Antiferromagnet-Ferromagnet Transition in Fe1-xCuxNbO4.

Iron niobates, pure and substituted with copper (Fe1-xCuxNbO4 with x = 0-0.15), were prepared by the solid-state method and characterized by X-ray diffraction, Raman spectroscopy, and magnetic measurements. The results of the structural characterizations revealed the high solubility of Cu ions in the structure and better structural stability compared to the pure sample. The analysis of the magnetic properties showed that the antiferromagnetic-ferromagnetic transition was caused by the insertion of Cu2+ ions into the FeNbO4 structure. The pure FeNbO4 structure presented an antiferromagnetic ordering state, with a Néel temperature of approximately 36.81K. The increase in substitution promoted a change in the magnetic ordering, with the state passing to a weak ferromagnetic order with a transition temperature (Tc) higher than the ambient temperature. The origin of the ferromagnetic ordering could be attributed to the increase in super-exchange interactions between Fe/Cu ions in the Cu2+-O-Fe3+ chains and the formation of bound magnetic polarons in the oxygen vacancies.

A clinical study of Japanese patients with ulcer induced by low-dose aspirin and other non-steroidal anti-inflammatory drugs.

BACKGROUND: The incidence and severity of non-steroidal anti-inflammatory drugs (NSAIDs)-induced gastro-duodenal ulcer have not been extensively studied in Japan. AIM: We performed a prospective study to clarify NSAIDs-induced gastro-duodenal injury, focusing especially on low-dose aspirin (L-A). METHODS: Two hundred and thirty-eight patients with bleeding peptic ulcers admitted to our hospital. History of taking NSAIDs and anti-ulcer drugs was obtained from all patients who underwent endoscopic examinations. The lesion scores of patients taking L-A were classified numerically from zero (no lesion) to five (ulcer). RESULTS: The NSAIDs were associated with 28.2% of hemorrhagic ulcers. The rates of patients using L-A, loxoprofen, diclofenac, and combination of two of these drugs were 27, 16, 10 and 9%, respectively. Co-administered anti-ulcer drugs were cytoprotective anti-ulcer drugs (27%), H2 receptor antagonists (16%), PPI (4%), and none (53%). In patients taking L-A, H2 receptor antagonists were used most frequently. The HP was positive in 63% of L-A-induced ulcer cases and in 69% of NSAIDs other than low-dose aspirin-induced ulcer cases. The lesion scores of patients taking L-A with H2 receptor antagonists or PPI were significantly lower than those of patients who were taking only L-A (P < 0.05). CONCLUSIONS: Approximately one-third of hospitalized patients with NSAIDs-induced hemorrhagic ulcer showed an association with L-A. Prospective randomized controlled trials including H2 receptor antagonists are required to establish preventive efforts aimed at L-A-induced gastro-duodenal injury.

Transfer of ciprofloxacin to bile and determination of biliary metabolites in humans.

1-Cyclopropyl-6-fluoro-1,4-dihydro-4-oxo-7-piperazin-1-ylquinol ine-3-carboxylic acid (ciprofloxacin, Bay o 9867; designated tradename: Ciprobay) is a new synthetic pyridone-carboxylic acid antimicrobial agent for oral use which has high activity against gram-positive and gram-negative bacteria and anaerobes. In 8 patients with T-tube drainage, the biliary excretion of ciprofloxacin and its metabolites including the glucuronide were determined by bioassay and HPLC. After single oral administration of ciprofloxacin 400 mg in 5 patients, the biliary excretion of the drug was investigated for 12 h. The peak biliary concentration of ciprofloxacin was 15.0 +/- 6.3 micrograms/ml by bioassay and 11.0 +/- 4.0 micrograms/ml by HPLC. The biliary concentration of the drug was 10 times as high as its serum concentration, indicating a good biliary excretion. The proportion of ciprofloxacin glucuronide in the biliary excretion, calculated from the difference between the concentration before beta-glucuronidase hydrolysis and that after the hydrolysis, was 30%. In 3 patients, biliary metabolites of ciprofloxacin were investigated. Main metabolites were the sulfone compound (Bay s 9435) and the oxo compound (Bay q 3542) and, in addition, a minor metabolite was detected.