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Biomedical subjects

R D Barnes

Publications and source records attributed to R D Barnes.

At least 73 records · Page 4Linked to original sources
PubMed1975

The lack of association of theta status and murine leukaemia virus content in the AKR.

Two AKR sublines appear atypical in possessing theta C3H. One of these two sublines - AKR/FuA - is notably resistant to lymphomata and is also characterized by reduced levels of the group specific murine leukaemia viral (MuLV) antigen. This suggested a possible association between theta status tumour susceptibility and viral content. Results here show no reduction in viral antigen titres in the other theta C3H tumour susceptible subline AKR/Cum, thus eliminating the possible association of theta status with the extent of MuLV replication.

Animals↗
PubMed1975

Virus-specific neutralization by a soluble non-immunoglobulin factor found naturally in normal mouse sera.

A low-molecular-weight substance found naturally in mouse serum neutralizes mouse xenotropic C-type virus. It has no effect on endogenous ecotropic viruses. This neutralizing factor does not belong to the known immunogloblin classes, and its activity is not associated with the antivirus immunoglobulins that can be detected by radioimmunoprecipitation. Preparations of xenotropic virus absorb out this neutralizing activity in mouse sera. The specificity of this factor for X-tropic virus suggests that it represents a newly recognized type of response of the host to an endogenous virus. Its possible role in the regulation of endogenous C-type viruses is considered.

Adsorption↗
PubMed1975

Fetal wastage as a consequence of Mycoplasma pulmonis infection in mice.

The effect of Mycoplasma pulmonis, strain JB, on the outcome of pregnancy in TO mice was studied. The mice were infected intravenously before or after mating and the fetuses were examined at autopsy just before parturition. An increase in the number of abnormal pregnancies was noted in mice infected about 2 weeks before mating, and there was a significant increase in the number of fetuses which died mid-way through pregnancy. Mycoplasmas were not isolated from any of the fetuses although the organisms reached the joints of the pregnant mice and caused arthritis. It is possible, therefore, that maternal upset was a factor in these abnormal pregnancies. In mice infected at various times after mating, abnormal pregnancies were most frequently seen in those infected 9 days after mating. There was an increase in the number of both mid- and late-stage fetal deaths in these mice and also an increase in the number of late-stage fetal deaths in mice infected 5 days after mating. Mycoplasmas were isolated not only from most of the dead fetuses but also from living ones which suggests that in most instances death was probably due to maternal infection and disturbance rather than fetal infection per se. The possibility of modifying this mouse model by establishing a chronic genital tract infection is discussed as a means of investigating the role of mycoplasmas in human abortion.

Animals↗
PubMed1975

Investigation of NZB mice born to BALB/c immunized against NZB allotype.

Allotype suppression is held to be an example of T-cell suppressor function. Failure of generalized suppressor T-cell function is considered to be responsible for the chronic and progressive disease of the NZB. The possible association of allotype suppression and autoimmune disease has been investigated here in a group of NZB mice, transplanted and born from BALB/c recipients whilst producing anti-NZB allotype. In this situation it was anticipated that if allotype suppression should fail this would coincide with the development of autoimmune disease; both processes reflecting failure of T-cell suppressor function. However, in spite of the fact that allotype suppression was not achieved, certain observations seem important. The fact that NZB born the BALB/c were in no way different from normally derived NZB confirms that the cause of the NZB disease is established prior to the stage of implantation. Maternal influence at or beyond this stage appears of little consequence in terms of effecting the development or progression of the NZB disease. The failure to induce allotype suppression in the NZB is important. In this context this strain appears to be no different from the majority of other strains that have been tested as homozygotes. The suppression obtained with (BALB/c X SJL/J)F1 hybrids in which chronic suppression has been achieved therefore seems to represent an exceptional situation and this suggests that it is perhaps unwise to base general assumptions as to the universal adaptability of T-cell control mechanisms upon unusual findings. It must be remembered that only homozygotes were examined here. Earlier attempts to induce allotype suppression in homozygotes also failed, even in the SJL/J. Since allotype suppression has only been demonstrated in heterozygote mice there is a distinct possibility that this phenomenon never occurs in the homozygote situation. The significance of this possibility is discussed.

Age Factors↗
PubMed1975

Failure to detect anti-group-specific murine leukemia virus activity in tetraparental AKR-CBA chimeras.

Tetraparental AKR-CBA/H-T6 chimeras were primarily derived and investigated to determine whether factors associated with the tumor resistance of the CBA/H-T6 could overcome the innate lymphoma susceptibility of the AKR. Evidence has since shown that, on comparison with the AKR, lymphomas were not only delayed but were also less common in a group of 18 early embryo aggregation derived AKR-CBA/H-T6 tetraparental chimeras. Evidence here has shown other clear differences between the AKR and AKR-CBA/H-T6 chimeras. Whereas murine group-specific murine leukemia viral antigens were detected in the sera in both situations, immunoabsorption studies showed that, in the AKR, the antigens exist complexed to the corresponding antibodies. The situation in the chimeras was in complete contrast, since here antigens exist as a "free" form. This in turn has led us to suggest that the advantage in respect to tumor immunity in the AKR-CBA/H-T6 chimeras is due to the tolerance to oncogenic virus being maintained. In this situation and in contrast to the AKR, in the absence of "masking" antibody-viral antigenic complexes, "normal" tumor immunity can be effected. It has to be assumed that tolerance to the oncogenic Gross virus in the AKR-CBA/H-T6 chimeras reflects the influence of the CBA component. How this has possibly been achieved is discussed.

AKR murine leukemia virus↗