• Tuberculosis and Respiratory Diseases
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• v.45 no.4
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• pp.846-860
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• 1998

Background: Endotoxin (LPS : lipopolysaccharide), a potent activator of immune system, can induce acute and chronic inflammation through the production of cytokines by a variety of cells, such as monocytes, endothelial cells, lymphocytes, eosinophils, neutrophils and fibroblasts. LPS stimulate the mononucelar cells by two different pathway, the CD14 dependent and independent way, of which the former has been well documented, but not the latter. LPS binds to the LPS-binding protein (LBP), in serum, to make the LPS-LBP complex which interacts with CD14 molecules on the mononuclear cell surface in peripheral blood or is transported to the tissues. In case of high concentration of LPS, LPS can stimulate directly the macrophages without LBP. We investigated to detect the generation of proinflammatory cytokines such as interleukin 1 (IL-1), IL-6 and TNF-$\alpha$ and fibrogenic cytokine, TGF-$\beta$, by peripheral blood mononuclear cells (PBMC) after LPS stimulation under serum-free conditions, which lacks LBPs. Methods : PBMC were obtained by centrifugation on Ficoll Hypaque solution of peripheral venous bloods from healthy normal subjects, then stimulated in the presence of LPS (0.1 ${\mu}g/mL$ to 100 ${\mu}g/mL$ ). The activities of IL-1, IL-6, TNF, and TGF-$\beta$ were measured by bioassaies using cytokines - dependent proliferating or inhibiting cell lines. The cellular sources producing the cytokines was investigated by immunohistochemical stains and in situ hybridization. Results : PBMC started to produce IL-6, TNF-$\alpha$ and TGF-$\beta$ in 1 hr, 4 hrs and 8hrs, respectively, after LPS stimulation. The production of IL-6, TNF-$\alpha$ and TGF-$\beta$ continuously increased 96 hrs after stimulation of LPS. The amount of production was 19.8 ng/ml of IL-6 by $10^5$ PBMC, 4.1 ng/mL of TNF by $10^6$ PBMC and 34.4 pg/mL of TGF-$\beta$ by $2{\times}10^6$ PBMC. The immunoreactivity to IL-6, TNF-$\alpha$ and TGF-$\beta$ were detected on monocytes in LPS-stimulated PBMC. Some of lymphocytes showed positive immunoreactivity to TGF-$\beta$. Double immunohistochemical stain showed that IL-1$\beta$, IL-6, TNF-$\alpha$ expression was not associated with CD14 postivity on monocytes. IL-1$\beta$, IL-6, TNF-$\alpha$ and TGF-$\beta$mRNA expression were same as observed in immunoreactivity for each cytokines. Conclusion: When monocytes are stimulated with LPS under serum-free conditions, IL-6 and TNF-$\alpha$ are secreted in early stage of inflammation. In contrast, the secretion of TGF-$\beta$ arise in the late stages and that is maintained after 96 hrs. The main cells releasing IL-1$\beta$, IL-6, TNF-$\alpha$ and TGF-$\beta$ are monocytes, but also lymphocytes can secret TGF-$\beta$.

• The Korean Journal of Physiology
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• v.18 no.1
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• pp.51-65
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• 1984

In an effort to elucidate the effect of physical training on the electrocardiographic amplitudes, QRS vector, axis and QRS vector amplitude, electrocardiograms were recorded before and 1, 5 and 10 minutes after 3 minute rebounder exercise in 23 healthy male students aged between 18 and 21 years in two groups of athletes and non-athletes. ECG amplitudes were measured from lead I, $V_1$ and $V_5$ and axis and amplitudes of QRS vectors were measured from lead I and III in frontal plane, from lead $V_2$ and lead $V_6$ in horizontal plane. The results obtained are summarized as follows. ECG amplitudes: The R wave amplitude was $23.38{\pm}1.14\;mm$ in athletes which was higher than $17.91{\pm}2.00\;mm$ in non-athletes. After exercise, the difference in two groups remained significant throughout the recovery period. The S wave amplitude was increased significantly, and the T wave amplitude was decreased in both groups after exercise. The P wave amplitude was increased in both groups after exercise, and it was lower in athletes than in non-athletes. The PQ segment amplitude was zero in athletes but negative in non-athletes than in the resting state. The J point amplitude was positive in resting state and was negative after exercise in both groups. J+0.08 sec point amplitude was also lowered after exercise, and it was higher in athletes than in non-athletes. Therefore the whole ST segment was proved to be decreased after exercise. The summated amplitude of R in $V_5$ plus S in $V_1$ was $38.74{\pm}2.71\;mm$ in athletes which was higher than $32.82{\pm}2.90\;mm$ in non-athletes. After exercise, it was also significantly higher in athletes than in non-athletes. Axis of QRS vector: In frontal plane, axis of QRS vector was $62.7{\pm}7.36^{\circ}$ in athletes, it showed no significant difference between the two groups. In horizontal plane, axis of QRS vector was $-23.5{\pm}7.2^{\circ}$ in athletes which was significantly higher than $-38.8{\pm}8.2^{\circ}$ in non-athletes. After exercise, it was significantly higher than the resting state in both groups. Amplitude of QRS vector : In frontal plane, amplitude of QRS vector was $13.86{\pm}1.44\;mm$ in athletes which was significantly higher than $9.62{\pm}0.97\;mm$ in non-athletes. After exercise, it was also significantly higher in athletes than in non-athletes. In horizontal plane, amplitude of QRS vector was $19.82{\pm}2.10\;mm$ in athletes which was significantly higher than $16.90{\pm}1.39\;mm$ in non-athletes. After exercise, it was also significantly higher in athletes than in non-athletes. From the above, these results indicate that R wave amplitude in athletes was significantly higher than in non-athletes before and after exercise, and that the summated amplitude of R in $V_5$ plus S in $V_1$ in athletes was also $38.74{\pm}2.71\;mm$ suggesting a left ventricular hypertrophy We should note that the PQ segment and ST segment amplitude were higher in athletes than in non-athletes, and they were decreased with exercise in both groups. In particular, the fact that amplitudes of QRS vector in frontal plane or in horizontal plane were significantly greater in athletes than in non-athletes may be an index in evaluating athletes.