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Search Results: 1 - 10 of 462317 matches for " Dawn A. Lowe "
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Skeletal Muscle-Specific Ablation of γcyto-Actin Does Not Exacerbate the mdx Phenotype
Kurt W. Prins, Dawn A. Lowe, James M. Ervasti
PLOS ONE , 2008, DOI: 10.1371/journal.pone.0002419
Abstract: We previously documented a ten-fold increase in γcyto-actin expression in dystrophin-deficient skeletal muscle and hypothesized that increased γcyto-actin expression may participate in an adaptive cytoskeletal remodeling response. To explore whether increased γcyto-actin fortifies the cortical cytoskeleton in dystrophic skeletal muscle, we generated double knockout mice lacking both dystrophin and γcyto-actin specifically in skeletal muscle (ms-DKO). Surprisingly, dystrophin-deficient mdx and ms-DKO mice presented with comparable levels of myofiber necrosis, membrane instability, and deficits in muscle function. The lack of an exacerbated phenotype in ms-DKO mice suggests γcyto-actin and dystrophin function in a common pathway. Finally, because both mdx and ms-DKO skeletal muscle showed similar levels of utrophin expression and presented with identical dystrophies, we conclude utrophin can partially compensate for the loss of dystrophin independent of a γcyto-actin-utrophin interaction.
Estrogen Regulates Estrogen Receptors and Antioxidant Gene Expression in Mouse Skeletal Muscle
Kristen A. Baltgalvis,Sarah M. Greising,Gordon L. Warren,Dawn A. Lowe
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0010164
Abstract: Estrogens are associated with the loss of skeletal muscle strength in women with age. Ovarian hormone removal by ovariectomy in mice leads to a loss of muscle strength, which is reversed with 17β-estradiol replacement. Aging is also associated with an increase in antioxidant stress, and estrogens can improve antioxidant status via their interaction with estrogen receptors (ER) to regulate antioxidant gene expression. The purpose of this study was to determine if ER and antioxidant gene expression in skeletal muscle are responsive to changes in circulating estradiol, and if ERs regulate antioxidant gene expression in this tissue.
Transgenic overexpression of γ-cytoplasmic actin protects against eccentric contraction-induced force loss in mdx mice
Kristen A Baltgalvis, Michele A Jaeger, Daniel P Fitzsimons, Stanley A Thayer, Dawn A Lowe, James M Ervasti
Skeletal Muscle , 2011, DOI: 10.1186/2044-5040-1-32
Abstract: We transgenically overexpressed γ-cyto actin, specifically in skeletal muscle of mdx mice (mdx-TG), and compared skeletal muscle pathology and force-generating capacity between mdx and mdx-TG mice at different ages. We investigated the mechanism by which γ-cyto actin provides protection from force loss by studying the role of calcium channels and stretch-activated channels in isolated skeletal muscles and muscle fibers. Analysis of variance or independent t-tests were used to detect statistical differences between groups.Levels of γ-cyto actin in mdx-TG skeletal muscle were elevated 200-fold compared to mdx skeletal muscle and incorporated into thin filaments. Overexpression of γ-cyto actin had little effect on most parameters of mdx muscle pathology. However, γ-cyto actin provided statistically significant protection against force loss during eccentric contractions. Store-operated calcium entry across the sarcolemma did not differ between mdx fibers compared to wild-type fibers. Additionally, the omission of extracellular calcium or the addition of streptomycin to block stretch-activated channels did not improve the force-generating capacity of isolated extensor digitorum longus muscles from mdx mice during eccentric contractions.The data presented in this study indicate that upregulation of γ-cyto actin in dystrophic skeletal muscle can attenuate force loss during eccentric contractions and that the mechanism is independent of activation of stretch-activated channels and the accumulation of extracellular calcium.Duchenne muscular dystrophy (DMD) is a severe muscle-wasting disease caused by mutations in the dystrophin gene. Dystrophin localizes primarily to costameres, where it links the cortical actin cytoskeleton to the sarcolemma and the extracellular matrix [1]. It is part of the dystrophin-glycoprotein complex (DGC), a large oligomeric complex of proteins thought primarily to stabilize the sarcolemma during muscle contraction. In the absence of a functional dy
Functional Substitution by TAT-Utrophin in Dystrophin-Deficient Mice
Kevin J. Sonnemann,Hanke Heun-Johnson,Amy J. Turner,Kristen A. Baltgalvis,Dawn A. Lowe,James M. Ervasti
PLOS Medicine , 2009, DOI: 10.1371/journal.pmed.1000083
Abstract: Background The loss of dystrophin compromises muscle cell membrane stability and causes Duchenne muscular dystrophy and/or various forms of cardiomyopathy. Increased expression of the dystrophin homolog utrophin by gene delivery or pharmacologic up-regulation has been demonstrated to restore membrane integrity and improve the phenotype in the dystrophin-deficient mdx mouse. However, the lack of a viable therapy in humans predicates the need to explore alternative methods to combat dystrophin deficiency. We investigated whether systemic administration of recombinant full-length utrophin (Utr) or ΔR4-21 “micro” utrophin (μUtr) protein modified with the cell-penetrating TAT protein transduction domain could attenuate the phenotype of mdx mice. Methods and Findings Recombinant TAT-Utr and TAT-μUtr proteins were expressed using the baculovirus system and purified using FLAG-affinity chromatography. Age-matched mdx mice received six twice-weekly intraperitoneal injections of either recombinant protein or PBS. Three days after the final injection, mice were analyzed for several phenotypic parameters of dystrophin deficiency. Injected TAT-μUtr transduced all tissues examined, integrated with members of the dystrophin complex, reduced serum levels of creatine kinase (11,290±920 U versus 5,950±1,120 U; PBS versus TAT), the prevalence of muscle degeneration/regeneration (54%±5% versus 37%±4% of centrally nucleated fibers; PBS versus TAT), the susceptibility to eccentric contraction-induced force drop (72%±5% versus 40%±8% drop; PBS versus TAT), and increased specific force production (9.7±1.1 N/cm2 versus 12.8±0.9 N/cm2; PBS versus TAT). Conclusions These results are, to our knowledge, the first to establish the efficacy and feasibility of TAT-utrophin-based constructs as a novel direct protein-replacement therapy for the treatment of skeletal and cardiac muscle diseases caused by loss of dystrophin.
