Medical service system integration follows the logic of system innovation and development.Case studies of the UK,the USA and Australia found that medical delivery system integration is the product of a series of mixed factors.Health care financing and payment mechanism reform,physician team building,stair-cased movement to grassroots of healthcare service,shared clinical norms utilization as well as its gradual development constitute the general logic of such an integration.In the evolution process,the check and balance between the government and market,equity and efficiency have been affecting the integration process all the way.In light of these logics,China should speed up its transform of the integration concept,improve the integration elements,and strengthen the guidance of integration principles during its integration of the medical service integration.

OBJECTIVETo study the molecular mechanism of Yangjing Zhongyu Decoction (YZD) n-butanol extracts (ZDC) and ethyl acetate extracts (YSYZ) in reducing androgen in porcine granulose cells by mitogen-activated protein kinase (MAPK) pathway.

METHODSPorcine granulose cells were isolated and cultured. They were inoculated by MAPK inhibitor PD98059 at different concentrations, and then they were divided into the blank control group (0), 1, 3, 10, and 25 micromol/L groups. After 24-h culture the cytochrome P450c17a (CYP17) mRNA expression level was detected using Real-time fluorescent quantitative PCR. Contents of androgen (testosterone) in the supernate were detected using RIA and optimal PD98059 concentration screened. After intervened by 10 micromol/L PD98059 for 24 h, the culture solution was intervened by effective ingredients of with or without YZD or YSYZ at various concentrations (0, 1 , 5, 25, 50 mg/mL) at various time points (3, 6, 18, 24 h). Expression levels of p-ERK1/2, c-Fos and CYP17 were detected by Western blot. Testosterone content in the supernate was determined by radioimmunoassay (RIA).

RESULTSTen pLmol/L PD98059 could obviously decrease p-ERK1/2 protein expression and increase CYP17 mRMA expression, and elevate testosterone content in the supernate (P < 0.05). ZDC and YSYZ at 25 ng/mL could increase p-ERK1/2 protein expression and c-Fos levels, and reduce CYP17 protein expression, and lower testosterone content in the supernate after 6-h intervention (P < 0.01).

CONCLUSIONEffective ingredients of YZD could reduce androgen production in porcine granulose cells through increasing activities of MAPK.

Androgens ; Animals ; Drugs, Chinese Herbal ; pharmacology ; Female ; Flavonoids ; Granulosa Cells ; metabolism ; Mitogen-Activated Protein Kinase 3 ; metabolism ; Mitogen-Activated Protein Kinases ; metabolism ; RNA, Messenger ; Swine

Nowadays,oil-pollution of seawater in the world has severely threatened the security of sea entironment.Bioremediation offers one available option for an oil spill response.The aspects as follows are introduced some evolvement of microbial ecology,including new method of survey of microbial diversity without cultivation,new isolated method and the properties of main hydrocarbon degradated strain.But we have little or no understanding of the vast majority of marine bacteria that remain uncultured,and more efforts should be made to improve current methods for isolating oil-degrading or oil-emulsifying bacteria,not only for assessing the fate and effects of the spilled oil,but also for isolating novel bacteria that would be useful for the petroleum industry.

A low-temperature hydrocarbon-degrading strain T7-2, isolated from sea-mud of Bohai polluted area and identified as Rhodococcus erythropolis, was found to produce an extracellular, nondialyzable emul- sifying agent (referred to as bioemulsifier) when grew with hexadecane as carbon source. The results showed that, this bioemulsifier which could remarkably emulsify hydrocarbons such as diesel oil, is consisted of three parts-carbohydrates, lipids and proteins, the proportion of which was 55.43:31.24:12.65. The mono- saccharide compositions were identified as mannose and rhamnose; the lipid compositions included de- canoic acid, lauric acid, hexadecanoic acid and stearic acid, and the protein constituents were composed of sixteen amino acids. Besides, according to the study of the physic-chemical properties of the bioemulsifier, it possesses the obvious advantages of character stability, high function efficiency and wide adaptation range, therefore this bioemulsifier is believed to have extensive application values for bioremediation of marine oil pollution, petroleum exploitation and etc.

