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Biomedical subjects

R Olsen

Publications and source records attributed to R Olsen.

At least 73 records · Page 4Linked to original sources
PubMed1977

Diagnosis of experimental encephalitozoonosis in rabbits by complement fixation.

A complement-fixation (CF) test has been developed for detection of experimental encephalitozoonosis in rabbits. The antigen consisted of disrupted homogenates of Encephalitozoon cuniculi spores grown in and released from rabbit choroid plexus tissue culture cells. The test was sensitive and capable of detecting experimental encephalitozoonosis in rabbits as early as 15 days after intracerebral infection. The test was specific for infected animals, and no cross-reactivity was demonstrated between E. cuniculi antigen and Nosema apis, Trypanosoma congolese, Trypanosoma cruzi, rabbit liver powder, rabbit brain powder, and rabbit choroid plexus cell culture. Sera from rabbits infected with Toxoplasma gondii, Eimeria stiedai, and Eimeria perforans did not exhibit antibodies to E. cuniculi. No CF-inhibition activity was detected.

Animals↗
PubMed1975

Serologic response to canine distemper viral antigens in gnotobiotic dogs infected with canine distemper virus.

The humoral immune response to canine distemper viral antigens in gnotobiotic dogs experimentally infected with canine distemper virus was studied by the complement fixation and serum neutralization tests. Antibody titers measured by both serologic methods varied inversely with the severity of disease produced. Recovered dogs demonstrated the highest titers of antibody, whereas fatally infected dogs had little or no antibody activity in their sera. A third group of dogs, characterized by chronic persistent infection, had intermediate levels of anitbody to canine distemper virus. Preliminary characterization of the viral antigens involved in the complement fixation test indicated that at least two antigenic components were involved. One antigen was soluble in ether and was heat-labile, whereas the other was relatively heat-stable and was unaffected by treatment with ether. No evidence for serologic cross-reaction between viral and central nervous system components was found. A vigorous antibody response to envelope antigen determinants in addition to core determinants distinguished immune dogs from persistently infected dogs. The results of this study suggest that the inability to produce antibodies to envelope antigens may be a crucial factor in the establishment of a persistent infection with canine distemper virus in these dogs.

Animals↗
PubMed1973

Myelin-specific autoantibodies associated with central nervous system demyelination in canine distemper virus infection.

Sera from dogs with spontaneously occurring and experimentally produced canine distemper virus-associated demyelinating encephalitis were examined for antibodies to central nervous system myelin by the complement fixation and indirect immunofluorescent methods. Complement-fixing immunoglobulin M antibodies and non-complement-fixing immunoglobulin G antibodies were found in 97% of the spontaneous cases. In comparison, only 28% of control sera contained these antibodies; furthermore, mean antibody titers in the control groups were significantly lower (P < 0.005) when compared to the distemper group. Complement-fixing antimyelin antibodies were also demonstrated in gnotobiotic dogs with experimentally induced distemper virus-associated demyelination. The antibody response could be correlated with clinicopathological features of the disease produced. Results of this study indicate that demyelination in canine distemper may proceed by immune mechanisms.

Absorption↗
PubMed1969

Conditioned suppression as a sensitive baseline for social facilitation.

The key pecking of pigeons maintained on a variable-interval schedule of food reinforcement was suppressed during occasional presentations of a warning stimulus paired with electric shock. On alternate sessions, a co-actor pigeon was visible in an adjoining chamber where it emitted the same food-reinforced key peck during the warning stimulus that signalled shock for the subject. With no shock and at low shock intensities, where the subject's responding was not suppressed or suppressed only slightly, the co-actor had little effect. At the higher shock intensities, where the subject's responding was reduced by at least 40%, the response rate during the warning stimulus was consistently higher when the co-actor was present. One explanation of these results assumes a special relationship between social stimuli and aversive stimuli in which the presence of another animal reduces emotional reactions and thereby allows operant responses to increase. This was not the case here because the mere presence of the co-actor did not maintain social facilitation. Rather, the present results, taken in conjunction with previous findings, suggest that changes in social and non-social variables which affect the rate of food-reinforced responding may produce proportionately larger changes in responding when that responding is suppressed by aversive stimulation than when it is not.

Journal Article↗
PubMed1968

Expression and localization of Escherichia coli alkaline phosphatase synthesized in Salmonella typhimurium cytoplasm.

The Escherichia coli structural gene for alkaline phosphatase was inserted into Salmonella typhimurium by episomal transfer in order to determine whether this enzyme would continue to be localized to the periplasmic space of the bacterium even though it was formed in a cell that does not synthesize alkaline phosphatase. The S. typhimurium heterogenote synthesized alkaline phosphatase under conditions identical to that observed with E. coli. This enzyme appeared to be identical to that synthesized by E. coli, and was quantitatively released from the bacterial cell by spheroplast formation with lysozyme. These results showed that localization is not a property unique to the E. coli cell and suggested that, in E. coli, enzyme location is related to the structure of the protein. Formation of alkaline phosphatase in the S. typhimurium heterogenote was repressed in cells growing in a medium with excess inorganic phosphate, even though only one of the three regulatory genes for this enzyme is on the episome. Thus, S. typhimurium can supply the products of the other two regulatory genes essential for repression even though this bacterium seems to lack the structural gene for alkaline phosphatase.

Alkaline Phosphatase↗
PubMedDate not supplied

Microvascular perturbations in rats receiving the maximum tolerated dose of methotrexate or its major metabolite 7-hydroxymethotrexate.

Methotrexate (MTX) is a clinically important cytostatic antifolate. The study describes the acute effects of maximum tolerated doses of MTX or its major metabolite 7-hydroxymethotrexate (7-OH-MTX) on the ultrastructure of rat liver and kidneys. The ultrastructural changes in rats receiving MTX or 7-OH-MTX were, in principle, indistinguishable and their severity and extension increased with time of survival or doses of medication. All lesions were focal, microvascular, or parenchymal. Microvascular changes were more severe in nature when blood cells were present. The endothelial cells were swollen with loss of pinocytotic vesicles, their luminal plasma membrane formed blebs or were disrupted. Partly detached endothelial cells or deendothelialized areas, various types of white blood cells, in particular, neutrophil granulocytes, were observed in the microcirculation. Single platelets or small platelet aggregates were found either in the lumen or adhering to deendothelialized areas of injured endothelial cells. Hepatocytes exhibited steatosis, edema, and manifest single cell necrosis. There were also nuclear changes, marked proliferation of smooth endoplasmatic reticulum, increased amounts of intracellular lipid vacuoles, and a decrease in glycogen particles in hepatocytes. The kidney presented the major changes in the tubules and in the interstitial part. MTX and 7-OH-MTX acute toxicity may primarily be related to microvascular perturbation.

Animals↗