• Development and Reproduction
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• v.6 no.2
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• pp.123-129
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• 2002

Leptin, a product of the obese gene, is associated not only with obesity but also with female reproductive function, but it has not yet been ascertained whether leptin acts directly on the ovary or indirectly via the hypothalamus-pituitary pathway. Therefore, the object of this study was to investigate the expession of leptin and its receptor in the rat ovary by immunohistochemistry and RT-PCR during the estrous cycle. Immunohistochemistry results showed that leptin was stained in the theca cells and in part of granulosa cells in atretic follicles, whereas leptin receptor was localized in the interstitial cells and ova in preantral follicies. In particular, leptin and its receptor in atretic follicles displayed more intensive staining compared to those in normal follicles. During the estrous cycle, the mRNA expression of leptin and its receptor in the ovary was detected by RT-PCR and estradiol, progesterone, and leptin levels in the serum was measured by ELISA. The leptin level in the serum on metestrous phase was significantly higher than that on estrous phase. Similar to leptin level, progesterone level increased on metestrous phase. Leptin mRNA was not detected throughout the estrous cycle, whereas leptin receptor mRNA was expressed on all phases of estrous cycle excepting the diestrous phase. These results suggest that leptin might be directly involved in the regulation of ovarian function in rat.

• Journal of Chest Surgery
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• v.39 no.5 s.262
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• pp.376-381
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• 2006

Background: The Ki-67 protein is a biomarker associated with cell proliferation and a valuable negative prognostic factor in non-small cell lung cancer. We investigated the Ki-67 protein expression in resected non-small cell lung cancer to evaluate the impact on clinicopathological characteristics and postoperative prognosis. Material and Method: Using monoclonal antibody Ki-67, we immunohistochemically examined 38 surgically resected non-small ceil lung cancers to determine Ki-67 Labeling Index (LI). We analysed the differences of clinicopathological characteristics and postoperative recurrence and survival between High Ki-67 Group $(LI{\ge}20%)$ and Low Ki-67 Group (LI<20%). Result: The Ki-67 LIs were heterogenous and a mean values was $20.0{\pm}20.05%$. There were no significant differences in age, sex, smoking, TNM stage, and vascular invasion between High Ki-67 Group and Low Ki-67 Group. A High Ki-67 Group was significantly associated with squamous cell type, poor differentiation, and lymphatic invasion $(p{\le}0.05)$. High Ki-67 Group showed a trend of lower survival (median 47.2 vs. 90.5 months, p=0.312) and lower disease-free survival (median 18.2 vs. 72.3 months, p=0.327) than Low Ki-67 Group. Conclusion: These results indicate that increased Ki-67 protein expression may be a negative prognostic factor and showed a trend of shortened survival and disease-free survival. To evaluate the pivotal role of Ki-67 protein expression, a long-term follow-up and further study are required.

• Tuberculosis and Respiratory Diseases
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• v.47 no.6
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• pp.786-796
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• 1999

Background: It has been anticipated that the amount and composition of mucin are changed in patients with chronic airway diseases. We evaluated whether RTO3(mAb against rat tracheal mucins) could quantify the amount of mucin from the airway in the patients with chronic airway diseases. Methods and results; 1) RTO3 was bound to high molecular weight of mucin based on Western blot in sputum and BALF from patients with chronic airway diseases. 2) The goblet cells and submucosal glands in main bronchus from human were observed by PAS stain. And immunohistochemical stain with RTO3 showed immunoreactivity on some goblet cells. 3) The amount of mucin was more increased in patients with chronic airway diseases compared to those in normal subjects. 4) In the exacerbation of asthmatics, mucin amounts were more increased than stable asthmatics. Conclusion: We suggested that secreted mucin in chronic airway diseases can be quantified by ELISA with RTO3.

• Clinical and Experimental Pediatrics
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• v.51 no.1
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• pp.73-77
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• 2008

