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Biomedical subjects

R T Johnson

Publications and source records attributed to R T Johnson.

At least 181 records · Page 10Linked to original sources
PubMed1982

Selective vulnerability of neural cells to viral infections.

A number of viruses selectively infect neurons and, in some cases, specific populations of neurons. The susceptible neuron need not be permissively infected to cause acute or chronic disease; therefore, infectious virus may not be recoverable and morphologically identifiable viral structures may not be detectable by ultrastructural structures. Polioviruses and the neurotropic murine retrovirus both cause paralytic disease with major pathological changes in motor neurons of the spinal cord. Both produce disease more readily in later life; in poliovirus because the mature animals are more susceptible to acute infection, and in the neurotropic retrovirus infections because of the long incubation period of the natural infection. In the acute inflammatory poliovirus infections, the motor neurons appear to be selectively infected and lysed by the virus, whereas in the chronic noninflammatory retrovirus infection, the effect may be indirect or may result from nonpermissive infection.

Animals↗
PubMed1981

Effect of cooperative, competitive, and individualistic experiences on self-esteem of handicapped and nonhandicapped students.

Compared are the effects of cooperative, competitive, and individualistic learning experiences on the self-esteem and perceived personal acceptance by the teacher of nonhandicapped and severely handicapped students in a mainstream setting. Thirty students (18 nonhandicapped and 12 trainable retarded) were randomly assigned to conditions stratified on the basis of handicap and sex. They participated in a bowling class which met for one hour per week for eight weeks. The results indicate that those in the cooperative condition had higher self-esteem and perceived more personal acceptance from the teacher than did the students in the competitive and individualistic conditions. Handicapped students reported higher self-esteem than nonhandicapped students.

Adolescent↗
PubMed1981

Studies of immune responses during recovery from Sindbis virus encephalitis in selectively reconstituted, thymectomized, lethally irradiated mice.

Recovery from acute Sindbis virus encephalitis was studied in selectively reconstituted, thymectomized, irradiated mice. Intact mice cleared virus from the brain by day 10 and developed inflammation along with immunoglobulin M (IgM) and IgG antibodies 4 to 6 days after infection. Unreconstituted mice died by day 11, with virus still present but decreasing, no detectable antibody, and no evidence of inflammation. Mice reconstituted with bone marrow cells alone produced only IgM antibody and no inflammation, but cleared virus by day 14. Mice reconstituted with sensitized T cells alone cleared virus by day 10, produced very small amounts of antibody, and developed a prompt inflammatory response.

Animals↗
PubMed1981

Experimental viral polymyositis: age dependency and immune responses to Ross River virus infection in mice.

Ross River virus (RRV) causes an age-dependent myositis in mice. Infected 4-week-old mice develop no clinical signs, but 1-week-old mice develop weakness and myositis. Humoral and cell-mediated immune responses to RRV in the two age groups are comparable, and immunosuppression does not alter age-dependent resistance to clinical disease. Immunosuppression of 1-week-old mice protracts clinical signs and reduces muscle inflammation but does not alter muscle necrosis or regeneration. These studies suggest that immune responses do not determine age dependency of RRV myositis and that muscle necrosis results from direct viral lysis of muscle fibers.

Age Factors↗
PubMed1981

Correlations of DNA damage and repair with nuclear and chromosomal damage in HeLa cells caused by methylnitrosamides.

N-Methyl-N-nitrosourethan induces breaks or alkali-labile sites in cellular DNA, many if not all of which are repaired rapidly. Other DNA lesions are repaired by an excision process. Hydroxyurea and 1-beta-D-arabinofuranosylcytosine cause an accumulation of DNA breaks after N-methyl-N-nitrosourethan treatment, probably by inhibiting the DNA-synthetic (but not the nucleolytic) stage of excision repair. Chromosome damage (fragmentation or attenuation of interphase chromosomes and decondensation and radial rearrangement of metaphase chromosomes) is present soon after treatment with N-methyl-N-nitrosourethan and is not reversed during further incubation. It is apparently associated with the longer-lived DNA lesions, probably those which are removed by excision, and is enhanced by incubation with hydroxyurea and 1-beta-D-arabinofuranosylcytosine. N-Methyl-N-nitrosourethan also inhibits cellular protein and the loss of nucleolar structure. N-Methyl-N-nitrosourea is less potent than N-methyl-N-nitrosourethan in causing DNA or chromosome damage and is less cytotoxic.

Cell Cycle↗
PubMed1980

Cerebrospinal-fluid lymphocyte populations and immune complexes in active multiple sclerosis.

A specific subpopulation of mononuclear cells bearing a surface receptor for the Fc portion of IgG was considerably reduced in the cerebrospinal fluid (CSF) of multiple sclerosis (MS) patients during exacerbation, but returned toward normal levels as the patient entered remission. Low concentrations of immune complexes were found in the CSF in nearly 50% of MS patients during exacerbations but immune complexes were not found in patients with stable MS.

Acute Disease↗
PubMed1980

Cell cycle-related variations in UV damage and repair capacity in Chinese hamster (CHO-K1) cells.

UV damage to CHO cell DNA, measured by formation of thymine-containing dimers, increases from mitosis to early S phase. Computer simulation of UV absorption by the DNA of an idealized CHO cell at different stages in the cell cycle resembles the cycle dependence of UV damage. Incision at UV damage sites, measured by the accumulation of breaks in preexisting DNA during 30 minutes' post-irradiation incubation with the DNA synthesis inhibitors 1-beta-D arabinofuranosylcytosine and hydroxyurea, increases from mitosis to interphase. Analysis of the dose dependence of DNA break accumulation indicates that both the affinity of the endonuclease for dimer sites and the maximum enzyme activity at saturating levels of dimers are significantly lower in mitosis than in interphase. The killing of CHO cells by UV is enhanced if repair is temporarily inhibited by are C. The DNA gyrase inhibitor novobiocin prevents UV-induced incision.

Animals↗
PubMed1980

Comparative studies of five strains of mumps virus in vitro and in neonatal hamsters: evaluation of growth, cytopathogenicity, and neurovirulence.

The growth and cytopathogenicity of five strains of mumps virus were examined in six types of cell cultures and in neonatal hamsters. These strains included the MJ and RW strains, both recent cerebrospinal fluid isolates: the neuroadapted Kilham strain; the Enders strain adapted to chick embryo; and the Jeryl Lynn vaccine strain adapted to chick cell culture. The MJ, RW, and Kilham strains all produced infectious virus without restriction in vitro, but the RW strain did not cause obvious cytopathic effect; the MJ and Kilham strains were cytopathic. The Enders and Jeryl Lynn strains adapted to chick embryo cells were cytopathic and productive in chick cell culture but were restricted in ability to grow productively in vitro on mammalian cell types, even failing to produce noninfectious particles in some cases. In vitro cytopathogenicity was a host-independent property of a specific virus strain, but the type of cytopathic effect manifest in culture (eg, fusion, cytoplasmic vacuoles) depended on both the strain and the host cell. The ability of a virus strain to invade the brain parenchyma and infect neurons in vivo appeared to correlate with the strain's cytopathogenicity and not with passage history or adaptive status.

Animals↗