• Journal of the korean academy of Pediatric Dentistry
• /
• v.36 no.2
• /
• pp.281-287
• /
• 2009

An eruption failure can be observed for child and adolescent periods when the primary dentition is changed to the permanent dentition through the mixed dentition frequently. The eruption failure can lead to miss erupting times of the tooth, then it will cause a lot of problems including root resorption, esthetic problem, transposition of adjacent tooth, malocclusoin and etc. Especially, the maxillary first molar is importantly concerned with occlusion and growth and is an essential tooth for development and maintenance of occlusion. So, it is a momentous part of more proper occlusal management to find these abnormal cases at the early stage and solve the problems. The sorts of eruption failures of the maxillary first molars can be divided into delayed eruption, impaction and the primary retention and the secondary retention. When physical obstacles cause impaction, first of all they must be removed then we can treat the impaction with observation after removal, surgical exposure or orthodontic traction. If the source of impaction is an ectopic eruption, the treatment can be a brasswire, a pendulum appliance, a space maintainer or space regainer after the extraction of the second deciduous tooth and etc. These cases are made a diagnosis of eruption failures of the maxillary first molars in mixed dentition period and have good prognosises after my treatments. So I reported them.

• Tuberculosis and Respiratory Diseases
• /
• v.56 no.5
• /
• pp.550-554
• /
• 2004

A paragonimiasis infestation is caused by the paragonimus species. It is commonly found in the lung but has also been found to exist extrapulmonary infestations including cerebral, spinal, subcutaneous, hepatic, splenic, abdominal, urinary, and gynecologic infestation. On the other hand, a cutaneous infestation is extremely rare. Human infestation is caused by ingesting raw or undercooked intermediate hosts. Because paragonimus westermani larva mature to an adult worm in the lung, the possibility of identifying the adult worm of paragonimus westermani at extrapulmonary region is very rare. Case : After ingesting a fresh-water crab 1 month prior to the hospital visit, a 45-year old female patient was suffering from right pleuritic chest pain during that 1 month. The patient also complained of a palpable mass that was movable and migrating, and it was localized at the right upper quadrant of the abdomen. The eosinophil fraction of the white blood cell of peripheral blood and pleural fluid was elevated to 55.1% and 90%, respectively. Parasite eggs were not found in her sputum and stool examination. By using the enzyme-linked immunosorbent assay (ELISA), the paragonimus-specific IgG antibody titer was elevated to 0.28. During incisional biopsy, we were able to find the young adult worm of paragonimus westermani. We experienced the rare case of ectopic paragonimiasis with pleural effusion that was confirmed by identifying the adult worm of paragonimus westermani within the abdominal subcutaneous tissue. We report a case with brief literature reviews.

• The Korean Journal of Nuclear Medicine
• /
• v.23 no.1
• /
• pp.41-48
• /
• 1989

