No abstract available.
Nasal Bone*

No abstract available.
Adhesives* ; Dental Pulp Cavity* ; Dentin* ; Gutta-Percha*

The purpose of this study was to compare the cytotoxicity by MTT test and genotoxicity by Ames test of new calcium phosphate-based root canal sealers (CAPSEAL I, CAPSEAL II) with commercially available resin-based sealers (AH 26, AH Plus), zinc oxide eugenol-based sealers (Tubliseal EWT, Pulp Canal Sealer EWT), calcium hydroxide-based sealer (Sealapex), and tricalcium phosphate based sealers (Sankin Apatite Root Canal Sealer I, II, III). According to this study, the results were as follows: 1. The extracts of freshly mixed group showed higher toxicity than those of 24 h set group in MTT assay (p < 0.001). 2. CAPSEAL I and CAPSEAL II were less cytotoxic than AH 26, AH Plus, Tubliseal EWT, Pulp Canal Sealer EWT, Sealapex and SARCS II in freshly mixed group (p < 0.01). 3. AH 26 in freshly mixed group showed mutagenicity to TA98 and TA100 with and without S9 mix and AH Plus extracts also were mutagenic to TA100 with and without S9 mix. 4. Tubliseal EWT, Pulp Canal Sealer EWT and Sealapex in freshly mixed group were mutagenic to TA100 with S9 mix. 5. Among those of 24 h set groups, the extracts of SARCS II were mutagenic to TA98 with and without S9 mix and AH 26 showed mutagenic effects to TA98 with S9 mix. 6. No mutagenic effect of CAPSEAL I and CAPSEAL II was detected. 7. There is no statistically significant difference between CAPSEAL I and CAPSEAL II at MTT assay and Ames test in both freshly mixed group and 24 h set group.
Calcium* ; Dental Pulp Cavity* ; Zinc Oxide

No abstract available.
Dental Pulp Cavity

No abstract available.
Calcium* ; Dental Pulp Cavity*

BACKGROUND: It has been known that most of thyroid stimulating antibodies (TSAbs) may interact with epitopes near N-terminal, and thyroid stimulation blocking antibodies (TSBAbs) near C-terminal on the extracellular domain of TSH receptor. However, many authors have reported different results about epitopes reacting with TSH receptor autoantibody (TRAb). TSBAbs inhibit thyroid stimulation of TSH and TSAbs at the receptor level. However, it has been reported that there are some TSBAbs which bind to the other sites, not TSH receptor, or block post-reeeptor process. These findings raise the possibility that TRAbs may be heterogeneous according to the mechanism of action. In order to investigate the heterogeneity of TRAb, we undertook immuno-precipitation using synthetic peptides of TSH receptor and measured TRAb activities by FRTL-5 cells and chimeric CHO cells. METHODS: We studied 102 patients with autoimmune thyroid disease (Graves disease 32, Hashimotos thyroiditis 29, atrophic thyroiditis 41) and 35 healthy persons. Three synthetic peptide fragments of TSH receptor were used to perform immunoprecipitation with serum or IgG of patients and healthy persons, TSAb and TSBAb activities were measured by FRTL-5 cells and CHO cells transfected with wild-type and 2 mutant TSH receptor cDNA (Mc2, Mc1+2). Mc2 and Mcl+2 were rnade to substitute amino acid residues of 90-165, 8-165 of the TSH receptor with corresponding residues of LH/CG receptor, respectively. RESULTS: Two out of 10 IgGs extracted from Graves disease and 2 out of 9 IgGs from atrophic thyroiditis had specific bidings over 0.84% in immunoprecipitation with peptide I (amino acid residue 35-50). Four out of 18 IgGs from Graves disease, 9 out of 41 IgGs from atrophic thyroiditis, and 6 out of 14 IgGs from Hashimotos thyroiditis had specific bidings over 0.84% in immunoprecipitation with peptide II (amino acid residue 317-332). Only 2 out of 10 IgGs from Graves disease had specific bidings over 0.84% in immunoprecipitation with peptide III (amino acid residue 341-358). When 10 IgGs extracted from Graves disease were reacted with wild-type, Mc2, and Mcl+2 CHO cells, 7 IgGs in wild-type and 4 IgGs in Mc2 had positive for TSAb activities. In 10 IgGs from atrophic thyroiditis, 5 in wild-type, 5 in Mc2, and 3 in Mcl+2 CHO cells had positive for TSBAb activities. In Hashimoto's thyroiditis, only 1 with hyperthyroidism had positive for TSAb activity in wild-type and 1 with hypothyroidism had positive for TSBAb activities in both of wild-type and Mc2 CHO cells. Therefore, patients with Graves disease were divided into at least 3 groups according to the TSAb activities measured by wild-type, Mc2, Mcl+ 2 CHO cells and TBII activities. And patients with atrophic thyroiditis were divided into at least 4 groups according to the TBII activities, TSBAb activities by wild-type, Mc2, Mcl+2 CHO cells and FRTL-5 cells. CONCLUSION: From these results, epitopes of TSH receptor reacting with TSAb or TSBAb in autoimmune thyroid disease may be scattered in the TSH receptor, although epitopes of TSAb tend to be near N-terminal and those of TSBAb near C-terminal. Graves disease or atrophic thyroiditis were divided into 3 or 4 groups according to the TBII and TRAb activities. Therefore, TRAb detected in autoimmune thyroid disease may be heterogenous.
Animals ; Antibodies, Blocking ; Autoantibodies* ; CHO Cells ; Cricetinae ; DNA, Complementary ; Epitopes ; Graves Disease ; Humans ; Hyperthyroidism ; Hypothyroidism ; Immunoglobulin G ; Immunoglobulins, Thyroid-Stimulating ; Immunoprecipitation ; Peptide Fragments ; Peptides ; Population Characteristics* ; Receptors, Thyrotropin* ; Thyroid Diseases* ; Thyroid Gland* ; Thyroiditis

