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Biomedical subjects

B Russell

Publications and source records attributed to B Russell.

At least 55 records · Page 3Linked to original sources
PubMed1993

A myogenic regulatory gene, qmf1, is expressed by adult myonuclei after injury.

Myogenic regulatory factors (MRFs) induce differentiation in developing muscle. We examined the role of MRFs in the repair of adult muscle using a model of stretch-induced injury in 5-wk-old chickens. The anterior latissimus dorsi muscle was stretched by loading the wing with 10% of body weight, while the contralateral muscle served as a control. At various intervals (0.5-72 h), chickens were killed by CO2 asphyxiation and the muscles were frozen. Slot hybridizations showed that the onset of high qmf1 expression occurred as early as 0.5 h, which was before regenerative processes involving satellite cell proliferation were observed. Maximal qmf1 expression varied among animals from 3 to 16 h and returned to control levels by 72 h. Within a muscle, in situ hybridization showed that maximal qmf1 expression varied spatially with > 60% of the nuclei within active fascicles being positive. We interpret this high percentage to mean that many of the nuclei of preexisting muscle fibers must be expressing qmf1. The expression of the protooncogene c-myc (presumably by proliferating cells such as satellite cells, fibroblasts, and capillary epithelial cells) and the MRF qmf1 (by myoblasts and adult muscle nuclei) are among the early molecular responses of injured muscle. We conclude that myogenic regulatory factors are not permanently repressed after embryonic development and that derepression plays a role in the repair of terminally differentiated myofibers.

Animals↗
PubMed1992

Mechanisms for intracellular distribution of mRNA: in situ hybridization studies in muscle.

The intracellular distribution of mRNA in striated muscle fibers is highly ordered, as is the structural organization of the fibers' contractile apparatus. Results from in situ hybridization of muscle mRNA are reviewed in an attempt to discern the mechanisms involved in mRNA distribution and to determine its relationship to developmental, growth, and repair processes in muscle. Nonradioactively labeled complementary RNA probes allow anatomic localization of mRNA at the light and electron microscopic level. Myosin mRNA in striated muscle is concentrated around transcriptionally active nuclei, myosin mRNA is excluded by the myofibrillar mass, myosin mRNA distribution correlates with that of cytoskeletal elements, and myosin mRNA is concentrated in regions of rapid growth and repair. The even distribution of myosin mRNA along the length of myofibrils gives no indication of specific association with either the thick or thin filaments. Of the possible mechanisms directing mRNA distribution, results from in situ hybridization and other analyses support a restricted diffusion model. Diffusion of mRNA (and polysomes) is severely limited by the myofibrillar lattice. It is possible that myosin mRNA is also associated with a cytoskeletal element, which may direct the mRNA to specific intracellular locations and affect translational activity.

Animals↗
PubMed1992

Remodeling of myofibrils: subcellular distribution of myosin heavy chain mRNA and protein.

Myofibril remodeling occurs during the normal life, in growth and development, and in the special case when isoform switching occurs. In this review we concentrate on the ultrastructural aspects of how myosin is incorporated into the A-band. Anatomic methods of study are emphasized that include isotope and immunochemical labeling as well as in situ hybridization. We conclude that the mechanism of remodeling is one of continual orderly exchange between a monomeric myosin pool and the thick filament. Myosin mRNA distribution is intermyofibrillar and nonsarcomeric, which suggests that newly translated myosin is released before diffusion and insertion in the A-band of the myofibrillar lattice.

Animals↗
PubMed1992

Growth hormone-binding proteins of human serum: developmental patterns in normal man.

The binding of GH by a low affinity binding protein (LA-BP) was measured from birth into adulthood and compared with binding of a high affinity binding protein (HA-BP) in human serum. Pooled serum samples for each year of age from birth to 16.5 yr were formed from 2500 separate samples and assayed for both binding proteins using a Sephadex chromatographic method. Individual samples in this age range and those from adults were assayed in a similar manner. Binding of [125I]GH was minimal by both binding proteins in cord blood (binding by LA-BP, 2.77 +/- 0.32%; binding by HA-BP, 2.58 +/- 0.35% mean +/- SEM). A 4-fold increase to maximal binding for LA-BP occurred by the age of 5 yr and remained relatively constant through adolescence, except for a transient decrease at puberty. From 16.5-20 yr of age, binding by LA-BP decreased to a level no greater than that seen at birth. Binding by the HA-BP, which increased 6- to 8-fold reached maximal binding between 23-25 yr of age. Binding by HA-BP did not decrease in adults between the ages of 20-30 yr. Whereas pregnancy increased LA-BP activity, GH binding by HA-BP was unaltered.