$^{99m}Tc-Pertechnetate\;(TcO_4^-)$ is concentrated by the stomach after intravenous injection, allowing the detection of ectopic gastric mucosa. It has been used to develop a noninvasive test of gastric secretion. However the cellular site of concentration is still controversial, that is whether mucin-secreting epithelial cell or acid-secreting parietal cell. This study is planned to investigate the effects of cimetidine and gastric acidity on the retention of $TcO_4^-$ in the gastric wall of the rat. Also we further attempted to clarify the uptake and secreting cell of $TcO_4^-$ in the gastric mucosa. One hundred rats were divided into two groups, preliminary (40 rats) and main examination group (60 rats). Preliminary examination group was composed of fasting group (20 rats) for the detection of the time for reaching stable $TcO_4^-$ retention ratio in gastric wall and post-prandial group (20 rats) for the detection of the time for reaching the maximal gastric acidity. Main examination group was composed of fasting group (30 rats), which was subdivided into control group (10 rats), cimetidine group (10rats), $Mylanta^{(R)}$ group (10 rats) and post?prandial group (30 rats), which was subaivided into 90 min group (10 rats), 90 min cimetidine group (10 rats), and 120 min group (10 rats). Retention ratio (%) of $TcO_4$ in the gastric wall and the pH of the gastric contents were measured in the extracted stomach of the six groups. Gastric wall retention ratio of $TcO_4^-$ was calculated by the gastric wall radioactivity (cpm) divided by total gastric radioactivity (cpm) at 30 mins after intravenous injection of 0.4 mCi of $TcO_4^-$. The results were as follows: 1) The time required for reaching stable $TcO_4$ retention ratio and the lowest gastric PH were 30 min and 90 min, respectively. 2) In the fasting group, the gastric wall retention ratio of $TcO_4^-$ was significantly increased in the cimetidine group, compared with the control group (P < 0.01). However there was no significant difference between the control and $Mylanta^{(R)}$ group 3) The $TcO_4^-$ retention ratios of 90 min and 120 min groups were lower than that of the fasting control group (p < 0.05), either. After administration of cimetidine, the retention ratio was significantly increased in 90 min group (p < 0.01). 4) While $TcO_4^-$ retention ratio and gastric pH were well correlated in the post-prandial 120 min group (r=0.7112, p<0.05), in the post-prandial 90 min and 90 min cimetidine groups correlated poorly. However, there was no correlation in the three fasting groups at all. Referring the above results, we infer that $TcO_4^-$ is secreted into the gastric lumen by both parietal and non-parietal cells, with dominant non-parietal $TcO_4^-$ secretion in the fasting state and dominant parietal $TcO_4^-$ secretion in the stimulated state.

• Journal of Life Science
• /
• v.19 no.2
• /
• pp.163-168
• /
• 2009

To understand cytotoxic activity of Rubia cordifolia L. (Rubiaceae), which has been used as a traditional oriental medicine, the mechanism underlying cytotoxic effect of its extract on human acute Jurkat T cells was investigated. The methanol extract of roots (3 kg) of R. codifolia was evaporated, dissolved in water, and then extracted by dichloromethane. The substances in the chloroform extract showing the most cytotoxic activity were further purified by a series of preparative HPLC. The extracted active substance (65 mg) was designated as CCH1. When Jurkat T cells were treated with CCH1 at concentration ranging from 0.5 to 2.0 ${\mu}g$/ml, apoptotic phenomena of cells companying several subsequent biochemical reactions such as mitochondria cytochrome c release, activation of casapase-8, -9, and caspase- 3, degradation of PARP and DNA fragmentation occurred via mitochondria-dependent pathway. However, abrogation of apoptosis was observed in an ectopic expression of Bcl-xL, which is a suppressor for mitochondrial cytochrome c release. These results demonstrate that the cytotoxicity of CCH1 against Jurkat T cells is attributable to apoptosis mediated by mitochodria-dependent death-signaling regulated by Bcl-xL. In addition, the CCH1 is more potent to leukemia Jurkat T cell than to human peripheral blood monocyte cells (PBMC).

• Journal of Life Science
• /
• v.26 no.11
• /
• pp.1345-1354
• /
• 2016

Alopecia areata (AA) is a common and tissue-specific autoimmune disease of hair follicle resulting in the loss of hair on the scalp and elsewhere on the body. Hair follicles is a unique organ because it has its own immune system and hormonal milieu and has a different immune state at each hair cycle stage. The collapses of anagen-dependent hair follicle immune privilege arise autoimmune attack, inducing ectopic MHC class I expression in the hair follicle epithelium and autoantigen presentation to autoreactive CD8+T cells, which results in AA. Clinical and experimental studies have pointed that psychological stress may also influence the hair follicle immune/hormone systems and contribute to the induction of AA. The key pathogenesis of AA is associated with immune privilege guardians (including ACTH, ${\alpha}-MSH$, and $TGF-{\beta}$), natural killer group 2D-positive (NKG2D+) cells (including NK and CD8+T cells), and stress hormones (including CRH and substance P). Effective treatments for AA are still demanded. One of the future targets of treatment will be the modification of hair follicle immune privilege including stress. Recent studies have reported that JAK inhibitors and immunomodulators used in other autoimmune disease, such as psoriasis, atopic dermatitis, and rheumatoid arthritis, Tregs, platelet-rich plasma therapy, statins, and prostaglandin anaolgues are effective for AA. Here the article reviews the recent understanding in the pathogenesis associated with perifollicular endocrine/immunology and new treatments of AA.

