Hyperexcitability of pyramidal neurons in field CA1 in hippocampal slices from rats evoked by episodes of hypoxia: the roles of GABAA and GABAB receptors.
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Biomedical subjects
Publications and source records attributed to S G Levin.
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This paper presents an estimate of the median lethal dose for humans exposed to total-body irradiation and not subsequently treated for radiation sickness. The median lethal dose was estimated from calculated doses to young adults who were inside two reinforced concrete buildings that remained standing in Nagasaki after the atomic detonation. The individuals in this study, none of whom have previously had calculated doses, were identified from a detailed survey done previously. Radiation dose to the bone marrow, which was taken as the critical radiation site, was calculated for each individual by the Engineering Physics and Mathematics Division of the Oak Ridge National Laboratory using a new three-dimensional discrete-ordinates radiation transport code that was developed and validated for this study using the latest site geometry, radiation yield, and spectra data. The study cohort consisted of 75 individuals who either survived > 60 d or died between the second and 60th d postirradiation due to radiation injury, without burns or other serious injury. Median lethal dose estimates were calculated using both logarithmic (2.9 Gy) and linear (3.4 Gy) dose scales. Both calculations, which met statistical validity tests, support previous estimates of the median lethal dose based solely on human data, which cluster around 3 Gy.
A disturbing characteristic of methylmercury (MeHg) intoxication is the preclinical "silent" stage. This stage is followed by the sometimes rapid onset of clinical signs such as peripheral sensory loss, motor difficulties, and visual and auditory impairment. The objective of this study was to search for "preclinical" changes in the electrophysiological activity of the central nervous system of dogs exposed to methylmercury chloride. Because of the prominence of the visual system in the MeHg literature, the visual evoked response (VER) was selected for evaluation. A dose rate of 500 microgram/kg/day po was expected to cause clinically apparent toxicosis in about 2 mon. After 1 week of exposure, a subtle distortion of the VER occurred. In a parallel group of dogs, blood mercury was 0.74 microgram/ml at this time, and brain mercury content was 1.28 microgram/g at the occipital cortex. Although the dogs continued to receive MeHg, VERs remained remarkably stable for the next 5 to 8 weeks, and then rapidly degraded during the nest few days as the dogs exhibited visual and motor disabilities. In many species, when brain Hg is about 15 microgram/g, clinical and histopathologic changes are usually present, and may even be detected at 8 microgram/g. Distortion of the VER at 1.28 microgram/g Hg at the visual cortex demonstrates that CNS changes exist during the "silent" stage of toxicosis, and at a brain Hg content suggesting physiologic dysfunction of neurons rather than neuronal death.
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The present study is based on the hypothesis that a humoral agent produced in inflammatory exudates is transported to the bone marrow where it stimulates CFU-S to differentiate into leukocytic precursors. Inflammatory exudates were produced by the subcutaneous implantation of a sterile acrylic cup filled with bacteria-free Hanks' balanced salt solution (HBSS) into B6D2F1 mice. The cups were removed 24 h later and the cells were separated from the supernatant. Cells collected from individual mice were pooled, as was the supernatant. Thereafter, normal mice received via tail vein either exudate cells, supernatant, plasma from cup-implanted or from normal mice, bone marrow cells or splenic cells from normal animals or HBSS. Another 24 h later bone marrow was removed from all mice and injected into previously lethally irradiated mice or suspended in vitro in agar-supported media. Nine days later the mice were euthanatized, the spleens removed, and colonies (CFU-S) counted. At the same time, colonies (CFU-C) were enumerated from the agar plates. The results clearly indicate that the bone marrow obtained from mice stimulated with either exudate cells or with super-natant or plasma obtained from cup-implanted mice contained a significantly greater number of CFU-S and CFU-C than did any one of the four control groups. These findings appear to substantiate the hypothesis.
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