• The Journal of Korea Assosiation for Disability and Oral Health
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• v.13 no.2
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• pp.108-113
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• 2017

Moyamoya disease is a disorder in which certain arteries in the brain are constricted. Blood flow can be blocked by the constriction and blood clots. The patients frequently experience transient ischemic attacks (TIA), cerebral hemorrhage, or may not experience any symptoms at all. It is reported that they have a higher risk of recurrent stroke and a distinct underlying pathophysiology. A 3-year-8-month old boy with moyamoya disease experienced cerebral infarctions five times, and he underwent a cerebrovascular anastomosis surgery four years ago. He showed swallow disturbance, general delayed development, hemiplegia, and strabismus. Also he had hypocalcified teeth with or without multiple caries lesions in all dentitions. Dental treatment under general anesthesia using sevoflurane was performed due to his lack of cooperation. Moyamoya disease is associated with various medical conditions requiring a thoughtful deliberation and a careful examination before and during dental treatment. Pain and anxiety control during dental treatment is important because hyperventilation induced by crying has been seen to trigger TIA. Both isoflurane and sevoflurane are commonly used in patients with MMD, but dynamic autoregulation is better preserved during sevoflurane than isoflurane anesthesia. So sevoflurance general anesthesia may be recommendable to manage dental patients having multiple caries with moyamoya disease.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.5
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• pp.2073-2080
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• 2015

Background: The human papillomavirus (HPV) and its variants show wide geographical distribution and have been reported to cause cervical lesions. With cervical neoplasia as the leading cancer in Indian women, the aim of the present study was to evaluate the multiple infection HPV type distribution and variant genotypes in cervical samples from the coastal Karnataka region, India. Materials and Methods: A total of 212 samples were screened by nested polymerase chain reaction using PGMY9/11 and GP5+/6+ primers. HPV positive samples were sequenced to identify the types and a phylogenetic tree was constructed using the neighbor-joining method. Results: Sequence analysis identified a total of 14 HPV types distributed in 20%, 73.3% and 82.5% of non-malignant, pre-malignant [low grade squamous intraepithelial lesion (LSIL) and high grade squamous intraepithelial lesion (HSIL)] and cervical cancer samples. The distribution of high risk HPV in cancer samples was HPV 16, 76.4%, HPV18, 11.7%, HPV81, 2.9%, HPV31, 1.4%, HPV35, 1.4% and HPV 45, 1.4%. Multiple infections were observed in 11.8% of tumor samples with HPV 16 contributing to 62.5% of cases. In non-malignant samples, 20% of HPV positive samples were detected with HPV16, 82.3%, HPV33, 5.8% and HPV58, 5.8% and very low incidence of multiple infections. Comparative phylogenetic analysis of HPV variants identified 9 HPV sequences as new papillomavirus species, predominantly classified as European lineage type. Conclusions: The findings for HPV infections associated with progression of cervical cancer in coastal Karnataka region and HPV variant analysis provide baseline data for prevention and HPV vaccination programs.

• Journal of The Korean Society of Inherited Metabolic disease
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• v.16 no.2
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• pp.102-108
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• 2016

