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Biomedical subjects

J A Powell

Publications and source records attributed to J A Powell.

At least 55 records · Page 3Linked to original sources
PubMed1989

Restoration of dysgenic murine (mdg) myotube contraction after addition of Schwann cells from normal mice in vitro.

Muscular dysgenesis in mutant mice is characterised by failure of excitation-contraction (E-C) coupling and consequent loss of skeletal muscle contraction. Contractile activity is restored in vitro by the addition of normal mice cells (11) (18) (7). In the present study we show a new model: contraction and ultrastructural organization of dysgenic myotubes are restored by coculture with Schwann cells from normal mice.

Animals↗
PubMed1988

Restoration of excitation-contraction coupling and slow calcium current in dysgenic muscle by dihydropyridine receptor complementary DNA.

Microinjection of an expression plasmid that carries complementary DNA encoding the receptor for dihydropyridine calcium channel blockers of skeletal muscle restores both excitation-contraction coupling and slow calcium current in cultured skeletal muscle cells from mice with muscular dysgenesis. This suggests that the dihydropyridine receptor in the transverse tubule membrane of skeletal muscle functions both as the voltage sensor for excitation-contraction coupling and as the slow calcium channel.

Animals↗
PubMed1988

Biological activities of nerve growth factor bound to nitrocellulose paper by Western blotting.

We have previously developed a cell-blot technique to visualize directly in tissue extracts molecules that display the biological activity of ciliary neuronotrophic factors (CNTFs). This technique involves SDS-PAGE of the tissue extract, Western blotting on nitrocellulose paper, neuronal cell culture on the paper, and, using a vital dye, visualization of the neurons that selectively survive on the trophic factor band. In this report, we show that (1) NGF, either purified or in a crude extract from submaxillary glands, can also be successfully recognized using a slightly modified cell-blot technique; (2) a variety of ganglionic neurons can respond to distinct nitrocellulose-anchored trophic factors; (3) while CNTF and NGF can both support the survival of their common target cells, only NGF also promotes neuritic extension; and (4) both the dimeric and the monomeric forms of immobilized beta-NGF are active.

Animals↗
PubMed1986

Acetylcholinesterase is regulated by action potential generation and not by muscle contractile activity per se in mouse muscle in vitro.

Dysgenic (mdg/mdg) skeletal muscle of the mouse, grown in primary cell culture, fires action potentials in the absence of contractions, thus allowing analysis of the role of electrical activity (without contraction) on the specific activity and molecular forms of acetylcholinesterase (AChE). Specific activity of AChE was assessed by the spectrophometric method of Ellman (Biochem. Pharmacol., 7 (1961) 88-95) and found to increase by 2-5 times in the active myotubes (contraction and action potentials in normal and action potentials, alone in dysgenic muscle) compared to quiescent muscle. Sucrose density sedimentation analysis of muscle homogenates revealed an increase, by 2-3 times, in the proportion of the asymmetric (16S) molecular form of AChE in active muscle of both genotypes. Thus, electrical membrane activity, and not contraction per se, is directly involved in the regulation of levels of specific activity of and accumulation of the asymmetric (16S) form of AChE in muscle cells in culture.

Acetylcholinesterase↗
PubMed1986

The development of motoneurons in the embryonic spinal cord of the mouse mutant, muscular dysgenesis (mdg/mdg): survival, morphology, and biochemical differentiation.

Motoneuron development was studied in the spinal cord of the mouse mutant, muscular dysgenesis, between embryonic days (E) 13 and 18. Dysgenic embryos are characterized by the absence of neuromuscular activity (motility) and exhibit a number of other striking changes in neuromuscular development. Many of these changes have also been observed in chick embryos chronically treated with neuromuscular blocking agents that suppress motility. Motoneuron survival, as well as several other aspects of neuronal development, was examined in the thoracic and lumbar spinal cords of mutant and control embryos. There was a significant decrease in motoneuron numbers in control embryos indicating the presence of naturally occurring cell death in the mouse spinal cord. At all ages examined, the dysgenic embryos had significantly more healthy and significantly fewer degenerating motoneurons than controls. There were no differences in the number of dorsal root ganglion neurons or in any of the other morphometric parameters examined between mutant and control embryos. Creatine kinase activity, a marker for myofiber maturation, was significantly reduced in the limb musculature of mutant embryos. Choline acetyltransferase activity was significantly increased in the spinal cord of mutant embryos. No significant differences were observed in spinal cord levels of acetylcholinesterase activity between control and mutant embryos. The absence of muscle contractions in the dysgenic mouse is associated with a number of changes in neuromuscular development, including a substantial reduction of naturally occurring motoneuron death.

