This paper takes the Traditional Chinese Medicine health population science as a social service . From the theoretical perspective .There's a clue that using the models of Perceived Service Quality , Determinants of Quality of Service , 5 Gaps Mode to find out the invisible zone of the continuous improvement of TCM populational sci -ence services.With the further analysis , this zone refers to the 5 gaps of the recognition differential .By minimizing the recognition differential , we form up a strategic program package for TCM populational science , which makes it dif-ferent.Besides, the real case of Guangdong Provincial hospital of TCM has verified that the good TCM populational Science service had demonstrated a positive influence to the Harmonious Relationship of doctor -patient.

Objective To investigate the clinical significance of ambulatory blood pressure monitoring in short-term prognosis of acute inferior myocardial infarction patients .Methods A total of 80 patients with acute inferior myocardial infarction received 24 hours ambulatory blood pressure monitoring after enrolled .According to the results of 24 hours ambulatory blood pressure monito-ring ,eligible patients were divided into dipper model group(n=29) and non-dipper model group(n=51) .Clinical information was collected and all patients were followed-up for major adverse cardiovascular events (MACE) .Results The rate of intravenous thrombolysis in dipper model group was significantly higher than that in non-dipper model group(t=4 .120 ,P=0 .021) .Night mean systolic blood pressure and night mean diastolic blood pressure were all significantly lower in dipper model group than in non-dipper model group(t=2 .032 ,P=0 .040 ;t=3 .175 ,P=0 .002) .The rate of cumulative MACE in non-dipper model group was significant-ly higher than that in dipper model group(t=2 .626 ,P=0 .041) .Multivariate logistic regression analysis showed that ,daytime mean systolic blood pressure(<90 mm Hg) was independent risk factor of MACE(P=0 .018 ,OR=1 .298) ,dipper model blood pressure (P=0 .019 ,OR=0 .769) and intravenous thrombolysis(P=0 .007 ,OR=0 .520) were protective factors for MACE .Conclusion Parameters of ambulatory blood pressure monitoring are closely correlated with prognosis of acute inferior myocardial infarction pa-tients ,and the change of blood pressure model is an important factor for short-term prognosis .

Objective To investigate the effect of Xiexin Decoction(XXD) on the early diabetic nephropathy(DN) of diabetic rats induced by high-fat diet with injection of streptozotocin(STZ).MethodsMale Sprague-Dawley rats were divided into two groups and fed with normal pellet diet(NPD) or high-fat diet(HFD),respectively,for a period of four weeks and then HFD-fed rats were ip injected with STZ.The diabetic rats were divided into three groups: model group,XXD group,and metformin group.After 13-weeks ig administration,fasting blood glucose(FBG),glycated hemoglobin(HbAlc),blood lipids(TG and TC),serum insulin(INS),renal function,kidney index,albumin in urine,and the renal histology and ultrastructure were observed.Results Compared with the model group,XXD reduced the levels of water intake,food consumption,urine volume,HbAlc,insulin resistance index(IRI),creatinine clearance rate(CCr),albumin in urine and blood lipids(P

Objective To investigate the effects and mechanism of magnetic microsphere combination of cisplatin with nano or micron ferric oxide particle on human hepatoma cell(HHC). Methods A human hepatoma cell line BEL-7402 was used in this study, 0.04?g/ml～8?g/ml of cisplatin(CDDP), cisplatin nano-ferric oxide magnetic microsphere(nCDDPmm) and micro-ferric oxide magnetic microsphere(mCDDPmm) were administered to the culture solution for culturing the BEL-7402 cell as the experimental groups,and in the control groups were administered with cisplatin 0?g/ml and magnetic microsphere without cisplatin respectively. The optic density of viable cell, cytotoxity index, growth curve of cell, cell cycle, proliferation index and apoptosis were assayed by MTT method, cell count and flow cytometry respectively. Results (1)The viable cell's optic density decreased and the cytotoxity index increased in human hepatoma cell following increasing dosages of CDDP, nCDDPmm and mCDDPmm in culture solution,presenting a dose-dependent manner(r value of three drugs were 0.95, 0.91 and 0.89 respective, P 0.05)between nCDDPmm and mCDDPmm. (3)Apoptosis rate of hepatoma cell increased ( P

