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Biomedical subjects

M C Rice

Publications and source records attributed to M C Rice.

9 recordsLinked to original sources
PubMed1996

Correction of the mutation responsible for sickle cell anemia by an RNA-DNA oligonucleotide.

A chimeric oligonucleotide composed of DNA and modified RNA residues was used to direct correction of the mutation in the hemoglobin betaS allele. After introduction of the chimeric molecule into lymphoblastoid cells homozygous for the betaS mutation, there was a detectable level of gene conversion of the mutant allele to the normal sequence. The efficient and specific conversion directed by chimeric molecules may hold promise as a therapeutic method for the treatment of genetic diseases.

Alleles↗
PubMed1980

Genetic variance of laboratory outbred Swiss mice.

The extent of allelic variation has been estimated at 46 structural gene loci within three major colonies of Swiss mice and between inbred derivative strains. The colonies have retained nearly the same amount and type of variation found in natural murine or human populations despite laboratory propagation for more than 50 years (175 generations). The population genetic structures of the Swiss mouse colonies were comparable to an island population in which random fixation, and not inbreeding or population bottlenecks, is apparently responsible for slight losses in genetic variance.

Alleles↗
PubMed1980

Genetic diversity in leukemia-prone feral house mice infected with murine leukemia virus.

The Lake Casitas (LC) mouse population located in south western Ventura county in California is unusual insofar as 85% of these mice are persistently viremic with congenitally transmitted murine leukemia virus (MuLV). The virus has been identified as the etiological agent responsible for lymphoma and neuromotor paralysis in large numbers of the mice. The majority of other wild mouse populations are generally free of infectious MuLV despite the presence of endogenous cellular DNA sequences homologous to infectious virus isolated from wild mice. Electrophoretic variation in 46 gene-enzyme systems was surveyed using mice from Lake Casitas and from a virus-negative population located in Bouquet Canyon (BC) approximately 40 miles from Lake Casitas. The LC and BC populations are genetically very similar to each other and to feral mouse populations previously studied in California and Europe. In the LC population 24% of the loci are polymorphic compared to 17% in the BC population. The average heterozygosities for the LC and Bc populations are 0.094 and 0.073, respectively. The large amount of genic variation in LC fails to support the concept of the derivation of the colony from a small number of founders. Tests for linkage disequilibrium and/or selective association of viremia and polymorphism at 15 loci located on nine mouse chromosomes did not reveal any nonrandom assortments. The viremic LC population, then, appears indistinguishable within the limits of experimental resolution from the virus-negative BC population in its population genetic structure.

Animal Population Groups↗
PubMed1977

Studies of urticaria and acute serum sickness with the C1q precipitin test.

The C1q precipitin test was performed in serum samples from five groups of patients: (1) 20 patients with acomplementemic systemic lupus erythematosus glomerulonephritis (SLE), (2) 2 patients with serum sickness due to the administration of horse serum, (3) 2 patients with serum sickness preceding hepatitis B, (4) 50 patients with chronic urticaria, and (5) 30 normal controls. Positive C1q precipitin tests were found in all patients with SLE and the four cases of serum sickness. Positive tests correlated with depressed serum complement (C3 and C4) levels and were found only in the early phase of serum sickness. Urticaria patients uniformly had negative C1q precipitin tests and normal serum complement levels.

Acute Disease↗
PubMedDate not supplied

In vitro complement consumption by contrast materials and analogues: reactors vs. nonreactors.

Blood samples from previous contrast reactors and nonreactor controls were incubated with diatrizoate and several contrast analogues. Total complement levels were assayed. All the agents caused complement activation generally proportional to their concentration. Reactors' sera responded to lower concentrations of contrast or analogues than did control sera. Such studies might be of value in predicting contrast reactors.

Acetamides↗
PubMedDate not supplied

Iodinated contrast material: studies relating to complement activation, atopy, cellular association, and antigenicity.

There are multiple problems of iodinated contrast physiology and iodinated contrast reactions that remain unresolved. The author's recent work has included studies in four of these areas. (I) In evaluating complement activation following contrast reactions, significant drops in total hemolytic complement were found, as well as that the reactors had lower baseline complement levels than nonreactors. (II) The leukocytes of atopics and of nonatopics were incubated with contrast and a greater release of histamine was found among the atopics than among the normal subjects. (III) Since histamine can be shown to be released from leukocytes by contrast, I-125-sodium diatrizoate was incubated with blood to detect any cellular association for the contrast. Significant retention of radioactivity was demonstrated by the leukocytes and not the erythrocytes. (IV) The gluteraldehyde technique was used to conjugate diatrizoate bovine serum albumen. After injection of this conjugate into a rabbit, antibody activity in the rabbit serum to the diatrizoate was demonstrated via the enzyme-linked immunospecific assay system.

Antibody Formation↗