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Takeshi Ueda

Publications and source records attributed to Takeshi Ueda.

40 records · Page 3Linked to original sources

Measurement of ventilatory threshold by respiratory frequency.

This study was conducted to assess whether respiratory frequency can be used as a valid parameter for estimating ventilatory threshold and for examining differences in exercise modes such as a cycle ergometer and a treadmill. 24 men and 12 women performed an incremental exercise test to exhaustion on a cycle ergometer and on a treadmill. Oxygen uptake, carbon dioxide output, pulmonary ventilation, ventilatory frequency, and heart rate were measured continuously every 30 sec. during the test. Three different and independent reviewers detected the ventilatory threshold point and break point of respiratory rate, which were then compared. Analysis indicated that (1) ventilatory threshold was well correlated with break point of respiratory rate for both cycle (r=.88, p<.001) and treadmill exercise (r=.96, p<.001). However, on the average, ventilatory threshold was only 71% (cycle) or 88% (treadmill) of break point of respiratory rate. (2) The regression equation for treadmill exercise was more accurate than that for cycling, but the detected data samples were smaller. The break point of respiratory rate was more easily detected for the cycle ergometer test 33 of 36 subjects) than for the treadmill test (only 15 of 36). The cycle ergometer test identified the break point of respiratory rate more easily than did the treadmill test. (3) There was an association between physical fitness and whether the break point of respiratory rate was detectable, and the more fit the subject (above average), the more likely the break point was to be undetected. Our study demonstrates that the break point of respiratory rate is closely associated with ventilatory threshold and that the cycle ergometer test is more conducive than the treadmill test to the detectability of break point of respiratory rate.

Adolescent↗

Suppression of metastasis of rat prostate cancer by introduction of human chromosome 13.

AIM: Chromosome 13 is one of the most frequently altered chromosomes in prostate cancer. The present study was undertaken to examine the role of human chromosome 13 in the progression of prostate cancer. METHODS: Human chromosome 13 was introduced into highly metastatic rat prostate cancer cells via microcell-mediated chromosome transfer. RESULTS: Microcell hybrid clones containing human chromosome 13 showed suppression of metastasis to the lung without any suppression of tumorigenicity, except for one clone, which contained the smallest sized human chromosome 13 and did not show any suppression on lung metastasis. Expression of two known tumor suppressor genes, BRCA2 and RB1, which map to chromosome 13, was examined by reverse transcription- polymerase chain reaction analysis. BRCA2 was expressed only in the metastasis-suppressed microcell-hybrid clones, whereas RB1 was expressed in all clones. CONCLUSION: Human chromosome 13 contains metastasis suppressor gene(s) for prostate cancer derived from rat. Furthermore, the RB1 gene is unlikely to be involved in the suppression of metastasis evident in this system.

Animals↗

Activation of the androgen receptor N-terminal domain by interleukin-6 via MAPK and STAT3 signal transduction pathways.

The androgen receptor (AR) is a ligand-activated transcription factor that mediates the biological responses of androgens. However, non-androgenic pathways have also been shown to activate the AR. The mechanism of cross-talk between the interleukin-6 (IL-6) and AR signal transduction pathways was investigated in LNCaP human prostate cancer cells. IL-6 induced several androgen-response element-driven reporters that are dependent upon the AR, increased the phosphorylation of mitogen-activated protein kinase (MAPK), and activated the AR N-terminal domain (NTD). Inhibitors to MAPK and JAK decreased the IL-6-induced phosphorylation of MAPK and activation of the AR NTD. Immunoprecipitation and transactivation studies showed a direct interaction between amino acids 234-558 of the AR NTD and STAT3 following IL-6 treatment of LNCaP cells. These results demonstrate that activation of the human AR NTD by IL-6 was mediated through MAPK and STAT3 signal transduction pathways in LNCaP prostate cancer cells.

Amino Acids↗