Relevant bibliographies by topics / Myogenic

Academic literature on the topic 'Myogenic'

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Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Myogenic"

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Cheng, T. C., T. A. Hanley, J. Mudd, J. P. Merlie, and E. N. Olson. "Mapping of myogenin transcription during embryogenesis using transgenes linked to the myogenin control region." Journal of Cell Biology 119, no. 6 (December 15, 1992): 1649–56. http://dx.doi.org/10.1083/jcb.119.6.1649.

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During vertebrate embryogenesis, the muscle-specific helix-loop-helix protein myogenin is expressed in muscle cell precursors in the developing somite myotome and limb bud before muscle fiber formation and is further upregulated during myogenesis. We show that cis-acting DNA sequences within the 5' flanking region of the mouse myogenin gene are sufficient to direct appropriate temporal, spatial, and tissue-specific transcription of myogenin during mouse embryogenesis. Myogenin-lacZ transgenes trace the fate of embryonic cells that activate myogenin transcription and suggest that myogenic precursor cells that migrate from the somite myotome to the limb bud are committed to a myogenic fate in the absence of myogenin transcription. Activation of a myogenin-lacZ transgene can occur in limb bud explants in culture, indicating that signals required for activation of myogenin transcription are intrinsic to the limb bud and independent of other parts of the embryo. These results reveal multiple populations of myogenic precursor cells during development and suggest the existence of regulators other than myogenic helix-loop-helix proteins that maintain cells in the early limb bud in the myogenic lineage.
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Higashioka, Koki, Noriko Koizumi, Hidetoshi Sakurai, Chie Sotozono, and Takahiko Sato. "Myogenic Differentiation from MYOGENIN-Mutated Human iPS Cells by CRISPR/Cas9." Stem Cells International 2017 (2017): 1–9. http://dx.doi.org/10.1155/2017/9210494.

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It is well known that myogenic regulatory factors encoded by the Myod1 family of genes have pivotal roles in myogenesis, with partially overlapping functions, as demonstrated for the mouse embryo. Myogenin-mutant mice, however, exhibit severe myogenic defects without compensation by other myogenic factors. MYOGENIN might be expected to have an analogous function in human myogenic cells. To verify this hypothesis, we generated MYOGENIN-mutated human iPS cells by using CRISPR/Cas9 genome-editing technology. Our results suggest that MYOD1-independent or MYOD1-dependent mechanisms can compensate for the loss of MYOGENIN and that these mechanisms are likely to be crucial for regulating skeletal muscle differentiation and formation.
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Wang, Y., and R. Jaenisch. "Myogenin can substitute for Myf5 in promoting myogenesis but less efficiently." Development 124, no. 13 (July 1, 1997): 2507–13. http://dx.doi.org/10.1242/dev.124.13.2507.

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The myogenic basic Helix-Loop-Helix transcription factors, including Myf5, MyoD, myogenin (myg) and MRF4, play important roles in skeletal muscle development. The phenotypes of mutant mice deficient in either gene are different, suggesting that each gene may have a unique function in vivo. We previously showed that targeting myogenin into the Myf5 locus (Myf5(myg-ki)) rescued the rib cage truncation in the Myf5-null mutant, hence demonstrating functional redundancy between Myf5 and myogenin in skeletal morphogenesis. Here we present the results of crossing myogenin knock-in (myg-ki) mice with either MyoD-null or myogenin-null mutants. The Myf5(myg-ki) allele rescued early myogenesis, but Myf5(myg-ki/myg-ki);MyoD(−/−) mutant mice died immediately after birth owing to reduced muscle formation. Therefore, myogenin, expressed from the Myf5 locus, is not able to completely replace the function of Myf5 in muscle development although it is capable of determining and/or maintaining myogenic lineage. Myf5(myg-ki/myg-ki);myg(−/−) mutant mice displayed the same phenotype as myg(−/−) mutants. This indicates that the earlier expression of myogenin cannot promote myogenic terminal differentiation, which is normally initiated by the endogenous myogenin. Thus, our results are consistent with the notion that Myf5 and myogenin are functionally interchangeable in determining myogenic lineage and assuring normal rib formation. Our experiment revealed, however, that some aspects of myogenesis may be unique to a given myogenic factor and are due to either different regulatory sequences that control their temporal and spatial expression or different functional protein domains.
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Rawls, A., M. R. Valdez, W. Zhang, J. Richardson, W. H. Klein, and E. N. Olson. "Overlapping functions of the myogenic bHLH genes MRF4 and MyoD revealed in double mutant mice." Development 125, no. 13 (July 1, 1998): 2349–58. http://dx.doi.org/10.1242/dev.125.13.2349.

