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Biomedical subjects

R E Allen

Publications and source records attributed to R E Allen.

At least 55 records · Page 3Linked to original sources
PubMed1990

Does 3,5,dibromo-4-nitrosobenzene sulphonate spin trap superoxide radicals?

Pulse radiolysis studies show that the spin trap 3,5,dibromo-4-nitrosobenzene sulphonate (I) reacts rapidly with O2.- but the product formed is very unstable. No radicals were detected in ESR studies of solutions of I after reaction with O2.- formed by gamma-radiolysis. Evidence is presented that the stable radical observed by some, but not all workers, following exposure of I to the O2.(-)-generating xanthine/xanthine oxidase system, is produced by a peroxidatic oxidation using hydrogen peroxide formed by O2-. dismutation and that formation of this radical depends on the presence of peroxidase activity in the xanthine oxidase sample employed.

Benzenesulfonates↗
PubMed1990

The effects of bFGF, IGF-I, and TGF-beta on RMo skeletal muscle cell proliferation and differentiation.

A new skeletal muscle cell line, rat myoblast omega or RMo, has been characterized with regard to the effects of three growth factors: basic fibroblast growth factor (bFGF), insulin-like growth factor I (IGF-I), and transforming growth factor beta (TGF-beta). Results indicate a differential response of these factors on both cell proliferation and differentiation. Exposure to bFGF and IGF-I stimulate proliferation, while TGF-beta has no effect on cell number. RMo cell differentiation, as indicated by skeletal myosin synthesis, is enhanced by IGF-I, whereas both bFGF and TGF-beta suppress differentiation. These responses are in agreement with the effects of bFGF, IGF-I, and TGF-beta on myogenic cells cultured from fetal and postnatal muscle, thereby suggesting that RMo cells can serve as a model system for the study of growth factor effects on skeletal muscle cells.

Animals↗
PubMed1990

Pelvic floor damage and childbirth: a neurophysiological study.

Ninety six nulliparous women were investigated to establish whether childbirth causes damage to the striated muscles and nerve supply of the pelvic floor. The techniques used were concentric needle electromyography (EMG), pudendal nerve conduction tests and assessment of pelvic floor contraction using a perineometer. There was EMG evidence of re-innervation in the pelvic floor muscles after vaginal delivery in 80% of those studied. Women who had a long active second stage of labour and heavier babies showed the most EMG evidence of nerve damage. Forceps delivery and perineal tears did not affect the degree of nerve damage seen. We conclude that vaginal delivery causes partial denervation of the pelvic floor (with consequent re-innervation) in most women having their first baby. In a few this is severe and is associated with urinary and faecal incontinence. For some it is likely to be the first step along a path leading to prolapse and/or stress incontinence.

Action Potentials↗
PubMed1990

Control of oxidative damage in rheumatoid arthritis by gold(I)-thiolate drugs.

The roles of anti-arthritic gold(I)-thiolate drugs such as disodium aurothiomalate ('Myocrisin') in the modulation or promotion of oxygen radical-mediated oxidative damage in vivo are reviewed. In particular, the precise molecular mechanisms by which these novel second-line agents exert their therapeutic effects are discussed in terms of (i) the direct and indirect control of enzymes involved in the generation or scavenging of reactive oxygen species (ROS) such as superoxide ion, hydrogen peroxide and hydroxyl radical, (ii) the protection of proteins and relevant enzyme systems against attack by ROS and (iii) their direct involvement in the production (at appropriate 'target' sites) or scavenging of ROS in vivo. In addition, the role of the orally-effective gold(I)-phosphine complex auranofin in the control of oxidative damage in rheumatoid arthritis is also discussed.

Antirheumatic Agents↗
PubMed1990

Regulation of satellite cells during skeletal muscle growth and development.

Satellite cells are myogenic cells attributed with the role of postnatal growth and regeneration in skeletal muscle. Following proliferation and subsequent differentiation, these cells will fuse with one another or with the adjacent muscle fiber, thereby increasing myonuclei numbers for fiber growth and repair. The potential factors which could regulate this process are many, including exercise, trauma, passive stretch, innervation, and soluble growth factors. Three classes of growth factors in particular (fibroblast growth factor, insulin-like growth factor, and transforming growth factor-beta) have been studied extensively with respect to their effects on satellite cell proliferation and differentiation in culture. Fibroblast growth factor has been shown to stimulate proliferation but depress differentiation. Insulin-like growth factor stimulates both proliferation and differentiation, although the latter to a much greater degree. Transforming growth factor-beta slightly depresses proliferation but inhibits differentiation. When administered in combination, these factors can induce satellite cell activities in culture which mimic those typical of satellite cells found in vivo in growing, regenerating, or healthy mature muscle. Alterations in the concentrations of these growth factors in the muscle environment as well as alterations in the cell's sensitivity or responsiveness to these factors represent potential mechanisms for regulating satellite cell activity in situ.