Unitarity Relations in c=1 Liouville Theory
David A. Lowe
Physics , 1992, DOI: 10.1142/S0217732392004122
Abstract: We consider the S-matrix of c=1 Liouville theory with vanishing cosmological constant. We examine some of the constraints imposed by unitarity. These completely determine (N,2) amplitudes at tree level in terms of the (N,1) amplitudes when the plus tachyon momenta take generic values. A surprising feature of the matrix model results is the lack of particle creation branch cuts in the higher genus amplitudes. In fact, we show the naive field theory limit of Liouville theory would predict such branch cuts. However, unitarity in the full string theory ensures that such cuts do not appear in genus one (N,1) amplitudes. We conclude with some comments about the genus one (N,2) amplitudes.
Causal Properties of Free String Field Theory
D. A. Lowe
Physics , 1993, DOI: 10.1016/0370-2693(94)91314-5
Abstract: This paper examines the causal structure of the commutator of two string fields, in free light-cone string field theory. By treating the commutator as a distribution on infinite dimensional loop space, it is shown that the commutator vanishes when $\int d\ss (\delta X(\ss))^2 <0$. Of more direct physical interest is the commutator of finite mass fields, obtained by smearing the string fields with appropriate wave functions. This is shown to vanish at spacelike separations, reproducing the usual point particle field theory result. The implications of this for the information spreading mechanism proposed by Susskind to solve the black hole information problem are discussed. Finally, it is verified that the above conclusions also hold for the superstring.
Bound States of Type I' D-particles and Enhanced Gauge Symmetry
David A. Lowe
Physics , 1997, DOI: 10.1016/S0550-3213(97)00345-3
Abstract: Duality between the E_8 x E_8 heterotic string and Type I' theory predicts a tower of D(irichlet)-particle bound states corresponding to perturbative heterotic string states. In the limit of infinite Type I' coupling, some of these bound states become massless, giving rise to enhanced E_8 x E_8 gauge symmetry. By taking a different infinite coupling limit, one can recover the E_8 x E_8 gauge bosons of M-theory, compactified on S^1/Z_2. In this paper we use the matrix model description of the D-particle dynamics to study these bound states. We find results consistent with the chain of dualities and clarify a number of issues that arise in the application of the matrix mechanics to this system.
E_8 x E_8 Small Instantons in Matrix Theory
David A. Lowe
Physics , 1997, DOI: 10.1016/S0550-3213(98)00040-6
Abstract: A formulation of new six-dimensional theories with (1,0) supersymmetry and E_8 global symmetry is proposed. The model is based on the large n theory describing n D-strings interacting with parallel D-fivebranes in Type I string theory.
Eleven-Dimensional Lorentz Symmetry from SUSY Quantum Mechanics
David A. Lowe
Physics , 1998, DOI: 10.1088/1126-6708/1998/10/003
Abstract: The supermembrane in light-cone gauge gives rise to a supersymmetric quantum mechanics system with SU(N) gauge symmetry when the group of area preserving diffeomorphisms is suitably regulated. de Wit, Marquard and Nicolai showed how eleven-dimensional Lorentz generators can be constructed from these degrees of freedom at the classical level. In this paper, these considerations are extended to the quantum level and it is shown the algebra closes to leading nontrivial order at large N. A proposal is made for extending these results to Matrix theory by realizing longitudinal boosts as large N renormalization group transformations.
The Planckian Conspiracy: String Theory and the Black Hole Information Paradox
David A. Lowe
Physics , 1995, DOI: 10.1016/0550-3213(95)00521-9
Abstract: It has been argued that the consistency of quantum theory with black hole physics requires nonlocality not present in ordinary effective field theory. We examine the extent to which such nonlocal effects show up in the perturbative S-matrix of string theory.
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