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The myogenic basic helix-loop-helix (bHLH) genes - MyoD, Myf5, myogenin and MRF4 - exhibit distinct, but overlapping expression patterns during development of the skeletal muscle lineage and loss-of-function mutations in these genes result in different effects on muscle development. MyoD and Myf5 have been shown to act early in the myogenic lineage to establish myoblast identity, whereas myogenin acts later to control myoblast differentiation. In mice lacking myogenin, there is a severe deficiency of skeletal muscle, but some residual muscle fibers are present in mutant mice at birth. Mice lacking MRF4 are viable and have skeletal muscle, but they upregulate myogenin expression, which could potentially compensate for the absence of MRF4. Previous studies in which Myf5 and MRF4 null mutations were combined suggested that these genes do not share overlapping myogenic functions in vivo. To determine whether the functions of MRF4 might overlap with those of myogenin or MyoD, we generated double mutant mice lacking MRF4 and either myogenin or MyoD. MRF4/myogenin double mutant mice contained a comparable number of residual muscle fibers to mice lacking myogenin alone and myoblasts from those double mutant mice formed differentiated multinucleated myotubes in vitro as efficiently as wild-type myoblasts, indicating that neither myogenin nor MRF4 is absolutely essential for myoblast differentiation. Whereas mice lacking either MRF4 or MyoD were viable and did not show defects in muscle development, MRF4/MyoD double mutants displayed a severe muscle deficiency similar to that in myogenin mutants. Myogenin was expressed in MRF4/MyoD double mutants, indicating that myogenin is insufficient to support normal myogenesis in vivo. These results reveal unanticipated compensatory roles for MRF4 and MyoD in the muscle differentiation pathway and suggest that a threshold level of myogenic bHLH factors is required to activate muscle structural genes, with this level normally being achieved by combinations of multiple myogenic bHLH factors.
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Gómez, JoséA, Mahul B. Amin, Jae Y. Ro, Michael D. Linden, Min W. Lee, and Richard J. Zarbo. "Immunohistochemical Profile of Myogenin and MyoD1 Does Not Support Skeletal Muscle Lineage in Alveolar Soft Part Sarcoma." Archives of Pathology & Laboratory Medicine 123, no. 6 (June 1, 1999): 503–7. http://dx.doi.org/10.5858/1999-123-0503-ipomam.

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Abstract Background.—The histogenesis of alveolar soft part sarcoma remains elusive. Myogenic origin is favored, although conflicting data on immunohistochemical demonstration of muscle-associated markers exist. Myogenin and MyoD1, transcription factors of the myogenic determination family, have crucial roles in commitment and differentiation of mesenchymal progenitor cells to myogenic lineage and in maintenance of skeletal muscle phenotype. Their immunohistochemical detection is specific in characterization of rhabdomyosarcoma. Methods.—Antibodies for myogenin, MyoD1, desmin, and muscle-specific actin were employed on a large series of cases (n = 19) of formalin-fixed, paraffin-embedded alveolar soft part sarcoma. Results.—Minimal scattered nuclear staining was seen with myogenin. All cases had pronounced, nonspecific granular cytoplasmic immunostaining with MyoD1; nuclei were negative. All tumors were negative for desmin and muscle-specific actin. Ultrastructural study in 10 cases failed to reveal features of skeletal muscle differentiation. Conclusions.—Cytoplasmic staining with MyoD1 in alveolar soft part sarcoma may correspond to cross-reactivity with an undetermined cytoplasmic antigen. The lack of immunostaining with myogenin, MyoD1, desmin, and muscle-specific actin provides evidence against a myogenic origin for alveolar soft part sarcoma.
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Bergstrom, Donald A., and Stephen J. Tapscott. "Molecular Distinction between Specification and Differentiation in the Myogenic Basic Helix-Loop-Helix Transcription Factor Family." Molecular and Cellular Biology 21, no. 7 (April 1, 2001): 2404–12. http://dx.doi.org/10.1128/mcb.21.7.2404-2412.2001.

