Unitarity and electron pair production in peripheral ultrarelativistic heavy-ion collisions.
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Biomedical subjects
Publications and source records attributed to G Baur.
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Nonphagocytic, nonadherent mononuclear cells from canine peripheral blood (PBMC) were shown to suppress colony formation in agar of autologous and allogeneic bone marrow granulocyte-macrophage progenitor cells (CFU-GM). Suppression required previous cell-to-cell contact in liquid culture between PBMC and bone marrow cells (BMC) and was time- and dose-dependent and resistant to x-irradiation with 20 Gy. Small BMC were less susceptible than large BMC, whereas day-7 and day-14 CFU-GM were equally suppressed. Cryo-preservation of BMC did not enhance CFU-GM inhibition. Spontaneous inactivation during liquid culture of CFU-GM or accessory cells by PBMC is the likely effector mechanism. Possible recognition structures are different from dog leukocyte antigens A and B. Canine PBMC or subpopulations thereof might participate in the regulation of normal hemopoiesis and in the rejection of hemopoietic stem cell grafts by natural killer cell-like mechanisms as has been suggested for human and murine natural killer cells.
Human erythrocytes were separated into three groups according to their density and age by centrifugation in a continuous Percoll gradient. The specific activities of glucose-6-phosphate dehydrogenase, catalase, glutathione peroxidase, glutathione reductases as well as the glutathione and selenium content were highest in the youngest cell and uniformly decreased by about 20-30% in the eldest group. The age-dependence of superoxide dismutase was much more pronounced. The malondialdehyde content taken as an estimate for lipid peroxidation showed an inverse age dependence and increased by 35% in the eldest cell population. Red blood cells from 10 anemic patients exhibited less glutathione and also less malondialdehyde, while GSH-peroxidase and GSSG-reductase contents were higher. The parameters showed similar age profiles as in healthy subjects. The findings support the concept of lipid peroxidation as one of the causal events in red cell aging, but do not allow to deduce the involvement of a single enzyme related to the glutathione redox cycle in this process.
Studies on 42 patients (38 women, 4 men) with chronic-destructive non-purulent cholangitis or primary biliary cirrhosis demonstrated that the duration of symptoms does not correlate with the histological stages. The shortest duration of symptoms was found in patients in the cirrhotic stage. Enzyme levels measured at the time of diagnosis indicated that--contrary to serum bilirubin and serum copper levels--they did not correlate with the stage of the disease. There was an increased frequency of allergic signs in the past history of this group of patients. Furthermore, in all the women (average age 45) there was a 29% abortion rate. Among the three control groups (no liver disease, chronic-aggressive hepatitis, other forms of liver disease), the one with chronic-aggressive hepatitis also showed a high abortion rate (19.5%).
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The major parameters of the peroxide-metabolizing system were investigated in eight human colon carcinoma excisions and compared with apparently non-neoplastic colon tissue from the same patients. The mean malondialdehyde level as an index of lipid peroxidation was 147 pmol/mg protein in carcinoma compared to 40 pmol/mg in healthy tissue. The following relations of specific activities in carcinoma and healthy tissue were found: superoxide dismutase 3.9 micrograms/mg protein (carcinoma): 2.4 micrograms/mg (healthy), glutathione peroxidase 23 mU/mg:10 mU/mg; GSH-transferase 38 mU/mg:25 mU/mg; catalase 2.3 mK/mg:4.1 mK/mg. The mean selenium concentration in carcinoma was 36 ng/mg protein compared to 24 ng/mg. The difference between carcinoma and normal tissue showed an overall-significance of p < 0.002 for the whole set of data. No significant differences were found in GSH levels (12.6 nmol/mg protein in carcinoma: 9.4 nmol/mg in normal colon), GSSG levels (0.6 nmol/mg:0.7 nmol/mg) and in the protein content (70 +/- 23.5 mg/g wet tissue: 66 +/- 20 mg/g). It is concluded that the enhanced lipid peroxidation in tumor tissue may be due to peroxisomally generated H2O2 in conjunction with a lowered catalase activity.
The influence of the storage of plasma preparations on binding was studied in different drugs. No alteration on only a slight alteration of binding was found if the plasma preparations were kept deep-frozen, or at temperatures between +3 degrees and +4 degrees C, for up to 12 months. More marked changes were found for some drugs if the plasma preparations were lyophilized or stored at +32 degrees C, for 6 and 12 months.