• The Journal of Korean Physical Therapy
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• v.14 no.4
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• pp.163-171
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• 2002

Neuromuscular junction consist of presynaptic membrane, synaptic cleft and postsynaptic membrane. In the neuromuscular junction, presynaptic membrane is the motor nerve terminal, have many synaptic vesicle. Postsynaptic membrane is the motor end plate of muscle fiber and the most striking structural features are the deep infolding of the sarcolemma. Between the nerve and muscle cells, there is a synaptic cleft of some 50-100nm. This review shows the ultrastructure and function of neuromuscular junction, summarizes the current knowledge.

• The Journal of Korean Academy of Orthopedic Manual Physical Therapy
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• v.13 no.1
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• pp.58-66
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• 2007

The purpose of this study is to understand the structure and biomechanics of the skeletal muscle. The skeletal muscle takes 40 to 45% of the whole body. Stable posture requires a balance of muscle. However, when the muscle strength is unbalanced, movement initiates. The power generated by the muscle is a primary means to adjust the equilibrium of posture and movement. The structural unit of the skeletal muscle is a long cylindrical type muscle fiber which contains hundreds of nucleus. The thickness of muscle fiber is about $10-100{\mu}m$, and its length is about 1-50cm. Muscle fiber is composed of myofibril that is covered with plasma membrane which is called sarcolemma. In understanding the movement of human body, it is important to comprehend the movement of bone and joint and the tension of muscle. Understanding the structure and biomechanics of muscle also provides basic information on clinical treatment of patients.

• Archives of Pharmacal Research
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• v.8 no.2
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• pp.49-57
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• 1985

The effect of ginseng components on the potassium depleted cardiomyopathic rat heart was investigated. In the perfused heart experiment using Langendorff apparatus, the deterioration rate of contriactile force of potassium depleted rat heart (low potassium diet group) was faster than that of normal rat heart and ginseng components showed the ability to slow the deterioration rate of potassium depleted hearts. Both sialic acid contents in carcolemmal ghost and sialyltransferase activity of 40,000 * g subcellular fraction prepared from cardiac ventricular tissue of low potassium diet group were significantly decreased compared to those of normal group. The decrease of the sialic acid content and sialyltransferase activity in sarcolemma of low potassium diet group was inhibited when ginseng was concomitantly administered. Calcium uptake of sarcoplasmic reticulum prepared from low potassium diet group was significantly greaterthan that of normal group. Ginseng extract or total saponin showed the tendency to inhibit the increase of cacium uptake.

• Applied Microscopy
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• v.19 no.1
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• pp.1-18
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• 1989

It has been debated whether postischemic reperfusion is necessarily beneficial to salvage the myocardium after ischemic insult or not. Therefore, this study was undertaken to compare the ultrastructural changes as well as the distribution of $Ca^{2+}$ in the ventricular myocardial cells after transient ischemia and after postischemic reperfusion, and to suspect to what extent the postischemic reperfusion is beneficial. After 10 minutes of ischemia, the heart developed wide I bands, glycogen depletion, intramyofibrillar edema, mitochondrial swelling, clumping and migration of chromatin, ghosts of lipid droplets, disintegration of cell junctions, sarcolemmal disruption, and loss of $Ca^{2+}$ binding capacity of the sarcolemma and the mitochondria. In spite of reperfusion, in a large number of cells, the ultrastructure was more severely damaged, however, $Ca^{2+}$ binding capacity of the sarcolemma and the mitochondria restored. These results suggest that postischemic reperfusion may help the myocardial cells to restore their function to control $Ca^{2+}$ to a certain extent, but that it could aggravate the ischemic insult.

• The Korean Journal of Pharmacology
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• v.22 no.2
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• pp.151-156
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• 1986

There are some evidence for the presence of more than one type of calcium channels. To investigate whether organic calcium antagonist sensitive calcium channels exist in the isolated sarcolemmal membrane, we prepared high KCl-loaded sarcolemmal vesicle from the procine small instine, and induced calcium transport by high $K^+$ concentration or by electrical stimulation after preincubation of KCl-loaded vesicle in the low potassium solution. Calcium transport induced by high $K^+$ concentration (84.7mM) was significantly increased (p<0.05), compared with that by low $K^+$ concentration (2.08 mM), and not inhibited by diltiazem $(10^{-6}\;M)$. Calcium transport was inactivated with time. By continuous electrical stimulation (3V, 15Hz, 25m see), calcium transport was markedly increased, and inhibited significantly by dilltiazem $(10^{-6}\;M)$ and nifedipine $(10^{-6}\;M)$ (p<0.005), compared with the value of control without electrical stimulation. Calcium transport by electrical stimulation was not inactivated with time for at least 2 min. From these results, it was concluded that there was organic calcium antagonist sensitive channel in the isolated intestinal sarcolemma membrane, which was activated by electrical stimulation.

• Biomedical Science Letters
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• v.12 no.4
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• pp.303-310
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• 2006

Ankyrins are a ubiquitously expressed family of intracellular adaptor proteins involved in targeting diverse proteins to specialized membrane domains in both the plasma membrane and the endoplasmic reticulum. We described here that the C-terminal domain of ankyrin-B interact specifically with Z-line portion of titin in yeast two-hybrid analysis, in vitro pull-down assays and localization experiments in COS-7 cells. In this study we provide the first experimental evidence that Z-line portion of titin is necessary for the localization of ankyrin-B and ankyrin-B links between the sarcolemma and the myofibril in costameres.