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ABSTRACT The myogenic basic helix-loop-helix (bHLH) proteins regulate both skeletal muscle specification and differentiation: MyoD and Myf5 establish the muscle lineage, whereas myogenin mediates differentiation. Previously, we demonstrated that MyoD was more efficient than myogenin at initiating the expression of skeletal muscle genes, and in this study we present the molecular basis for this difference. A conserved amphipathic alpha-helix in the carboxy terminus of the myogenic bHLH proteins has distinct activities in MyoD and myogenin: the MyoD helix facilitates the initiation of endogenous gene expression, whereas the myogenin helix functions as a general transcriptional activation domain. Thus, the alternate use of a similar motif for gene initiation and activation provides a molecular basis for the distinction between specification and differentiation within the myogenic bHLH gene family.
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Schwarz, J. J., T. Chakraborty, J. Martin, J. M. Zhou, and E. N. Olson. "The basic region of myogenin cooperates with two transcription activation domains to induce muscle-specific transcription." Molecular and Cellular Biology 12, no. 1 (January 1992): 266–75. http://dx.doi.org/10.1128/mcb.12.1.266.

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Myogenin is a skeletal muscle-specific transcription factor that can activate myogenesis when introduced into a variety of nonmuscle cell types. Activation of the myogenic program by myogenin is dependent on its binding to a DNA sequence known as an E box, which is associated with numerous muscle-specific genes. Myogenin shares homology with MyoD and other myogenic regulatory factors within a basic region and a helix-loop-helix (HLH) motif that mediate DNA binding and dimerization, respectively. Here we show that the basic region-HLH motif of myogenin alone lacks transcriptional activity and is dependent on domains in the amino and carboxyl termini to activate transcription. Analysis of these N- and C-terminal domains through creation of chimeras with the DNA-binding domain of the Saccharomyces cerevisiae transcription factor GAL4 revealed that they act as strong transcriptional activators. These transcription activation domains are dependent for activity on a specific amino acid sequence within the basic region, referred to as the myogenic recognition motif (MRM), when an E box is the target for DNA binding. However, the activation domains function independent of the MRM when DNA binding is mediated through a heterologous DNA-binding domain. The activation domain of the acidic coactivator VP16 can substitute for the myogenin activation domains and restore strong myogenic activity to the basic region-HLH motif. Within a myogenin-VP16 chimera, however, the VP16 activation domain also relies on the MRM for activation of the myogenic program. These findings reveal that DNA binding and transcriptional activation are separable functions, encoded by different domains of myogenin, but that the activity of the transcriptional activation domains is influenced by the DNA-binding domain. Activation of muscle-specific transcription requires collaboration between the DNA-binding and activation domains of myogenin and is dependent on events in addition to DNA binding.
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Schwarz, J. J., T. Chakraborty, J. Martin, J. M. Zhou, and E. N. Olson. "The basic region of myogenin cooperates with two transcription activation domains to induce muscle-specific transcription." Molecular and Cellular Biology 12, no. 1 (January 1992): 266–75. http://dx.doi.org/10.1128/mcb.12.1.266-275.1992.

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Myogenin is a skeletal muscle-specific transcription factor that can activate myogenesis when introduced into a variety of nonmuscle cell types. Activation of the myogenic program by myogenin is dependent on its binding to a DNA sequence known as an E box, which is associated with numerous muscle-specific genes. Myogenin shares homology with MyoD and other myogenic regulatory factors within a basic region and a helix-loop-helix (HLH) motif that mediate DNA binding and dimerization, respectively. Here we show that the basic region-HLH motif of myogenin alone lacks transcriptional activity and is dependent on domains in the amino and carboxyl termini to activate transcription. Analysis of these N- and C-terminal domains through creation of chimeras with the DNA-binding domain of the Saccharomyces cerevisiae transcription factor GAL4 revealed that they act as strong transcriptional activators. These transcription activation domains are dependent for activity on a specific amino acid sequence within the basic region, referred to as the myogenic recognition motif (MRM), when an E box is the target for DNA binding. However, the activation domains function independent of the MRM when DNA binding is mediated through a heterologous DNA-binding domain. The activation domain of the acidic coactivator VP16 can substitute for the myogenin activation domains and restore strong myogenic activity to the basic region-HLH motif. Within a myogenin-VP16 chimera, however, the VP16 activation domain also relies on the MRM for activation of the myogenic program. These findings reveal that DNA binding and transcriptional activation are separable functions, encoded by different domains of myogenin, but that the activity of the transcriptional activation domains is influenced by the DNA-binding domain. Activation of muscle-specific transcription requires collaboration between the DNA-binding and activation domains of myogenin and is dependent on events in addition to DNA binding.
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Heidt, Analeah B., Anabel Rojas, Ian S. Harris, and Brian L. Black. "Determinants of Myogenic Specificity within MyoD Are Required for Noncanonical E Box Binding." Molecular and Cellular Biology 27, no. 16 (June 11, 2007): 5910–20. http://dx.doi.org/10.1128/mcb.01700-06.

