[Objective] To establish n HPLC method for analysis of ginsenoside Rb1 in AITONG capsules. [Method]The HPLC system consists of G1314A variable wavelength un-visible detector,Hypersil ODS(4.6mm?250mm,5?m),HP chemstation, Hp1100 Series Quaternary Pump and Vacuum degasser (G1322A). The mobile phase was: Acetonitrile:Water (30∶70,v/v). The flowrate was 1.0ml?min-1,the injection volume was 20?l,and the detector wavelength was 203nm. [Results] The method was linear at the ginsenoside Rb1 ranging from 0.04?g to 2?g. The recovery of method was 98.26%(n=5),the average RSD was 1.41% .

Objective To study the effect of glutamine (Gln) on the intestinal mucosa inflammatory reaction and permeability after intestine ischemia-reperfusion injury in rats.Methods The rat model of intestinal ischemia-reperfusion injury was established by clamping the mesenteric superior artery and then restoring blood flow.Forty-eight model rats were divided into control group (n =24) and model + Gln group (n =24)according to the stochastic indicator method.Both groups were given enteral nutrition with equal energy and nitrogen [energy 125.4 kJ/ (kg · d) and nitrogen 0.2 g/ (kg · d)].The model +Gln group was fed with enteral nutrition plus 3％ Gln,while the control group was fed with enteral nutrition plus 3％ soybean protein.The experiment lasted 8 days after modeling.The intestinal mucosa and the plasma levels of nuclear factor-κB (NF-κB),tumor necrosis factor-α (TNF-α),interleukin-6 (IL-6),Gln,D-LACtic acid and diamine oxidase (DAO) were observed in rats before and after modeling and on the 3rb and 8rd day of the experiment.Changes in the morphology of intestinal mucosa were observed by electron microscopy.Results After modeling in control and model + Gln group,the level of NF-κB in intestinal mucosa [18 cases (75.0％) and 17 cases (70.8％)] were significantly higher than those before modeling [0 case (0.0％),P =0.013,P =0.019],the level of IL-6 in intestinal mucosa [(313.27±75.28) pg/g and (321.75±76.46) pg/g] were significantly higher than those before modeling [(227.52 ±58.13) pg/g,P =0.023,P =0.043],and the level of TNF-α in intestinal mucosa [(241.28 ±65.29) pg/g and (240.35 ±64.86) pg/g] were significantly higher than those before modeling [(172.45 ±33.76) pg/g,P=0.036,P=0.011].The plasma level of IL-6 [(150.32 ± 18.74) ng/L and (148.21 ±20.19) ng/L] were significantly higher than those before modeling [(116.37 ± 14.59) ng/L,P =0.032,P =0.025],the plasma level of TNF-α [(127.62 ± 14.24) ng/Land (123.86 ± 13.75) ng/L] were significantly higher than those before modeling [(85.18 ± 8.84) ng/L,P =0.018,P =0.035],and the plasma level of D-LAC [(0.46 ±0.03) mmol/L and (0.51 ±0.04) mmol/L]were significantly higher than those before modeling [(0.27 ±0.02) mmol/L,P =0.041,P =0.018],and the plasma level ofDAO [(2.76±0.57) U/ml and (2.58 ±0.51) U/ml] were significantly higher than those before modeling [(1.52±0.24) U/ml,P=0.015,P=0.037],while the plasma level of Gln [(0.18 ±0.01) g/L and (0.21 ± 0.01) g/L] were significantly lower than those before modeling [(0.39 ± 0.03) g/L,P =0.026,P =0.031].On the 3rd and 8th days of the experiment in the control group,the level of NF-κB in intestinal mucosa [16 cases (66.7％),15 cases (62.5％)] were significantly higher than those before modeling (P =0.027,P =0.002),the level of TNF-α in intestinal mucosa [(226.23 ±55.35) pg/g and (214.76 ±54.82) pg/g] were significantly higher than those before modeling (P=0.042,P =0.038)],the level of IL-6in intestinal mucosa [(297.56 ± 71.39) pg/g and (291.49 ± 68.46) pg/g] were significantly higher than those before modeling (P =0.031,P =0.012).On the 3rd and 8th days in the control group,the plasma level of IL-6[(147.38 ± 17.25) ng/L and (144.65 ± 15.32) ng/L] were significantly higher than those before modeling (P =0.016,P =0.034),the plasma level of TNF-α [(121.75 ± 13.72) ng/L and (113.83 ± 11.69) ng/L] were significantly higher than those before modeling (P =0.025,P =0.041),the plasma level of D-LAC [(0.41 ±0.03) mmol/L and (0.53 ±0.05) mmol/L)] were significantly higher than those before modeling (P =0.029,P =0.030),the plasma level of DAO [(2.51 ± 0.52) U/ml and (1.76 ± 0.34) U/ml] were significantly higher than those before modeling (P =0.034,P =0.016).The plasma level of Gln [(0.22 ±0.01) g/L and (0.21 ±0.03) g/L] were significantly lower than those before modeling (P =0.042,P =0.035).On the 3rd day of the experiment in the model + Gln group,the levels of NF-κB,TNF-α,and IL-6 in intestinal mucosa [14 cases (58.3％),(213.78 ±43.76) pg/g,(293.72 ±69.86) pg/g] were significantly higher than those before modeling (P =0.038,P =0.026,P =0.013) ; the plasma level of IL-6,TNF-α,D-LAC,and DAO [(135.61 ±14.25) ng/L,(117.35 ±11.29) ng/L,(0.45 ±0.03) mmol/L,and (2.26 ± 0.43) U/ml] were significantly higher than those before modeling (P =0.021,P =0.032,P =0.032,P =0.025).On the 8th day of the experiment in the model + Gln group,the levels of NF-κB,TNF-α,and IL-6 in intestinal mucosa [9 cases (37.5％),(184.53 ± 42.16) pg/g,and (236.83 ±66.52) pg/g] were significantly lower than those after modeling and those in the control group (P =0.024,P=0.027; P=0.026,P=0.039; P=0.013,P=0.028) ; the plasma levels of IL-6,TNF-α,D-LAC,and DAO [(126.35±12.74) ng/L,(92.76±9.42) ng/L,(0.31 ±0.02) mmol/L,and (1.76±0.34) U/ml]were significantly lower than those after modeling and those in the control group (P =0.021,P =0.030; P =0.032,P =0.025 ; P =0.024,P =0.037 ; P =0.022,P =0.036) ; the plasma level of Gln [(0.40 ±0.03) g/L] was significantly higher than those after modeling and in the control group (P =0.028,P =0.032).Under the electron microscope,the structure of villus and recess was damaged after modeling,villi were sparse and short,with a lot of inflammatory cell infiltration in the lamina propria.Lymphangiectasia and edema occured after modeling.On the 8th day,compared with after modeling and the control group,intestinal villi and recess structure were significantly restored in the model + Gln group; compared with the after-modeling status,the recovery of intestinal mucosa villi and recess structure was not obvious,and the inflammatory cell infiltration in the lamina propria persisted in the control group.Conclusion Gln repairs ischemia-reperfusion injury in the intestinal mucosa by regulating intestinal mucosa inflammatory cytokine release,inhibitng inflammatory response,and reducing the permeability of the intestinal mucosa.

