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Helicobacter pylori as the second most common cause of gastric cancer in the world infects approximately half of the developed countries population and 80% of the population living in developing countries. Integrons as genetic reservoirs play major roles in dissemination of antimicrobial resistance genes. To the best of our knowledge, this is the first study to report carriage of class 1 and 2 integrons and associated gene cassettes in H. pylori isolates from Iran. This crosssectional study was conducted in Tehran among 110 patients with H. pylori infection. Antimicrobial susceptibility testing (AST) for H. pylori strains were assessed by the micro broth dilution method. Class 1 and 2 integrons were detected using PCR. In order to determine gene cassettes, amplified fragments were subjected to DNA sequencing of both amplicon strands. The prevalence of resistance to clarithromycin, metronidazole, clarithromycin, tetracycline, amoxicillin, rifampin, and levofloxacin were 68.2% (n=75), 25.5% (n=28), 24.5% (n=27), 19.1% (n=21), 18.2% (n=20) and 16.4% (n=18), respectively. Frequency of multidrug resistance among H. pylori isolates was 12.7%. Class 2 integron was detected in 50 (45.5%) and class 1 integron in 10 (9.1%) H. pylori isolates. The most predominant gene cassette arrays in class 2 integron bearing H. pylori were included sateraaadA1, dfrA1sat2aadA1, blaoxa2 and, aadB whereas common gene cassette arrays in class 1 integron were aadBaadA1cmlA6, aacA4, blaoxa2, and catB3. The high frequency of class 2 integron and multidrug resistance in the present study should be considered as a warning for clinicians that continuous surveillance is necessary to prevent the further spread of resistant isolates.

Nine different β-thioxoketones of general formula R(1)C(=O)CH2C(=S)R(2) (R(1) = C6H5, R(2) = C6H5L1; R(1) = C6H5, R(2) = p-CF3C6H4L2; R(1) = p-MeOC6H4, R(2) = C6H5L3; R(1) = p-MeOC6H4, R(2) = p-CF3C6H4L4; R(1) = C5H4N, R(2) = C6H5L5; R(1) = p-IC6H4, R(2) = C6H5L6; R(1) = C6H5, R(2) = p-IC6H4L7; R(1) = C6H5, R(2) = C10H7L8 and R(1) = CH3, R(2) = C6H5L9) and their tris-substituted bismuth(III) complexes having the general formula [Bi{R(1)C(=O)CHC(=S)R(2)}3] were synthesised and fully characterised. The solid state structure of [Bi{C5H4NC(=O)CHC(=S)C6H5}3] B5 was determined by crystallography and revealed that the three β-thioxoketonato ligands are bound to bismuth(III) centre in a bidentate fashion through O and S atoms. The bismuth(III) complexes and the corresponding thioxoketones were assessed for their activity against H. pylori. All of the bismuth(III) complexes were highly active against H. pylori having a MIC of greater than or equal to 3.125 μg mL(-1), while the free acids were essentially not toxic to the bacteria. The anti-leishmanial activity of all the bismuth(III) β-thioxoketonates and the corresponding free acids were assessed against L. major promastigotes. The toxicity towards human fibroblast cells was also assessed. All of the free β-thioxoketones were selectively toxic to the L. major promastigotes displaying some potential as anti-leishmanial agents. Among these [C6H5C(=O)CH2C(=S)C6H5] L1 and [C5H4NC(=O)CH2C(=S)C6H5] L5 showed comparable activity to that of Amphotericin B, killing about 80% of the L. major promastigotes at a concentration of 25 μM (6.0 μg mL(-1)). The bismuth(III) β-thioxoketonate complexes were toxic to both the L. major promastigotes and fibroblast cells at high concentrations, but gave no improvement in anti-leishmanial activity over the free β-thioxoketones.

Background and Study Aims: Uraemic patients show susceptibility to gastrointestinal mucosal lesions and colonisation by Helicobacter pylori (HP). Antibiotic resistance constitutes a problem in treatment and bismuth preparations are toxic in uraemic patients. This study aimed to assess the correlation between creatinine clearance (CrCl) and eradication of HP infection with new sequential and standard triple therapeutic regimens., Patients and Methods: A total of 120 HP-positive patients with renal function impairment and 60 control patients with HP infection were enrolled in this study. Patients were divided into four groups on the basis of CrCl and were randomly assigned to one of the two different regimens: A 14-day standard triple therapy with 20mg omeprazole bid, 1000mg amoxicillin bid and 500mg clarithromycin bid and a new sequential regimen with 20mg omeprazole bid and 1000mg amoxicillin bid both for 14 days, 500mg ciprofloxacin bid for the first 7 days and 200mg furazolidone bid for the last 7 days. Doses of amoxicillin, clarithromycin and ciprofloxacin were reduced to 50% in the cases of CrCl <30mgdl(-1)., Results: One hundred and sixty two out of 180 HP-positive patients (54.3% male, 51.6±12.1 years) completed treatment in the four groups and were studied. According to renal function they were classified into group A (n=39), haemodialysis (HD) patients; group B (n=37), CrCl <30mgdl(-1) without HD; group C (n=36), CrCl between 30 and 60mgdl(-1); and group D (n=50), control subjects with CrCl >90mgdl(-1). HP was successfully eradicated in 77.7% of patients with standard triple therapy and in 81.4% of patients with the sequential therapy. There was no significant difference among the study groups in the rate of HP-infection eradication with both regimens., Conclusion: HP eradication rates did not differ with both sequential and standard therapeutic regimens in uraemic and non-uraemic patients. We, therefore, prefer the standard triple therapy due to its simplicity and reported., (Copyright © 2011 Arab Journal of Gastroenterology. Published by Elsevier Ltd. All rights reserved.)