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ABSTRACT The MyoD family of basic helix-loop-helix (bHLH) transcription factors has the remarkable ability to induce myogenesis in vitro and in vivo. This myogenic specificity has been mapped to two amino acids in the basic domain, an alanine and threonine, referred to as the myogenic code. These essential determinants of myogenic specificity are conserved in all MyoD family members from worms to humans, yet their function in myogenesis is unclear. Induction of the muscle transcriptional program requires that MyoD be able to locate and stably bind to sequences present in the promoter regions of critical muscle genes. Recent studies have shown that MyoD binds to noncanonical E boxes in the myogenin gene, a critical locus required for myogenesis, through interactions with resident heterodimers of the HOX-TALE transcription factors Pbx1A and Meis1. In the present study, we show that the myogenic code is required for MyoD to bind to noncanonical E boxes in the myogenin promoter and for the formation of a tetrameric complex with Pbx/Meis. We also show that these essential determinants of myogenesis are sufficient to confer noncanonical E box binding to the E12 basic domain. Thus, these data show that noncanonical E box binding correlates with myogenic potential, and we speculate that the myogenic code residues in MyoD function as myogenic determinants via their role in noncanonical E box binding and recognition.
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Arnold, H. H., C. D. Gerharz, H. E. Gabbert, and A. Salminen. "Retinoic acid induces myogenin synthesis and myogenic differentiation in the rat rhabdomyosarcoma cell line BA-Han-1C." Journal of Cell Biology 118, no. 4 (August 15, 1992): 877–87. http://dx.doi.org/10.1083/jcb.118.4.877.

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Two clonal rat rhabdomyosarcoma cell lines BA-Han-1B and BA-Han-1C with different capacities for myogenic differentiation have been examined for the expression of muscle regulatory basic helix-loop-helix (bHLH) proteins of the MyoD family. Whereas cells of the BA-Han-1C subpopulation constitutively expressed MyoD1 and could be induced to differentiate with retinoic acid (RA), BA-Han-1B cells did not express any of the myogenic control factors and appeared to be largely differentiation-defective. Upon induction with RA, BA-Han-1C cells expressed also myogenin, in contrast to BA-Han-1B cells which never activated any of the genes encoding muscle bHLH factors. The onset of myogenin transcription in BA-Han-1C cells required de novo protein synthesis and DNA replication suggesting that RA probably did not act directly on the myogenin gene. Although MyoD1 was expressed in proliferating BA-Han-1C myoblasts, muscle-specific reporter genes were not activated indicating that MyoD was biologically inactive. However, transfections with plasmid expressing additional MyoD1 protein resulted in the transactivation of muscle genes even in the absence of RA. mRNA encoding the negative regulatory HLH protein Id was expressed in proliferating BA-Han-1C cells and disappeared later after RA induction which suggested that it may be involved in the regulation of MyoD1 activity. The myogenic differentiation of malignant rhabdomyosarcoma cells strictly correlated with the activation of the myogenin gene. In fact, stable transfections of BA-Han-1C cells with myogenin expressing plasmids resulted in spontaneous differentiation. Together, our results suggest that the transformed and undifferentiated phenotype of BA-Han-1C rhabdomyosarcoma cells is associated with the inactivation of the myogenic factor MyoD1 as well as lack of myogenin expression. RA alleviates the inhibition of myogenic differentiation, probably by activating MyoD protein and myogenin gene transcription. BA-Han-1B cells did not respond to RA and the differentiated phenotype could not be restored by overexpression of MyoD1 or myogenin.
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Dissertations / Theses on the topic "Myogenic"

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Murnane, Owen D. "Vestibular Evoked Myogenic Potentials." Digital Commons @ East Tennessee State University, 2011. https://dc.etsu.edu/etsu-works/1933.