Objective: To explore safety and effects of exercise rehabilitation in aged patients with chronic heart failure (CHF). Methods: A total of 83 aged CHF patients were randomly divided into exercise rehabilitation group (n=42, received exercise training based on usual care) and usual care group (n=41, received usual care). Period of treatment was eight weeks and patients were followed up for 12 months. New York heart association (NYHA) classification was used to represent cardiac function. Left ventricular ejection fraction (LVEF), left ventricular end-diastolic dimension (LVEDd) were determined by ultrasound cardiography, 6 min walking distance (6MWD) and oxygen metabolic equivalent (METs) also were determined , plasma level of brain natriuretic peptide (BNP) was examined. Minnesota living with heart failure questionnaire (MLHFQ) was used to represent quality of life. Rehospitalization rate and mortality rate within 12 months were recorded in all patients. Results: On 8 th weeks after treatment, the LVEF, LVEDd and NYHA class of two groups all significantly improved（P＜0.05 all）,compared with usual care group, there were significant improvement in LVEF [（54.7±6.2）% vs. 65.4±8.7）%], LVEDd [（49.6±8.3）mm vs.（40.2±9.3）mm] and NYHA class [（2.7±0.8）classes vs.（1.9±0.9）classes], P<0.05 all; 6MWD [(122.7±9.2) m vs. (175.6±8.7) m] and METs [(5.8±1.8) vs. (8.4±2.4)] also significantly increased (P<0.01), and plasma level of BNP [(43.4±9.8) pg/ml vs. (31.7±8.9) pg/ml, P<0.05] significantly decreased in exercise rehabilitation group. No severe adverse events occurred in exercise rehabilitation group. After 12 months, compared with usual care group, there were significant increase in MLHFQ score [(45.6±8.2) scores vs. (68.9±7.9) scores], significant decrease in rehospitalization rate caused by heart failure (24.4% vs. 9.5%) , P<0.05 all in exercise rehabilitation group. Conclusion: Exercise rehabilitation is safe and effective in aged patients with chronic heart failure, which can significantly improve cardiac function, enhance exercise capacity and increase quality of life.

