The Experts below are selected from a list of 129 Experts worldwide ranked by ideXlab platform
Adelino V M Canário - One of the best experts on this subject based on the ideXlab platform.
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Hormonal control of swimbladder sonic muscle dimorphism in the Lusitanian toadfish Halobatrachus didactylus.
Journal of Experimental Biology, 2003Co-Authors: Teresa Modesto, Adelino V M CanárioAbstract:SUMMARY The swimbladder and associated sonic muscle of the Lusitanian toadfish Halobatrachus didactylus increase in size throughout life and are, respectively, 25% and 30% larger in type I (nest-holder) males than females, which may generate sexual differences in sound production. Sexual dimorphism in swimbladder is also evident in the morphological features of sonic muscle fibers. During the breeding season, type I males have smaller myofibril contracting zones surrounded by larger Sarcoplasm areas compared with females, possibly an adaptation to speed and fatigue resistance for the production of long mating calls. Type II (floater) males show characteristics that are intermediate, but statistically not significantly different, between type I males and females. Six weeks after castration and androgen (testosterone and 11-ketotestosterone) replacement in type I and type II males there were no alterations either in swimbladder mass or fiber morphology. However, 17β-estradiol induced a significant decrease in swimbladder mass and Sarcoplasm area/myofibril area ratio. Six months after castration there was a clear reduction in the seasonal swimbladder hypertrophy in males and induction of sonic fiber morphological characteristics that resemble those occurring in females (low Sarcoplasm area/myofibril area ratio). These results suggest that testicular factors are required to initiate sonic muscle hypertrophy and type I sonic fiber phenotype in H. didactylus , but a specific involvement of androgens has not been completely clarified.
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Hormonal control of swimbladder sonic muscle dimorphism in the Lusitanian toadfish Halobatrachus didactylus.
The Journal of experimental biology, 2003Co-Authors: Teresa Modesto, Adelino V M CanárioAbstract:The swimbladder and associated sonic muscle of the Lusitanian toadfish Halobatrachus didactylus increase in size throughout life and are, respectively, 25% and 30% larger in type I (nest-holder) males than females, which may generate sexual differences in sound production. Sexual dimorphism in swimbladder is also evident in the morphological features of sonic muscle fibers. During the breeding season, type I males have smaller myofibril contracting zones surrounded by larger Sarcoplasm areas compared with females, possibly an adaptation to speed and fatigue resistance for the production of long mating calls. Type II (floater) males show characteristics that are intermediate, but statistically not significantly different, between type I males and females. Six weeks after castration and androgen (testosterone and 11-ketotestosterone) replacement in type I and type II males there were no alterations either in swimbladder mass or fiber morphology. However, 17beta-estradiol induced a significant decrease in swimbladder mass and Sarcoplasm area/myofibril area ratio. Six months after castration there was a clear reduction in the seasonal swimbladder hypertrophy in males and induction of sonic fiber morphological characteristics that resemble those occurring in females (low Sarcoplasm area/myofibril area ratio). These results suggest that testicular factors are required to initiate sonic muscle hypertrophy and type I sonic fiber phenotype in H. didactylus, but a specific involvement of androgens has not been completely clarified.
M. J. Wranicz - One of the best experts on this subject based on the ideXlab platform.
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Trichinella spiralis : induction of the basophilic transformation of muscle cells by synchronous newborn larvae. II. Electron microscopy study
Parasitology research, 1998Co-Authors: Błotna-filipiak M, Gabryel P, Gustowska L, E. Kucharska, M. J. WraniczAbstract:The present ultrastructure observations apply to the same experimental groups that were investigated in the first part of the study. The results of electron microscopy investigations correspond to those obtained using light microscopy methods. The ultrastructure data demonstrated that 1-h-old sNBL (group I) penetrated into the Sarcoplasm of the muscle cells and transformed it basophilically, finally creating the "nurse cell-muscle larva complex." These larvae also caused transformation of the same muscle cells without being present in the Sarcoplasm. The larvae of group II (9-h-old sNBL) preserved transformation potential as well, but it was less intensive. Not all NBL settled in the muscle cells; some of them remained in the intercellular spaces. Group II larvae present in the muscle cells underwent early degeneration and necrosis more often than did group I larvae; the inflammatory cell reactions in the vicinity of the larvae were more intensive. The basophilic transformation of muscle cells that did not contain larvae in their Sarcoplasm was not intensive and often stopped at the level of cell nuclei. The larvae of group III (6-day-old sNBL) neither settled in the muscle cells nor transformed the cell Sarcoplasm.
