Objective To investigate the possible effects of aspirin and indomethacin on the growth of Helicobacter pylori(H.pylori) and the effects of aspirin on the susceptibility of H.pylori to some antimicrobials. Methods Kinetic studies of H.pylori were performed by inoculating strains in Brucella broth with different concentrations of aspirin and indomethacin. Growth of bacteria in the broth was assessed spectrophotometrically and by viable colony count after incubation for 24 and 48 hours. Bacteria morphology was studied by Gram stain under light microscopy. MICs of aspirin and indomethacin were determined by standard agar dilution method. MICs of amoxicillin, clarithromycin and metronidazole were measured in the presence and in the absence of aspirin by E test method. Results Kinetic studies revealed that aspirin and indomethacin inhibited the growth of H.pylori in a dose dependent manner and the bactericidal activities of these agents were due to cell lysis. Aspirin at 400 ?g/ml produced about 2 logs decrease in CFU per milliliter at 48 hours. The assemble inhibition effects were obtained when 100 ?g/ml indomethacin tested. The MIC 90 of H.pylori for aspirin and indomethacin were 512 ?g/ml and 128 ?g/ml, respectively. Increased susceptibility to amoxicillin, clarithromycin and metronidazole of H. pylori were induced by aspirin. Conclusions Aspirin and indomethacin could significantly inhibit the growth of H.pylori when incubated in Brucella broth in vitro. A subinhibitory concentration of aspirin enhanced the susceptibility of H. pylori to antimicrobial agents.

Objective: To investigate whether initial periodontal therapy may affect the presence of oral Helicobacter pylori(Hp), and to compare the genotype of Helicobacter pylori in oral cavity and that in stomach. Methods: 56 patients with gastric Hp and periodontitis were enrolled in this study. PCR was carried out to identify the presence of Hp in the samples before and after initial periodontal therapy(group 1) or medicine therapy(group 2). DNA sequence of PCR products of 5 patients and 1 Hp infected patient's relative was compared and analyzed. Results: Four weeks after medicine therapy, the rate of Hp in oral cavity was singnificantly lower in group 1 than that in group 2 (3.0% vs 26.1%, P

Objective To compare the efficacy of pantoprazoh based short-term quadruple regimens in the treatment of Helicobacter pylori (H. Pylori) infection for 4 days,5 days or 7days. Methods 166 patients with H. Pylori associated severe gastritis were randomly divided into pantoprozole quadruple regimens of 4-day group (n =61) ,5-day group (n = 54) or 7-day group (n = 51). The regimen was pantoprazole 40 mg,bismuth potassium citrate 220 mg,elarithromycin 250 mg and amoxicillin 1 g twice daily. The patients received pantoprazole for 1 week, bismuth potassium citrate for 2 weeks,clarithromycin and amoxicillin for 4 days,5 days or 7 days respectively. The H. Pylori eradication and symptomatic relief was determinded by 13C-UBT at least 4 weeks after the therapy. Results The H. Pylori eradication rates of 4-day,5-day or 7-day panteprazole quadruple regimens were 73.8% (45/61) ,75.9% (41/54) and 80.4% (41/51) respectively. The pain relief rates were 82.4% (42/51) ,85.1% (40/47) and 88.9% (40/45) in 4-day,5-day and 7 day group. Conclusion The 4-day and 5- day pantoprazoh based quadrual therapy is a short- term, effective, safe and lower therapeutic- cost regimen for H. Pylori eradication.

Gastric cancer (GC) is one of the most frequent malignant tumors. In order to systematically characterize the cellular and molecular mechanisms of intestinal GC development, in this study, we used 22 K oligonucleotide microarrays and bioinformatics analysis to evaluate the gene expression profiles of GC in 45 tissue samples, including 20 intestinal GC tissue samples,20 normal appearing tissues (NATs) adjacent to tumors and 5 noncancerous gastric mucosa tissue samples. These profiles allowed us to explore the transcriptional characteristics of GC and determine the change patterns in gene expression that may be of clinical significance. 1519 and 1255 differentially- expressed genes (DEGs) were identified in intestinal GC tissues and NATs, respectively, as determined by Bayesian analysis (P < 0.001). These genes were associated with diverse functions such as mucosa secretion, metabolism, proliferation, signaling and development, which occur at different stages of GC development.

OBJECTIVETo elucidate the impact of Hes1 on the proliferation and apoptosis of acute myeloid leukemia (AML) cells.

METHODSThe expression levels of Hes1 and p21 in AML patient samples and myeloid leukemia cell lines were analyzed by real-time PCR. Hes1 was up-regulated by retrovirus transfection in AML cell lines and the proliferation capacity were assayed by MTT, cell cycle by Hoechst/PY, apoptosis by AnnexinV.

RESULTSThe expression of Hes1 in primary AML cells and HL-60, U937, KG1a cell lines were 0.67 ± 0.24, 0.59 ± 0.43, 0.42 ± 0.03, and 0.32 ± 0.26, respectively, and p21 were 0.54 ± 0.01, 0.44 ± 0.12, 0.36 ± 0.12, and 0.59 ± 0.43, respectively. Hes1 expression levels after transduction in HL-60, U937, KG1a were 4.9 ± 0.2, 5.2 ± 0.4, 5.8 ± 0.5, respectively. Induced activation of Hes1 led to AML cells growth arrest and apoptosis, which was associated with an enhanced p21 expression. Besides, activated Hes1 led to AML cells growth inhibition in vivo.

CONCLUSIONHes1 could mediate growth arrest and apoptosis in AML cells, which may be a novel target for AML.

Apoptosis ; Basic Helix-Loop-Helix Transcription Factors ; Cell Cycle ; Cell Line, Tumor ; Homeodomain Proteins ; Humans ; Leukemia, Myeloid, Acute ; Transcription Factor HES-1 ; Up-Regulation