Background: Studies showed that aberrant activation of JAK/STAT3 signaling pathway promoted the tumorigenesis and progression of hepatocellular carcinoma (HCC), and transforming growth factor-β1 (TGF-β1) has either tumor-suppressing or tumor-promoting effect in regulation of tumor progression.Aims: To investigate the effect of specific inhibition of JAK/STAT3 signaling pathway on HCC and whether TGF-β1 signaling pathway is involved in this process or not.Methods: Thirty Wistar rats were randomly divided into three groups: control group, HCC group, and HCC+AG490 group.In the latter two groups, diethylnitrosamine was administered in drinking water to induce HCC model, and in HCC+AG490 group, AG490, a specific inhibitor of JAK was injected intraperitoneally in the first week of model establishment.At the end of the 16th week, all rats were sacrificed.The maximum diameter of tumor nodules in the liver was recorded and the number of tumors with maximum diameter greater than 1 cm was counted.Expression and distribution of STAT3 and TGF-β1 in liver tissue were determined by real-time PCR, immunohistochemistry, and immunofluorescence.Results: Compared with the control group, expressions of STAT3 and TGF-β1 mRNA in liver tissue were significantly increased in HCC group (P<0.05).Phosphorylated STAT3 (p-STAT3) and TGF-β1 proteins were absent in liver tissue in control group, and both were up-regulated and co-expressed in HCC group.While in HCC+AG490 group, expressions of STAT3 and TGF-β1 mRNA were significantly lower than those in HCC group (P<0.05);the liver tissue was weakly positive for p-STAT3 and TGF-β1 proteins, and the number of tumor nodules greater than 1 cm and the maximum diameter were markedly reduced when compared with the HCC group [1.20±1.03 and (1.14±0.18) cm vs.4.30±1.06 and (1.78±0.27) cm, P all<0.05].Conclusions: Specific inhibition of JAK/STAT3 signaling pathway may restrain the tumorigenesis and progression of HCC partially by interfering TGF-β1 signaling pathway.

OBJECTIVE:To improve community pharmaceutical care so as to promote the rational drug use of community resi-dent and improve the quality of life. METHODS:By analyzing the situation of community pharmaceutical care,the pharmaceutical care of community pharmacists was improved by changing pharmaceutical care mode,actively developing the propaganda of ratio-nal drug use,strengthening retraining of clinical pharmacists. RESULTS:With the help of Hongkou district quality control group, many hospitals of the district signed thepharmaceutical linkage assistance agreement. Through the efforts of Hongkou district quality control group and many hospitals,community pharmaceutical care was improved and the propaganda of rational drug use has achieved certain results. CONCLUSIONS:Through exploration and practice,the pharmaceutical care levels of community phar-macists have been improved and the rational drug use of community residents has been promoted.

The antioxidative capability and Na+-K+-ATPase α1-subunit mRNA expression in myocardium of hypothyroid rats induced by low-iodine diet were observed. The results showed that the antioxidative capability of myocardium decreased, resulting in lipid peroxidative damage, atrophy of myocardial cells and chondrification of tunica intima, along with decreased expression of sodium pump α1 subunit mRNA in hypothyroid rats.