Alleles↗
PubMed1985

Antibodies to Newcastle disease virus in various human diseases.

Sera of patients with infectious mononucleosis (IM) and various other diseases were studied for agglutinins against Newcastle disease virus (NDV)-modified human group O red blood cells (NDVO) and antibodies to the NDV preparations. In agreement with previous studies, the NDVO antibodies are found in a wide variety of diseases in addition to IM, including Japanese IM-like syndrome (22%), syphilis (24%), lepromatous leprosy (30%), systemic lupus erythematosus (29%), multiple sclerosis (18%) and cancer (17%); these antibodies were also found in patients with renal allografts (29%). It was also noted that the Victoria (VIC), Roakin and Herts strains, but not B1 strain of NDV are active in the NDVO agglutination, and VIC and Roakin strains, but not B1 strain in the immunodiffusion. Immunodiffusion and enzyme immunoassay with various preparations of the VIC strain revealed that the major antigen(s) of the virus under study is carried by the hemagglutinin-neuraminidase (H-N) glycoproteins. The H-N molecule was also shown to be able to modify human erythrocytes for the agglutination by the pathologic sera.

ABO Blood-Group System↗
PubMed1985

Specificity of antibodies to Newcastle disease virus.

Specificity of antibodies to Victoria strain of Newcastle disease virus (NDV) found in infectious mononucleosis (IM) and other pathologic sera was investigated by agglutination of NDV-modified human O red blood cells, as well as by immunodiffusion and enzyme immunoassay with various preparations of the virus. These studies clearly demonstrated that the NDV antibodies are distinct from P-B or H-D antibodies. The unexpected observation that guinea pig kidney (GPK) tissues absorbed NDV antibodies allowed their classification into a group of 'GPK-positive' heterophile antibodies. The simultaneous occurrence of the NDV antibodies and H-D antibodies in IM and other diseases suggests the possibility that multiple new antigenic determinants, especially those of carbohydrate nature, may appear due to the alteration of self-antigens as a result of various pathologic processes.

Antibodies, Viral↗
PubMed1985

Monoclonal antibodies to T-2 toxin. In vitro neutralization of protein synthesis inhibition and protection of rats against lethal toxemia.

A murine monoclonal antibody (15H6) against the trichothecene mycotoxin T-2 was capable of neutralizing the in vitro protein synthesis inhibitory effect of T-2 toxin in human B lymphoblastoid cultures. It was further shown that 15H6 given to rats (250 mg/kg) 30 min before or 15 min after a lethal dose (1 mg/kg) of T-2 toxin conferred 100% survival. A lower dose of 15H6 (125 mg/kg), given 15 min after the lethal dose of T-2 toxin, protected 25% of the rats. An increased time to death and 45% survival was seen in rats given the full dose of 15H6 antibody 60 min after lethal toxin. These data are the first demonstration of effective prophylaxis and therapy for T-2 toxemia.

Animals↗
PubMed1984

Distribution and quantification of ACh receptors and innervation in diaphragm muscle of normal and mdg mouse embryos.

Muscular dysgenesis (mdg) in the mouse is an autosomal recessive mutation, expressed in the homozygous state (in vivo and in vitro) as an absence of skeletal muscle contraction. The distribution of acetylcholine receptors (ACh R) in the diaphragms of phenotypically normal and dysgenic (mdg/mdg) embryos was studied from the 14th to 19th day of gestation by binding of 125I-alpha-bungarotoxin to the muscle, followed by autoradiography of longitudinally sectioned hemidiaphragms and/or of isolated muscle fibers. Localization of ACh R at putative motor end-plate regions begins 14 to 15 days in utero in both normal and dysgenic diaphragms. The distribution of high ACh R density patches is aberrantly scattered beyond the normal innervation pattern in dysgenic diaphragms. Isolated mutant fibers possess (1) multiple ACh R clusters, up to five per single fiber, (2) larger clusters of more variable morphology and variable receptor density than normal clusters, and (3) higher levels of extrajunctional receptors than normal fibers. These autoradiographic results correlate well with higher total level of toxin binding sites per diaphragm and per milligram protein in dysgenic vs normal muscle, as quantified from gamma counting of sucrose density gradient isolation of 125I-toxin-ACh R complexes. The dispersed distribution of ACh R patches on dysgenic muscle may be correlated with extensive phrenic nerve branching as demonstrated by silver impregnation technique. We suggest that the aberrant ACh R cluster distribution is a result of multiple innervation of single fibers from the branched nerve terminals. Possible causes of the excessive nerve branching in the mutant are discussed in light of generalized nerve sprouting found in paralyzed muscle.

