巻号一覧
55 巻, 4 号
選択された号の論文の5件中1～5を表示しています
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Regular Papers
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Shu-Ming Chen, Cheng-Deng Kuo, Low-Tone Ho, Jyh-Fei Liao2005 年 55 巻 4 号 p. 211-219
発行日: 2005年
公開日: 2006/01/28
[早期公開] 公開日: 2005/10/29ジャーナル フリーBoth hypothyroid (Hypo) and hypozincemia are commonly observed in patients and animals with chronic renal failure (CRF). In CRF whether the hypothyroid plays a role in the pathogenesis of hypozincemia is unclear. This study is designed to investigate the effects of hypothyroid on intestinal zinc absorption and urinary zinc excretion in 5/6 nephrectomized (Nx) rats, because plasma zinc balance is attained through a controlled rate of intestinal uptake as well as renal reabsorption. Intestinal zinc absorption was carried out in jejunum and ileum segments by an in vivo perfusion technique and the renal zinc disposal was evaluated by a conventional method using a standard formula to calculate the zinc tubular reabsorption and the excretion of urinary zinc in 5/6 Nx rats with hypothyroidism. The Hypo-NxT rats showed a significant decrease in the rate of intestinal zinc absorption and in the response of plasma zinc levels during intestinal zinc perfusion compared with Eu-NxT rats. They also had significantly lower levels of mucosal zinc and MT as well as lower content of liver zinc than Eu-NxT rats after intestinal zinc perfusion for 80 min. Hypo-NxT rats showed low plasma zinc levels, but had a similar output of pancreaticobiliary zinc and excretion of 24-h urine zinc compared with the Eu-NxT rats. When 2% alcohol intestinal perfusion was used to produce water diuresis, the Hypo-NxT rats presented a higher excretion of urinary zinc than the Eu-NxT rats did, especially during 2% alcohol intestinal zinc perfusion. In the Hypo-NxT rats, the lower plasma zinc levels may thus result from the hypothyroid because it reduces intestinal zinc absorption. Increasing the urine flow rate may aggravate the reduction of plasma zinc level in Hypo-NxT rats because of the increased excretion of urinary zinc.
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Meng Cao, Long Chen, Xiao Xiao Shan, Shuang Quan Zhang2005 年 55 巻 4 号 p. 221-227
発行日: 2005年
公開日: 2006/01/28
[早期公開] 公開日: 2005/10/29ジャーナル フリーThe B cell activating factor of the TNF family (BAFF, also known as BLyS, TALL-1, THANK, and zTNF4) is an important survival factor for B lymphocytes. Our previous study has demonstrated that the final purified material of human soluble BAFF (refolded hsBAFF) synthesized in Escherichia coli is biologically active in a validated induced human B lymphocyte proliferation bioassay. In this study, the administration of refolded hsBAFF to isolated mouse B lymphocytes and mice was carried out to study the immunological effects of hsBAFF on in vitro and in vivo B lymphocytes. The results showed that splenic B lymphocyte proliferation significantly increased after hsBAFF administration (in vitro 1, 2, 3, 5 µg/ml and in vivo 0.01, 0.5, 1.0 mg/kg body mass). An oppositely elevated immune response of B lymphocyte to LPS stimulation after hsBAFF administration (1, 2.5, 5 µg/ml) and a significantly elevated change after treatment with hsBAFF and costimulation with anti-IgM (2.5 µg/ml) was observed in vitro, respectively. A similar change existed also in hsBAFF-treated mice on the 8th postexperiment day, but the value with anti-IgM alone didn't increase compared to normal control in vitro. We found that the treatment of mice with hsBAFF resulted in a developmental maturation of T1 B lymphocytes to T2 and mature B lymphocytes by detecting distributions of splenic CD21lo with CD45R/B220+ and CD21hi with CD45R/B220+ subsets. These results suggest that the refolded hsBAFF synthesized in Escherichia coli may enhance immune responses in the body by regulating the proliferation, differentiation, and immune response of B lymphocytes.
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Short Communications
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Shuang Gao, Kunihiko Tanaka, Taro M. Gotoh, Hironobu Morita2005 年 55 巻 4 号 p. 229-234
発行日: 2005年
公開日: 2006/01/28
[早期公開] 公開日: 2005/10/26ジャーナル フリーThe Na+ receptor that exists in the hepatoportal region plays an important role in postprandial natriuresis and the regulation of Na+ balance during NaCl load. Thus it would be considered that a dysfunction of the hepatic Na+ receptor might result in the elevation of arterial pressure under a condition of high NaCl diet. To elucidate this hypothesis, arterial pressure was continuously measured during three weeks of high NaCl diet (8% NaCl) in four groups of rats: (i) intact rats, (ii) rats with hepatic denervation (HD), (iii) rats with sinoaortic denervation (SAD), and (iv) rats with SAD+HD. During a 1-week normal NaCl diet period, there was no difference in arterial pressure among the four groups. A high NaCl diet had no influence on arterial pressure in intact or HD rats; however, it significantly increased by 11 ± 3 mmHg in SAD rats. The addition of HD to SAD had no synergistic effect on arterial pressure; i.e., in SAD+HD rats, mean arterial pressure increased by 13 ± 1 mmHg. In conclusion, sinoaortic baroreceptor, but not hepatic Na+ receptor, has a significant role in the long-term regulation of arterial pressure on a high NaCl diet.
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Koichiro Hayashi, Jun Sugawara, Hidehiko Komine, Seiji Maeda, Takashi ...2005 年 55 巻 4 号 p. 235-239
発行日: 2005年
公開日: 2006/01/28
[早期公開] 公開日: 2005/10/27ジャーナル フリーAortic pulse wave velocity (PWV) significantly decreased after 16 weeks of moderate-intensity exercise training (walking/jogging) in 17 sedentary middle-aged men, whereas leg PWV did not. These results suggest that in contrast with central arterial stiffness, peripheral arterial stiffness is difficult to change with aerobic exercise training.
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Technical Note
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Michael J. Buono, Paul W. Miller, Clifford Hom, Robert S. Pozos, Fred ...2005 年 55 巻 4 号 p. 241-244
発行日: 2005年
公開日: 2006/01/28
[早期公開] 公開日: 2005/10/04ジャーナル フリーSkin blood flow affects NIRS. Leg skin blood flow (SkBF) was increased and decreased following local heating and intradermal epinephrine injection. Epinephrine decreased muscle saturation (StO2), and heating the leg increased StO2. The results suggest that changes in SkBF can significantly affect resting StO2 as measured by near-infrared tissue spectroscopy.
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