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Biomedical subjects

J E Clements

Publications and source records attributed to J E Clements.

141 records · Page 8Linked to original sources
PubMed1980

Pyridoxine (pyridoxamine) phosphate oxidase activity in the red cell.

A method has been developed for the measurement of red cell pyridoxine (pyridoxamine) phosphate oxidase activity. The more stable substrate, pyridoxamine phosphate, was incubated with a red cell haemolysate and the product pyridoxal phosphate was measured by Lactobacillus casei microbiological assay. A wide range of oxidase activities was found in control subjects (6-136 ng pyridoxal phosphate/g Hb x 10(-2)). There is a close correlation between the rate of conversion of pyridoxine to pyridoxal phosphate in whole blood and the oxidase activity. There was a marked increase in both after oral riboflavin. These results suggest that the oxidase plays a large part in the regulation of vitamin B-6 metabolism in red cells.

Adult↗
PubMed1980

Genomic changes associated with antigenic variation of visna virus durig persistent infection.

Visna virus undergoes antigenic change during persistent infection of sheep. Antigenic variants of visna virus were compared by using the genomic RNA and analyzing the large RNase T1-resistant oligonucleotides. Mutants isolated from a persistently infected sheep contained a small number of changes in their oligonucleotide patterns when compared with parental virus. To determine whether the changes in the nucleotide structure were clustered in one region of the genome, we determined the order of the oligonucleotides of the parental and mutant RNAs along the genome with respect to the 3' polyadenylylated end. All but one difference between the parental strain and the antigenic mutant used for mapping were located within 2 kilobases from the 3' terminus. Nucleotide sequence analyses showed that several of the oligonucleotides that differed in the parental and mutant RNAs could be accounted for by single base changes.

Animals↗
PubMed1980

Biological characterization of the virus causing leukoencephalitis and arthritis in goats.

This study describes the biological properties of a strain of virus isolated from tissues of a goat with leukoencephalomyelitis-arthritis. The agent is a retrovirus, having a virion-associated reverse transcriptase enzyme and an antigenic determinant(s) which cross-reacts with the p30 of visna-maedi viruses. Morphogenesis of the virus is also similar to visna virus in terms of virus assembly and the multinucleated giant cell formation which accompanies replication of the latter virus. Despite its cytopathogenic property the goat agent was not lytic in goat cell culture, causing instead a productive infection which persisted through multiple subcultures of the cells. The virus replicated incompletely in sheep cell cultures but could be rescued from the latter, weeks after inoculation, by co-cultivation with goat cells. Our data suggest that this strain of goat leukoencephalitis virus is a variant of the ovine retroviruses with a host range limited to the goat.

Animal Diseases↗
PubMed1980

Biochemical characterization of the virus causing leukoencephalitis and arthritis in goats.

Goat leukoencephalitis-arthritis virus (GLV) has the density of a retrovirus in sucrose and contains an endogenous RNA-dependent DNA polymerase (reverse transcriptase). The virion reverse transcriptase utilizes the synthetic RNA template poly(rA). (dT)12 but not the synthetic DNA template poly(dA). (dT)12. A high mol. wt. RNA similar in size to visna virus RNA was isolated from 3H-uridine-labelled virions. The major structural protein of GLV has the same mol. wt. as that of visna virus. From these data the GLV appears to be a retrovirus.

Animal Diseases↗
PubMed1978

A DNase for apurinic/apyrimidinic sites associated with exonuclease III of Hemophilus influenzae.

An endonuclease purified from Hemophilus influenzae made single strand breaks in DNA containing apurinic or apyrimidinic sites but had no detectable endonuclease activity on untreated native DNA. The new 5'-termini created at the cleavage sites were base-free deoxyribose 5-phosphate residues. The enzyme preparation also catalyzed the exonucleolytic release of 5'-mononucleotides from bihelical DNA and the hydrolysis of DNA 3'-terminal phosphomonoesters. The phosphatase-exonuclease activity was indistinguishable from that reported by Gunther and Goodgal (J. Biol. Chem. (1970) 245, 5341-5349) and resembled that of exonuclease III of Escherichia coli. The endonucleolytic and exonucleolytic activities could not be separated by electrophoresis, sedimentation, or gel filtration, and they were also affected simultaneously by mutation. The enzymatic activities appear to be functions of a single monomeric protein (M(r) = 30,000).

Apurinic Acid↗
PubMed1978

Virus mutation during 'slow infection': temporal development and characterization of mutants of visna virus recovered from sheep.

