• Nuclear Engineering and Technology
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• v.5 no.1
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• pp.38-43
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• 1973

The spin-rotation constants of the proton and tile fluorine nucleus in C $H_4$, Si $H_4$, Ge $H_4$, C $F_4$, Si $F_4$ and Ge $F_4$ were determined experimentally by the molecular beam magnetic resonance method. From the Hamiltonian and the high field approximation, the quantized energy level is given by the following equation. W $m_{I}$ $m_{J}$=- $g_{I}$ $m_{I}$H- $g_{J}$ $m_{J}$H- $C_{av}$ $m_{I}$ $m_{J}$, where $c_{av}$ is one third of the trace of the C tensor. In the nuclear resonance experiment, the proton and the fluorine nuclear resonance curves consist of many unresolved lines given by v=- $g_{J}$H- $C_{av}$ $m_{I}$, and a Gaussian approximation is made to correlate $c_{av}$ to the experimentally obtained half-width of the resonance curve. In the rotational resonance experiment, the five resonance peaks as predicted by v=- $g_{I}$H- $c_{av}$ $m_{I}$, $m_{I}$=0, $\pm$1 and $\pm$2, were all observed. The magnitude of car was determined by measuring the frequency distance between two adjacent peaks. The sign of $c_{av}$ was determined by the side peak suppression technique. The technique is described, and the sign and magnitude of the spin-rotation constant cav are summarized as following: for C $H_4$ -10.3$\pm$0.4tHz(from the rotational resonance), for SiH +3.71$\pm$0.08kHz(from the nuclear resonance), for Ge $H_4$+3.79$\pm$0.13kHz(from the nuclear resonance), for C $F_4$, -6.81$\pm$0.08kHz(from the rotational resonance), for Si $F_4$, -2.46$\pm$0.06kHz(from the rotational resonance), and finally for Ge $F_4$-1.84$\pm$0.04kHz(from the rotational resonance).onal resonance).esonance).

• Journal of the korean academy of Pediatric Dentistry
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• v.33 no.2
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• pp.290-303
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• 2006

Tooth eruption is a complex and tightly regulated process that involves cells of the tooth organ and the surrounding alveolus. Osteoclast precursors must be recruited into the dental follicle prior to the onset of eruption. This function of dental follicle may be regarded as the ability of bone remodeling characterized by the interaction of osteoclasts and osteoblasts. This is because tooth eruption is a localized event in which many of the genes required for eruption are expressed in the dental follicle. RANKL is a membrane-bound protein that is a member of the TNF ligand family. which is present on bone marrow stromal cells and osteoblasts, and induces osteoclast formation and activation from precursor cell. The biologic effect of RANKL is inhibited by OPG and, in bone, the relative ratio of RANKL and OPG modulates osteoclastogenesis. To evaluate the roles of RANKL and OPG in tooth eruption and the relations with the expression pattern of Runx2, in situ hybridization was performed with mandibles of mice at postnatal stage 1, 3, 5, 7, 9 and 11. mRNA of RANKL, OPG, and Runx2 are expressed in dental follicle and surrounding tissue from P1 to 11. To determine the sites of osteoclastic activity during tooth eruption, mandibles were dissected. Peak osteoclastic activity in alveolar bone along the occlusal and basal regions was observed from P5 to 9, with osteoclasts in these regions being large and strongly TRAP-positive The specific spatio-temporal expression patterns of RANKL, OPG, and Runx2 in our study suggest that tooth eruption could be progressed through the interactions of molecular signaling among dental follicle, dental organ and alveolar bone, furthermore it means that dental follicle is quite important in tooth eruption In addition, it indicates that these genes (RANKL, OPG, and Runx2) play critical roles in tooth eruption.