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Trichinella spiralis : induction of the basophilic transformation of muscle cells by synchronous newborn larvae
Parasitology research, 1998Co-Authors: M. J. Wranicz, Gabryel P, Gustowska L, E. Kucharska, Władysław CabajAbstract:The present ultrastructure observations apply to the same experimental groups that were investigated in the first part of the study. The results of electron microscopy investigations correspond to those obtained using light microscopy methods. The ultrastructure data demonstrated that 1-h-old sNBL (group I) penetrated into the Sarcoplasm of the muscle cells and transformed it basophilically, finally creating the “nurse cell-muscle larva complex.” These larvae also caused transformation of the same muscle cells without being present in the Sarcoplasm. The larvae of group II (9-h-old sNBL) preserved transformation potential as well, but it was less intensive. Not all NBL settled in the muscle cells; some of them remained in the intercellular spaces. Group II larvae present in the muscle cells underwent early degeneration and necrosis more often than did group I larvae; the inflammatory cell reactions in the vicinity of the larvae were more intensive. The basophilic transformation of muscle cells that did not contain larvae in their Sarcoplasm was not intensive and often stopped at the level of cell nuclei. The larvae of group III (6-day-old sNBL) neither settled in the muscle cells nor transformed the cell Sarcoplasm.
Teresa Modesto - One of the best experts on this subject based on the ideXlab platform.
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Hormonal control of swimbladder sonic muscle dimorphism in the Lusitanian toadfish Halobatrachus didactylus.
Journal of Experimental Biology, 2003Co-Authors: Teresa Modesto, Adelino V M CanárioAbstract:SUMMARY The swimbladder and associated sonic muscle of the Lusitanian toadfish Halobatrachus didactylus increase in size throughout life and are, respectively, 25% and 30% larger in type I (nest-holder) males than females, which may generate sexual differences in sound production. Sexual dimorphism in swimbladder is also evident in the morphological features of sonic muscle fibers. During the breeding season, type I males have smaller myofibril contracting zones surrounded by larger Sarcoplasm areas compared with females, possibly an adaptation to speed and fatigue resistance for the production of long mating calls. Type II (floater) males show characteristics that are intermediate, but statistically not significantly different, between type I males and females. Six weeks after castration and androgen (testosterone and 11-ketotestosterone) replacement in type I and type II males there were no alterations either in swimbladder mass or fiber morphology. However, 17β-estradiol induced a significant decrease in swimbladder mass and Sarcoplasm area/myofibril area ratio. Six months after castration there was a clear reduction in the seasonal swimbladder hypertrophy in males and induction of sonic fiber morphological characteristics that resemble those occurring in females (low Sarcoplasm area/myofibril area ratio). These results suggest that testicular factors are required to initiate sonic muscle hypertrophy and type I sonic fiber phenotype in H. didactylus , but a specific involvement of androgens has not been completely clarified.
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Hormonal control of swimbladder sonic muscle dimorphism in the Lusitanian toadfish Halobatrachus didactylus.
The Journal of experimental biology, 2003Co-Authors: Teresa Modesto, Adelino V M CanárioAbstract:The swimbladder and associated sonic muscle of the Lusitanian toadfish Halobatrachus didactylus increase in size throughout life and are, respectively, 25% and 30% larger in type I (nest-holder) males than females, which may generate sexual differences in sound production. Sexual dimorphism in swimbladder is also evident in the morphological features of sonic muscle fibers. During the breeding season, type I males have smaller myofibril contracting zones surrounded by larger Sarcoplasm areas compared with females, possibly an adaptation to speed and fatigue resistance for the production of long mating calls. Type II (floater) males show characteristics that are intermediate, but statistically not significantly different, between type I males and females. Six weeks after castration and androgen (testosterone and 11-ketotestosterone) replacement in type I and type II males there were no alterations either in swimbladder mass or fiber morphology. However, 17beta-estradiol induced a significant decrease in swimbladder mass and Sarcoplasm area/myofibril area ratio. Six months after castration there was a clear reduction in the seasonal swimbladder hypertrophy in males and induction of sonic fiber morphological characteristics that resemble those occurring in females (low Sarcoplasm area/myofibril area ratio). These results suggest that testicular factors are required to initiate sonic muscle hypertrophy and type I sonic fiber phenotype in H. didactylus, but a specific involvement of androgens has not been completely clarified.
Mohammad Salajegheh - One of the best experts on this subject based on the ideXlab platform.
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Sarcoplasmic redistribution of nuclear tdp 43 in inclusion body myositis
Muscle & Nerve, 2009Co-Authors: Jack L Pinkus, Anthony A Amato, Mohammad Salajegheh, Paul J Taylor, Remedios Nazareno, Robert H Baloh, Steven A GreenbergAbstract:The nucleic acid binding protein TDP-43 was recently identified in normal myonuclei and in the Sarcoplasm of inclusion body myositis (IBM) muscle. Here we found TDP-43 Sarcoplasmic immunoreactivity in 23% of IBM myofibers, while other reported IBM biomarkers were less frequent, with rimmed vacuoles in 2.8%, fluorescent Congo red material in 0.57%, SMI-31 immunoreactivity in 0.83%, and focal R1282 beta-amyloid immunoreactivity in 0.00% of myofibers. The presence of as little as > 1% of myofibers with non-nuclear Sarcoplasmic TDP-43 was highly sensitive (91%) and specific (100%) to IBM among 50 inflammatory myopathy patient samples, though some patients with hereditary inclusion body myopathies and myofibrillar myopathy also had Sarcoplasmic TDP-43. TDP-43 mutations were sought, and none were identified. TDP-43 could be one of many nucleic acid binding proteins that are abnormally present in IBM Sarcoplasm. They could potentially interfere with the normal function of extranuclear RNAs that maintain myofiber protein production.