• Journal of Chest Surgery
• /
• v.35 no.1
• /
• pp.48-51
• /
• 2002

The conversion of failing Fontan circuit to total cavopulmonary connection(TCPC) is recommended as a therapeutic option in patients with late Fontan complications such as atrial arrhythmia, atrial enlargement, pulmonary venous obstruction, and ventricular dysfunction. Combined TCPC with extracardiac conduit and cryoablation of arrhythmia circuit is preferred for treatment of failing Fontan coulection with atrial lachyarrhythrnia. We report a case of conversion of atriopulmonary connection to extracardiac conduit Fontan and cryoablation of atrial arrhythmia circuit in a patient with tricuspid atresia, who also had ectopic atrial tachycardia, right atrial thrombi, pulmonary venous obstruction, and ventricular dysfunction. This patient and the parents were Jehovah's Witnesses; therefore, the patient underwent the procedure without blood transfusion.

• Clinical and Experimental Pediatrics
• /
• v.51 no.7
• /
• pp.760-765
• /
• 2008

Paragonimiasis is a parasitic infection that occurs following the ingestion of infectious Paragonimus metacercariae from crabs or crayfish. Pulmonary paragonimiasis is the most common clinical manifestation of this infection, but several ectopic paragonimiasis cases have also been reported. Among them, cases of subcutaneous paragonimiasis are rare, especially in children. We report a case of subcutaneous paragonimiasis of the right abdominal wall with pleural effusion with hepatic involvement and without abnormal pulmonary infiltration in a boy aged 2 years and 5 months. He had eaten soybean sauce-soaked freshwater crabs (kejang) 6 months prior to complaining of right abdominal wall distension. On evaluation, right pleural effusion without abnormal pulmonary infiltration was detected, as well as blood eosinophilia, an elevated serum IgE level, pleural fluid eosinophilia and a positive enzyme-linked immunosorbent assay that detected P. westermani antibody in the serum. Thoracentesis, praziquantel administration, and excision of subcutaneous lesions were performed. After treatment, the eosinophil count and serum IgE level were decreased, and the subcutaneous lesions did not recur. The frequency of paragonimiasis has decreased recently, but it is still prevalent in Korea. Paragonimiasis should be suspected if pleural fluid eosinophilia is associated with blood hypereosinophilia and a high level of serum IgE; however clinicians should obtain a thorough history of travel and food habits.

• Journal of Microbiology and Biotechnology
• /
• v.15 no.4
• /
• pp.756-766
• /
• 2005

The signaling mechanism underlying aburatubolactam C-induced FasL upregulation was investigated in human Jurkat T cells. After treatment with aburatubolactam C, the src-family PTKs $p56^{lck}\;and\;p59^{fyn}$, and MAP kinases ERK2 and JNK1, were activated prior to FasL upregulation; Both $p56^{lck}\;and\;p59^{fyn}$ were directly activated 2.4- and 2.2-fold, respectively, in vitro by aburatubolactam C. The aburatubolactam C-induced cellular changes, including the activation of ERK2 and INK1, and FasL upregulation, were completely prevented by the PTK inhibitor genistein. The activation of protein kinase C (PKC$\delta,\;\epsilon\;and\;\mu$ was also induced following aburatubolactam C treatment. Although the activation of $p56^{lck}$ and tyrosine phosphorylation of the cellular proteins were not blocked by the PKC inhibitor GFl09203X, the activation of ERK2 was completely abrogated, along with a detectably enhanced JNK1 activation; FasL upregulation, and apoptosis. However, the FasL upregulation and apoptosis were significantly inhibited by the PKC activator PMA, with a remarkable increase in the ERK2 activation. The cytotoxic effect of aburatubolactam C was reduced in the presence of the anti-Fas neutralizing antibody ZB-4. Although ectopic expression of Bcl-2 failed to completely block the cytotoxicity of aburatubolactam C, it was clearly suppressed. The c-Fos mRNA expression was upregulated in a biphasic manner, where the second phasic expression overlapped with the FasL upregulation. Accordingly, these results demonstrate that aburatubolactam C-induced apoptosis is exerted, at least in part, by FasL upregulation dictated by activation of the PTK ($p56^{lck}\;and\;p59^{fyn}$) /JNKI pathway, which is negatively affected by the concurrent activation of the PKC/ERK2 pathway proximal to PTK activation.

