Biomedical subjects

D Morrell

Publications and source records attributed to D Morrell.

28 records · Page 2Linked to original sources

PubMed1986

Mortality and cancer incidence in 263 patients with ataxia-telangiectasia.

Mortality and cancer incidence were measured retrospectively in 263 ataxia-telangiectasia (A-T) homozygotes. For white and black A-T patients, respectively, all-cause mortality was 50 and 147 times higher than expected based on U.S. mortality rates. There were 52 primary cancers, representing a 61-fold cancer excess for white probands and a 184-fold excess for black probands. The cancer excess was most pronounced for lymphoma, with 252- and 750-fold excesses observed for whites and blacks, respectively. All the age-specific mortality and cancer incidence rates for blacks exceeded those for whites, and overall mortality was 3.0 times higher for black probands than for whites (P less than .001), whereas cancer incidence was 2.2 times higher (P less than .06). Among the white A-T patients, 36% of those who had died had lived at least until 20 years of age, and 33% of those still living were at least 20 years old.

Adolescent↗

PubMed1986

The incidence and gene frequency of ataxia-telangiectasia in the United States.

Ataxia-telangiectasia (A-T) is an autosomal recessive neurological syndrome of considerable interest because homozygotes are highly predisposed to cancer. Vigorous casefinding in the United States in 1970-72 and 1980-84 identified 231 white, 29 black, and three Oriental A-T cases that provide information about the incidence and gene frequency of A-T. White patients identified in this study were born at the rate of 3.0 per million live births in the U.S. in the years 1965-69. The highest observed incidence was in the state of Michigan for 1965-69, where identified white A-T patients were born at the rate of 11.3 per million births. Based on the incidence data, the minimum frequency of a single hypothetical A-T gene in the U.S. white population was estimated to be .0017. Pedigree analysis, which estimates the gene frequency from the proportion of affected close blood relatives of homozygous probands, estimated the most likely gene frequency to be .007 on the assumption that A-T is a single homogeneous genetic syndrome, with 95% confidence limits of .0012-.02. Given that complementation analysis has demonstrated the genetic heterogeneity of A-T, the A-T heterozygote frequency will probably fall between 0.68% and 7.7%, with 2.8% being the most likely estimate.

Ataxia Telangiectasia↗

PubMed1985

Fetal rat myoblasts release both rat somatomedin-C (SM-C)/insulin-like growth factor I (IGF I) and multiplication-stimulating activity in vitro: partial characterization and biological activity of myoblast-derived SM-C/IGF I.

The relative release of rat somatomedin-C (SM-C)/insulin-like growth factor I (IGF I) and multiplication-stimulating activity (MSA) immunoreactivity and bioactivity from isolated fetal rat myoblasts was assessed by a partial characterization of the SM peptides present in concentrated myoblast-conditioned culture medium (MCM). The SM bioactivity of MCM, measured by [3H]thymidine or [35S]sulfate uptake by fetal rat cartilage explants, eluted with an apparent size of 50-80K on Sephadex G-200 at pH 7.5, and was associated with SM-C/IGF I immunoreactivity. Chromatography of MCM on Bio-Gel P-10 or Sephadex G-75 at acidic pH resulted in a peak of SM bioactivity associated with both SM-C/IGF I and MSA immunoreactivity in the 6-9K region. SM-binding activity, measured by competition with activated charcoal for [125I]SM-C or MSA, eluted in the void volume. When these fractions were incubated with [125I]SM-C and chromatographed on Sephadex G-200 at neutral pH, a heterogeneous pattern of binding proteins was seen, with a major component of 50-80K. After chromatofocusing of proteins in the 6-9K region from Bio-Gel P-10, three peaks of SM bioactivity were recovered, each associated with SM-C immunoreactivity, with pI values of 8.5, 7.1, and 6.5. Although both the basic and neutral peaks enhanced [3H]thymidine uptake by growth-restricted fetal rat myoblasts in vitro, only the bioactivity of the former could be blocked by incubation with a monoclonal antibody to human SM-C. Both human SM-C/IGF I and MSA purified from Buffalo rat liver cell-conditioned medium enhanced thymidine incorporation by growth-restricted fetal rat myoblasts. The results suggest that unlike reports of other fetal rat tissues, fetal rat myoblasts released approximately equal amounts of rat SM-C/IGF I and MSA during culture. The myoblast-derived SM-C/IGF I was biologically active on the cell type of origin and may play a paracrine role in muscle development.

Animals↗

PubMed1984