1.Full mouth rehabilitation of class III patient with disharmonious occlusal plane: A case report.
Hayeong KIM ; Janghyun PAEK ; Kung Rock KWON ; Ahran PAE
The Journal of Korean Academy of Prosthodontics 2016;54(4):451-457
Prosthodontic decision-making process is done through analysis of clinical information and mutual communication between patient and dentist. When opposing teeth are extruded due to missing tooth or tooth defects, selection of appropriate treatment plan and predictory prognosis can be complicated in functional rehabilitation. In case of severely disharmonious occlusal plane result from extruded teeth, re-establishment of the occlusal plane is required, if necessary via prudent evaluation. In this case, class III patient had unesthetic appearance and mastication discomfort caused by disharmonious occlusal plane due to severe extrusion. Through a structured diagnostic process, appropriate treatment plan was selected. Esthetic and functional results were obtained through from full mouth rehabilitation with re-establishment of the occlusal plane.
Dental Occlusion*
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Dentists
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Humans
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Mastication
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Mouth Rehabilitation*
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Mouth*
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Prognosis
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Rehabilitation
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Tooth
2.Modulation of the caveolin-3 localization to caveolae and STAT3 to mitochondria by catecholamine-induced cardiac hypertrophy in H9c2 cardiomyoblasts.
Kyuho JEONG ; Hayeong KWON ; Chanhee MIN ; Yunbae PAK
Experimental & Molecular Medicine 2009;41(4):226-235
We investigated the effect of phenylephrine (PE)- and isoproterenol (ISO)-induced cardiac hypertrophy on subcellular localization and expression of caveolin-3 and STAT3 in H9c2 cardiomyoblast cells. Caveolin-3 localization to plasma membrane was attenuated and localization of caveolin-3 to caveolae in the plasma membrane was 24.3% reduced by the catecholamine-induced hypertrophy. STAT3 and phospho-STAT3 were up-regulated but verapamil and cyclosporin A synergistically decreased the STAT3 and phospho-STAT3 levels in PE- and ISO-induced hypertrophic cells. Both expression and activation of STAT3 were increased in the nucleus by the hypertrophy. Immunofluorescence analysis revealed that the catecholamine-induced hypertrophy promoted nuclear localization of pY705-STAT3. Of interest, phosphorylation of pS727-STAT3 in mitochondria was significantly reduced by catecholamine-induced hypertrophy. In addition, mitochondrial complexes II and III were greatly down-regulated in the hypertrophic cells. Our data suggest that the alterations in nuclear and mitochondrial activation of STAT3 and caveolae localization of caveolin-3 are related to the development of the catecholamine-induced cardiac hypertrophy.
Animals
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Catecholamines/*pharmacology
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Caveolae/*metabolism
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Caveolin 3/*metabolism
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Cell Line
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Hypertrophy/metabolism
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Mitochondria/*metabolism
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Myocardium/cytology/*pathology
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Myocytes, Cardiac/cytology/*drug effects/metabolism
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Rats
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STAT3 Transcription Factor/*metabolism