High-dose ecabet sodium improves the eradication rate of helicobacter pylori in dual therapy with lansoprazole and amoxicillin

AIM: The additive effect of ecabet sodium in combination with dual therapy on Helicobacter pylori eradication was evaluated. METHODS: H. pylori-positive chronic gastritis patients were randomly assigned to one of the following three groups and medicated for 2 weeks. Group LA: dual therapy (lansoprazole 30 mg o.d. plus amoxicillin 750 mg b.d.). Group LA1E: dual therapy plus ecabet sodium (1 g b.d.). Group LA2E: dual therapy plus ecabet sodium (2 g b.d.). Patients were evaluated 4 weeks after the cessation of treatment by culture and 13C-urea breath test. RESULTS: Seventy-one patients (mean age, 56.6 years; range, 26-79 years; 40 males, 31 females) were enrolled in this prospective, single-blind study, and 68 completed the protocol. The eradication rates per protocol patient were 43% in group LA, 62% in group LA1E, and 79% in group LA2E, and those on the intention-to-treat basis were 42% in group LA, 57% in group LA1E and 79% in group LA2E. The eradication rate in group LA2E was significantly higher than group LA (P=0.032 in per protocol, P=0.022 in intention-to-treat). Adverse effects were observed in 10 patients in this study. There were no severe adverse effects caused by ecabet sodium. CONCLUSION: High-dose ecabet sodium increases eradication rates of H. pylori in dual therapy with lansoprazole and amoxicillin.     

Prediction of curve progression in idiopathic scoliosis based on initial roentgenograms. A proposal of an equation

A retrospective study was conducted in 122 patients with idiopathic scoliosis who were followed for more than 2 years. There were 58 patients who showed 5 degrees (Cobb) or more progression, and 41 patients who showed no progression. Only those who did not receive any treatment or who failed to comply with brace treatment were selected, to eliminate the effect of treatment. In the early phase of the study, 12 parameters were put into a multivariate analysis to observe the relative weight of each of them, which led the authors to eliminate the following five parameters: 1) Cobb angle, 2) rotation of the apical vertebra, 3) deviation of the apical vertebra, 4) Risser's expected correction: (standing angle--supine angle) X 3, and 5) maturation index of the iliac apophysis. Through a multiple regression analysis, an equation was obtained to correlate the predictive and the real progression within 10 degrees deviation.     

Immunological cross-reactivities of sulfocephalosporins.

The immunological cross-reaction among sulfocephalosporins (cefsulodin, SFC-I, SFC-II), cephaloridine, sulbenicillin, penicillin G and 7-aminocephalosporanic acid has been investigated. A specific antibody was produced in rabbits against several structurally related haptens. The sensitization was conducted with a hapten-human serum albumin conjugate, which was prepared in an alkaline solution, with Freund's complete adjuvant. A cross-reaction was claraly demonstrated between sulfocephalosporins and sulbenicillin, but not between sulfocephalosporins and cephaloridine, penicillin G or 7-aminocephalosporanic acid.     

Overexpression of Aurora-A potentiates HRAS-mediated oncogenic transformation and is implicated in oral carcinogenesis

Aurora kinases are known to play a key role in maintaining mitotic fidelity, and overexpression of aurora kinases has been noted in various tumors. Overexpression of aurora kinase activity is thought to promote cancer development through a loss of centrosome or chromosome number integrity. Here we observed augmentation of G12V-mutated HRAS-induced neoplastic transformation in BALB/c 3T3 A31-1-1 cells transfected with Aurora-A. Aurora-A-short hairpin RNA (shRNA) experiments showed that the expression level of Aurora-A determines susceptibility to transformation. Aurora-A gene amplification was noted in human patients with tongue or gingival squamous carcinoma (4/11). Amplification was observed even in pathologically normal epithelial tissue taken at sites distant from the tumors in two patients with tongue cancer. However, overexpression of Aurora-A mRNA was observed only within the tumors of all patients examined (11/11). Our data indicate that Aurora-A gene amplification and overexpression play a role in human carcinogenesis, largely due to the effect of Aurora-A on oncogenic cell growth, rather than a loss of maintenance of centrosomal or chromosomal integrity.     

Aurora-B/AIM-1 kinase activity is involved in Ras-mediated cell transformation

Aurora-B, previously known as AIM-1, is a conserved eukaryotic mitotic protein kinase. In mammals, this kinase plays an essential role in chromosomal segregation processes, including chromosome condensation, alignment, control of spindle checkpoints, chromosome segregation, and cytokinesis. Aurora-B is overexpressed in various cancer cells, suggesting that the kinase activity perturbs chromosomal segregation processes. Its forced overexpression induces chromosomal number instability and progressive tumorigenicity in rodent cells in vitro and in vivo. Nevertheless, based on focus formation in BALB/c 3T3 A31-1-1 cells, Aurora-B is not oncogenic. Here, we show that Aurora-B kinase activity augments Ras-mediated cell transformation. RNA interference with short hairpin RNA inhibits transformation by Ras and its upstream oncogene Src, but not by the downstream oncogene Raf. In addition, the inner centromere protein, which is a passenger protein associated with Aurora-B, has a similar ability to potentiate the activity of oncogenic Ras. These data indicate that elevated Aurora-B activity promotes transformation by oncogenic Ras by enhancing oncogenic signaling and by converting chromosome number-stable cells to aneuploid cells.