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R Todorov

Publications and source records attributed to R Todorov.

5 recordsLinked to original sources
PubMed2001

Electric light scattering from single-stranded DNA in linear polyacrylamide solutions.

The electric light scattering (ELS) of ssDNA (calf thymus, 10 kbp, 55 micrograms/mL) in denaturing polyacrylamide (PAA) solutions was studied as a function of applied sinusoidal electric field and polymer concentration. Electric fields of strengths up to 300 V/cm and of frequencies between 100 and 5000 Hz were applied. It was found that the ELS effect increases with the field strength and decreases at high frequencies. The dependence of the ELS effect of ssDNA on polymer concentration passes through a maximum at 1% PAA. The relaxation times of decay of the ELS effect increase with increasing polymer concentrations. It was demonstrated that ELS is a useful method for investigation of ssDNA behavior in the course of pulse-field electrophoresis in polymer solutions.

Acrylic Resins↗
PubMed1998

Peroxynitrite is not a major mediator of endothelial cell injury by activated neutrophils in vitro.

OBJECTIVE: Human polymorphonuclear leukocytes (PMN) produce nitric oxide (NO), superoxide (O2.-) and peroxynitrite (ONOO-) upon stimulation. We investigated the role of ONOO- in PMN-induced injury to cultured bovine aortic endothelial cells (BAEC). METHODS: BAEC were cocultured with phorbol 12-myristate 13-acetate (PMA)-activated human PMN (effector-to-target ratio, 10:1) and injury to BAEC was evaluated at intervals by 51Cr release assay. The levels of NO, O2.-, ONOO- and nitrotyrosine, a reaction product of ONOO-, were also measured, and the influence of NO synthase inhibitors, O2.- and hydroxyl radical scavengers and other effectors was examined. RESULTS: In BAEC cocultured with PMA-activated PMN, 51Cr release was significantly increased [14.6 +/- 2.2% at 2 h (p < 0.05) and 42.6 +/- 2.7% at 4 h (p < 0.01); control (nonactivated PMN), < 4%]. Superoxide dismutase (100 U/ml) reduced 51Cr release to 4.6 +/- 2.2% at 2 h (p < 0.05). N-Iminoethyl-L-ornithine (L-NIO, 0.1 mM) potentiated 51Cr release (30.6 +/- 3.8% at 2 h, p < 0.01), and the potentiation was eliminated by anti-CD18 monoclonal antibody. The 51Cr release was completely prevented by dimethyl sulfoxide or by deferoxamine. Treatment of PMN with L-NIO inhibited NO generation and increased O2.- production. The nitrotyrosine level did not increase in BAEC cocultured with PMA-activated PMN. CONCLUSION: NO-derived ONOO- is not a major cytotoxic mediator in BAEC injury by activated PMN. NO may have a cytoprotective effect by inhibiting PMN adherence to endothelial cells.

Animals↗
PubMed1987

[Infusion treatment with nitrites of patients with acute myocardial infarct and unstable angina pectoris].

The results of prolonged infusion treatment with Trinitrosan and Isoket of 29 patients with acute myocardial infarction and unstable angina pectoris are reported. The drug action on the anginal syndrome, accompanying cardiac failure, heart rate and arterial tension is analysed. The action on the dynamic of enzyme activity and of the electrocardiograms during the treatment is compared with a control group of healthy persons. The results show full therapeutic efficacy in relation to the anginal syndrome and cardiac failure without any other medication in 1/2 of the patients; a partial antianginal effect is found in 1/4 of the patients treated. The examinations did not show any favourable action of the drugs on the enzymes and ECGs followed up in dynamics. The nitrites in the doses applied show no negative action on the heart rate and arterial tension and no special hemodynamics control is required.

Angina Pectoris↗