Magnetic isotope effect of magnesium (25)Mg on E. coli resistance to antibiotics.

Effects of synergism and antagonism of antibacterial drugs and magnetic isotope of magnesium (25)Mg on antibiotic resistance of bacteria E. coli were discovered. Fourteen antibiotics from seven different groups were tested. The increase in antibiotic resistance in the presence of the ion (25)Mg(2+) was discovered in E. coli cells incubated with quinolones/fluoroquinolones, indicating the inhibiting effect of the magnetic moments of nuclei (25)Mg on DNA synthesis. The change in antibiotic resistance was also detected in bacteria affected by magnesium (25)Mg and certain antibiotics from aminoglycoside and lincosamide groups.

[Role of endothelial dysfunction, the interface between hemostatic and system inflammatory responses in the pathogenesis of an infectious inflammation-dependent exacerbation of chronic obstructive pulmonary disease].

AIM: To analyze the systemic manifestations of vascular endothelial damage, the activation of hemostatic and inflammatory responses in patients with an infectious inflammation-dependent exacerbation of chronic obstructive pulmonary disease (COPD). SUBJECTS AND METHODS: The paper provides the data of examinations of 111 patients with the clinical signs of an infectious inflammation-dependent exacerbation of COPD who had 2 or 3 positive criteria elaborated by N. Anthonisen et al. (1987). The patients were divided into 2 phenotypically different subgroups: 1) 92 (82.9%) COPD patients without clinical manifestations of bronchoectasis; 2) 19 (17.1%) patients with COPD concurrent with documented bronchiectasis. The patient subgroups were matched for smoking status and the characteristics of COPD and respiratory failure. The investigators assessed the time course of changes in the serum level of endothelin-1 (ET-1), the aggregation function of platelets, and the plasma concentrations of D-dimers and homocysteine in patients with COPD compared to healthy, never smokers (n = 35) and smokers (n = 27). RESULTS: An increase in the levels of the endothelial dysfunction markers ET-1 and homocysteine was found in patients with COPD, which was comparable with the changes in these indicators in the group of smokers. In both subgroups, the rise in plasma D-dimer levels was more pronounced in the patients with a COPD exacerbation than in the smokers. Its therapy with systemic and inhaled glucocorticosteroids reduced C-reactive protein and ET-1 levels in both patient subgroups and in D-dimers in subgroup 1. Elevated D-dimer levels remained when achieving remission, which points to the risk of thrombogenic and thromboembolic events in the patients with an infectious inflammation-dependent exacerbation of COPD and concomitant circulatory system diseases. CONCLUSION: The patients with an infectious inflammation-dependent exacerbation of COPD are observed to have elevated peripheral blood markers of endothelial dysfunction and thrombinemia. These changes are pathogenetically caused by smoking or neutrophilic inflammation and associated with a higher risk of thrombogenic events.

[Low-dose cytosine-arabinoside (Ara-C) therapy for chronic myeloid leukemia]. / Primenenie malykh doz tsitozin-arabinozida (Ara-C) dlia lecheniia bol'nykh khronicheskim mieloleikozom.

The effects of low doses of cytosine-arabinoside (Ara-C) were studied in 17 patients with chronic myeloid leukemia: chronic, resistant to IFN and hydroxyurea therapy (including 4 cases of advanced chronic disease)--7, and tumor progression--10. Hematologic effect was recorded in 7 chronic patients tolerant to hydroxyurea and alpha-interferon therapy. Among 10 cases of tumor progression, chronic stage II was observed in 3, stabilization (tumor progression short of blastic crisis)--5, and without effect--1. Low-dose Ara-C treatment was considered effective in 15 (88%) out of 17 patients.