Mineral trioxide aggregate (MTA) would influence healing of periapical tissues by modulating the production of growth factors and cytokines from PDL fibroblasts, however, the studies are insufficient. Therefore, the purpose of this study was to monitor the expression of transforming growth factor-beta1 (TGF- beta1), fibroblast growth factor-2 (FGF-2), and interleukin-6 (IL-6) from PDL fibroblasts in the presence of MTA. The human PDL fibroblasts were seeded onto the set MTA or IRM at a level of 1 x 10(5) cells per unit well, and further incubated for 6, 12, 24, and 48 hours. The levels of TGF-beta1, FGF-2, and IL-6 from the supernatant were measured by enzyme-linked immunosorbent assay (ELISA). The data were analyzed using one-way ANOVA. The level of TGF-beta1 was down-regulated when the cells were grown in the presence of MTA except at 6 hours. The levels of FGF-2 release were significantly suppressed when PDL fibroblasts were grown in the presence of MTA or IRM at all time intervals (p < 0.05). The expressions of IL-6 from MTA treated cells were comparable to those of untreated control cells throughout the observation periods. We presume that this material inhibits the stimulatory function of growth factors on granulation tissue formation and in turn, it promotes the healing process modulated by other bone-remodeling cells.
Cytokines ; Enzyme-Linked Immunosorbent Assay ; Fibroblast Growth Factor 2 ; Fibroblasts* ; Granulation Tissue ; Humans* ; Intercellular Signaling Peptides and Proteins* ; Interleukin-6 ; Periapical Tissue ; Periodontal Ligament* ; Transforming Growth Factor beta1 ; Pemetrexed

Mineral trioxide aggregate (MTA) would influence healing of periapical tissues by modulating the production of growth factors and cytokines from PDL fibroblasts, however, the studies are insufficient. Therefore, the purpose of this study was to monitor the expression of transforming growth factor-beta1 (TGF- beta1), fibroblast growth factor-2 (FGF-2), and interleukin-6 (IL-6) from PDL fibroblasts in the presence of MTA. The human PDL fibroblasts were seeded onto the set MTA or IRM at a level of 1 x 10(5) cells per unit well, and further incubated for 6, 12, 24, and 48 hours. The levels of TGF-beta1, FGF-2, and IL-6 from the supernatant were measured by enzyme-linked immunosorbent assay (ELISA). The data were analyzed using one-way ANOVA. The level of TGF-beta1 was down-regulated when the cells were grown in the presence of MTA except at 6 hours. The levels of FGF-2 release were significantly suppressed when PDL fibroblasts were grown in the presence of MTA or IRM at all time intervals (p < 0.05). The expressions of IL-6 from MTA treated cells were comparable to those of untreated control cells throughout the observation periods. We presume that this material inhibits the stimulatory function of growth factors on granulation tissue formation and in turn, it promotes the healing process modulated by other bone-remodeling cells.
Cytokines ; Enzyme-Linked Immunosorbent Assay ; Fibroblast Growth Factor 2 ; Fibroblasts* ; Granulation Tissue ; Humans* ; Intercellular Signaling Peptides and Proteins* ; Interleukin-6 ; Periapical Tissue ; Periodontal Ligament* ; Transforming Growth Factor beta1 ; Pemetrexed