Objective To investigate the effects of arsenic trioxide plus thalidomide on immune function of patients with myelodysplastic syndrome (MDS).Methods Fifty-seven MDS patients (Low risk,medium risk and high risk) and 30 healthy volunteers were selected as our subjects.Thirty-four cases with medium risk Ⅱ and high risk MDS patients were randomly divided into A and B groups.Seventeen MDS patients in A group were treated with arsenic trioxide plus thalidomide,and 17 MDS patients in B group were treated with low-dose cytarabine.Lymphocyte subsets in peripheral blood were examined by flow cytometry (FCM).The adverse effect of arsenic trioxide and thalidomide were recorded.Results Compared with control group,the number of T lymphocytes(CD3 +),B lymphocytes (CD3-CD19 +) and NK cell (CD3-(CD16 CD56) +) of patients with MDS were significantly lower,and the differences were statistically significant (t =2.157,2.349,2.958 ; P ＜ 0.05 or P ＜ 0.01).The helper CD3 + CD4 + T cell (Th) ratio decreased in MDS patients than that of control group (t =2.412,P ＜ 0.05).The inhibition CD3 + CD8 + T cells (Ts) ratio increased (t =2.749,P ＜ 0.01).Th/Ts ratio inversion was seen in MDS patients.As the progression of MDS increase,Ts cell expression gradually increased and NK cells ratio gradually decreased.However,there was no significant difference among three groups.Th cells and B lymphocytes in the risk group were lower than that in the low risk group,and the difference was statistically significant (F =4.896 and 4.516,P ＜0.05),but there was no significant difference in the terms of the number of T lymphocytes,Th cell,ratio of Th/Ts and B lymphocytes among MDS groups.Number of T lymphocytes,B lymphocytes and NK cell count in group A after treatment were increased than that before treatment (t =2.435,2.468,2.653,P ＜ 0.05).In group A,2 cases were complete remission,4 cases with partial remission,and 5 cases with hematologic improvement.The total effective rate was 64.71％ (11/17),and curative effect is obviously better than that of B group (x2 =4.253,P ＜ 0.05).Meanwhile adverse effect was mild.Conclusion The cellular and humoral immune function decreased in MDS patients.The treatment of arsenic trioxide plus thalidomide on MDS is proved safety and efficacy,which might work by improving immune function of MDS patients.

Objective Analysis of myocardial microvascular perfusion in patients with chronic total coronary occlusion (CTO) who underwent a coronary artery bypass graft (CABG) use real-time myocardial contrast echocardiography (RTMCE),to provide an effective method of detecting viable myocardium and a reference for the choice of CABG indications.Methods Twenty-seven patients with CTO underwent RTMCE 1 week before CABG,they underwent follow-up echocardiography and coronary artery 256-slice multislice computed tomography aagiography 1 year after CABG.Myocardial viability was defined as a postoperative ultrasound wall motion significantly improved ≥ 1 point.Semi-quantitative analysis of contrast images,myocardial viability was defined as myocardial perfusion score ≤ 2 points.Viable myocardium by quantitative assessment of myocardial blood flow (MBF) was determined by analyses of receiver-operating characteristic (ROC) curves.Results Patients with LVEF increased significantly after CABG (P ＜ 0.01),Of 259 segments with wall motion abnormality,149 (58％) showed wall motion significantly improved ≥ 1 point after CABG,considered viable myocardium,110 (42％) were not observed in wall motion improved,considered to be non-viable.The viable myocardial segments were significantly greater than non-viable myocardial segments in A,β,A × β value (P ＜ 0.01).Compared with the semi-quantitative analysis,quantitative analysis of MBF increased the sensitivity and accuracy of RTMCE for detecting viable myocardium (P ＜ 0.05).Conclusion RTMCE could accurately assess myocardial viability and provide a strong reference for clinical decision making and judging prognosis.