Nine different β-thioxoketones of general formula R1C(vO)CH2C(vS)R2 (R1 = C6H5, R2 = C6H5 L1; R1 = C6H5, R2 = p-CF3C6H4 L2; R1 = p-MeOC6H4, R2 = C6H5 L3; R1 = p-MeOC6H4, R2 = p-CF3C6H4 L4; R1 = C5H4N, R2 = C6H5 L5; R1 = p-IC6H4, R2 = C6H5 L6; R1 = C6H5, R2 = p-IC6H4 L7; R1 = C6H5, R2 = C10H7 L8 and R1 = CH3, R2 = C6H5 L9) and their tris-substituted bismuth(III) complexes having the general formula [Bi{R1C(vO)CHC(vS)R2}3] were synthesised and fully characterised. The solid state structure of [Bi{C5H4NC(vO)CHC(vS)C6H5}3] B5 was determined by crystallography and revealed that the three β-thioxoketonato ligands are bound to bismuth(III) centre in a bidentate fashion through O and S atoms. The bismuth(III) complexes and the corresponding thioxoketones were assessed for their activity against H. pylori. All of the bismuth(III) complexes were highly active against H. pylori having a MIC of greater than or equal to 3.125 μg mL-1, while the free acids were essentially not toxic to the bacteria. The anti-leishmanial activity of all the bismuth(III) β-thioxoketonates and the corresponding free acids were assessed against L. major promastigotes. The toxicity towards human fibroblast cells was also assessed. All of the free β-thioxoketones were selectively toxic to the L. major promastigotes displaying some potential as anti-leishmanial agents. Among these [C6H5C(vO)CH2C(vS)C6H5] L1 and [C5H4NC(vO)CH2C(vS)C4H5] L5 showed comparable activity to that of Amphotericin B, killing about 80% of the L. major promastigotes at a concentration of 25 μM (6.0 μg mL-1). The bismuth(III) β-thioxoketonate complexes were toxic to both the L. major promastigotes and fibroblast cells at high concentrations, but gave no improvement in anti-leishmanial activity over the free β-thioxoketones. [ABSTRACT FROM AUTHOR]

Two new substituted thiobenzoic acids, m-nitrothiobenzoic and m-sulfothiobenzoic acid, and six (four new) homo- and heteroleptic bismuth(iii) compounds derived from thiobenzoic acid and substituted thiobenzoic acid have been synthesised and fully characterised using both solvent free and solvent mediated methods; Bi(SC(=O)C[sub 6]H[sub 5])[sub 3] (3), PhBi(SC(=O)C[sub 6]H[sub 5])[sub 2] (4), Ph[sub 2]Bi(SC(=O)C[sub 6]H[sub 5]) (5), Bi(SC(=O)C[sub 6]H[sub 4]-m-NO[sub 2])[sub 3] (6), PhBi(SC(=O)C[sub 6]H[sub 4]-m-NO[sub 2])[sub 2] (7), and PhBi(SC(=O)C[sub 6]H[sub 4]-m-SO[sub 3]) (8). The solid-state structures of the previously reported Bi(SC(=O)C[sub 6]H[sub 5])[sub 3] (3) and PhBi(SC(=O)]C[sub 6]H[sub 5])[sub 2] (4) complexes have now been confirmed by X-ray crystallography. In the solid-state complex 3 forms a column-like polymeric structure resembling stacked bowls through pyramidal intermolecular Bi-S[sub 3] bonds of distance 3.359 , providing a Bi(iii) centre with a nine coordinate environment. Complex 4 forms discrete tetrameric units cemented by long intermolecular Bi-S (3.774 ), Bi-O(= C) (3.030, 3.071 ) and Bi-C bonds (3.627 ). The complexes were assessed for their activity against three strains of Helicobacter pylori and all show a minimum inhibitory concentration of 6.25 μg mL[sup -1], indicating that the high level of bactericidal activity is insensitive to the degree of substitution at the Bi(iii) centre. Six homo- and heteroleptic bismuth(iii) thiobenzoates of form Ph[sub 3-n]BiL[sub n] (n = -3) have been synthesised by solvent-mediated and solvent-free methods. The structures of the compounds derived from thiobenzoic acid have been determined by X-ray crystallography. Bactericidal studies against three strains of Helicobacter pylori show a minimum inhibitory concentration of 6.25 μg mL[sup -1] for all compounds, indicating that the high activity is independent of ligand type and degree of substitution at the Bi(iii) centre. [ABSTRACT FROM AUTHOR]