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Murnane, Owen D. "Vestibular Evoked Myogenic Potentials." Digital Commons @ East Tennessee State University, 2004. https://dc.etsu.edu/etsu-works/1948.

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Murnane, Owen D. "Vestibular Evoked Myogenic Potentials." Digital Commons @ East Tennessee State University, 2005. https://dc.etsu.edu/etsu-works/1947.

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Murnane, Owen D. "Vestibular Evoked Myogenic Potentials." Digital Commons @ East Tennessee State University, 2013. https://dc.etsu.edu/etsu-works/1932.

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Akin, Faith W. "Vestibular Evoked Myogenic Potentials." Digital Commons @ East Tennessee State University, 2006. https://dc.etsu.edu/etsu-works/2452.

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Akin, Faith W., and Owen D. Murnane. "Vestibular Evoked Myogenic Potentials." Digital Commons @ East Tennessee State University, 2008. https://dc.etsu.edu/etsu-works/1939.

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Murnane, Owen D., and Faith W. Akin. "Vestibular-Evoked Myogenic Potentials." Digital Commons @ East Tennessee State University, 2009. https://dc.etsu.edu/etsu-works/1795.

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Cervical vestibular-evoked myogenic potentials (cVEMPs) are recorded from the sternocleidomastoid muscle using air conduction or bone conduction acoustic stimuli, skull taps, or transmastoid current. The diagnostic usefulness of the cVEMP has been examined for various peripheral and central vestibulopathies. Recent reports indicate that it is possible to record short-latency ocular vestibular-evoked myogenic potentials (oVEMPs) from surface electrodes below the eyes in response to air conduction and bone conduction stimuli. Both methods provide diagnostic information about otolith function. This article provides an overview of each method and highlights the similarities and differences. Several cases are presented to illustrate the relation between the results for cVEMPs and oVEMPs in patients with well-defined audiovestibular disorders.
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Akin, Faith W., and Owen D. Murnane. "Vestibular Evoked Myogenic Potentials." Digital Commons @ East Tennessee State University, 2001. https://dc.etsu.edu/etsu-works/1916.

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Akin, Faith W., and Owen D. Murnane. "Vestibular Evoked Myogenic Potentials." Digital Commons @ East Tennessee State University, 2007. https://dc.etsu.edu/etsu-works/1944.

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Akin, Faith W. "Vestibular Evoked Myogenic Potentials." Digital Commons @ East Tennessee State University, 2007. https://dc.etsu.edu/etsu-works/2450.

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Books on the topic "Myogenic"

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Murofushi, Toshihisa, and Kimitaka Kaga. Vestibular Evoked Myogenic Potential. Tokyo: Springer Japan, 2009. http://dx.doi.org/10.1007/978-4-431-85908-6.

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Barlas, Panagiotis. An investigation of the effects of acupuncture upon experimentally-induced myogenic pain. [s.l: The Author], 1997.

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Yamaguchi, Terence P. The regulation of myogenic determination and differentiation by growth factors and oncogenes. Ottawa: National Library of Canada, 1990.

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Tai, Helen H. Inhibition of myogenic differentiation in Harvey ras-transfected BCb3sH1 muscle cells. Ottawa: National Library of Canada, 1990.

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Miller, Mathew Gordon. Integrin-Linked Kinase 1 (ILK1) is necessary for myogenic differentiation in rat L6 myoblasts. Ottawa: National Library of Canada, 2000.

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Osepchook, Claire C. Expression patterns of muscle growth factors and myogenic regulatory factors in response to undernutrition in ovine skeletal muscle. Ottawa: National Library of Canada, 2002.

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Myers, Bre Lynn. Vestibular learning manual. San Diego: Plural Pub., 2011.

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Vestibular Evoked Myogenic Potential. Springer, 2008.

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Kaga, Kimitaka, and Toshihisa Murofushi. Vestibular Evoked Myogenic Potential: Its Basics and Clinical Applications. Springer, 2010.

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Endlich, Karlhans, and Rodger Loutzenhiser. Tubuloglomerular feedback, renal autoregulation, and renal protection. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0209.