• Clinical and Experimental Pediatrics
• /
• v.52 no.9
• /
• pp.991-998
• /
• 2009

Purpose : Thyroid hormone is essential for development of the brain in early life. Thyroid dysfunction is more common in the first 2-4 postnatal weeks of life in premature infants than in term infants. This study aimed to identify the prevalence and clinical course of thyroid dysfunction in prematurity. Methods : Premature infants admitted to and given neonatal screenings at Dankook University Hospital between April 1999 and March 2008 were included in this study. We retrospectively reviewed medical records and categorized subjects into six groups: normal, hypothyroidism, hyperthyrotropinemia, hypothyroxinemia, delayed onset of hypothyroidism, and delayed onset of hyperthyrotropinemia. Results : Among 599 subjects, 136 (23%) had initially abnormal thyroid function test (TFT); transient hypothyroxinemia was the most frequent condition (118, 20%). In addition, 8 (17%) of 46 subjects with initially normal TFT levels showed delayed onset of hyperthyrotropinemia with or without low free thyroxine ($fT_4$). Thyroxine was prescribed for 10 patients (1.7%) due to low $fT_4$ levels but was discontinued in 9 patients during follow-up. Thyroid scan confirmed ectopic thyroid in one patient. Conclusion : Thyroid dysfunction was frequently seen in premature infants, but most of the conditions were transient. In addition, some infants showed delayed TSH elevation on routine follow-up. Therefore, a recheck of the thyroid function of premature infants at 3-4 weeks is recommended, even if normal thyroid function is initially seen, especially in prematurity of less than 33 weeks of gestational age or birth weight of less than 2,500 grams.

• Asian Pacific Journal of Cancer Prevention
• /
• v.15 no.16
• /
• pp.6949-6954
• /
• 2014

Background: Recent studies have indicated that microRNA-15a (miR-15a) is dysregulated in breast cancer (BC). We aimed to evaluate the expression of miR-15a in BC tissues and corresponding para-carcinoma tissues. We also focused on effects of miR-15a on cellular behavior of MDA-MB-231 and expression of its target gene synuclein-${\gamma}$ (SNCG). Materials and Methods: The expression levels of miR-15a were analysed in BC formalin fixed paraffin embedded (FFPE) tissues by microarray and quantitative real-time PCR. CCK-8 assays, cell cycle and apoptosis assays were used to explore the potential functions of miR-15a in MDA-MB-231 human BC cells. A luciferase reporter assay confirmed direct targets. Results: Downregulation of miR-15a was detected in most primary BCs. Ectopic expression of miR-15a promoted proliferation and suppressed apoptosis in vivo. Further studies indicated that miR-15a may directly interact with the 3'-untranslated region (3'-UTR) of SNCG mRNA, downregulating its mRNA and protein expression levels. SNCG expression was negatively correlated with miR-15a expression. Conclusions: MiR-15a has a critical role in mediating cell cycle arrest and promoting cell apoptosis of BC, probably by directly targeting SNCG. Thus, it may be involved in development and progression of BC.