Objective To investigate the effects of atorvastatin on C-reactive protein (CRP)induced Toll-Like receptor 4(TLR4)expression on CD14+ monocyte, and the production of proinflammatory cytokines tumor necrosis factor α (TNFα), interleukin-6 (IL-6), matrix metalloproteinases-9 (MMP-9), and to study the anti-inflammatory mechanisms of statins. Methods The monocytes were isolated from blood of healthy volunteers by the Ficoll density gradient and stimulated by CRP with different doses (5, 25, 50, 100 μg/ml)and different exposure time (6, 12, 24, 48 h). Cells were also incubated with atorvastatin of different doses (1.0, 2.5, 5.0, 7.5, 10.0 μmol/L)in the presence of CRP 50 μg/ml. The protein expression of TLR4 was measured by flow cytometry, mRNA expression of TLR4 and of myeloid differentiation protein (MD2)was detected by quantitative PCR. TNFα, IL-6, MMP-9 concentrations in supernatants of cultured medium were measured by ELISA.Results (1)Compared with the un-stimulated control group, enhanced TLR4 protein expression was already detected at a concentration of 5 μg/ml of CRP and increased in a dose-dependent manner (32.22±2.80)%, (49.94±5.58)%, (74.82±3.24)% and (90.82±2.88)% at 5, 25, 50 and 100 μg/ml CRP. (2)TLR4 protein expression on 50 μg/ml CRP stimulated cells also increased in a time-dependent manner (29.80±2.70)%, (47.44±4.41)%, (81.71±2.92)% and (50.57±3.34)% after 6 h, 12 h, 24 h, 48 h.(3)When monocytes were incubated with CRP 50 μg/ml and atorvastatin (1.0, 2.5, 5.0, 7.5, 10.0 μmol/L), protein expression [(68.17±1.71)%, (52.43±1.38)%, (27.72±4.55)%, (17.46±3.20)%, (9.99±2.81)%］and mRNA expression (82.72%, 67.34%, 48.16%, 30.88%, 13.85%)of TLR4 as well as mRNA expression of MD2 (81.78%, 71.04%, 47.85%, 27.06%, 18.30%)were reduced in a dose-dependent manner. (4)Level of TNFα, IL-6 and MMP-9 in supernatants was significantly reduced by atorvastatin (2.5 μmol/L)compared with control group(P<0.01). When monocyte incubated with CRP 50 μg/ml and atorvastatin 10.0 μmol/L, the level of TNFα, IL-6, MMP-9 decreased to (25.8±2.5)pg/ml, (128.2±14.7)pg/ml, (65.2±12.3)ng/ml, respectively.Conclusion CRP increased the protein expression of TLR4 on CD14+ monocyte in a dose-dependent and time-dependent manner. Atorvastatin can inhibit the signal transduction of TLR4 and reduce proinflammatory cytokines release induced by CRP on CD14+ monocyte, and this might be one of the anti-inflammatory mechanisms of atorvastatin.

OBJECTIVETo explore the correlation between pathological characteristics of target organs and excess evil syndrome in IgA nephropathy.

METHODSData were collected in multicenter cooperation. Totally 266 IgA nephropathy patients were typed into exogenous wind-heat affection syndrome (49 cases), lower energizer damp-heat syndrome (100 cases), damp-phlegm syndrome (43 cases), and blood stasis syndrome (74 cases). Meanwhile, percutaneous renal biopsy was performed in all patients for Hass classification, Oxford classification, Katafuchi integral, and Jiang's classification methods. The correlation between excess evil syndrome and pathological index was analyzed.

RESULTSFour syndrome types were correlated with their Hass levels (r = 0. 341, P <0. 01). Affection of exogenous wind-heat syndrome was correlated with segmental proliferation of endothelial cells and damaged active lesions of segmental capillary loops. Lower-energizer damp-heat syndrome was associated with Hass III level, destroying active lesions of capillary loops, segmental proliferation of endothelial cells, glomerular segmental lesions, focal interstitial infiltration of inflammatory cells, focal interstitial fibrosis and tubular atrophy. Blood stasis syndrome was associated with Hass IV level, glomerular sclerosis, segmental glomerulosclerosis (S)/adhesion, mesangial hypercellularity (M), angiohyalinosis, multi-foci interstitial infiltration of inflammatory cells, multi-foci interstitial fibrosis and tubular atrophy. Phlegm-damp syndrome had higher proportions of Hass I and III levels, but with no association with other pathological parameters.

CONCLUSIONSExcess evil syndrome was associated with partial pathological characteristics of IgA nephropathy. It could reflect pathological damage degree of target organs, activities, chronic lesions, and prognosis of IgA nephropathy to certain extent. Correlated pathological characteristics and its evolution could indicate excess evil syndrome types and their evolution rules.

Capillaries ; Fibrosis ; Glomerulonephritis, IGA ; pathology ; Glomerulosclerosis, Focal Segmental ; Humans ; Kidney Glomerulus ; Medicine, Chinese Traditional ; Prognosis ; Syndrome

The distribution of shear stress on the bottom of the parallel plate flow chamber under different inlet velocities was analyzed by numerical simulation. In the present experimental study, the projection planes of the relative errors at 0.7% level were obtained, and then the efficient region and the actual entrance length were further corrected by introducing the concept of relative error. The results showed that the efficient region of the chamber increased with the direction of length while the inlet velocity was increased, and the actual entrance length was much greater than that of the theoretical entrance length. Therefore, in accordance to the needed range of shear stress in experiment and to the needed efficient region area, the optimum design of the flow chamber is necessary.
Algorithms ; Blood Flow Velocity ; Blood Pressure ; physiology ; Computer Simulation ; Humans ; Models, Cardiovascular ; Numerical Analysis, Computer-Assisted ; Pulsatile Flow ; Rheology ; Shear Strength ; Stress, Mechanical