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Vascular tone of glomerular blood vessels is controlled dynamically in response to a number of stimuli of which tubuloglomerular feedback and blood flow (and glomerular filtration rate) autoregulation are the most prominent. Both tubuloglomerular feedback- and myogenic-mediated pre-glomerular vasoconstriction are important in the response to reduced pressure. The renal myogenic mechanism, which has the potential to adjust steady-state tone in response to the oscillating systolic pressure signal, additionally plays an essential role in protecting the kidney from the damaging effects of hypertension.
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Book chapters on the topic "Myogenic"

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Rowe, Fiona J. "Myogenic Disorders." In Clinical Orthoptics, 354–61. West Sussex, UK: John Wiley & Sons, Ltd., 2013. http://dx.doi.org/10.1002/9781118702871.ch16.

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Kahn, Natan D., and David A. Weinberg. "Myogenic Ptosis." In Evaluation and Management of Blepharoptosis, 79–106. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-0-387-92855-5_10.

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Johnson, Paul C. "The Myogenic Response." In The Resistance Vasculature, 159–68. Totowa, NJ: Humana Press, 1991. http://dx.doi.org/10.1007/978-1-4612-0403-9_10.

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Nishimura, Takamichi, Ikuo Mineo, Takao Shimizu, Masanori Kawachi, Akira Ono, Hiromu Nakajima, Masamichi Kuwajima, Norio Kono, and Seiichiro Tarui. "Myogenic Hyperuricemia in Hypoparathyroidism." In Advances in Experimental Medicine and Biology, 213–16. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4899-2638-8_48.

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Mattingly, Jameson K., William J. Riggs, and Oliver F. Adunka. "Vestibular Evoked Myogenic Potentials." In Diagnosis and Treatment of Vestibular Disorders, 107–11. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-97858-1_8.

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Michaels, L. "Vascular Neoplasms; Myogenic Neoplasms." In Ear, Nose and Throat Histopathology, 203–9. London: Springer London, 1987. http://dx.doi.org/10.1007/978-1-4471-3332-2_19.

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Michaels, Leslie, and Henrik B. Hellquist. "Vascular Neoplasms; Myogenic Neoplasms." In Ear, Nose and Throat Histopathology, 218–27. London: Springer London, 2001. http://dx.doi.org/10.1007/978-1-4471-0235-9_19.

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Rundle, Paul, and Hardeep Singh Mudhar. "Uveal Myogenic, Fibrous and Histiocytic Tumors." In Clinical Ophthalmic Oncology, 331–39. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-54255-8_26.

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Applebaum, Mordechai, and Chaya Kalcheim. "Mechanisms of Myogenic Specification and Patterning." In Results and Problems in Cell Differentiation, 77–98. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-662-44608-9_4.

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Murofushi, Toshihisa. "Vestibular Neuropathy and Vestibular Evoked Myogenic Potential." In Neuropathies of the Auditory and Vestibular Eighth Cranial Nerves, 85–92. Tokyo: Springer Japan, 2009. http://dx.doi.org/10.1007/978-4-431-09433-3_10.

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Conference papers on the topic "Myogenic"

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Torfs, T., R. F. Yazicioglu, P. Merken, B. Gyselinckx, R. Puers, R. Vanspauwen, F. L. Wuyts, and C. Van Hoof. "Wireless Vestibular Evoked Myogenic Potentials System." In 2007 IEEE Sensors. IEEE, 2007. http://dx.doi.org/10.1109/icsens.2007.4388600.

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Drummond, Catherine J., Matthew R. Garcia, Daniel J. Devine, Jennifer Peters, Victoria Frohlich, David Finkelstein, and Mark E. Hatley. "Abstract 1036: Non-myogenic origin of embryonal rhabdomyosarcoma." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-1036.

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Li, Yali, and N. C. Goulbourne. "Electro-Chemo-Mechanical Modeling of the Artery Myogenic Transient and Steady-State Response." In ASME 2014 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2014. http://dx.doi.org/10.1115/imece2014-39237.