BACKGROUND: Platelet plays an important role in the pathogenesis of acute coronary syndrome. Platelet glycoprotein IIb III a is the receptor for fibrinogen, and it plays an important role in the platelet aggregation. It was reported that polymorphism of the platelet glycoprotein III a (PlA1/A2) is related to acute coronary syndrome, especially in young patients. The aims of this study is to evaluate the relationship between platelet glycoprotein III a polymorphism and acute coronary syndrome in Koreans. METHOD: We studied total 208 patients (M: F=131 : 77, mean ages : 57.2+/-9.7). Acute coronary group comprised 110 patients, who underwent coronary angiography with the impression of acute myocardial infarction or unstable angina. Normal group comprised 98 patients who had no significant angiographic lesion. Genomic DNA was extracted from peripheral blood. To determine the frequency of PlA1/A2 genotype, polymerase chain reaction (PCR) was done and the product was restricted with Msp I. 3% gel electrophoresis showed Restriction Fragment Length Polymorphism (RFLP). Clinical profile and risk factor were also reviewed. RESULT: One patient in the acute coronary group is PlA1/A2 heterozygote and all the other are PlA1 homozygote. In normal group, all patients are PlA1 homozygote. The genotypic frequency of PlA1/A2 is consistent with the previous study. CONCLUSION: The genotype frequency of platelet glycoprotein III a gene polymorphism in Koreans is different from that of Caucasian. The allele frequencies of platelet glycoprotein III a is not different between acute coronary syndrome patient and normal control group. Platelet glycoprotein III a polymorphism may not be an hereditary risk factor in Koreans.
Acute Coronary Syndrome* ; Angina, Unstable ; Blood Platelets* ; Coronary Angiography ; DNA ; Electrophoresis ; Fibrinogen ; Gene Frequency ; Genes, vif ; Genotype ; Glycoproteins* ; Heterozygote ; Homozygote ; Humans ; Integrin beta3 ; Myocardial Infarction ; Platelet Aggregation ; Polymerase Chain Reaction ; Polymorphism, Restriction Fragment Length ; Risk Factors

BACKGROUND: Platelet plays an important role in the pathogenesis of acute coronary syndrome. Platelet glycoprotein IIb III a is the receptor for fibrinogen, and it plays an important role in the platelet aggregation. It was reported that polymorphism of the platelet glycoprotein III a (PlA1/A2) is related to acute coronary syndrome, especially in young patients. The aims of this study is to evaluate the relationship between platelet glycoprotein III a polymorphism and acute coronary syndrome in Koreans. METHOD: We studied total 208 patients (M: F=131 : 77, mean ages : 57.2+/-9.7). Acute coronary group comprised 110 patients, who underwent coronary angiography with the impression of acute myocardial infarction or unstable angina. Normal group comprised 98 patients who had no significant angiographic lesion. Genomic DNA was extracted from peripheral blood. To determine the frequency of PlA1/A2 genotype, polymerase chain reaction (PCR) was done and the product was restricted with Msp I. 3% gel electrophoresis showed Restriction Fragment Length Polymorphism (RFLP). Clinical profile and risk factor were also reviewed. RESULT: One patient in the acute coronary group is PlA1/A2 heterozygote and all the other are PlA1 homozygote. In normal group, all patients are PlA1 homozygote. The genotypic frequency of PlA1/A2 is consistent with the previous study. CONCLUSION: The genotype frequency of platelet glycoprotein III a gene polymorphism in Koreans is different from that of Caucasian. The allele frequencies of platelet glycoprotein III a is not different between acute coronary syndrome patient and normal control group. Platelet glycoprotein III a polymorphism may not be an hereditary risk factor in Koreans.
Acute Coronary Syndrome* ; Angina, Unstable ; Blood Platelets* ; Coronary Angiography ; DNA ; Electrophoresis ; Fibrinogen ; Gene Frequency ; Genes, vif ; Genotype ; Glycoproteins* ; Heterozygote ; Homozygote ; Humans ; Integrin beta3 ; Myocardial Infarction ; Platelet Aggregation ; Polymerase Chain Reaction ; Polymorphism, Restriction Fragment Length ; Risk Factors