• Journal of Korean Theatre Studies Association
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• no.52
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• pp.319-357
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• 2014

Formation of 'body schema' is the start for actor to create role and becomes the root and the foundation of existing as a role on the stage. For this, an actor needs to form 'scheme of role' with escaping from own 'body schema.' 'Schema of role' is formed by acquiring through synthesizing daily basic actions, namely, walking, standing, sitting, hand stretching, bending, and touching. The body schema, which was made with simple and usual actions, has fundamental significance in a sense of becoming the body in which the past traces in a role are habituated while energy as a role flows. As for the process of forming body schema, an actor first needs to obtain the visualized materials like photo, magazine, picture and image available for seeing a role specifically and clearly based on what analyzed a character. An actor needs to have three-dimensional image available for always recalling it in the head during acting. To do this, image data available for fundamentally capturing routine actions along with body structure are still more useful. Next, the body schema is formed by interaction with environment. Thus, there is a need of passing through the two-time process of forming body schema. Firstly, the body schema is made on routine actions in a role as physical condition of a role in actor's own everyday life. Secondly, the body schema is made on routine actions available for moving efficiently and economically in line with the environment of performance. A theatrical stage is the temporal space of rhythm and rule different from routine space. What forms body schema immediately in the second phase without body schema in the first phase ultimately becomes what exists as actor's own body, not the body of a role. The body schema, which was formed as the second process, is what truly has identity as a role in the ontological aspect, comes to experience the oppositional force in muscle, a qualitative change in energy, and emotional agitation in the physical aspect, and experiences perception, thinking, volition, and even consciousness with the entire body in the cognitive dimension. Thus, the formation of body schema can be known to be just a method of changing even spiritual and emotional layer. Body schema cannot be made if there is no process of embodiment and habit. Embodiment and habit are not simply the repeated, empty and mechanical action in the body. But, habit itself has very important meanings for forming body schema for role creating. First, habit allows the body itself to learn and understand a meaning. Second, habit relies upon environment, thereby allowing an actor of making the habituated body schema to recognize environment. Third, habit makes the mind. The habituated body schema is just the mind and the ego of a person who possesses the body schema. Fourth, habit comes to experience the expansion in energy and the expansion in existence. It may be experienced through interrelation among actor's body, tool, and environment. Fifth, habit makes identity of the body. Hence, this just becomes what secures identity of a role. These implications of habit are the formation of body schema, which is maintained with the body of being remembered firmly through being closely connected with the process of neural adaptation. Finally, it sought for possibility of practice as one method of forming body schema for role creating through Deleuze's '-becoming' theory. As 'actual animal-becoming' is real '-becoming' of forming structural transformation in the physical dimension, it meets with what the formation of body schema pursues actuality and reality. This was explained with a concept as saying of 'all '-becoming' molecular' by Deleuze/Guattari. 'Animal of having imitated animal's characteristic- becoming' is formed by which the body schema relies upon environment. In this way, relationship among the body, tool and environment has influence even upon a change in consciousness, thinking, and emotion, thereby being able to be useful for forming body schema in a sense of possibly experiencing ultimately expansion in role, namely, expansion in existence.

• Journal of Life Science
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• v.32 no.3
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• pp.189-195
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• 2022

Kinesin-2 comprises two subfamilies of the heterotrimeric or homodimeric motors found in mammalian cells. Heterotrimeric kinesin-2 consists of kinesin superfamily proteins (KIFs) 3A and 3B and kinesin-associated protein 3 (KAP3), which is a molecular motor protein that moves along microtubules. It plays diverse roles in cargo transport, including anterograde trafficking in cilia, and interacts with many different cargoes and proteins, but their binding proteins have not yet been fully identified. In this study, the yeast two-hybrid assay was used to identify the proteins that interact with the cargo-binding domain (CBD) of KIF3A, and an interaction between KIF3A and brain expressed X-linked 2 (Bex2) was found. Bex2 bound to the CBD-containing C-terminal tail region of KIF3A but did not interact with the same region of KIF3B or KIF5A (a motor protein of kinesin-1). KIF3A interacted with another isoform, Bex1, but did not interact with Bex3. In addition, glutathione S-transferase (GST) pull-downs showed that KIF3A specifically interacts with GST-Bex1 and GST-Bex2 but not with GST alone. When co-expressed in HEK-293T cells, Bex2 co-localized with KIF3A and co-immunoprecipitated with KIF3A and KIF3B but not KIF5B. In combination, these results suggest that Bex2 is capable of binding to heterotrimeric kinesin-2 and may serve as an adaptor protein that links heterotrimeric kinesin-2 with cargo.

