• Korean Journal of Head & Neck Oncology
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• v.20 no.2
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• pp.181-188
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• 2004

Background: About 3% of all cancer patients suffer from cancer of unknown primary origin. Generally, carcinoma of unknown primary (CUP) carries a grave prognosis, but primary tumor presented to the neck is exception to this. The aims of study are to determine the role of chemotherapy and to find the prognostic factors in unknown primary tumor presented to the neck. Method and Material: Eighty-four patients were diagnosed with unknown primary tumor presented to the neck between January 1996 and June 2002. Among 84 patients, 43 patients (52%) received chemotherapy, radiation or surgery were performed in 20 patients (23%), 21 patients (25%) had no treatment. Results: The response rates to chemotherapy were 87.5% in CUP only localized to the neck and 44.0% in CUP systemically involved (p=0.012). A median follow-up duration was 6.4 years and overall median survival time was 9 months. The median overall survival time of patients treated with chemotherapy were 17 months and that of patients who received surgery or radiation were 20 months (p=0.3548). The important prognostic factors were performance status and the number of involved organ. Conclusion: The prognosis of patients with CUP presented to the neck is more favorable than that of patients with CUP of other localization. The effectiveness of chemotherapy for CUP only localized to the neck was similar to that of surgery or radiation. The important prognostic factors were performance status and the number of involved organ.

• Archives of Pharmacal Research
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• v.28 no.4
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• pp.421-432
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• 2005

In order to understand the renal reabsorption mechanism of neutral amino acids via amino acid transporters, we have isolated human L-type amino acid transporter 2 (hLAT2) and human T-type amino acid transporter 1 (hTAT1) in human, then, we have examined and compared the gene structures, the functional characterizations and the localization in human kidney. Northern blot analysis showed that hLAT2 mRNA was expressed at high levels in the heart, brain, placenta, kidney, spleen, prostate, testis, ovary, lymph node and the fetal liver. The hTAT1 mRNA was detected at high levels in the heart, placenta, liver, skeletal muscle, kidney, pancreas, spleen, thymus and prostate. Immunohistochemical analysis on the human kidney revealed that the hLAT2 and hTAT1 proteins coexist in the basolateral membrane of the renal proximal tubules. The hLAT2 transports all neutral amino acids and hTAT1 transports aromatic amino acids. The basolateral location of the hLAT2 and hTAT1 proteins in the renal proximal tubule as well as the amino acid transport activity of hLAT2 and hTAT1 suggests that these transporters contribute to the renal reabsorption of neutral and aromatic amino acids in the basolateral domain of epithelial proximal tubule cells, respectively. Therefore, LAT2 and TAT1 play essential roles in the reabsorption of neutral amino acids from the epithelial cells to the blood stream in the kidney. Because LAT2 and TAT1 are essential to the efficient absorption of neutral amino acids from the kidney, their defects might be involved in the pathogenesis of disorders caused by a disruption in amino acid absorption such as blue diaper syndrome.

• Tuberculosis and Respiratory Diseases
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• v.43 no.1
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• pp.54-62
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• 1996

Background: $^{99m}Tc$ MIBI(Methoxyisobutylisonitrile complex), a member of the isonitrile class of coordination compounds, is a lipophilic cation presently under investigation for clinical use as myocardial perfusion imaging agent and is widely used to detect myocardial infarction. Preliminary reports indicate that $T_1$-201 accumulate in human neoplasm and several authors reported $^{99m}Tc$ MIBI may also localized in primary malignant tumor and metastatic deposits from lung cancer. We evaluated the uptake of $^{99m}Tc$ MIBI in lung cancer and localization of mediastinal and other site metastasis, and compared the benign lesion of the lung. Method: Thirty four patients of lung cancer and ten patients of benign lung lesion were studied with chest CT and $^{99m}Tc$ MIBI Lung SPECT. $^{99m}Tc$ MIBI uptake ratio was assessed by TR/NL(Lung lesion/ Normal area), HT/NL (Heart/Normal area) and HT/TR(Heart/Lung lesion). Results: 1) All lung cancer patients showed increased uptakes of $^{99m}Tc$ MIBI in malignant lung lesion and Tc-99m MIBI uptake was also increased in mediastinal and lymph node metastasis except two cases. 2) There was significant different ratio of TR/NL between malignant and benign lesion, $3.79{\pm}1.82$ and $1.67{\pm}0.63$ on planar images, respectively(p<0.001). 3) There was no significant difference of $^{99m}Tc$ MIBI uptake ratio between squamous cell carcinoma, small cell carcinoma and adeno carcinoma($3.64{\pm}1.66$, $3.57{\pm}0.72$, $4.31{\pm}2.28$ respectively). Conclusion: $^{99m}Tc$ MIBI lung SPECT was useful in the localization of tumor and mediastinal or other site metastatic lesion in lung cancer and also in the differential diagnosis between benign and malignant lesion.

• 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.

• Nuclear Medicine and Molecular Imaging
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• v.41 no.5
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• pp.350-358
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• 2007

Purpose: Localizing and differentiating a metastatic lesion of differentiated thyroid cancer (DTC) by using radio iodine whole body scan could be difficult because a whole body scan (WBS) lacks anatomic information. This study was performed to evaluate the usefulness of radio-iodine SPECT/CT for differentiating equivocal lesions. Materials & Methods: Among 253 patients with DTC who had undergone radio-iodine scan between February and July 2006, 26 patients were enrolled (M:F = 8:18, Age $50.7{\pm}12.5$ years) in this study. The patients had abnormal uptakes in the WBSs that necessitated precise anatomical localization for differentiating between a metastatic lesion and a false-positive lesion. SPECT/CT was performed for the region with abnormal uptake in the WBS. WBS and SPECT/CT were evaluated visually. Metastases were diagnosed based on the results of the radio-iodine scan along with the results of other radiological examinations and serological tests. Results: Based on the WBS images, 13 were suspected with cervical lymph node (LN) metastases in 16 patients with abnormal neck uptake, and in the 11 patients with abnormal extra-cervical uptakes, extra-cervical metastases were doubtful in all. After SPECT/CT was performed, the diagnostic results were altered for 16 patients (62%). SPECT/CT revealed that only 5 patients had cervical LN metastases, while 3 patients had extra-cervical (mediastinal) LN metastases. Overall, there was a 58% (15/26) change in diagnoses and plans for treatment due to SPECT/CT. Among 8 patients suspected with metastases on SPECT/CT, 6 patients underwent another radio-iodine therapy. In 96% (24/25) of the patients, the results of SPECT/CT corresponded with those of further radiological examinations and with other clinical information. Conclusion: Radio-iodine SPECT/CT images permitted the differentiation of abnormal radio-iodine uptake and improved anatomical interpretation in DTC.