The Experts below are selected from a list of 519 Experts worldwide ranked by ideXlab platform
Koichi Osawa - One of the best experts on this subject based on the ideXlab platform.
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POSTNATAL CHANGES IN THE Extrafusal Muscle Fiber AND Muscle SPINDLE IN THE MASSETER Muscle OF THE DYSTROPHIC MOUSE
Biomedical Research, 1993Co-Authors: Morito Ukai, Norihiko Maeda, Koichi OsawaAbstract:In dystrophic (C57BL/6J-dy/dy) mice, postnatal changes in the masseter Muscle were analyzed morphometrically and histochemically. From the 6th to 14th postnatal week, the superficial portion of the masseter Muscle, which was composed of white and intermediate Muscle Fibers, was atrophied in dystrophic mice. The atrophy was severest in the most lateral component of the Muscle. On the contrary, distinct hypertrophy was evident in red Muscle Fibers in the deep portion. These changes increased with time in the diseased animals. The distribution of formazan particles produced by succinate dehydrogenase (SDH) staining was irregular in the Muscle of dystrophic mice. In Muscle spindles, mean diameters of intrafusal Muscle Fibers and outer capsule were significantly decreased in the diseased mice
Patrick E. Crago - One of the best experts on this subject based on the ideXlab platform.
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Structural Model of the Muscle Spindle
Annals of Biomedical Engineering, 2002Co-Authors: Patrick E. CragoAbstract:A model of the Muscle spindle was developed based on its anatomical structure. The model contains three intrafusal Fibers (bag1, bag2, and chain), two efferents (dynamic γ efferent to the bag1 Fiber and static γ efferent to bag2 and chain Fibers), and two afferents [primary (Ia) and secondary (II)]. As in the real Muscle spindle, the spindle model, under the modulation of γ efferents, responds to the Extrafusal Muscle Fiber length. Both outputs (Ia and II afferents) of the model were compared extensively with published data, under both sinusoidal stretch (with different stretch amplitudes and frequencies) and ramp and hold stretch (with different stretch amplitudes and velocities) in three different fusimotor activation conditions (dynamic γ stimulation, static γ stimulation, and without γ stimulation). Model Ia afferent responses fit the published data well with active gamma input, but less well in the passive state. Model II afferent responses also fit the published data, although less quantitative data were available for comparison. The model correctly predicted the fractional power dependence of the primary and secondary ending responses on stretch velocity. The current model provides a powerful tool for simulation studies of neuromusculoskeletal systems, and demonstrates the feasibility of using a structural approach to model complex neurophysiological systems. © 2002 Biomedical Engineering Society. PAC02: 8719Ff, 8719La, 8719St
Morito Ukai - One of the best experts on this subject based on the ideXlab platform.
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POSTNATAL CHANGES IN THE Extrafusal Muscle Fiber AND Muscle SPINDLE IN THE MASSETER Muscle OF THE DYSTROPHIC MOUSE
Biomedical Research, 1993Co-Authors: Morito Ukai, Norihiko Maeda, Koichi OsawaAbstract:In dystrophic (C57BL/6J-dy/dy) mice, postnatal changes in the masseter Muscle were analyzed morphometrically and histochemically. From the 6th to 14th postnatal week, the superficial portion of the masseter Muscle, which was composed of white and intermediate Muscle Fibers, was atrophied in dystrophic mice. The atrophy was severest in the most lateral component of the Muscle. On the contrary, distinct hypertrophy was evident in red Muscle Fibers in the deep portion. These changes increased with time in the diseased animals. The distribution of formazan particles produced by succinate dehydrogenase (SDH) staining was irregular in the Muscle of dystrophic mice. In Muscle spindles, mean diameters of intrafusal Muscle Fibers and outer capsule were significantly decreased in the diseased mice
Norihiko Maeda - One of the best experts on this subject based on the ideXlab platform.
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POSTNATAL CHANGES IN THE Extrafusal Muscle Fiber AND Muscle SPINDLE IN THE MASSETER Muscle OF THE DYSTROPHIC MOUSE
Biomedical Research, 1993Co-Authors: Morito Ukai, Norihiko Maeda, Koichi OsawaAbstract:In dystrophic (C57BL/6J-dy/dy) mice, postnatal changes in the masseter Muscle were analyzed morphometrically and histochemically. From the 6th to 14th postnatal week, the superficial portion of the masseter Muscle, which was composed of white and intermediate Muscle Fibers, was atrophied in dystrophic mice. The atrophy was severest in the most lateral component of the Muscle. On the contrary, distinct hypertrophy was evident in red Muscle Fibers in the deep portion. These changes increased with time in the diseased animals. The distribution of formazan particles produced by succinate dehydrogenase (SDH) staining was irregular in the Muscle of dystrophic mice. In Muscle spindles, mean diameters of intrafusal Muscle Fibers and outer capsule were significantly decreased in the diseased mice
Das Mainak - One of the best experts on this subject based on the ideXlab platform.