• Biomedical Science Letters
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• v.8 no.1
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• pp.21-27
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• 2002

To investigate an effect of bum on the cardiac function, we studied some biochemical assay, ultrastructural changes and stereological analysis in heart tissue. Sprague-Dawley rats were induced a 15% total body surface area scald burn. 5 and 24 hours later, the heart was excised. Burned rats showed the decrease of heart weight per body weight (%) compared with control. The activity of serum aspartate aminotransferase was significantly increased at 5 (p＜0.001) and 24 hours (p＜0.01) after burn compared with control. And the activity of serum LDH was decreased at 5 hours after burn but increased at 24 hours compared with control. Ultrastructurally, enlargement of interstitium and destruction of sarcolemma were observed at 5 and 24 hours after burn. Especially at 5 hours postburn, hypercontraction band was noted and at 24 hours, wavy fiber and muscle fraying were noted. In stereological changes, volume density of mitochondria and myofibril was significantly decreased at postburn 5 and 24 hours. But volume density of sarcoplasmic reticulum was significantly increased at postburn 5 hours. Our data suggest that dermal scald bum causes myocardial dysfunction.

• The Journal of Korean Physical Therapy
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• v.3 no.1
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• pp.175-188
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• 1991

A study was performed to investigate the effect of electrical stimulation on disused rat soleus muscle, of male rat. The animal's hindlimbs were immobilized 4weeks by plaster of paris, and stimulated with E. S. T for 4weeks (20min/day) The changes on soleus were examined with histochemical, histological, and morphometric method. The results are summarized as follows. 1. Disued atrophy group from immobilization, which margin of sarcolemma and myofibril in sarcoplasm were not cleared, also degenerated from necrosis with phagocytosis. 2. The numbers of nuclear were much increased and accumulation of nuclear were finded, and relatively muscular atrophic changed. 3. Increased inflammatory cyte, also finded neutrophil and macrophage. 4. Relatively atrophic changed from severe fibrosis by incleased connectivetissue. 5. The glycogen granules were much decreased in E. S. T group. It means that electrical stimulation effected the muscle exercise. 6, The activity of the NADH-TR reaction of E. S. T. Tgroup were white muscle group are transformed into red muscle fiber than normal group. 7. These results indicate that the electrical stimulation effected to soleus also prevention and delayed muscular atrophy.

• Annals of Clinical Neurophysiology
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• v.6 no.2
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• pp.65-74
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• 2004

Limb-girdle muscular dystrophy (LGMD) is a heterogeneous group of inherited muscle disorders caused by the mutations of different genes encoding muscle proteins. In the past, when the molecular diagnostic techniques were not available, the subtypes of muscular dystrophies were classified by the pattern of muscle weakness and the mode of inheritance, and LGMD had been considered as a 'waste basket' of muscular dystrophy because many unrelated heterogeneous cases with 'limb-girdle' weakness were put into the category of LGMD. With the advent of molecular genetics at the end of the last century, it has been known that there are many subtypes of LGMD caused by the mutation of different genes, and now, LGMD is classified according to the results of the linkage analysis and the genes or proteins affected. Only small proportion (probably less than 10%) of LGMD is dominantly inherited, and autosomal dominant LGMD (AD-LGMD) consists of six subtypes (LGMD1A to 1F) so far. In autosomal recessive LGMD (AR-LGMD), more than 10 subtypes (LGMD2A to 2J) have been linked and most of the causative genes have been identified. Among AR-LGMDs, LGMD2A (calpain 3 deficiency), 2B (dysferlin deficiency), and sarcoglycanopathy (LGMD2C-2F) are major subtypes. The defective proteins in LGMDs are components of nuclear envelope, cytosol, sarcomere, or sarcolemma, and seem to play a different role in the pathogenesis of muscular dystrophy. It is notable that many causative genes of LGMDs are also responsible for other categories of muscular dystrophy or diseases affecting other tissue. However, by which mechanism they produce such a broad phenotypic variability is still unknown. The identification of mutation in the relevant gene is confirmative for the diagnosis, and is essential for genetic counseling and antenatal diagnosis of LGMD. Because many different genes are responsible for LGMD, differentiation of subtypes using immunohistochemistry and western blotting is the essential step toward the detection of mutation. For the effective research and medical care of the patients with muscular dystrophy in Korea, a research center with a medical facility supported by the government seems to be needed.

• The Journal of Korean Physical Therapy
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• v.6 no.1
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• pp.61-74
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• 1994

This study was carried out to determine effects of electrical stimulation on the soleus, target muscle of the sciatic newt, of white rat normal muscles. The biometric, histochemical, ultrastructural observations were made. The following results were obtained. A daily electrical stimulation of the skeletal muscle of the normally-functioning rat caused an increase of girth and weight of the muscle fibers for 2 weeks. No noticeable change was observed afterwards. More specifically, the density of volume of the red muscle fiber increased. whereas the density of the white muscle fiber decreased. The electrical stimulation group(experimental group) showed hypertrophy of the muscle fibers and narrowing of the space between perimysium and endomysium. Normally, glycogen granules are accumulated regardless of classification of muscle fibers. In addition, the NADH-TR reaction results were in agreement with the biometric findings, in that the red muscle fibers significantly increased. The ultrastructural observations revealed that mitochondria was formed in the red muscle fiber parallel to the muscle fibers of normal muscle, while mitochondria was observed in the sarcomere region of the white muscle fiber. However, activation of mitochondria took place in the sarcolemma region of the muscle fiber, and generation of mitochondria was observed in the sarcomere region of the white muscle fiber.