Mitochondrial encephalopathy, lactic acidosis, and stroke-like episode (MELAS) syndrome is one of mitochondrial encephalopathy. As the early clinical manifestations can be variable, it is important to suspect the disease, especially in patients with multiple organ dysfunctions. A boy was diagnosed with epilepsy when he was 9 years old. Two years later, severe headache and blurred vision developed suddenly. On examination, left homonymous hemianopsia was detected with corresponding cerebral parenchymal lesions in right temporo-occipito-parietal areas. MELAS syndrome was confirmed by genetic test, which showed m.3243 A>G mitochondrial DNA mutation. Multivitamins including coenzyme Q10 were added to anticonvulsant. He experienced 4 more events of stroke-like episodes over 5 years, but he is able to perform normal daily activities. A 13-year-old boy was brought to the hospital due to suddenly developed respiratory arrest and asystole associated with pneumonia. Past medical history revealed that he had multiple medical problems such as epilepsy, failure-to-thrive, optic atrophy, and deafness. He has been on valproic acid as an anticonvulsant which was prescribed from local clinic. He recovered after the resuscitation, but his cognition and motor function were severely damaged. He became bed-ridden. He was diagnosed with MELAS syndrome by brain MRI, muscle biopsy, and clinical features. Genetic test did not reveal any mitochondrial gene mutation. Four years later, he expired due to suddenly developed severe metabolic acidosis combined with hyperglycemic hyperosmolar nonketotic coma. The clinical features of MELAS syndrome are variable. Early diagnosis before the presentation to the grave clinical course may be important for the better clinical outcome.

• Korean Journal of Head & Neck Oncology
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• v.22 no.1
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• pp.8-14
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• 2006

Objectives: The p53 tumor suppressor gene has a key role in cellular control mechanisms involving apoptosis and DNA repair, leading to the G1 arrest following DNA damage. Its mutation is one of the most frequent alterations in human cancers. Ki-67 is identified in replicating cells of both benign and malignant lesions, so it can be the predictor of proliferative activity. The aim of this study is to evaluate the expression of p53 and Ki-67 in salivary gland tumors. Materials and Methods: Immunohistochemical analysis was used to detect expression of p53 and Ki-67 in paraffin-embedded samples from 31 benign and 27 malignant salivary gland tumors. Results were analyzed between benign and malignant tumors and compared with the clinical parameters such as stage and recurrence in malignant tumors. Results: p53 overexpression was detected in 19.6% of benign tumors and 40.7% of malignant tumors, but there was no statistical significance. p53 was significantly expressed in Warthin's tumor(45.5%) compared with pleomorphic adenoma(5.9%). Only 5.9% of pleomorphic adenoma were positive for p53, while 60% of carcinoma ex pleomorphic adenoma were positive for p53. Ki-67 was expressed in 3.2% of benign tumors and 51.9% of malignant tumors, which showed significant higher expression in malignant tumors. In malignant tumors, p53 and Ki-67 expressions bore no correlation to stage and recurrence. Conclusion: p53 overexpression is not associated with the progression of malignant tumors, and Ki-67 overexpression can be used as biologic indicator of malignant salivary gland tumors.

• Maxillofacial Plastic and Reconstructive Surgery
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• v.30 no.1
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• pp.41-51
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• 2008

Mucoepidermoid carcinoma (MEC) is the most common malignant salivary gland tumor which compromises about 6$\sim$8% of all tumors followed by the adenoid cystic carcinoma (ACC) and adenocarcinoma. Most deaths from salivary carcinomas are caused by recurrent or metastatic lesions that are resistant to conventional therapy. Therefore, knowledge of cellular properties and tumor-host interactions that influence the vascular metastasis is important for the design of more effective therapy of salivary carcinomas. Neoangiogenesis is essential for tumor growth, which is postulated to be fundamentally dependent on the induction of stromal neovascularization. However, how neovascularization takes place in live tissue has not been fully established, especially in recruitment and differentiation of endothelial cells in the salivary gland tumors. Vascular endothelial growth factor (VEGF) is a heparin-binding, dimeric polypeptide growth factor known to exert its mitogenic activity specifically on endothelial cells. VEGF has been shown th be directly involved in angiogenesis, which in essential for the pathogenesis of many solid tumors. von Willebrand factor (vWF) is a large multimeric protein synthesized by megakaryocytes and endothelial cells that enable platelets to adhere to exposed subendothelium and, as well, to respond to changes in the blood flow. Recent studies suggest that increased levels of vWF correlate with progression of disease, metastasis, or survival time and thus may have a prognostic significance. vWF is explained as an acute phase proteins which is increased in cancer or as a result of increased endothelial cell synthesis associated with tumor-induced angiogenesis. Due to adhesive properties of vWF, its increased concentrations may also contribute metastasis of tumor. In this study, we determined the mRNA expression of VEGF and vWF in salivary ACC, MEC and pleomorphic adenoma by in situ hybridization. As a result, stronger expression of VEGF and vWF was seen in salivary ACC and MEC which has more invasive nature than the salivary benign tumor.