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Tissue Engineering The Motoneuron To Muscle Segment Of The Stretch Reflex Arc Circuit Utilizing Micro-fabrication, Interface Design And Defined Medium Formulation
'Information Bulletin on Variable Stars (IBVS)', 2008Co-Authors: Das MainakAbstract:The stretch reflex circuit is one of the most primitive circuits of mammalian system and serves mainly to control the length of the Muscle. It consists of four elements: the stretch sensor (Muscle spindle/ intrafusal Fiber lie parallel between Extrafusal, contractile musculature), Extrafusal Muscle Fiber, sensory neuron and motoneuron. The basic principle of the stretch reflex arc circuit is as follows: whenever there is a sudden stretch in a Muscle, it needs to compensate back to its original length so as to prevent any kind of injury. It performs this compensation process using a simple negative feed back circuit called the stretch reflex arc. Any form of stretch in a Muscle activates the stretch sensors (Muscle spindle/ intrafusal Fiber) lying deep in each Muscle. After the stretch sensors get activated, it sends a train of signals to the spinal cord through the sensory neurons. The sensory neurons relay this information to the motoneuron. The motoneuron performs the necessary information processing and sends the message to the Extrafusal Fibers so as to compensate for the sudden stretch action. The motoneuron conveys this message to the Extrafusal Fibers by communicating through the special synaptic junctions called neuromuscular junctions. Based on this information, the Extrafusal Fibers act accordingly so as to counter the effect of sudden stretch. This is also called the monosynaptic stretch reflex that involves a single synapse between a sensory neuron and a motoneuron. To date studying these stretch reflex circuits is only feasible in animal models. Almost no effort has been made to tissue engineer such circuits for a better understanding of the complex development and repair processes of the stretch reflex circuit formation. The long-term goal of this research is to tissue engineer a cellular prototype of the entire iii stretch reflex circuit. The specific theme of this dissertation research was to tissue engineer the motoneuron to Muscle segment of the stretch reflex arc circuit utilizing micro-fabrication, interface design and defined medium formulations. In order to address this central theme, the following hypothesis has been proposed. The first part of the hypothesis is that microfabrication technology, interface design and defined medium formulations can be effectively combined to tissue engineer the motoneuron to Muscle segment of the stretch reflex arc. The second part of the hypothesis is that different growth factors, hormones, nanoparticles, neurotransmitters and synthetic substrate can be optimally utilized to regenerate the adult mammalian spinal cord neurons so as to replace the embryonic motoneurons in the stretch reflex tissue engineered construct with adult motoneurons. In this body of work, the different tissue engineering strategies and technologies have been addressed to enable the recreation of a in vitro cellular prototype of the stretch reflex circuit with special emphasis on building the motoneuron to Muscle segment of the circuit. In order to recreate the motoneuron to Muscle segment of the stretch reflex arc, a successful methodology to tissue engineer skeletal Muscle and motoneuron was essential. Hence the recreation of the motoneuron to Muscle segment of the stretch reflex circuit was achieved in two parts. In the part 1 (Chapters 2-5), the challenges in skeletal Muscle tissue engineering were examined. In part 2 (Chapters 6-7), apart from tissue engineering the motoneuron to Muscle segment, the real time synaptic activity between motoneuron and Muscle segment were studied using extensive video recordings. In part 3 (Chapters 8-10), an innovative attempt had been made to tissue engineer the adult mammalian spinal cord neurons so that in future this technology could utilized to replace the iv embryonic neurons used in the stretch reflex circuit with adult neurons. The advantage of using adult neurons is that it provides a powerful tool to study older neurons since these neurons are more prone to age related changes, neurodegenerative disorders and injuries. This study has successfully demonstrated the recreation of the motoneuron to Muscle segment of the stretch reflex arc and further demonstrated the successful tissue engineering strategies to grow adult mammalian spinal cord neurons. The different cell culture technologies developed in these studies could be used as powerful tools in nerve-Muscle tissue engineering, neuro-prosthetic devices and in regenerative medicine