Visna virus could be recovered from peripheral blood leukocytes of sheep for years after intracerebral inoculation. Viruses recovered from sheep prior to and several months after development of antibody were antigenically identical to the parental strain used for inoculation. Subsequently, mutant viruses which were not neutralized by the animals' sera were obtained. Longitudinal studies of leukocyte viruses collected from two infected sheep showed that more than one strain of virus could co-exist in the animal. Virus neutralization tests using sequentially collected sera and the viruses recovered from leukocytes revealed a sequential development of antibody to parental and then to each strain of mutant virus. Characterization of two of the mutant viruses showed that they were antigenically stable, virulent in cell culture and when inoculated into new sheep, elicited antibodies which cross reacted with the parental virus from which they were derived. This continuous mutation of Visna virus in persistently infected sheep may be a mechanism for the production of chronic disease.

Animals↗
PubMed1978

Environmental and behavioral aspects of glue sniffing in a population of emotionally disturbed adolescents.

The following study used an eight question survey to explore some ecological and behavioral dimensions of glue sniffing in a population of emotionally disturbed adolescents. The results indicated that peer-based pressure was a dominant motivational aspect for engaging initially in glue-sniffing behavior. In addition, a significant number of adolescents in this survey revealed a trend toward experiencing unpleasantness with continual use.

Adolescent↗
PubMed1975

Inhibition of Bacillus subtilis deoxyribonucleic acid polymerase III by phenylhydrazinopyrimidines. Demonstration of a drug-induced deoxyribonucleic acid-enzyme complex.

The interaction of 6-(phenylhydrazino)-pyrimidines and Bacillus subtilis DNA polymerase III was examined in experiments exploiting agarose gel filtration of mixtures of drug, DNA, and purified enzyme. 6-(p-Hdroxyphenylhydrazino)-uracil and 6-(p-hydroxyphenylhydrazino)-isocytosine were used as model inhibitors; both drugs induced the formation of a distinct polymerase-DNA complex. Comples formation required the inhibitory, hydrazino forms of the drugs and a form of DNA suitable as a primer-template for DNA polymerase III. dGTP and dATP, which respectively, competitively antagonize the inhibitory effects of the uracil and isocytosine derivatives, antagonized in an equally specific manner the respective capacities of these compounds to induce complex formation. Experiments exploiting both wild type and drug-resistant, mutant polymerases indicated that drug concentrations required for the half-maximal induction of complex formation were nearly identical with the apparent inhibitor constants (Ki) determined independently by kinetic analysis of enzyme inhibition. These results and those of experiments exploiting defined homopolymer-oligomer combinations as template-primers support a model of inhibitor action in which arylhydrazinopyrimidine forms a reversible, ternary complex with the enzyme and an appropriate timplate pyrimidine residue in an area adjacent to the 3-hydroxyl primer terminus.

Bacillus subtilis↗
PubMedDate not supplied

Hypothesis on the molecular basis of nononcogenic retroviral diseases.

Oncogenic and nononcogenic retroviruses have similar structures and replicate by reverse transcription of their viral RNAs. The nononcogenic retroviruses are distinguished from the oncogenic retroviruses by virtue of the chronic inflammatory or degenerative disease they cause. These diseases include visna-maedi of sheep, caprine arthritis and encephalitis, equine infectious anemia, and chronic spongiform polioencephalomyelopathy of mice. The basis for the particular disease caused by the nononcogenic retroviruses seems to be the selective infection of specific end-stage cells. A common factor in these slowly progressing diseases is lifelong persistence of virus with viral spread either in the face of host immunity-antigenic drift or by modulation of the host immune response. The molecular basis for antigenic drift in visna virus and its biologic significance are discussed.

Animals↗
PubMedDate not supplied

A model for the maturation of protective antibody responses to SIV envelope proteins in experimentally immunized monkeys.

Studies using live attenuated virus vaccines in the simian immunodeficiency virus (SIV) rhesus macaque model have demonstrated broad protection against experimental challenge. Protection in these studies was found to be critically dependent on the length of time postvaccination, suggesting that protective immunity involves a necessary maturation of immune responses. The current study characterizes the evolution of protective envelope-specific antibody responses from monkeys inoculated with the highly attenuated SIV/17E-Cl virus vaccine. For comparison, the same antibody assays were used to characterize the properties of SIV envelope-specific antibodies elicited by inactivated whole virus and envelope subunit vaccines that failed to provide protection from experimental virus challenge. Results of these studies identify a continuous and complex maturation of envelope-specific antibody responses during the first six to eight months postinfection. Furthermore, the time required for maturation of SIV envelope-specific antibodies parallels the time required for the development of protective immunity against experimental challenge with heterologous strains of SIV. While no single immune correlate of protection has been identified, we suggest that a combination of antibody parameters may serve as prognostic indicators in the development of candidate AIDS vaccines.

AIDS Vaccines↗