• Korean Journal of Plant Resources
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• v.20 no.1
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• pp.43-49
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• 2007

This study was conducted to examine the pattern and characteristics of flowering and leaf emergence for twenty two kinds of the genus of Lycoris sp. One species of Lycoris was flowered on July to August, twelve species on August, and nine species on September. Shape of flowers were as follows : Nine species belong to L. radiara-shaped flower, seven species L. squamigera-shaped flower, and seven species the intermediate type. Flower color of three kind were an order of descent red and pink. seven kind white, four kind yellow, three kind orange, and two kind purple colors. Ten Lycoris species were good fertile, and two kinds were poor fertile. The average length of pollen grain was ranged from $48.53\;to\;88.62{\mu}m$, and the width from $22.87\;to\;33.67{\mu}m$. Eleven kinds were spring-leaf emergence type, and ten kind autumn-leaf emergence types. Hunter values in leaves were as follows : $L^*$ value was ranged from 31.6 to 45.2; $a^*$ values from -6.74 to -17.46; $b^*$ values from 6.19 to 21.89 Leaf width was ranged from 0.90 to 2.35cm, and its shape was oblong. The length of epidermal cells was 0.33 to 0.75mm, and the width was $38.53\;to\;90.00{\mu}m$. Most of stomata were distributed in the back side of leaves. The length of stomata was ranged from $67.12\;to\;104.89{\mu}m$, and its width was from $14.90\;to\;71.52{\mu}m$.

• Maxillofacial Plastic and Reconstructive Surgery
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• v.28 no.6
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• pp.499-510
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• 2006

Malignant tumors of the human salivary glands may arise from major or minor salivary glands. Adenoid cystic carcinoma (ACC) is the second most common malignant neoplasm in the salivary glands. ACC is occasionally highly aggressive tumor that readily invades adjacent tissues and metastasize to distant organs at early stages of the disease. Although ACC tends to grow slowly, treatment outcome may be poor due to wide local infiltration, perineural or intraneural spread and a propensity for hematogenous metastasis. Therefore, knowledge of cellular and molecular characteristics that influence the growth, survival and metastasis of tumor cells, is important for new treatment strategies of salivary ACC. I determined expressions of epiderma growth factor (EGF)-signaling molecules using surgical specimens of human ACCs. Protein expressions of EGF, transforming growth $factor(TGF)-{\alpha}$, EGF receptor (EGFR), phosphorylated EGFR (pEGFR), and human EGF receptor (HER)-2 were assessed in 18 cases of salivary ACC by immunohistochemical staining. Adjacent normal salivary tissues and mucosal tissues, uninvolved by the malignant tumor, served as internal controls. Most of the tumors, especially ACC with a tubulocribriform pattern, were positive for EGF signaling molecules. The overall percentages of the 18 specimens expressing EGF, $TGF-{\alpha}$, EGFR, pEGFR, and HER2 were 50, 89, 61, 61 and 83% respectively. Moreover, tumor-associated endothelial cells and infiltrating immune-related cells in the stroma of ACC, also expressed these biomarkers. Taken together, EGF-signaling molecules are actively expressed in salivary ACC. Therefore, we suggest that these biomarkers can be molecular targets for new treatment strategies of salivary tumors.

• The Journal of the Korean Society for Microbiology
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• v.21 no.3
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• pp.311-329
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• 1986

The experimental exposure of animals to sources of ultraviolet radiation (UVR) which emit their energy primarily in the UVB region (280-320nm) is known to result in a number of well-described changes in the recipient's immune competence. Two such changes include a depressed capacity to effectively respond immunologically to transplants of syngeneic UVR tumors and a markedly reduced responsiveness to known inducers of delayedtype (DTH) and contact hypersensitivity (CH) reactions. The results of experiments that were designed to elucidate the mechanisms responsible for UVR-induced immunomodulation have implicated: 1) an altered pattern of lymphocyte recirculation, 2) suppressor T cells(Ts), 3) deviations in systemic antigen presenting cell (APC) potential. 4) changes in the production of interleukin-1-like molecules, and 5) the functional inactivation of epidermal Langerhans cells in this process. The exposure of skin to UVR, therefore, causes a number of both local and systemic alterations to the normal host immune system. In spite of this seeming complexity and diversity of responses, our recent studies have established that each of the UVR-mediated changes is probably of equal importance to creating the UVR-induced immunocompromised state. Normal animals were exposed to low dose UVR radiation on their dorsal surfaces under conditions where a $3.0\;cm^2$ area of skin was physically protected from the light energy. Contact sensitization of these animals with DNFB, to either the irradiated or protected back skin, resulted in markedly reduced CH responses. This was observed in spite of a normal responsiveness following the skin sensitization to ventral surfaces of the UVR-exposed animals. Systemic treatment of the low dose UVR recipients with the drug indomethacin (1-3 micrograms/day) during the UVR exposures resulted in a complete reversal of the depressions observed following DNFB sensitization to "protected" dorsal skin while the altered responsiveness found in the group exposed to the skin reactive chemical through directly UVR-exposed sites was maintained. These studies implicate the importance of EC as effective APC in the skin and also suggest that some of the systemic influences caused by UVR exposure involve the production of prostaglandins. This concept was further supported by finding that indomethacin treatment was also capable of totally reversing the systemic depressions in CH responsiveness caused by high dose UVR exposure (30K joules/$m^2$) of mice. Attempts to analyze the cellular mechanisms responsible established that the spleens of all animals which demonstrated altered CH responses, regardless of whether sensitization was through a normal or an irradiated skin site, contained suppressor cells. Interestingly, we also found normal levels of T effector cells in the peripheral lymph nodes of the UVR-exposed mice that were contact sensitized through normal skin. No effector cells were found when skin sensitization took place through irradiated skin sites. In spite of such an apparent paradox, insight into the probable mechanisms responsible for these observations was provided by establishing that UVR exposure of skin results in a striking and dose-dependent blockade of the efferent lymphatic vessels in all peripheral lymph nodes. Therefore, the afferent phases of immune responses can apparently take place normally in UVR exposed animals when antigen is applied to normal skin. The final effector responses, however, appear to be inhibited in the UVR-exposed animals by an apparent block of effector cell mobility. This contrasts with findings in the normal animals. Following contact sensitization, normal animals were also found to simultaneously contain both antigen specific suppressor T cells and lymph node effector cells. However, these normal animals were fully capable of mobilizing their effector cells into the systemic circulation, thereby allowing a localization of these cells to peripheral sites of antigen challenge. Our results suggest that UVR is probably not a significant inducer of suppressor T-cell activity to topically applied antigens. Rather, UVR exposure appears to modify the normal relationship which exists between effector and regulatory immune responses in vivo. It does so by either causing a direct reduction in the skin's APC function, a situation which results in an absence of effector cell generation to antigens applied to UVR-exposed skin sites, inhibiting the capacity of effector cells to gain access to skin sites of antigen challenge or by sequestering the lymphocytes with effector cell potential into the draining peripheral lymph nodes. Each of these situations result in a similar effect on the UVR-exposed host, that being a reduced capacity to elicit a CH response. We hypothesize that altered DTH responses, altered alloresponses, and altered graft-versus-host responses, all of which have been observed in UVR exposed animals, may result from similar mechanisms.

