guide hospital electricity consumption and saving.