• Journal of the korean academy of Pediatric Dentistry
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• v.34 no.3
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• pp.490-497
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• 2007

Odontoma is defined as a benign odontogenic tumor containing enamel, dentin as well as cementum and constitued 22% of all odontogenic tumors. Although the lesions are commonly asymptomatic, they may be discovered routine radiographic examination. Odontomas often cause disturbances in the eruption of teeth such as, impaction or delayed eruption, retention of primary teeth, or abnomalities in the position of the teeth such as tipping or displacement of adjacent teeth. Radiologically, odontomas manifest as a dense radiopaque lesion surrounded by a thin radiotransparent halo. However, in some cases, radiopacity was not quite clear and images of the teeth shadowed very tiny odontomas. And at early development stages of odontoma, calcification remains immature and is difficult to diagnose on radiographs. This suggests that when delayed eruption of the teeth is found, periapical radiographs should be taken to clarify whether any small area of radiopaque material exists. This case report shows tiny odontomas involving an impacted tooth and crowding and we remove the tiny odontoma surgically.

• BMB Reports
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• v.51 no.11
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• pp.584-589
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• 2018

Secondary prevention via earlier detection would afford the greatest chance for a cure in premalignant lesions. We investigated the exomic profiles of non-malignant and malignant changes in head and neck squamous cell carcinoma (HNSCC) and the genomic blueprint of human papillomavirus (HPV)-driven carcinogenesis in oropharyngeal squamous cell carcinoma (OPSCC). Whole-exome (WES) and whole-genome (WGS) sequencing were performed on peripheral blood and adjacent non-tumor and tumor specimens obtained from eight Korean HNSCC patients from 2013 to 2015. Next-generation sequencing yielded an average coverage of $94.3{\times}$ for WES and $35.3{\times}$ for WGS. In comparative genomic analysis of non-tumor and tumor tissue pairs, we were unable to identify common cancer-associated early mutations and copy number alterations (CNA) except in one pair. Interestingly, in this case, we observed that non-tumor tonsillar crypts adjacent to HPV-positive OPSCC appeared normal under a microscope; however, this tissue also showed weak p16 expression. WGS revealed the infection and integration of high-risk type HPV16 in this tissue as well as in the matched tumor. Furthermore, WES identified shared and tumor-specific genomic alterations for this pair. Clonal analysis enabled us to infer the process by which this transitional crypt epithelium (TrCE) evolved into a tumor; this evolution was accompanied by the subsequent accumulation of genomic alterations, including an ERBB3 mutation and large-scale CNAs, such as 3q27-qter amplification and 9p deletion. We suggest that HPV16-driven OPSCC carcinogenesis is a stepwise evolutionary process that is consistent with a multistep carcinogenesis model. Our results highlight the carcinogenic changes driven by HPV16 infection and provide a basis for the secondary prevention of OPSCC.

• Molecules and Cells
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• v.43 no.10
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• pp.889-897
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• 2020

