• Clinical and Experimental Pediatrics
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• v.49 no.12
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• pp.1348-1353
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• 2006

Purpose : The reticuloendothelial system is composed of sinusoidal capillaries, through which even large protein molecules are freely movable between plasma and interstitial space, including the lymphatic system. Therefore, high-dose intravenous immunoglobulin (IVIG) would cause a redistribution of proteins between two compartments. To investigate this hypothesis, we measured plasma protein and lipid levels in patients with Kawasaki disease before and after high-dose IVIG treatment. Methods : Thirty four children with Kawasaki disease who had complete responses to high-dose IVIG treatment (1 g/kg/day for two consecutive days), were analyzed. Before and after the administration of IVIG, serum analyses were performed for such parameters as total protein, albumin, ${\gamma}$-globulins (IgG, IgM, IgA), ${\alpha}1-$, ${\alpha}2-$, and ${\beta}-$ globulin fractions, and lipid profiles (total cholesterol, HDL-cholesterol, LDL-cholesterol and triglyceride). Results : The levels of ${\gamma}$-globulins including IgG, IgM, IgA were significantly increased, and IgG was increased by $1,779{\pm}304mg/dL$ after two-dose of IVIG infusion. The levels of albumin, ${\alpha}1-$, ${\alpha}2-$, and ${\beta}$ globulin fractions were significantly decreased by 18 percent, 24 percent, 19 percent and 12 percent, respectively. HDL-cholesterol level was significantly decreased by 20 percent, while LDL-cholesterol and triglyceride levels were significantly increased by 21 percent and 50 percent, respectively. The total cholesterol level was not changed. Conclusion : High-dose IVIG treatment decreased the levels of a variety of proteins except immunoglobulins, and the increase of IgG after IVIG treatment was lower than expected. Our results suggest that a part of infused IVIG and plasma proteins, including etiologic proteins for Kawasaki disease, may be distributed to the extravascular compartments. The rapid improvement of symptoms induced by IVIG in Kawasaki disease might be explained by this mode of action of IVIG.

• 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.

• Journal of Chest Surgery
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• v.41 no.1
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• pp.68-73
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• 2008

Background: The presence of infiltrated mediastinal lymph nodes is a crucial factor for the prognosis of lung cancer. The aim of our study is to investigate the pattern of metastatic non-small cell lung cancer that spreads to the mediastinal lymph nodes, in relation to the primary tumor site, in patients who underwent major lung resection with complete mediastinal lymph node dissection. Material and Method: We retrospectively. studies 293 consecutive patients [mean age $63.0{\pm}8.3$ years (range $37{\sim}88$) and 220 males (75.1%)] who underwent major lung resection due to non-small cell lung cancer from January 1998 to December 2005. The primary tumor and lymph node status was classified according to the international TNM staging system reported by Mountain. The histologic type of the tumors was determined according to the WHO classification. Fisher's exact test was used; otherwise the chi-square test of independence was employed. A p-value < 0.05 was considered significant. Result: Lobectomy was carried out in 180 patients, bilobectomy in 50, sleeve lobectomy in 10 and pnemonectomy in 53. The pathologic report revealed 124 adenocarcinomas, 138 squamous-cell tumors, 14 adenosquamous tumors, 1 carcinoid tumor, 8 large cell carcinomas, 1 carcinosarcoma, 2 mucoepidermoid carcinomas and 5 undifferentiated tumors. The TNM stage was IA in 51 patients, IB in 98, IIB in 41, IIIA in 71, IIIB in 61 and IV in 6. 25.9 % of the 79 patients had N2 tumor. Most common infiltrated mediastinal lymph node was level No.4 in the right upper lobe, level No. 4 and 5 in the left upper lobe and level No. 7 in the other lobes, but no statistically significant difference was observed. Thirty-six patients (12.3%) presented with skip metastasis to the mediastinum. Conclusion: Mediastinal lymph node dissection is necessary for accurately determining the pTNM stage. It seems that there is no definite way that non-small cell lung cancer spreads to the lymphatics, in relation to the location of the primary cancer. Further, skip metastasis to the mediastinal lymph nodes was present in 12.3% of our patients.

• Radiation Oncology Journal
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• v.22 no.2
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• pp.124-129
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• 2004

Purpose : To evaluate the clinical findings, prognosis and treatment strategy of patients with neuroendocrine carcinoma of cervix. Materials and Methods: Thirteen patients with neuroendocrine carcinoma of cervix were included in this study, as confirmed histologically and immunohistochemically at the Dongsan Medical Center, Keimyung University, between May 1944 and October 2001. The mean age of patients was 56 years with a range of 32 to 78 years of age. According to the FIGO staging system, there were 5 patients with stage IB carcinoma, 5 patients with IIA, and 3 patients with stage IIB. Four patients underwent radical hysterectomy with pelvic lymphadenectomy, 3 of these patients also received postoperative radiotherapy, and one patient underwent extrafascial hysterectomy after radiotherapy. Primary radiotherapy was done in 9 patients, and 3 were irradiated postoperatively. Nine patients received chemotherapy, 7 received neoadjuvant and 2 received concurrent chemoradiotherapy. The radical purpose of radiotherapy consisted of external irradiation to the whole pelvis (4,500 $\~$5,400 cGy) and intracavitary irradiation (3,000 $\~$ 3,500 cGy). Results : The mean follow up duration was 36 months with a range of 3 to 104 months. The overall 5-year survival rate was 61.5$\%$ and the 5-year survival rates for stage IB, IIA, IIB were 60.0$\%$, 60.0$\%$, and 66.7$\%$ respectively (p=0.99). Eight patients are still alive without disease, and all of the 5 patients with recurrence are dead due to distant metastasis. Conclusion : Neuroendocrine carcinoma of cervix is highly aggressive, with early lymphatic dissemination and a high rate of distant recurrence. Therefore, an aggressive therapeutic strategy Is required to obtain pelvic and distant disease control. Multimodal therapy should be considered at the time of Initial diagnosis.