• Tuberculosis and Respiratory Diseases
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• v.45 no.4
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• pp.861-869
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• 1998

Backgrounds: The injury of a tissue results in the infalmmation, and the imflammed tissue is replaced by the normal parenchymal cells during the process of repair. But, constitutional or repetitive damage of a tissue causes the deposition of collagen resulting in the loss of its function. These lesions are found in the lung of patients with idiopathic pulmonary fibrosis, complicated fibrosis after diffuse alveolar damage (DAD) and inorganic dust-induced lung fibrosis. The tissue from lungs of patients undergoing episodes of active and/or end-stage pulmonary fibrosis shows the accumulation of inflammatory cells, such as mononuclear cells, neutrophils, mast cells and eosinophils, and fibroblast hyperplasia. In this regard, it appears that the inflammation triggers fibroblast activation and proliferation with enhanced matrix synthesis, stimulated by inflammatory mediators such as interleukin-1 (IL-1) and/or tumor necrosis factor (TNF). It has been well known that TGF-$\beta$ enhance the proliferation of fibroblasts and the production of collagen and fibronectin, and inhibit the degradation of collagen. In this regard, It is likely that TGF-$\beta$ undergoes important roles in the pathogenesis of pulmonary fibrosis. Nevertheless, this single cytokine is not the sole regulator of the pulmonary fibrotic response. It is likely that the balance of many cytokines including TGF-$\beta$, IL-1, IL-6 and TNF-$\alpha$ regulates the pathogenesis of pulmonary fibrosis. In this study, we investigate the interaction of TGF-$\beta$, IL-1$\beta$, IL-6 and TNF-$\alpha$ and their effect on the proliferation of fibroblasts. Methods: We used a human fibroblast cell line, MRC-5 (ATCC). The culture of MRC-5 was confirmed by immunofluorecent staining. First, we determined the concentration of serum in cuture medium, in which the proliferation of MRC-5 is supressed but the survival of MRC-5 is retained. Second, we measured optical density after staining the cytokine-stimulated cells with 0.5% naphthol blue black in order to detect the effect of cytokines on the proliferation of MRC-5. Result: In the medium containing 0.5% fetal calf serum, the proliferation of MRC-5 increased by 50%, and it was maintained for 6 days. IL-1$\beta$, TNF-$\alpha$ and IL-6 induced the proliferation of MRC-5 by 45%, 160% and 120%, respectively. IL-1$\beta$ and TNF-$\alpha$ enhanced TGF-$\beta$-induced proliferation of MRC-5 by 64% and 159%, but IL-6 did not affect the TGF-$\beta$-induced proliferation. And lNF-$\alpha$-induced proliferation of MRC-5 was reduced by IL-1$\beta$ in 50%. TGF-$\beta$, TNF-$\alpha$ and both induced the proliferation of MRC-5 to 89%, 135% and 222%, respectively. Conclusions: TNF-$\alpha$, TGF-$\beta$ and IL-1$\beta$, in the order of the effectiveness, showed the induction of MRC-5 proliferation of MRC-5. TNF-$\alpha$ and IL-1$\beta$ enhance the TGF-$\beta$-induced proliferation of MRC-5, but IL-6 did not have any effect TNF-$\alpha$-induced proliferation of MRC-5 is diminished by IL-1, and TNF-$\alpha$ and TGF-$\beta$ showed a additive effect.