K-RAS is frequently mutated in human lung adenocarcinomas (ADCs), and the p53 pathway plays a central role in cellular defense against oncogenic K-RAS mutation. However, in mouse lung cancer models, oncogenic K-Ras mutation alone can induce ADCs without p53 mutation, and loss of p53 does not have a significant impact on early K-Ras-induced lung tumorigenesis. These results raise the question of how K-Ras-activated cells evade oncogene surveillance mechanisms and develop into lung ADCs. RUNX3 plays a key role at the restriction (R)-point, which governs multiple tumor suppressor pathways including the p14^ARF-p53 pathway. In this study, we found that K-Ras activation in a very limited number of cells, alone or in combination with p53 inactivation, failed to induce any pathologic lesions for up to 1 year. By contrast, when Runx3 was inactivated and K-Ras was activated by the same targeting method, lung ADCs and other tumors were rapidly induced. In a urethane-induced mouse lung tumor model that recapitulates the features of K-RAS-driven human lung tumors, Runx3 was inactivated in both adenomas (ADs) and ADCs, whereas K-Ras was activated only in ADCs. Together, these results demonstrate that the R-point-associated oncogene surveillance mechanism is abrogated by Runx3 inactivation in AD cells and these cells cannot defend against K-Ras activation, resulting in the transition from AD to ADC. Therefore, K-Ras-activated lung epithelial cells do not evade oncogene surveillance mechanisms; instead, they are selected if they occur in AD cells in which Runx3 has been inactivated.

• Korean Journal of Food Science and Technology
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• v.39 no.2
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• pp.181-188
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• 2007

This study examined the effects of green tea extract supplementation (500 or 1,000 mg/kg b.w. per day) in conjunction with an atherogenic diet (10% coconut oil (w/w), 0.1% cholesterol) on plasma lipid composition, regression of pre-existing foam cells, and on the mRNA levels of hepatic HMG-CoA reductase and LDL receptor. Compared to groups fed only with the atherogenic diet, the addition of green tea extract to atherogenic diet-fed groups significantly down-regulated plasma triglyceride and total cholesterol levels, dose-dependently. Supplementation of 1,000 mg/kg b.w. of green tea extract with the atherogenic diet induced significant up-regulation of both HMG-CoA reductase and LDL receptor messenger RNA levels in liver as compared to the group receiving green tea extract supplementation at 500 mg/kg b.w. The F1B hamsters fed the atherogenic diet had greater foam cell accumulation compared to those fed a normal diet, or the atherogenic diet supplemented with green tea extract. Regression of fatty streak lesions was achieved by atherosclerosis in fat- and cholesterol-fed hamsters and this effect was associated with down-regulation of plasma cholesterol and up-regulation of hepatic LDL receptor expression.

• Parasites, Hosts and Diseases
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• v.54 no.3
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• pp.281-289
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• 2016

Clonorchis sinensis is a Group-I bio-carcinogen, associated with cholangiocarcinoma (CCA). The hamster is the only experimental model of C. sinensis-mediated CCA, but we oblige another animal model. The present study intended to develop a C. sinensis (Cs) mediated CCA model using C3H/He mice, co-stimulated with N-nitrosodimethylamine (NDMA) and dicyclanil (DC). The mice were divided into 8 groups with different combinations of Cs, NDMA, and DC. Six months later the mice were sacrificed and subjected to gross and histopathological examination. The body weights were significantly reduced among the groups treated with 2 or more agents (eg. Cs+NDMA, Cs+DC, NDMA+DC, and Cs+NDMA+DC). In contrast, liver weight percentages to body weight were increased in above groups by 4.1% to 4.7%. A Change of the spleen weight was observed only in Cs+NDMA group. Though C. sinensis infection is evident from hyperplastic changes, only 1 worm was recovered. Two mice, 1 from Cs and the other from Cs+DC group, showed mass forming lesions; 1 ($281.2mm^3$) from the Cs group was a hepatocellular adenoma and the other ($280.6mm^3$) from the Cs+DC group was a cystic mass (peliosis). Higher prevalence of gray-white nodules was observed in Cs group (42.9%) followed by Cs+NDMA+DC group (21.4%). The mice of the Cs+NDMA+DC group showed hyper-proliferation of the bile duct with fibrotic changes. No characteristic change for CCA was recognized in any of the groups. In conclusion, C3H/He mice produce no CCA but extensive fibrosis when they are challenged by Cs, NDMA, and DC together.