Objective: To investigate the effect of protein ki nase C on signal transduction such as tyrosine phosphorylation, c-fos and c-ju n mRNA expression in antigen activated mast cells. Methods: RBL-2H3 cells either untreated or treated with phorbol 12-myristate 13 -acetate (PMA) were sensitized with anti-DNP IgE, and activated with DNP-BSA, histamine release and tyrosine phosphorylation were quantitatively measured by ELISA and flow cytometry, respectively. The effect of PKC on the ex pression of c-fos and c-jun in serum-deprived RBL-2H3 cells activated by DNP-BSA detected by ethidium staining of PCR-amplified cDNA, the amplified cDNA products were subjected to Southern blot hybridization using specific prob es to determine the veracity of amplification. Results: Tyr osine phosphorylation and histamine release were significantly reduced from (4.4 7±0.03)% to (2.79±0.07)% and (104.47±1.31) nmol/L to (60.75±1.38) nm ol/L, respectively, 45 min after DNP-BSA stimulation in sensitized cells pre treated with PMA for 48 h. Bands of the size predicted for the amplified cDNA we re obtained: 299 bp for c-fos, and 651 bp for c-jun, a decrease of 91% and 82% , respectively, for c-fos and c-jun mRNAs was observed in antigen stimulated c ells pretreated with PMA for 48 h. Conclusion: PKC plays an impo rtant role in modulating the tyrosine phosphorylation and histamine release resp onses and may upregulate the expression of c-fos and c-jun in antigen activate d mast cell.

Objective To investigate the expression of pSTAT5 in 7 pancreatic carcinoma cell lines,and the change of expression of pSTAT5 in pancreatic carcinoma cells SW1990 after growth hormone (GH) treatment, and explore its molecular mechanism. Methods Human pancreatic carcinoma cell lines (SW1990, Cap-1, Colo, Mia, AsPc, P3, PANC1) were cultured in vitro, and Western blotting was used to detect the expression of pSTAT5 in these cell lines. SW1990 in exponential growth phase was collected and nude Balb/c mice were inoculated with SW1990 cells. When tumors became palpable after inoculation, mice (normal saline group). 1 h, 2 h and 24 h after the last dose of GH treatment, the mice were sacrificed.Western blotting was used to detect the expression of pSTAT5 in SW1990 and inoculation tumor cells after GH injection. Results Positive expression of pSTAT5 was observed in all human pancreatic carcinoma cell lines (SW1990, Cap-1, Colo, Mia, Aspc, P3, PANC1). 5 minutes after GH (50 ng/ml) stimulation, the expression of pSTAT5 in SW1990 was 0.57 ±0.05, which was significantly increased; and it reached 0.64 ±0.04 at 10 minutes, then decreased to 0.39 ±0.03 at 15 minutes, however, it remained higher than that in the control group at 1 h (0.33 ± 0.02 vs 0.25 ± 0.06), and its expression at 2 h was 0.26 ± 0.03 and returned to the normal level. The expression of pSTAT5 in xenograft was not significantly changed. Conclusions GH could rapidly up-regulate the expression of pSTAT5 in SW1990 but the effect lasted for a relatively short period. GH had no significant effect on the expression of pSTAT5 in xenograft.

OBJECTIVE To investigate macrolide resistance and main molecular mechanisms in Mycoplasma pneumoniae. METHODS Thirty two throat swabs from children infected with M. pneumoniae were cultured by modified Hayflick medium. Antibiotic susceptibility test was used to screen the macrolide-resistant M. pneumoniae. The 23S rRNA gene sequences of the strains were determined with polymerase chain reaction and sequencing. RESULTS Nineteen strains were isolated from 32 throat swabs successfully.Fifteen strains were resistant to macrolide antibiotics according to the results of antibiotic susceptibility test. Once the strain was resistant to one of macrolide antibiotics,it would be resistant to the others. Sequencing results of the sensitive strains and the standard strain FH were completely same. Fifteen resistant strains presented A2063G point mutation in 23 SrRNA region Ⅴ, in which 2 examples showed the coexistence of the sensitive strain and the resistant strain. CONCLUSIONS Macrolide-resistant M. pneumoniae is common and serious at present. The antibiotic resistant isolate carries point mutations of the 23S rRNA region Ⅴ.

