Background A reliably highly effective high‐dose proton‐pump inhibitor plus amoxicillin (dual Helicobacter pylori therapy) has remained elusive. We compared whether the addition of bismuth to high‐dose dual therapy would improve the efficacy of high‐dose dual therapy as first‐line treatment. Methods This was an open‐label, randomized single‐center study of 160 treatment‐naive patients with H. pylori infection who were randomly assigned to 14‐day therapy with esomeprazole 40 mg twice a day plus amoxicillin 1 g three times a day with or without bismuth potassium citrate 600 mg (elemental bismuth 220 mg) twice a day. Antibiotic resistance was determined by agar dilution method and eradication by 13C‐urea breath test. Results The per‐protocol eradication rates were 96.1%; 95% CI = 88.9%‐99.2% (73/76) without bismuth vs 93.3%; 95% CI = 85.1%‐97.8% (70/75) with bismuth (P = 0.494). The intention‐to‐treat eradication rates were 92.5%; 95% CI = 84.4%‐97.2% (74/80) without bismuth and 88.8%; 95% CI = 79.7%‐94.7% (71/80) with bismuth (P = 0.416). Resistance to amoxicillin, clarithromycin, metronidazole, and levofloxacin was 0%, 31.7%, 81.4%, and 40.7%, respectively. Smoking reduced treatment effectiveness limited to those not receiving bismuth. The per‐protocol eradication rates were 70% (7/10) vs 100% (66/66) in smokers vs non‐smokers without bismuth (P = 0.002), and 100% (10/10) in smokers vs 92.3% (60/65) in non‐smokers with bismuth (P = 1.0). The adverse event rates were 7.5% (6/80) without bismuth vs 11.3% (9/80) with bismuth (P = 0.416). Conclusions Fourteen‐day high‐dose dual therapy was both effective and safe for first‐line treatment in a region of high prevalence antibiotic resistance. Adding bismuth only improved treatment effectiveness among smokers.
BackgroundMetabolic syndrome (MetS) is associated with carotid intima-media thickness (CIMT), which is a good predictor of cardiovascular disease (CVD). However, among individuals with MetS, direct comparative data regarding the utility of the apoB/apoAΙ ratio and the non-HDL-C/HDL-C ratio to diagnose carotid atherosclerosis are scarce, particularly in Chinese populations. We aimed to determine the relationship between the apoB/apoAΙ ratio and the non-HDL-C/HDL-C ratio and carotid atherosclerosis among Chinese individuals with MetS.MethodsWe performed a retrospective study of 5822 Chinese participants who underwent a routine health screening examination. Lipid profiles, fasting glucose, fasting insulin, CRP, apoB, apoAΙ and CIMT were measured.ResultsWe observed that among Chinese individuals with MetS, men (53.95 ± 0.58 ys) developed carotid atherosclerosis at a younger age than women (58.47 ± 1.17 ys) (P < 0.001). Both the apoB/apoAΙ ratio and the non-HDL-C/HDL-C ratio positively correlated with carotid atherosclerosis among Chinese individuals with MetS, particularly among women. Meanwhile, CIMT increased progressively across the quartiles of the non-HDL-C/HDL-C ratio (P for trend, < 0.05). Receiver Operating Characteristic (ROC) analysis indicated that the AUC of the apoB/apoAΙ ratio (0.561) was higher than that of the non-HDL-C/HDL-C ratio (0.522) in men (P < 0.05) and the AUC of the apoB/apoAΙ ratio (0.640) was lower than that of the non-HDL-C/HDL-C ratio (0.695) in women (P < 0.05). Among Chinese individuals with MetS, the AUC of the non-HDL-C/HDL-C ratio was more prominent among women compared with men (P < 0.05).ConclusionOur findings indicate that among individuals with MetS, Chinese men develop carotid atherosclerosis at a much younger age than women. There were no significant differences between the apoB/apoAΙ ratio and the non-HDL-C/HDL-C ratio for the prediction of carotid atherosclerosis among Chinese individuals with MetS. Among Chinese individuals with MetS, the utility of the non-HDL-C/HDL-C ratio was found to be greater among women than among men.
The aim of the present study was to investigate the effect of cantharidin (CTD) on human gastric cancer cells and to explore the underlying mechanisms of these effects. The human gastric cancer SGC-7901 and BGC-823 cell lines were treated with CTD. MTS assays were then employed to examine cellular proliferation, flow cytometry was used to analyze the cell cycle and apoptosis, and western blot analysis was used to determine protein expression levels. It was found that CTD inhibited the proliferation of the human gastric cancer SGC-7901 and BGC-823 cells in a dose- and time-dependent manner in vitro. CTD also induced G2/M phase arrest and cellular apoptosis in a dose-dependent manner. In addition, CTD increased the levels of p21, caspase-7, -8 and -9, activated caspase-3, poly ADP ribose polymerase and Bad, but decreased the levels of cyclin-dependent kinase 1, cyclin A and B, B-cell lymphoma-2 (Bcl-2) and Bid. The present results suggested that CTD may inhibit the proliferation of human gastric cancer SGC-7901 and BGC-823 cells in vitro by inducing G2/M phase arrest and cell apoptosis. CTD may induce cellular G2/M phase arrest by regulating cycle-associated proteins and induce apoptosis by activating a caspase cascade or regulating the Bcl-2 family proteins.
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