• The korean journal of orthodontics
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• v.31 no.1 s.84
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• pp.85-95
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• 2001

The purpose of this study was to evaluate the material for fixed type retainer, allowing physiologic tooth movement. and proper remodeling or periodontal tissue during retention period. The Present study was Performed to observe the histologic changes of periodontal tissue after application of different types of fixed type retainer after orthodontic tooth movement in young adult dogs. For this study, 4 young adult dogs were used as a experimental animal and experimental group was divided into three groups : experimental group 1 contained right side maxillayy third incisors and canines, experimental group 2 contained contralateral teeth of same animals, and control group contained mandibular premolars. And each dogs were applied the 4 different types of fixed type retainer to experimental group 1. The experimental teeth were ligated on the Sentalloy closed coil $spring^{\circledR}$(Tomy Co., Japan) from maxillary third incisors and canines and applied orthodontic force at initial 200gm-forced during 1 week. All the experimental animals were sacrificed on the 3rd week after the orthodontic teeth movement and then the specimens were taken, fixed in formalin, embeded in parafin, sectioned $6-8{\mu}m$ in thickness and stained with Hematoxylin-Eosin staining, and Masson's trichrome staining method. Examined under the light microscopy The following results were observed. 1. There were observed that decreased infiltration of giant tells in pressure side and increased the new bone forming in tension side on the specimen of 6-stranded 0.0195' $Respond^{\circledR}$(G&H Co., U.S.A.) group. Periodontal ligament fibers were much compressed or elongated in 3-stranded 0.018', 0.020' $Dentaflex^{\circledR}$(Dentarum Co., Germany), and Superbond $C&B^{\circledR}$(Sun Medical Co., Japan) groups. 2. In experimental group 1, necrotic bone inside the alveolar bone of pressure side, forming of the sharpey's fiber in osteoid tissue, and remodeling of the periodontal ligament were observed in all animals. 3. In experimental group 2, it was observed that the amount of bone resorption was equal or decreased in pressure side, and increased new bone forming and significantly decreased infiltration of giant cell than the experimental group 1. By this results, it considered that 6-stranded $Respond^{\circledR}$(G&H Co., U.S.A.) wire was the most useful material allowing early periodontal tissue remodeling.

• Journal of Life Science
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• v.31 no.10
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• pp.913-921
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• 2021

Limb-girdle muscular dystrophy (LGMD) which is characterized by progressive muscle weakening of the hip and shoulder shows both dominant and recessive inheritances with many pathogenic genes including TTN. This study performed to identify genetic causes of a male patient with late onset (45 years old) autosomal recessive LGMD and atrial flutter. By application of the whole exome sequencing, we identified bi-allelic variants of TTN gene in the patient. One allele had a single missense variant of [c.24124G>T (p.V8042F)], while the other allele consisted of three missense variants of [c.29222G>C (p.R9741P) + c.67490A>G (p.H22497R) + c.75376C>T (p.R25126C)]. The p.V8042F allele was transmitted from his mother, while the other haplotype allele was putatively transmitted from his father. His two unaffected sons had only the p.R9741P. These variants have been not reported or rarely reported in the public human genome databases (1,000 Genome, gnomAD, and KRGDB). Most variants were located in the highly conserved immunoglobulin or fibronectin domains and were predicted to be pathogenic by the in silico analyses. The TTN giant protein plays a key role in muscle assembly, force transmission at the Z-line, and maintenance of resting tension in the I-band. In conclusion, we think that these bi-allelic compound heterozygous mutations may play a role as the genetic causes of the LGMD phenotype.

• Tuberculosis and Respiratory Diseases
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• v.41 no.3
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• pp.231-238
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• 1994

Backgroud: Since the demonstration of the fact that vascular relaxation by acetylcholine(Ach) results from the release of relaxing factor from the endothelium, the identity and physiology of this endothelium-derived relaxing factor(EDRF) has been the target for many researches. EDRF has been identified as nitric oxide(NO). With the recent evidences that EDRF is an important mediator of vascular tone, there have been increasing interests in defining the role of the EDRF as a potential mediator of hypoxic pulmonary vasoconstriction. But the role of EDRF in modulating the pulmonary circulation is not compeletely clarified. To investigate the endothelium-dependent pulmonary vasodilation and the role of EDRF during hypoxic pulmonary vasoconstriction, we studied the effects of $N^G$-monomethyl-L-arginine(L-NMMA) and L-arginine on the precontracted pulmonary arterial rings of the rat in normoxia and hypoxia. Mothods: The pulmonary arteries of male Sprague Dawley(300~350g) were dissected free of surrounding tissue, and cut into rings. Rings were mounted over fine rigid wires, in organ chambers filled with 20ml of Krebs solution bubbled with 95 percent oxygen and 5 percent carbon dioxide and maintained at $37^{\circ}C$. Changes in isometric tension were recorded with a force transducer(FT.03 Grass, Quincy, USA) Results: 1) Precontraction of rat pulmonry artery with intact endothelium by phenylephrine(PE, $10^{-6}M$) was relaxed completely by acetylcholine(Ach, $10^{-9}-10^{-5}M$) and sodium nitroprusside(SN, $10^{-9}-10^{-5}M$), but relaxing response by Ach in rat pulmonary artery with denuded endothelium was significantly decreased. 2) L-NMMA($10^{-4}M$) pretreatment inhibited Ach($10^{-9}-10^{-5}M$)-induced relaxation, but L-NMMA ($10^{-4}M$) had no effect on relaxation induced by SN($10^{-9}-10^{-5}M$). 3) Pretreatment of the L-arginine($10^{-4}M$) significantly reversed the inhibition of the Ach ($10^{-9}-10^{-5}M$)-induced relaxation caused by L-NMMA($10^{-4}M$) 4) Pulmonary arterial contraction by PE($10^{-6}M$) was stronger in hypoxia than normoxia but relaxing response by Ach($10^{-9}-10^{-5}M$) was decreased, 5) With pretreatment of L-arginine($10^{-4}M$), pulmonary arterial relaxation by Ach($10^{-9}-10^{-5}M$) in hypoxia was reversed to the level of relaxation in normoxia. Conclusion: It is concluded that rat pulmonary arterial relaxation by Ach is dependent on the intact endothelium and is largely mediated by NO. Acute hypoxic pulmonary vasoconstriction is related to the suppression on NO formation in the vascular endothelium.