Objective: To investigate the effect of black currant extract on human esophageal squamous cancer cell Eca109 line to reveal its probable mechanism. Methods: The survival cells and protein synthesis of tumor cell lines treated with 10-1, 10 -2,10-3 g/ml of the water extracts of black currant for 24 h were determined by MTT and Bradford assays, and the cell-DNA ploidy distribution and apoptotic rate were measured by flow cytometry (FCM) and morphological observation. Results: There was significant inhibition of the cell survival and protein synthesis of cancer cells at dose of 10-1 g/ml of the extracts. In the normal rat liver cells, the cell survival was not affected. An apoptosis peak appeared before diploid peak in FCM and apoptotic rate was 49.6%, and morphological change of apoptosis was observed. Conclusion: Black currant could significantly inhibit growth of human esophageal squamous cancer cell Eca109 line through inducing apoptosis.

Objective To investigate the effect of GH on proliferation of pancreatic cancer cells and observe the features of IGF-IGFBP3 pathway in the host after GH administration. Methods Pancreatic cancer cells (SW-1990,PANC-1 and P3) during exponential growth stage were harvested and cultured in medium containing growth hormone (50 ng/ml). After 24, 48 and 72 hours, cells were counted using a Coulter Counter. Thirty-five Athymic nude Balb/c mice were inoculated with SW-1990cells. When tumors became palpable after inoculation, animals were randomized to receive GH points (1 h, 2 h, 6 h, 24 after the last injection), plasma samples were gathered for subsequent ELISA determination and liver was rapidly incised for immune blotting analysis. Results The results revealed that GH stimulated cell growth in vitro. GH elevated levels of IGF-Ⅰ , Ⅱ at the 1st , 2nd , 6th hour after the last injection. GH augmented the expression of IGFBP3 in the liver of the host in vivo (1 h, 2 h, 6 h, 24 h, respectively). Conclusion Such proteins as IGF- Ⅰ and Ⅱ might be associated with mechanism of last effect of GH on tumor host. The up-regulation of IGFBP3 by GH administration in the host may help to explain the phenomena that GH doesn't accelerate growth of pancreatic tumor in vivo.

Objective To study the impact of exogenous growth hormone (GH) on the levels of insulin-like growth factor-Ⅰ and -Ⅱ (IGF-Ⅰ, -Ⅱ) of the pancreatic cancer tissue and the small intestine mucosa of the host. Methods In situ hybridization was performed on pancreatic cancer cell lines (SW-1990) and inoculation tumor of the host to determine the location of the mRNA transcript encoding IGF R-Ⅰ,-Ⅱ. Athymic nude Balb/c mice were inoculated with SW-1990 cells. After inoculated tumors have become palpable, animals were randomized to receive GH (4 mg/kg once daily for 2 weeks) versus saline control. After the animals were killed at time point, tissues (tumor and small intestine) were rapidly incised for subsequent immune blotting analysis. Results Strong IGF R-Ⅰ,-Ⅱ mRNA hybridization signal could be detected in pancreatic cancer cell. There was no statistically significant difference between the level of IGF-Ⅰ, Ⅱ in the tumor of the GH and NS groups after 1 hours of GH injection (P>0.05). GH augmented the expression of IGF-Ⅰ(1 h : 0.33±0.05, P<0.05 ; 2 h : 0.34±0.04, P<0.05 ; 6 h:0.34±0.05, P<0.05), -Ⅱ(1 h : 0.36±0.05, P<0.05) in the small intestine mucosa of the host. Conclusions The expression of IGF-Ⅰ, Ⅱ in the small intestine mucosa of the host was elevated by GH, but not in the inoculation tumor in vivo. The discrepancy of GH-IGF pathway between inoculation tumor and small intestine of the host may help to explain the phenomena that GH doesn't accelerate growth of pancreatic tumor in vivo.