Animals↗
PubMed1984

Extensive nerve overgrowth and paucity of the tailed asymmetric form (16 S) of acetylcholinesterase in the developing skeletal neuromuscular system of the dysgenic (mdg/mdg) mouse.

In muscular dysgenesis (mdg) both skeletal muscle and motor innervation present an abnormal differentiation at birth (Rieger and Pinçon-Raymond. 1981). We establish in this report that the abnormalities of the motor innervation, extension of the innervation territory and nerve branching, and the low level of tailed asymmetric (16 S) acetylcholinesterase (AChE) are observed in the diaphragm as soon as the mutation is phenotypically expressed in the mdg/mdg embryo, at embryonic Day 13 1/2 or 14. The nerve-muscle interaction is thus abnormal at the very beginning of the formation of the neuromuscular system. The comparative electron microscopic study of normal and mutant muscle basal lamina shows that the newly formed mdg/mdg myotube lacks a basal lamina at Day 14. However, the biosynthesis of the basal lamina is not totally defective as, at Day 18, mdg/mdg myotubes possess basal lamina sheaths. Such delayed formation of extracellular material in the mutant may partly explain the abnormally low induction of 16 S AChE which is thought to be localized in the extracellular matrix and has potential important implications in nerve-muscle recognition and synapse stabilization.

Acetylcholinesterase↗
PubMed1984

Psychosocial health issues in pediatric practices: parents' knowledge and concerns.

Parents' general knowledge of child development and the demographic factors associated with that knowledge were studied. A questionnaire was completed by 230 parents of patients from three quite different pediatric practices in the south-central United States. Chi square analysis was used as the major statistical technique. Results indicated that age, educational level, and income were associated with level of child development knowledge. Parents reported the sources and educational techniques that were most helpful to them in the past and present. The majority (81%) of the questions that parents wished to direct to pediatricians, given sufficient time, were concerned with psycho- social issues. It appears that the pediatric practice is a logical means of providing information to parents about their children's health concerns, both behavioral and physical. These results emphasize the importance of training pediatricians in behavioral issues and in improving their communication skills. The results are presented to help pediatricians select the anticipatory guidance and educational techniques that might be provided to parents through the pediatric practice.

Adult↗
PubMed1983

Evidence for dysfunction in the regulation of cytosolic Ca2+ in excitation-contraction uncoupled dysgenic muscle.

In noncontracting, dysgenic murine muscle, excitation is uncoupled from contraction. To test whether the gene lesion is expressed as a defect in the regulation of the intracellular free Ca2+ levels, cultured normal and dysgenic muscle at various stages of development (proliferative myoblasts, early, late, and mature myotubes) were exposed to increasing increments (0.5-mM steps) of extracellular Ca2+ in ionophore A23187-Ca2+-EGTA-buffered media. Normal and dysgenic muscle at all stages (except myoblast) displayed contractures at approximately 500 microM free Ca2+ and higher. Experiments using finer increments of Ca2+ and different ionophore concentrations indicated an external Ca2+ threshold for contracture at 265 microM Ca2+ for early and late myotubes and 47-78 microM for mature normal and dysgenic myotubes. Low extracellular concentrations of calcium (14 microM and 0.76 nM) caused elongation of both normal and dysgenic myotubes. Mature cells were depolarized by exposure to increasing extracellular K+ and monitored by intracellular recording; normal and dysgenic myotubes showed similar reductions in membrane potentials. Depolarization to -35 mV elicited contractures in normal myotubes, but even depolarization to -9 mV in dysgenic cells elicited no response. Thus steady-state depolarization of dysgenic muscle does not cause contractures, which can, however, be elicited by increasing the intracellular free Ca2+. These results offer new evidence for a possible defect in the regulation of Ca2+ levels in dysgenic muscle.

Animals↗
PubMed1982

Factor analysis of reports of parental behavior by children living in divorced and married families.

To determine whether or not responses to the Child's Report of Parental Behavior Inventory (CRPBI) would yield similar factors for children living in divorced families and for children living in married families, responses to the 56-item six-scale version of the CRPBI were obtained from 29 children living with their divorced mothers and from 30 children living with their married parents. All children were between seven and 11 years of age. Socioeconomic characteristics of the two types of families were similar except for income. Each child completed the inventory for both the mother and the father. Scale totals for each family structure and sex of parent were intercorrelated separately and subjected to a principal axis factor analysis with Varimax rotation. Three factors emerged for children's reports of married mothers, married fathers, and divorced fathers; however, two factors emerged for children's reports of divorced mothers. While the unique factor structure observed for children's reports of divorced mothers may be a function of the instrument's being more valid for reports of parental behavior by children living with married parents, alternative explanations were discussed. Results of the study appear to lend empirical support to Weiss' theory of the structure and functioning of single-parent households.

Child↗