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Active contraction of smooth muscle results in the myogenic response and vasomotion of arteries, which adjusts the blood flow and nutrient supply of the organism. It is a multiphysic process coupled electrical and chemical kinetics with mechanical behavior of the smooth muscle. This paper presents a new constitutive model for the media layer of the artery wall to describe the myogenic response of artery wall for different transmural pressures. The model includes two major components: electrobiochemical, and chemomechanical parts. The electrochemical model is a lumped Hodgkin-Huxley-type cell membrane model for the nanoscopic ionic currents: calcium, sodium, and potassium. The calculated calcium concentration serves as input for the chemomechanical portion of the model; its molecular binding and the reactions with other enzyme cause the relative sliding of thin and thick filaments of the contractile unit. In the chemomechanical model, a new nonlinear viscoelastic model is proposed using a continuum mechanics approach to describe the time varying behavior of the smooth muscle. Specifically, this model captures the filament overlap effect, active stress evolution, initial velocity, and elastic recoil in the media layer. The artery wall is considered as a thin-walled cylindrical tube. Using the proposed constitutive model and the thin-walled equilibrium equation, the myogenic response is calculated for different transmural pressures. The integrated model is able to capture the pressure-diameter transient and steady-state relationship.
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Bedrov, Y. A., J. P. Dvoretsky, and G. V. Chernyavskaya. "Mechanosensitivity of vessel myocytes: role in formation of myogenic reactions." In Fourth International Workshop on Nondestructive Testing and Computer Simulations in Science and Engineering. SPIE, 2001. http://dx.doi.org/10.1117/12.417655.

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Tenente, Ines M., Myron Ignatius, Eleanor Chen, Madeline Hayes, and David M. Langenau. "Abstract 5153: Myogenic regulatory factors and their role in embryonal rhabdomyosarcoma." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-5153.

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Hashimoto, Takahiro, Takeshi Tsujimura, and Kiyotaka Izumi. "Myogenic potential pattern discernment method using genetic programming for hand gesture." In 2014 Joint 7th International Conference on Soft Computing and Intelligent Systems (SCIS) and 15th International Symposium on Advanced Intelligent Systems (ISIS). IEEE, 2014. http://dx.doi.org/10.1109/scis-isis.2014.7044713.

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Yohe, Marielle E., Berkley E. Gryder, Hsien-Chao Chou, Young K. Song, Xiaohu Zhang, Donna Butcher, Kristine A. Isanogle, et al. "Abstract B17: MEK inhibition induces myogenic differentiation in RAS-driven rhabdomyosarcoma." In Abstracts: AACR Special Conference on Targeting RAS-Driven Cancers; December 9-12, 2018; San Diego, CA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1557-3125.ras18-b17.

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Coulson, Rebecca J., Marilyn J. Cipolla, Lisa Vitullo, and Naomi C. Chesler. "Mechanical Properties of Active and Passive Rat Middle Cerebral Arteries." In ASME 2002 International Mechanical Engineering Congress and Exposition. ASMEDC, 2002. http://dx.doi.org/10.1115/imece2002-32508.

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Abstract:
Cerebral arteries play an important role in the regulation of cerebral blood flow through autoregulation, a well established phenomenon which is caused by a combination of myogenic, neuronal and metabolic mechanisms [1]. Myogenic reactivity is the ability of the vascular smooth muscle cells (SMC) to contract in response to stretch or to an increase in transmural pressure (TMP), and to dilate in response to a decrease in TMP [2]. It is this active constriction of arteries within the autoregulatory range that prompts studies of not just passive mechanical properties, but also active mechanical properties. Passive properties provide an understanding of the behavior of the extracellular matrix components of arteries (i.e. collagen and elastin); but, in order to understand how the artery behaves in vivo, it is necessary to understand the mechanical properties with smooth muscle cell activation. Mechanical properties might also be altered if the vessel is diseased or damaged. Ischemia has been shown to reduce vascular tone, which might lead to brain tissue damage during stroke [3]. Therefore studying the mechanical properties of vessels in disease states to determine if they are able to adequately take part in controlling local blood flow is also important.
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Mullen, M., C. Bahney, S. Ravuri, J. Huard, and Ehrhart NP. "Exosome Production in C2C12 Myoblasts Improves Proliferation and Myogenic Differentiation following Exercise." In Abstracts of the 47th Annual Conference of the Veterinary Orthopedic Society. Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1712884.

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Ilgner, Justus, TA Duong Dinh, and Martin Westhofen. "Position Sensitivity of Cervical Vestibular Evoked Myogenic Potentials on a Rotational Chair." In Abstract- und Posterband – 91. Jahresversammlung der Deutschen Gesellschaft für HNO-Heilkunde, Kopf- und Hals-Chirurgie e.V., Bonn – Welche Qualität macht den Unterschied. © Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1711235.

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Reports on the topic "Myogenic"

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Angov, Georgi, Maria Petrova, and Kateruna Stambolieva. Ocular and Cervical Vestibular Evoked Myogenic Potentials in Multiple Sclerosis Patients. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, December 2020. http://dx.doi.org/10.7546/crabs.2020.12.14.

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