Animals↗
PubMed1989

Effect of monoclonal antibodies on the properties of smooth muscle myosin.

Monoclonal antibodies were generated against turkey gizzard myosin, and their effects on some of the properties of myosin were assayed. Ca2+- and Mg2+-ATPase activities of myosin were enhanced by the anti-subfragment 2 antibodies at low ionic strength (i.e., with 10S myosin). Tryptic fragments of an anti-S2 IgM also activated these activities. Antibodies directed against subfragment 1 and light meromyosin had no effect. The Mg2+-ATPase activity of heavy meromyosin also was activated by an anti-S2 antibody. Actin-activated ATPase activity of phosphorylated myosin was enhanced by the anti-S2 IgM fragments at low MgCl2 concentrations. This increase was reflected by a 5-fold increase in Vmax and a slight decrease in the apparent dissociation constant for actin. The actin-activated ATPase of dephosphorylated myosin was not affected by intact anti-S2 antibody or its fragments. The rates of phosphorylation and dephosphorylation of the 20,000-dalton light chains were increased by interaction of myosin with anti-S2 antibody. Limited proteolysis of myosin was used as a conformational probe. Interaction of anti-S2 antibody with 10S myosin increased the extent of cleavage at the S1-S2 junction. Proteolysis of 6S myosin was rapid and was not influenced by anti-S2 antibody. Our interpretation of these results is that interaction of the anti-S2 antibodies with myosin alters the conformation in the S2 region and this in turn modifies some of the properties of myosin. This is consistent with the hypothesis that the S2 region of smooth muscle myosin is a determinant of its biological properties.

Animals↗
PubMed1989

Regulation of skeletal muscle satellite cell proliferation and differentiation by transforming growth factor-beta, insulin-like growth factor I, and fibroblast growth factor.

Skeletal muscle satellite cells were cultured from mature rats and were treated in vitro with various combinations of transforming growth factor (TGF)-beta, fibroblast growth factor (FGF), and insulin-like growth factor I (IGF-I). In serum-free defined medium the following observations were made: TGF-beta depressed proliferation and inhibited differentiation; FGF stimulated proliferation and depressed differentiation; IGF-I stimulated proliferation to a small degree but demonstrated a more pronounced stimulation of differentiation. In evaluating combinations of these three factors, the differentiation inhibiting effect of TGF-beta could not be counteracted by any combination of IGF-I or FGF. The proliferation-depressing activity of TGF-beta, however, could not inhibit the mitogenic activity of FGF. Maximum stimulation of proliferation was observed in the presence of both FGF and IGF-I. The highest percentage fusion was also observed under these conditions, but differentiation with minimal proliferation resulted from treatment with IGF-I, alone. By altering the concentrations of TGF-beta, FGF, and IGF-I, satellite cells can be induced to proliferate, differentiate, or to remain quiescent.

Animals↗
PubMed1989

Trenbolone alters the responsiveness of skeletal muscle satellite cells to fibroblast growth factor and insulin-like growth factor I.

The potential role of satellite cells in mediating the effect of trenbolone [17 beta-hydroxyestra-4,9-11-trien-3-one (TBOH)] on skeletal muscle hypertrophy was examined. Young female Sprague-Dawley rats received TBOH injections daily for 2 weeks; growth, body composition, and the composition of selected muscles were assessed. Treated rats grew more rapidly and deposited less body lipid and more protein. The semimembranosus muscle from treated rats was larger and had approximately 60% more DNA per muscle than muscles from control rats. The addition of trenbolone directly to the medium of cultured satellite cells did not stimulate cell proliferation, nor did it augment the stimulatory response of these cells to fibroblast growth factor (FGF) or insulin-like growth factor I (IGF-I). In contrast, satellite cells cultured from TBOH-treated rats exhibited greater proliferative responses to FGF and IGF-I than satellite cells from control rats. In addition, serum from TBOH-treated rats stimulated greater cell proliferation in satellite cell cultures than serum from control rats. These experiments suggest that one possible mechanism responsible for the ability of TBOH to stimulate skeletal muscle hypertrophy may be through enhanced proliferation and differentiation of satellite cells as a result of the increased sensitivity of these cells to IGF-I and FGF.