Objective To explore the effects of L?type calcium channel (LTCC) α1C and β3 subunits on that magnesium inhibited thoracic aortic calcification induced by β?glycerophosphate (β?GP). Methods Vascular smooth muscle cells (VSMCs) and aortic rings from rat aortic were cultured, then divided into control group, high phosphorus group (10 mmol/L β?GP), magnesium group (10 mmol/L β?GP+3 mmol/L MgSO4) and 2?APB (an inhibitor of magnesium transporter) group (10 mmol/L β?GP+3 mmol/L MgSO4+0.1 mmol/L 2?APB). Calcium deposition of VSMCs and aortic rings were respectively measured by alizarin red staining and Von Kossa staining, meanwhile the quantification of their calcium was tested by OCPC. The mRNA expressions of Runx2, LTCCα1C andβ3 in VSMCs were detected by RT?PCR, and their protein expressions were detected by Western blotting. Intracellular calcium ion of VSMCs was tested by fluorescence probe and alkaline phosphatase (ALP)activity was measured by ELISA. The Runx2 expression of aortic rings was detected by immunohistochemistry. Results After VSMCs stimulated for 7 days, calcium, ALP, mRNA and protein expressions of LTCCα1C, LTCCβ3 and Runx2, and intracellular calcium ion in high phosphorus group were higher than those in control group (all P<0.05). Moreover, calcium, ALP, mRNA and protein expressions of LTCCα1C, LTCCβ3 and Runx2, and intracellular calcium ion were decreased in magnesium group as compared with those in high phosphorus group (all P<0.05). In aortic rings, magnesium group had lower calcium and protein expression of Runx2 than high phosphorus group. No statistical difference between 2?APB group and high phosphorus group was observed in above indexes (all P>0.05). Conclusion Magnesium may down?regulate expressions of LTCCα1C andβ3 subunit, prevent calcium influx and then inhibit osteogenic differentiation so as to reduce β?glycerophosphate?induced VSMCs calcification.

Background Light-induced retinal damage results in the damage of retinl pigment epithelial (RPE) cells and therefore affects the pathogenesis and development of age-related macular degeneration (AMD).Studies showed that tissue factor (TF) is overexpressed in oxidative damaged RPE cells and the choroidal neovascularization (CNV) of AMD,speculating that the suppression of TF can prevent the damage of RPE cells and inhibit CNV.Objective This study was conducted to observe the protective effects of TF targeting peptide (TFTP),a new drug of autologous synthesis,on human RPE-cells induced by blue light.Methods Human RPE cells were isolated from donor eye and cultured.Cultured cells were divided into blank control group,model group and TFTP treated group.Light-induced RPE cell damage model was established by exposuring the cells in the blue light of (4.0±-0.5) mW/cm2 for 12 hours in the model group,and different concentrations (10,100,150,200,300 μmol/L) of TF-TP were added into the medium to pretreat the cells for 24 hours and then exposed the cells to the blue light for 12 hours in the TF-TP groups.The cell viability was determined by CCK-8 assay.The morphology and ultrastructure in the cells were observed under the inverted microscope and transmission electron microscope.The apoptosis of the cells was assayed by Hoechst staining.The expressions of TF and apoptosis-related protein bax,bcl-2 in the cells were determined by Western blot.Results CCK-8 assay showed that there was no significant difference in the cell viability among blank control group and different concentrations TF-TP groups (F=2.15,P =0.11).The cell survival rate of blank control group,model group and 150 μmol/L TF-TP group was (100.0±0.00) ％,(43.79±6.55) ％ and (63.45±3.57) ％,and the survial rate was increased in the 150 μmol/L TF-TP group compared with the model group (P =0.00),and 150 μmol/L was detemined as a optimal concentration of TF-TP.A lot of shrinkage,deformation,suspension cells were exhibited under the optical microscope,and decrease of microvilli structure,rupture of mitochondrial cristae and vacuolar degeneration of the cells were found in the model group,and the damage of the cells were evidently lightened in the 150 μ mol/L TF-TP group.The apoptosis rate of the cells were (0.98 ±0.19)％,(9.98 ±0.82) ％ and (5.73 ±0.88) ％ in the blank group,model group and 150 μmol/L TF-TP group,respectively,with a significant difference among the groups (F =206.18,P =0.00),and the apoptosis rate of the cells in the 150 μmol/L TF-TP group was significantly lower than that in the model group (P＜0.05).Compared with the blank control group,the relative expression of bax and TF was obviously increased and that of bcl-2 was decreased in the model group;while the expression of bax and TF was lower,and that of bcl-2 was higher in the 150 μmol/L TF-TP group compared with the model group (all at P ＜ 0.05).Conclusions Pretreation of TF-TP can lessen cell apoptosis and increase cell survival rate and therefore plays a protective role to blue light-induced human RPE cells possibly by inhibiting bax/bcl-2 apoptotic pathways mediated by TF.