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Sarcoplasmic redistribution of nuclear TDP‐43 in inclusion body myositis
Muscle & nerve, 2009Co-Authors: Mohammad Salajegheh, Jack L Pinkus, Anthony A Amato, Remedios Nazareno, Robert H Baloh, J. Paul Taylor, Steven A GreenbergAbstract:The nucleic acid binding protein TDP-43 was recently identified in normal myonuclei and in the Sarcoplasm of inclusion body myositis (IBM) muscle. Here we found TDP-43 Sarcoplasmic immunoreactivity in 23% of IBM myofibers, while other reported IBM biomarkers were less frequent, with rimmed vacuoles in 2.8%, fluorescent Congo red material in 0.57%, SMI-31 immunoreactivity in 0.83%, and focal R1282 beta-amyloid immunoreactivity in 0.00% of myofibers. The presence of as little as > 1% of myofibers with non-nuclear Sarcoplasmic TDP-43 was highly sensitive (91%) and specific (100%) to IBM among 50 inflammatory myopathy patient samples, though some patients with hereditary inclusion body myopathies and myofibrillar myopathy also had Sarcoplasmic TDP-43. TDP-43 mutations were sought, and none were identified. TDP-43 could be one of many nucleic acid binding proteins that are abnormally present in IBM Sarcoplasm. They could potentially interfere with the normal function of extranuclear RNAs that maintain myofiber protein production.
Steven A Greenberg - One of the best experts on this subject based on the ideXlab platform.
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Sarcoplasmic redistribution of nuclear tdp 43 in inclusion body myositis
Muscle & Nerve, 2009Co-Authors: Jack L Pinkus, Anthony A Amato, Mohammad Salajegheh, Paul J Taylor, Remedios Nazareno, Robert H Baloh, Steven A GreenbergAbstract:The nucleic acid binding protein TDP-43 was recently identified in normal myonuclei and in the Sarcoplasm of inclusion body myositis (IBM) muscle. Here we found TDP-43 Sarcoplasmic immunoreactivity in 23% of IBM myofibers, while other reported IBM biomarkers were less frequent, with rimmed vacuoles in 2.8%, fluorescent Congo red material in 0.57%, SMI-31 immunoreactivity in 0.83%, and focal R1282 beta-amyloid immunoreactivity in 0.00% of myofibers. The presence of as little as > 1% of myofibers with non-nuclear Sarcoplasmic TDP-43 was highly sensitive (91%) and specific (100%) to IBM among 50 inflammatory myopathy patient samples, though some patients with hereditary inclusion body myopathies and myofibrillar myopathy also had Sarcoplasmic TDP-43. TDP-43 mutations were sought, and none were identified. TDP-43 could be one of many nucleic acid binding proteins that are abnormally present in IBM Sarcoplasm. They could potentially interfere with the normal function of extranuclear RNAs that maintain myofiber protein production.
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Sarcoplasmic redistribution of nuclear TDP‐43 in inclusion body myositis
Muscle & nerve, 2009Co-Authors: Mohammad Salajegheh, Jack L Pinkus, Anthony A Amato, Remedios Nazareno, Robert H Baloh, J. Paul Taylor, Steven A GreenbergAbstract:The nucleic acid binding protein TDP-43 was recently identified in normal myonuclei and in the Sarcoplasm of inclusion body myositis (IBM) muscle. Here we found TDP-43 Sarcoplasmic immunoreactivity in 23% of IBM myofibers, while other reported IBM biomarkers were less frequent, with rimmed vacuoles in 2.8%, fluorescent Congo red material in 0.57%, SMI-31 immunoreactivity in 0.83%, and focal R1282 beta-amyloid immunoreactivity in 0.00% of myofibers. The presence of as little as > 1% of myofibers with non-nuclear Sarcoplasmic TDP-43 was highly sensitive (91%) and specific (100%) to IBM among 50 inflammatory myopathy patient samples, though some patients with hereditary inclusion body myopathies and myofibrillar myopathy also had Sarcoplasmic TDP-43. TDP-43 mutations were sought, and none were identified. TDP-43 could be one of many nucleic acid binding proteins that are abnormally present in IBM Sarcoplasm. They could potentially interfere with the normal function of extranuclear RNAs that maintain myofiber protein production.
