• Clinical and Experimental Pediatrics
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• v.50 no.1
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• pp.65-73
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• 2007

Purpose : Short stature is an important complication that impairs the quality of life in survivors of childhood brain tumors. We studied their final adult height (FAH) to evaluate risk factors for short stature. Methods : We reviewed the medical data of 95 survivors of childhood brain tumors (64 males and 31 females) who had been followed up from 1982 to 2006, reached FAH, and had a more than five year-disease-free survival. Results : Final adult height standard deviation score (FAHTSDS: $mean{\pm}SD$) of the patients was lower than those of general population ($-1.15{\pm}1.72$), HTSDS at diagnosis ($-0.13{\pm}1.57$), and target HTSDS ($-0.49{\pm}0.69$). FAHTSDS of craniopharyngioma patients did not decrease ($0.57{\pm}1.17$), but those of germ cell tumor and medulloblastoma patients were significantly reduced ($-1.20{\pm}1.45$, $-2.70{\pm}1.46$; P<0.05). The patients treated with craniospinal radiation or chemotherapy had lower FAHTSDS ($-1.93{\pm}1.58$, $-2.27{\pm}1.44$; P<0.01). In the spinal irradiation group, the younger the age at diagnosis was, the more the loss of FAH (r=0.442, P<0.01). Growth hormone replacement (GHR) didn't improve FAHTSDS, but starting GHR under 12 years was an independent factor for improving FAH once treatment methods were taken into account (P=0.01). Conclusion : The younger age at diagnosis, spinal radiation and chemotherapy were all important risk factors of height loss, and height gain was expected in patients who received GHR under the age of 12 years. Therefore, regular check-ups of growth and early intervention with growth hormones are needed for high risk groups to improve FAH.

• IMMUNE NETWORK
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• v.1 no.3
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• pp.244-249
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• 2001

The transforming growth $factor-{\beta}$ ($TGF-{\beta}$) is a multifunctional cytokine modulating the onset and course of autoimmune disease as shown in experimental models. In synovial inflammation, there is a potential role for $TGF-{\beta}$ in repairment, the inhibition of cartilage and bone destruction, and the down-regulation of immune response. The biologic effects of $TGF-{\beta}$ depend on the cell type, the isoform and the availability of active $TGF-{\beta}$. We investigated $TGF-{\beta}$ expression in patients with rheumatoid arthritis (RA) and compared to those of osteoarthritis (OA). And we determined a correlation between $TGF-{\beta}1$ and $TGF-{\beta}2$, and also the relationships between each $TGF-{\beta}$ isoform and the parameters for disease activity of RA. Methods: The study population consisted of 20 patients with RA and 20 patients with OA. The commercial ELISA kit was used to study $TGF-{\beta}1$ and $TGF-{\beta}2$ levels in peripheral blood (PB) and synovial fluids (SF). Results: 1) While PB $TGF-{\beta}1$ level was of no difference between RA and OA patient groups, SF $TGF-{\beta}1$ level was higher in RA group than OA group. Similarly, PB $TGF-{\beta}2$ levels of RA and OA groups was not different, but SF $TGF-{\beta}2$ levels was higher in RA group than OA group. 2) In patients with RA, the $TGF-{\beta}1$ levels were higher than $TGF-{\beta}2$ in both the PB and SF, while in patients with OA, there showed higher readings for $TGF-{\beta}1$ than $TGF-{\beta}2$ in SF but no difference between $TGF-{\beta}1$ and $TGF-{\beta}2$ levels in PB. 3) In patients with RA, there were no correlations between PB $TGF-{\beta}1$ and PB $TGF-{\beta}2$ levels, nor between SF $TGF-{\beta}1$ and SF $TGF-{\beta}2$ levels. At the same way, there was no correlation between PB $TGF-{\beta}1$ and SF $TGF-{\beta}1$ levels, nor between each levels of $TGF-{\beta}2$ in patients with RA. 4) There was also no correlation between each $TGF-{\beta}$ isoform and the parameters for disease activity such as ESR, CRP, tender joint count, swollen joint count, rheumatoid factor, and the duration of morning stiffness except between in PB $TGF-{\beta}1$ and disease duration of RA (r=0.637, p<0.01). Conclusion: Each $TGF-{\beta}$ isoforms were higher in synovial fluid of patients with RA than that of patients with OA. The data from the RA patients demonstrated different patterns of expressions of the isoforms depending on which compartment (PB or SF) was investigated. The quantification of different $TGF-{\beta}$ isoform is thought to be important when $TGF-{\beta}$ is measured under disease conditions of RA.