Purpose : p16 gene, mapped to the 9p21 chromosomal region, has emerged as a candidate tumor suppressor gene in human neoplasm. It is an inhibitor of cyclin-dependent kinase and inhibits Rb phosphorylation. In a variety of tumors including childhood acute lymphoblastic leukemia (ALL), deletion and/or mutation of the p16 gene has been found. Despite their high frequency, the prognostic importance of p16 alterations is still controversial in ALL and has been reported to be either unfavorable or similar to that of other patients. We studied the correlation between loss of p16 protein confirmed by immunohistochemical staining and clinical outcomes of patients diagnosed as ALL. Methods : We performed an immunohistochemical staining for p16 protein in 74 cases of bone marrow biopsy slide initially diagnosed as ALL between January 1998 and December 2006. We reviewed the clinical manifestations, laboratory findings, treatment outcomes retrospectively. Results : Of 74 slides, 12 were negative for p16 protein. Seven were males and 5 were females with a median age at diagnosis was 5.8 (1.3-18.8) years. Initial WBC were 17,225 $(500-403,300)/{\mu}L$. By immunologic surface marker analysis, 7 patients were early pre-B CALLA (+) and 5 patients were T-cell ALL. Two patients of intermediate risk group had relapsed and died. Three patients had family history of breast cancer. Four patients died and overall survival rates were $53.5{\pm}18.7%$. Conclusion : Loss of p16 protein is supposed to be an independent risk factor of childhood ALL associated with poor outcomes. In clinical setting, the clinician must take into account p16 status, not only at the genomic but also at the protein level. Further clinical experience on thoroughly investigated cases will help a better understanding between p16 status and clinical outcomes.

• Journal of Chest Surgery
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• v.35 no.4
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• pp.325-328
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• 2002

The neuroendocrine tumor is a rare thymic neoplasm, which has been regarded as a distinct tumor from thymoma and originates from Kultschizky cell. The pathologic diagnosis of thymic neuroendocrine tumor has been on findings from light microscopy, immunohistochemical studies, and electron microscopy. About 50% of thymic carcinoids are seen with endocrinopathies. Recurrence and extrathoracic metastasis are characteristics of thymic carcinoids. Surgical removal of the initial and recurred tumor is considered to be the most effective treatment. The role of the adjuvant chemotherapy and radiotherapy is still uncertain. Herein we report a case of thymic neuroendocrine tumor, which was resected surgically.

• Journal of the korean academy of Pediatric Dentistry
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• v.45 no.2
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• pp.144-153
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• 2018

The aim of this study was to understand the roles of Sonic Hedgehog (SHH) signaling during tooth root and periodontium formation. In this study, we generated the dental mesenchyme-specific Smoothened (Smo) activated/inactivated mice with the activity of Cre recombinase under the control of osteocalcin promoter. In the Smo activated mutant molar sections at the postnatal 28 days, we found extremely thin root dentin and widened pulp chamber. Picrosirius red staining showed loosely arranged fibers in the periodontal space and decreased cellular cementum with some root resorption. Immunohistochemical staining showed less localization of matrix proteins such as Bsp, Dmp1, Pstn, and Ank in the cementum, periodontal ligament, and/or cementoblast. In the Smo inactivated mutant mouse, there was not any remarkable differences in the localization of these matrix proteins compared with the wild type. These findings suggest that adequate suppressing regulation of SHH signaling is required in the development of tooth root and periodontium.

• Journal of Life Science
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• v.16 no.5
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• pp.780-787
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• 2006

Asthma is a chronic inflammatory disorder of the airways, which characterized by bronchial hyperresponsiveness, reversible airflow limitation and respiratory symptoms. Internationally, the prevalence of asthma has been increased over last 3 decades. Recently, several studies of asthma have been reported with gradually increasing importance. To tesify the hypothesis that interleukin (IL)-4 and IL-10 may be an important determinant of the severity of airway inflammation, their expression was studied in mouse model of asthma. BALB/c mouse, IL-4 Knockout (KO) mouse and IL-10 KO mouse were sensitized with intraperitoneal injection of ovalbumin adsorbed to aluminum potassium sulfate, followed by challenges with intranasal ovalbumin on 3 consecutive days. The severity of pulmonary inflammation was assessed by eosinophilia in BAL fluid, number of total BAL cells, histopathological changes in lung tissues, and immunohistochemical staining against IL-4 and IL-10. In BAL fluid, the number of total cells was significantly increased in asthma induced mouse compare to the control. In asthma induced mouse, eosinophil was increased to 56% and neutrophil was 0.2%. In H &E stains, eosinophilic infiltration and epithelium hyperplasia were clearly noticed in asthma induced mouse. In immunohistochemical staining for IL-4 and IL-10, there was no positive reaction in control group. However, very strong reactions were appeared in asthma induced group. In this research, IL-4 and IL-10, which seem to play a central role in allergic asthma, KO mouse was utilized to test the causative relationship between airway inflammation and role of specific cytokine. Asthma induced IL-4 and IL-10 KO mice showed much decreased inflammatory reactions in the number of total BAL cells, in eosinophilic infiltration, and in immunohistochemical stains against diverse inflammatory proteins. These results suggest that IL-4 and IL-10 increase the asthmatic reactions in vivo mice model.