Adult ; Aged ; Cell Cycle Proteins ; analysis ; Coal Mining ; Cyclin-Dependent Kinase Inhibitor p27 ; Female ; Humans ; Immunohistochemistry ; Lung ; chemistry ; pathology ; Male ; Middle Aged ; Occupational Diseases ; metabolism ; Pneumoconiosis ; metabolism ; Tumor Suppressor Proteins ; analysis

OBJECTIVETo investigate the dynamic changes in serum levels of hepatitis B surface antigen (HBsAg) and their relation to hepatic parenchyma cell volume (hepatic cell quantity) at different grades of liver inflammation and stages of hepatic fibrosis in patients with hepatitis B e antigen (HBeAg)-negative chronic hepatitis B.

METHODSSerum HBsAg levels were detected by electrochemilumineseence. Serum HBsAg levels were apportioned according to the hepatic parenchyma cell volume and compared among liver histological inflammation grade (1, 2, 3 and 4) and hepatic fibrosis stage ( I, II, III and IV), respectively.

RESULTSThe levels of serum HBsAg among the four liver histological inflammation grades were:1:6,036.4+/-2,729.4 COI/ml; 2:6,704.6+/-2,457.5 COI/ml; 3:6,332.2+/-2,409.0 COI/ml; 4:6,226.2+/-2,716.0 COI/ml. There were no differences among the groups before apportion (Fbefore apportion=0.564, P=0.640).Serum HBsAg levels apportioned by the hepatic parenchyma cell volume among liver histological inflammation grades were:1:9,174.8+/-4,142.0 COI/ml; 2:10,743.1+/-3,950.3 COI/ml; 3:11,078.0+/-4 230.0COI/ml; 4:11,540.5+/-5,058.8 COI/ml. There were significant differences among the groups after apportion (Fafter apportion =27.354, P<0.001). Serum HBsAg levels among hepatic fibrosis stages were: I: 6,222.1+/-2,665.4 COI/mL; II: 6,706.8+/-2,623.8 COI/ml; III:6 004.5+/-2,625.5 COI/ml; IV:6,455.6+/-2,344.4 COI/ml. There were no differences among groups before apportion (Fbefore apportion=0.768, P=0.513).Serum HBsAg levels apportioned by the hepatic parenchyma cell volume (hepatic cell quantity) among hepatic fibrosis stages were: I :9 417.5+/-4,034.2 COI/ml; II :10,093.3+/-4,183.4 COI/ml; III:10,177.1+/-4,445.0 COI/ml; IV:12,166.6+/-4,418.5 COI/ml. There were significant differences among the groups after apportion (Fafter apportion=57.077, P<0.001).

CONCLUSIONSerum HBsAg levels apportioned by the same hepatic parenchyma cell volume (hepatic cell quantity), rather than serum HBsAg levels, increased with hepatic pathological progress.

Hepatitis B ; Hepatitis B Surface Antigens ; Hepatitis B e Antigens ; Hepatitis B virus ; Hepatocytes ; Humans ; Inflammation ; Liver Cirrhosis

AIM:To investigate whether rebamipide repairs the small intestinal epithelial barrier in aspirin-induced small intestinal injury (SII) in mice and its mechanism.METHODS:Small intestinal injury was induced by aspirin (200 mg · kg-1 · d-1 for 5 d) in BALB/c mice.Based on the treatment with aspirin and/or rebamipide (320 mg ·kg-1 · d-1),the mice were divided into 4 groups (n =18 in each group).The living mice in each group (n =6) were sacrificed via cervical dislocation method at day 0,day 5,and day 10.The structure and function of intestinal barrier and the levels of the signaling pathway factors were measured by transmission electron microscopy,immunohistochemistry,qPCR,and Western blot.RESULTS:Tight junctions between intestinal epithelial cells improved significantly after rebamipide treatment.The expression of ZO-1 and occludin in the injured small intestine showed a gradually increasing trend after rebamipide administration (P ＜ 0.05).There was a decreased trend of D-lactate level in rebamipide-treated SII mice (P ＜ 0.05).The expression of cyolooxygenase-2 (COX-2),β-catenin,and c-Myc,and prostaglandin E2 concentration in small intestinal tissues were significantly increased in rebamipide treatment group (P ＜ 0.05).However,down-regulated COX-1 expression in the SII mice was sustained at a low level after rebamipide administration.CONCLUSION:Rebamipide repairs the injury of small intestinal mucosa and improves the structure and function of small intestinal barrier in aspirininduced SII mice by up-regulating the expression of COX-2.