Animals↗
PubMed1988

A randomized, double-blind, placebo-controlled trial of transfer factor as adjuvant therapy for malignant melanoma.

One hundred and sixty-eight evaluable patients participated in a randomized, double-blind study of transfer factor (TF) versus placebo as surgical adjuvant therapy of Stage I and Stage II malignant melanoma. Eighty-five patients received TF prepared from the leukocytes of healthy volunteer donors; eighty-three participants received placebo. Therapy was initiated within 90 days of resection of all evident tumor and continued until 2 years of disease-free survival or the occurrence of unresectable dissemination of melanoma. Known prognostic variables were similarly distributed in the treatment and control groups, documenting the randomization efficacy. Three endpoints were analyzed: disease-free interval, time to Stage III metastasis, and survival. After a median follow-up period of 24.75 months, there was a trend in favor of the placebo group with regard to all three endpoints and this was significant (P less than or equal to 0.05) for time to Stage III metastasis. These findings indicate that TF is not effective as surgical adjuvant therapy of malignant melanoma.

Clinical Trials as Topic↗
PubMed1988

Improvement of four patients with HIV-1 related symptoms after hyperimmunization with killed poliomyelitis (Salk) vaccine.

Four HIV-1 positive patients with characteristic symptoms of this infection experienced amelioration or resolution of symptoms after 2 months of hyperimmunization with inactivated (Salk) poliomyelitis vaccine. The patient who was initially the most symptomatic exhibited a marked improvement in T4/T8 ratio at the sixth month of continued hyperimmunization treatment. With two patients reported previously, six consecutive patients with lymphotropic retrovirus disease have benefited from hyperimmunization with inactivated polio vaccine.

Acquired Immunodeficiency Syndrome↗
PubMed1987

Inhibition of skeletal muscle satellite cell differentiation by transforming growth factor-beta.

Skeletal muscle satellite cells were cultured from mature rats and were treated in vitro with transforming growth factor-beta (TGF-beta). Muscle-specific protein synthesis and satellite cell fusion were used as indicators of muscle differentiation; a dose-dependent inhibition of differentiation was observed in response to TGF-beta. In addition, TGF-beta depressed cell proliferation in a dose-dependent manner. Half-maximal inhibition of differentiation was seen with a TGF-beta concentration of approximately 0.1 ng/ml. Although proliferation was not inhibited, it was depressed and half-maximal suppression of proliferation occurred in response to 0.1-0.5 ng TGF-beta/ml. Neonatal rat myoblasts were also subjected to TGF-beta treatment, and similar results were observed. Neonatal cells, however, were more sensitive to TGF-beta than satellite cells, as indicated by the reduced concentrations of TGF-beta required to inhibit differentiation and reduce the rate of proliferation. Under identical culture conditions proliferation of muscle-derived fibroblasts were also depressed. The differentiation inhibiting effect of TGF-beta on satellite cells was reversible. It has been suggested that TGF-beta could be an important regulator of tissue repair, and its in vitro effects on satellite cells suggest a possible role in regulation of muscle regeneration.

Animals↗
PubMed1987

Interaction of multiplication stimulating activity/rat insulin-like growth factor II with skeletal muscle satellite cells during aging.

Satellite cells were isolated from the skeletal muscle of 3-, 12- and 24-month-old Fischer 344 rats. In vitro growth of these cells was evaluated in serum-containing medium and in serum-free medium in response to multiplication stimulating activity/rat insulin-like growth factor II (MSA). Cells from 3-month-old rats exhibited a shorter lag phase of growth than cells from 12- or 24-month-old animals. Dose-response curves for MSA with each of the three age groups did not differ in the concentrations of MSA required for a half-maximal response or in the magnitudes of the response. Hormone-binding data using [125I]MSA, however, revealed the highest numbers of MSA-binding sites with lowest affinities in the 3-month-old rat muscle cells; cells from the 24-month-old rats were intermediate and cells from the 12-month-old rats had the highest affinity and lowest number of binding sites. The lower affinity and increased number of binding sites in the young rat cells may be due to greater numbers of IGF type I receptors in muscle from young growing rats.

Aging↗