No abstract available.
Myasthenia Gravis* ; Thymectomy*

BACKGROUND: Generalized aggressive periodontitis (GAP) is a destructive periodontal disease that can develop in young age. Only a few cases of full mouth rehabilitation, using dental implants, have been reported in a patient with aggressive periodontitis. CASE DESCRIPTION: This clinical report describes the treatment procedures and results of full mouth rehabilitation in a patient with aggressive periodontitis. After all teeth were extracted, 6 implants were placed in the maxilla and mandible, respectively. Fixed detachable implant prostheses were made. The patient was satisfied with the final results. She was followed for 10 months postloading. CLINICAL IMPLICATION: For a long-term success, continuous maintenance care is critical, as the contributing factors of the disease (such as immune factors or periodontal pathogens) may not be controlled adequately.
Aggressive Periodontitis ; Dental Implants ; Humans ; Immunologic Factors ; Mandible ; Maxilla ; Mouth ; Mouth Rehabilitation ; Periodontal Diseases ; Prostheses and Implants ; Tooth

No abstract available.
Panniculitis*

No abstract available.
Laurence-Moon Syndrome*

No abstract available.
Laurence-Moon Syndrome*

We have investigated the changes of DNA ploidy and S-phase fraction in proliferative lesions of rat liver. Proliferative lesions were induced by diethylnitrosamine and partial hepatectomy. DNA ploidy was measured by flow cytometer, and S-phase fraction was measured by in situ bromodeoxyuridine(BRdU)-anti BRdU monoclonal antibody techniques. Normal liver and initiated lesion revealed DNA diploidy or DNA tetraploidy. Hepatocyte nodule (NODULE) and hepatocelular carcinoma (HCC) revealed DNA diploidy, tetraploidy or aneuploidy. S-phase fraction was 1.0+/-0.9, 1.0+/-0.9m 3.7+/-2.3, 5.5+/-4.9, and 13.8+/-11.6 in normal liver, initiated lesion, NODULE not associated with HCC, NODULE associated with HCC, and HCC, respectively. In NODULE associated with HCC, it was widely distributed, ranging from 0.8 to 15.5%. In conclusion, S-phase fraction appeared to be increased as the hepatocarcinogenesis proceeded, but DNA ploidy did not. There was a heterogeneity of DNA ploidy and S-phase fraction in the proliferative hepatic lesions.
Rats ; Animals ; Carcinoma, Hepatocellular

OBJECTIVES: The definite cause of obsessive-compulsive disorder (OCD) is still unknown. Evidences from familial, twin and segregation studies support the role of a genetic factor. There also are growing evidences indicating that OCD has specific neurochemical and neuroanatomical basis. Derived from the effectiveness of serotonin reuptake inhibitors in OCD treatment, several candidate genes related to serotonin regulation have been hypothesized to play on important role in the development of OCD. One of them is the serotonin transporter gene. The aim of this study was to investigate the association between serotonin transporter gene and OCD. METHODS: 124 OCD patients and 119 normal controls participated in this study. Genomic DNA was extracted from their blood. The genotypes and allele frequencies of the 5-HTTLPR polymorphism between OCD group and control group were compared. And we investigated the association between 4 factors derived from YBOCS checklists and 5-HTTLPR polymorphism. RESULTS: In this case-control study, we could not find any association between 5-HTRLPR polymorphism and development of OCD. In OCD group, patients with L (l/s+s/s) genotype had higher scores for the religious/somatic factor than those with S genotype. CONCLUSION: In this study, there was no difference in genotype distributions of 5-HTTLPR between OCD and control groups. But, L genotype of 5-HTTLPR polymorphism had negative effects on some factors of the obsessive-compulsive symptoms.
Case-Control Studies ; Checklist ; DNA ; Gene Frequency ; Genotype ; Humans ; Obsessive-Compulsive Disorder* ; Serotonin Plasma Membrane Transport Proteins* ; Serotonin Uptake Inhibitors ; Serotonin*

OBJECTIVES: The definite cause of obsessive-compulsive disorder (OCD) is still unknown. Evidences from familial, twin and segregation studies support the role of a genetic factor. There also are growing evidences indicating that OCD has specific neurochemical and neuroanatomical basis. Derived from the effectiveness of serotonin reuptake inhibitors in OCD treatment, several candidate genes related to serotonin regulation have been hypothesized to play on important role in the development of OCD. One of them is the serotonin transporter gene. The aim of this study was to investigate the association between serotonin transporter gene and OCD. METHODS: 124 OCD patients and 119 normal controls participated in this study. Genomic DNA was extracted from their blood. The genotypes and allele frequencies of the 5-HTTLPR polymorphism between OCD group and control group were compared. And we investigated the association between 4 factors derived from YBOCS checklists and 5-HTTLPR polymorphism. RESULTS: In this case-control study, we could not find any association between 5-HTRLPR polymorphism and development of OCD. In OCD group, patients with L (l/s+s/s) genotype had higher scores for the religious/somatic factor than those with S genotype. CONCLUSION: In this study, there was no difference in genotype distributions of 5-HTTLPR between OCD and control groups. But, L genotype of 5-HTTLPR polymorphism had negative effects on some factors of the obsessive-compulsive symptoms.
Case-Control Studies ; Checklist ; DNA ; Gene Frequency ; Genotype ; Humans ; Obsessive-Compulsive Disorder* ; Serotonin Plasma Membrane Transport Proteins* ; Serotonin Uptake Inhibitors ; Serotonin*