Adolescent↗
PubMed1992

Repair of injured skeletal muscle: a molecular approach.

We review cellular and molecular processes involved in injury and repair of skeletal muscle with regard to the amount and location of damage produced. Discussion is based on advances made by use of newer techniques, including immunochemistry, in situ hybridization, molecular biology, ultrastructural analysis, and cell culture. Damage and repair processes after eccentric work, stretch, overload, chronic stimulation, cold injury, and other models are discussed for cellular and molecular components. Hypertrophy or hyperplasia can occur under certain conditions. After injury, satellite cells are activated by growth factors. These cells can also be activated during fiber-type transformation, probably to provide necessary DNA content rather than to supply cells of a new lineage. Emphasis is given to myosin mRNA studied by in situ hybridization to localize subcellular distribution. Increases in mRNA concentration are found near nuclei in damaged regions and at the subcellular sites being repaired in the middle of skeletal muscle fibers or near the myotendon junction. The activation of genes for muscle regulatory factors during development is compared with their activation in regeneration and response to injury.

Animals↗
PubMed1991

The growth hormone-insulin-like growth factor I axis: studies in man during growth.

Several major differences are noted between males and females in their patterns of growth at puberty. Accelerated pubertal growth in both males and females depends upon the integrity of the GH-receptor system. In males, acceleration of growth results primarily from enhanced sensitivity of the GH-receptor-IGF I system to GH brought about by testosterone. Whether testosterone itself is responsible for this observation is still unclear. Perhaps the initial GH, IGF I peak present in males and absent in females occurs at the time when sleep-related rises of gonadotropins and testosterone begin just prior to puberty. Though the pygmy data certainly supports a relationship between testosterone and the GH-receptor-IGF I axis, the undisputed tall stature of eunuchs remains a puzzle. It is possible that the maturing male gonad secretes another growth factor and/or growth inhibitor in conjunction with testosterone and that it is this unidentified factor which modulates growth. At any rate, acceleration of growth in males results from sensitization or the GH-receptor-IGF I system while growth acceleration in females results almost solely from increased secretion of GH and not sensitization of the system.

Adolescent↗
PubMed1991

Hormone and receptor studies: relationship to linear growth in childhood and puberty.

Preliminary data suggested different patterns of hormonal control of linear growth in males and females. To better define these patterns, serum samples were collected from 75-125 boys and a similar number from girls for each year of age between 3-16 yr (n = 2416). Fewer samples were collected from 2-yr-olds, newborns, and adults (n = 151). Samples for each age were aliquoted, combined, and assayed for GH, GH-binding protein (GHBP), insulin-like growth factor-I, and testosterone. GHBP, expressed as a percentage of the [125I]GH bound, increased yearly in males and females, with no relationship to the secretion of sex hormones. The increase in binding of [125I]GH and, by inference, GH receptors occurred at a greater rate between the ages of 2-10 yr than between 10-16 yr (in terms of absolute binding, 1.2 +/- 0.11% vs. 0.38 +/- 0.04% yearly; P less than 0.001). In each age group, however, the increase in GHBP exhibited a strong positive correlation with linear height (r = 0.96-0.98 in males; r = 0.92-0.99 in females). Before puberty, GH and insulin-like growth factor-I concentrations were consistently greater in females. Between 10-16 yr of age, height velocity (centimeters of growth per yr) correlated strongly with GH in girls (r = 0.86), but did not correlate with GH in boys of a similar age (r = -0.13). The major pubertal growth spurt in males strongly correlated with a rise in serum testosterone concentration beginning at age 11 yr (r = 0.92). Small peaks of GH secretion before and after the major period of accelerated growth in males possibly prolonged the major growth phase, but did not initiate it.

Adolescent↗
PubMed1991

Infection control.

"Universal precautions" and "strict infection control procedures" have become health-care facility as well as household terms. However, not much time has been given to explaining the specifics of exactly what they are or how and when they should be applied. The purpose, therefore, of this article is to review these specifics for practicing physicians, regardless of their specialty.

Acquired Immunodeficiency Syndrome↗
PubMed1990

The Yemenite deaf-blind hypopigmentation syndrome. A new oculo-dermato-auditory syndrome.

We have seen a Yemenite sister and brother with cutaneous hypomelanotic and pigmented spots and patches, microcornea, coloboma, severe hearing loss and normal karyotypes. Histopathological examinations of the skin showed absent melanocytes in the depigmented areas; in the normal and hyperpigmented skin there was abundant melanotic pigment. Similar patients have not been described previously, but there are corresponding mutations in mice and rats.

Abnormalities, Multiple↗