Publications by authors named "M A Ivin"

The complexes of La, Ce, Nd, Sm, Eu, Tb and Yb with benzoxazolyl-phenolate, benzothiazolyl-phenolate, benzoxazolyl-naphtholate, benzothiazolyl-naphtholate and 4,4,4-trifluoro-1-(2-thienyl)-1,3-butanedione ligands were treated with n,γ-irradiation upon a sustained (45 h, absorbed dose of 120 krad, flux of neutrons 5·10 n/cm) and a pulse mode (3 ms, absorbed dose of 130 krad, flux of neutrons 3.6·10 n/cm). It was found that main characteristics of the compounds (shape of substance, color, IR absorption and photoluminescent spectra) have not changed.

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A comparative study of the photoluminescence (PL) and radioluminescence (RL) of lanthanide complexes with benzimidazolylphenolate (NON), 4,4,4-trifluoro-1-(2-thienyl)-1,3-butanedionate (TTA) and 1,3-acetylacetonate (acac) ligands revealed significant differences in the total and relative intensity of emission. The PL spectra contain both bands of metal-centered and ligand centred emission while X-ray excited compounds display only the bands of Ln3+ ions, the relative intensity of which differs from that in UV excited analogues. The RL intensity of all the studied complexes is about 300 times lower than that of PL.

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Klebsiella pneumoniae is a significant cause of nosocomial pneumonia and an alarming pathogen owing to the recent isolation of multidrug resistant strains. Understanding of immune responses orchestrating K. pneumoniae clearance by the host is of utmost importance.

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Protective responses against pathogens require a rapid mobilization of resting neutrophils and the timely removal of activated ones. Neutrophils are exceptionally short-lived leukocytes, yet it remains unclear whether the lifespan of pathogen-engaged neutrophils is regulated differently from that in the circulating steady-state pool. Here, we have found that under homeostatic conditions, the mRNA-destabilizing protein tristetraprolin (TTP) regulates apoptosis and the numbers of activated infiltrating murine neutrophils but not neutrophil cellularity.

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Defense against bacterial infections requires activation of the immune response as well as timely reestablishment of tissue and immune homeostasis. Instauration of homeostasis is critical for tissue regeneration, wound healing, and host recovery. Recent studies revealed that severe infectious diseases frequently result from failures in homeostatic processes rather than from inefficient pathogen eradication.

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