The extracellular PH has been known to be lowered under the condition of chronic inflammation, and the tetrodotoxin-resistant sodium currents(TTX-r INa ) is thought to responsible for the inflammatory pain. We investigated the effects of PH and lidocaine on the TTX-r INa in sensory neurons derived from abolt rat trigeminal root ganglion(TRG) using whole-cell patch clamp technique to evaluate the underlying mechanisms of the poor analgesia following the administration of local anesthetic solutions into or around the area of the of inflammation. The results are as follows: 1. Two types of INa showing different sensitivity to TTX, TTX-sensitive and TTX-resistant INa , were expressed in the rat TRG neurons. 2. The amplitude and the current-voltage(I-V) relationship of TTX-r INa were significantly affected by the changes of extracellular pH. The acidification of external pH reduced the current amplitude and shifted the I-V relation to the depolarizing directions. 3. The change of extracellular PH also affected the voltage-dependence of activation and steady-state inactivation of TTX-r sodium channels. The voltage-dependence of the channel shifted to a depolarizing direction by the elevated concentration of external hydrogen ion. 4. Lidocaine suppressed TTX-r INa in a dose-dependent manner, and inhibitory effect of lidocaine decresed as the external PH lowered. 5. Lidocaine significantly shifted the activation and steady-state inactivation curves of TTX-r sodium channel to a hyperpolarizing direction by about -20 mV. 6. The effects of lidiocaine on TTX-r sodium channel producing an increase in the probability of channel inactivation greatiy decreased when the external pH was changed to 6.3 or 8.3 7. The 0.1mM lidocaine applied at PH 8.3 shifted the steady-state curve to a hyperpolazizing direction by -20mV compared to that obtained at lidocaine-free pH 7.3 condition. In contrast, the steady-state inactivation curve obtained in the presence of 0.1 mM lidocaine at pH 6.3 614 not showed any significant difference to that obtained at lldocaine-free pH 7.3 condition. These results suggest that the inhibitory action of lidocaine on the TTX-r sodium channel may be derived from the modificition of channel gating as well as blockade of channel pore. The reduced extracellular PH may reduce the TTX-rINa and increase the threshold for activation of TTX-r sodium channels. which may be responsible for the decresed neuronal excitability in the acidified environment. In the presence of lidocaine, however, the sensory neuron is thought to be more excitable in the acidic condition than in physiological PH, which may be due to the decreased lidocaine-induced inactivation of TTX-r sodoum channel as well as reduced amount of hydrophobic neutral from of lidocaine in acidosis.
Acidosis ; Analgesia ; Animals ; Ganglion Cysts* ; Hydrogen-Ion Concentration* ; Inflammation ; Lidocaine* ; Neurons* ; Protons ; Rats* ; Sensory Receptor Cells ; Sodium Channels ; Sodium*

PURPOSE: Few epidemiologic studies have investigated aggressive periodontitis in Koreans, but such studies of disease prevalence and other clinical characteristics would be invaluable in providing proper treatment. The aim of this study was to assess the prevalence of aggressive periodontitis and to measure the extent of associated periodontal breakdown. METHODS: The study population consisted of 1,692 patients who visited the Department of Periodontology, Wonkwang Daejeon Dental Hospital from January to December, 2010. Clinical parameters (probing depth, gingival recession, periodontal attachment loss) were measured by a single examiner, and radiographic examination was performed at the baseline. RESULTS: Twenty-eight (1.65%) patients showed clinical features of aggressive periodontitis, of which 27 patients exhibited the generalized form, and 1 exhibited the localized form. There was no significant difference between the percentage of male and female patients. The probing pocket depth of the maxillary first molar was deeper than that of the other teeth and gingival recession was also the most serious at the maxillary first molar. The periodontal attachment loss was the highest at the maxillary first molar. The average number of missing teeth was 1.29 per subject. Loss of the second molar was prominent. CONCLUSIONS: Within the limitations of this study, the periodontal breakdown evaluated by attachment loss was found to be most severe at the first molars of aggressive periodontitis patients. However, further large scale multicenter studies are necessary to access more precise data, including prevalence.
Aggressive Periodontitis ; Epidemiologic Studies ; Female ; Gingival Recession ; Humans ; Male ; Molar ; Periodontal Attachment Loss ; Prevalence ; Tooth