• Investigative Magnetic Resonance Imaging
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• v.14 no.2
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• pp.95-102
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• 2010

Purpose : To evaluate the magnetic resonance imaging (MRI) and clinicopathological features of triple negative breast cancer, and compare them with those of non-triple negative breast cancer. Materials and Methods : This study included 231 pathologically confirmed breast cancers from January 2007 to May 2008. We retrospectively reviewed the MRI findings according to the Breast Imaging Reporting and Data System (BI-RADS) lexicon: mass or non-mass type, mass shape, mass margin, non-mass distribution, and enhancement pattern. Histologic type, histologic grade, and the results for epidermal growth factor receptor, p53, and Ki 67 were reviewed. Results : Of 231 patients, 43(18.6%) were triple negative breast cancer. Forty triple negative breast cancers (93.0%) were mass-type lesion on MRI. A round or oval or lobular shape (p=0.006) and rim enhancement (p=0.004) were significantly more in triple negative breast cancer than non- triple negative breast cancer. In contrast, irregular shape (p=0.006) and spiculated margins (p=0.032) were significantly more in non-triple negative breast cancer. Old age (p=0.019), high histologic grade (p<0.0001), EGFR positivity (p<0.0001), p53 overexpression (p=0.038), and Ki 67 expression (<0.0001) were significantly associated with the triple negative breast cancer. Conclusion : MRI finding may be helpful for differentiation between triple negative and non-triple negative breast cancer.

• Tuberculosis and Respiratory Diseases
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• v.59 no.3
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• pp.286-297
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• 2005

Background : Non-small cell lung cancer (NSCLC) is a common cause of cancer-related death in North America and Korea, with an overall 5-year survival rate of between 4 and 14%. The TNM staging system is the best prognostic index for operable NSCLC . However, epidermal growth factor receptor (EGFR), matrix metalloproteinase-9(MMP-9), and C-erbB-2 have all been implicated in the pathogenesis of NSCLC and might provide prognostic information. Methods : Immunohistochemical staining of 81 specimens from a resected primary non-small cell lung cancer was evaluated in order to determine the role of the biological markers on NSCLC . Immunohistochemical staining for EGFR, MMP-9, and C-erbB-2 was performed on paraffin-embedded tissue sections to observe the expression pattern according to the pathologic type and surgical staging. The correlations between the expression of each biological marker and the survival time was determined. Results : When positive immunohistochemical staining was defined as the extent area>20%(more than Grade 2), the positive rates for EGFR, MMP-9, and C-erbB-2 staining were 71.6%, 44.3%, and 24.1% of the 81 patients, respectively. The positive rates of EGFR and MMP-9 stain for NSCLC according to the surgical stages I, II, and IIIa were 75.0% and 41.7%, 66.7% and 47.6%, and 76.9% and 46.2%, respectively. The median survival time of the EGFR(-) group, 71.8 months, was significantly longer than that of the EGFR(+) group, 33.5 months.(p=0.018, Kaplan-Meier Method, log-rank test).. The MMP-9(+) group had a shorter median survival time than the MMP-9(-) group, 35.0 and 65.3 months, respectively (p=0.2). The co-expression of EGFR and MMP-9 was associated with a worse prognosis with a median survival time of 26.9 months, when compared with the 77 months for both negative-expression groups (p=0.0023). There were no significant differences between the C-erbB-2(+) and C-erbB-2 (-) groups. Conclusion : In NSCLC, the expression of EGFR might be a prognostic factor, and the co-expression of EGFR and MMP-9 was found to be associated with a poor prognosis. However, C-erbB-2 expression had no prognostic significance.