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Results for “RADIATION SICKNESS”

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At least 955 records · Page 53Linked to original sources
PubMed2004

[Case of chronic radiation sickness with subsequent leukemia in track driver subjected to long-external gamma-irradiation (cesium-137)].

The article deals with consequences seen in track driver after prolonged exposure to radiation caused by "lost" gamma-source (cesium-137) that long remained in receptacle of the vehicle's left door. Radiation dose averaged 8 Gy. The authors presented clinical manifestations, changes in peripheral blood and bone marrow, cytogenetic data by progression of radiation hemopoiesis hypoplasy to myelodysplastic syndrome and to acute leukaemia.

Adult↗
PubMed1990

[Pyridoxal phosphate as an agent for normalizing the monoamine oxidase activity of the brain in radiation sickness].

A study was made of the influence of the coenzyme pyridoxal phosphate on the activity of mitochondrial monoaminoxidase (MAO) catalyzing oxidative deamination of serotonin at the exacerbation of acute radiation disease (on the 6th day after radiation exposure) in different parts of the brain (cerebral hemisphere, stem and cerebellum). Experiments were staged on rabbits, irradiated by x-ray at a dose of 4.5 Gy with a dose rate of 0.33 Gy/min. The peak of radiation disease was characterized by considerable changes in MAO activity resulting in catalysis of oxidative deamination of serotonin in different parts of the brain and in different mitochondrial subfractions. Pyridoxal phosphate produced a positive effect on monoaminoxidase activity, catalyzing serotonin deamination, and as a coenzyme it can be incorporated in a complex of drugs used for normalization of metabolism of mediators of the nervous system as well as for therapy of radiation injuries.

Animals↗
PubMed1987

[Interphase death of lymphoid cells: role in the genesis of radiation sickness and molecular mechanisms].

An analysis of the data on the effect of lymphoid cells on the proliferation and differentiation of hemopoietic stem cells has led to a conclusion that radiation injury of lymphocytes plays an important role in the pathogenesis of the cerebrospinal syndrome. The molecular mechanisms of lymphocyte interphase death were considered. It was shown that due to some peculiarities in the energy supply of these cells the appearance of breaks in DNA causes the development of biochemical processes resulting in a decrease in NAD, an increase in the activity of nucleases, a decrease in ATP, and the accumulation of active metabolites of glycolysis. These reactions result in an increase in the disintegration of DNA, chromatin and pyknosis of lymphocyte nuclei.

Animals↗
PubMedDate not supplied

[The use of recombinant human interleukin-1 alpha and -1 beta as agents in the early treatment of acute radiation sickness in an experiment].

Human recombinant interleukins 1 alpha and 1 beta (IL-1 alpha and IL-1 beta) have a good dose-dependent therapeutic effect for an acute radiation damage. For mice, the optimum therapy dose of IL-1 is 100.0 micrograms/kg-1 (survival rates: CD70--50%, CD100--17%; p < 0.05). For dogs, the dose is 1.0 microgram/kg-1 (survival rate: CD100 in combination with antibacterial therapy-up to 80%; p < 0.05).

Acute Disease↗