• Tuberculosis and Respiratory Diseases
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• v.48 no.3
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• pp.339-346
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• 2000

Background : The moot important prognostic factor in non-small cell lung cancer is the TNM stage. Even after complete resection in early non-small cell lung cancer, the five-year survival rate is still low. However, new prognostic factors, including molecular biologic factors, have recently been found to guide the treatment of patients with non-small cell lung cancer. We evaluated the prognostic value of the loss of blood-group antigen A in tumor tissue, which has been implicated as an important prognostic factor for overall survival and the timing of the disease progression. Methods : The loss of blood-group antigen A was assessed immunohistochemically in paraffin-embedded tumor samples from 26 patients with blood types A or AB, who had undergone curative surgery. Monoclonal antibody was used to detect the blood group antigen A expression. Results : Fifteen patients (58%) expressed antigen A in their tumor tissue, whereas 11 patients (42%) did not show antigen A. The median survival time of the blood A antigen positive group was 11 months, while the median survival time of the blood A antigen negative group was 18 months. The difference in survival between the two groups was not statistically significant. Conclusion : The loss of blood-group antigen A in tumor tissue was not found to be a significant prognostic factor in patients with non-small cell lung cancer. This study needs to be extended for further evaluation.

• The Korean Journal of Cytopathology
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• v.10 no.2
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• pp.121-126
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• 1999

The usefulness of E-cadherin immunostaining as a marker of malignancy in the body fluids was investigated in the present study. Thirty-three histologically proven cases of cell blocks from the pleural, peritoneal, and pericardial fluids were studied by immunocytochemistry for E-cadherin antibody using LSAB method. These cases were cytologically diagnosed as adenocarcinoma (25 cases) and atypical cells (8 cases). Tumor cells showed strong positive membranous staining for E-cadherin antibody in 21 out of 25 cases (84%) of adenocarcinoma. E-cadherin staining was not found in 6 of 8 cases of suspicious maligancy. The sensitivity and specificity were 84% and 75%, respectively. Reactive mesothelial cells and Inflammatory cells scattered were all negative. In conclusion, E-cadherin is an useful adjunctive marker to distinguish reactive mesothelial cells from the carcinoma cells in the body fluids.

• Journal of Chest Surgery
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• v.31 no.12
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• pp.1119-1126
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• 1998

Background: In this study, we investigated the early time course of expression of the major histocompatibility(MHC) antigens, intercellular adhesion molecule-1(ICAM-1), vascular cell adhesion molecule-1(VCAM-1), interleukin-6 and the histopathological changes in the coronary arteries of cardiac allografts exchanged between inbred mice strains that differ in one loci of class I major histocompatibility antigen (B10.BR to B10.A). Material and Method: No immunosuppressive therapy was used. Both allografts and the hearts of the recipients were harvested at 7(group 1, n=6), 15(group 2, n=6), 21(group 3, n=6), and 30(group 4, n=6) days after transplantation. They were examined by immunohistochemistry, microscopy and morphometry. All allografts had contractions at the time of harvest. Result: A strong MHC class I antigen expression was present on the endothelial and medial cells of the coronary arteries in group 1 and remained unchanged in the rest of the groups. However, MHC class II reactivity was none or very little at any time. Mild to moderate ICAM-1 expression was observed on the endothelial cells, but not on the medial cells at any time by 30 days. VCAM-1 expression was strong both on the endothelial and medial cells at any time. Moderate degree expression of interleukin-6 was observed from 7 to 30 day specimens. Histopathologically, percentage of affected vessels(vessels with intimal thickening) was less than 10 % in 7 day group and increased up to 50 % at 30 days. Mean percent narrowing of the lumen of the affected vessels revealed less than 20 % at 7 days and 40 % at 30 days. The area occupied by tropomyosin positive cells in the intimal lesion, graded from 0 to 3, showed gradual increase but remained between grade 0 to 1 by 30 days. Medial integrity was also well preserved at any time. Moderate perivascular mononuclear cell infiltration was observed at 7 days and it was progressively increased upto 30 days. Recipients' heart revealed no positive immunopathologic findings. Conclusion: In this study, the early time course of progression of the transplantation vasculopathy was demonstrated in the murine heterotopic heart transplant model.