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Articles by Y Imai
Total Records ( 3 ) for Y Imai
  T Masamune , H Sato , K Okuyama , Y Imai , H Iwashita , T Ishiyama , T Oguchi , D. I Sessler and T. Matsukawa
 

BACKGROUND: JM-1232(–) is a novel isoindoline derivative which shows sedative and hypnotic activities through the benzodiazepine site of -aminobutyric acid type A (GABAA) receptors. Typical doses of midazolam, another GABAA receptor agonist, slightly reduce the shivering threshold in humans. We thus determined the extent to which JM-1232(–) decreases the shivering threshold.

METHODS: Eighteen rabbits, lightly anesthetized with isoflurane 0.2 minimum alveolar anesthetic concentration (MAC), were randomly assigned to infusions of 1) saline (control), 2) 0.01 mg · kg–1 · min–1 JM-1232(–), or 3) 0.1 mg · kg–1 · min–1 JM-1232(–). Body temperature was reduced at a rate of 2-3°C/h by perfusing water at 10°C though a U-shaped plastic tube positioned in the colon. Cooling continued until shivering was observed by an investigator blinded to treatment, or until core temperature reached 34°C. Core temperatures were recorded from the distal esophagus, and core temperature at the onset of shivering defined the threshold. Data were analyzed by one-way analysis of variance with Student-Newman-Keuls tests. Results are presented as means ± sd; P < 0.05 was considered statistically significant.

RESULTS: The rabbits given a saline infusion shivered at 36.5 ± 0.3°C. Five of the six rabbits given JM-1232(–) at a rate of 0.01 mg · kg–1 · min–1 shivered at 35.7 ± 0.8°C, and one of these rabbits failed to shiver at 34.0°C. None of the rabbits given JM-1232(–) at a rate of 0.1 mg · kg–1 · min–1 shivered before reaching the 34.0°C cutoff temperature.

CONCLUSION: A low dose of JM-1232(–) reduced the shivering threshold in rabbits approximately 0.8°C which is similar to the effects in humans given premedication doses of midazolam. In contrast, a 10-fold larger dose reduced the threshold more than 2.5°C. This is a substantial decrement and might facilitate induction of therapeutic hypothermia.

  M Kuroda Morimoto , H Tanaka , N Hayashi , M Nakahira , Y Imai , M Imamura , K Yasuda , S Yumikura Futatsugi , K Matsui , T Nakashima , K Sugimura , H Tsutsui , H Sano and K. Nakanishi
 

We previously reported that intranasal challenge with ovalbumin (OVA) plus IL-18 induces airway hyperresponsiveness (AHR) and eosinophilic airway inflammation in mice with OVA-specific Th1 cells. These two conditions can be prevented by neutralizing anti-IFN- and anti-IL-13 antibodies, respectively. The mice develop AHR and eosinophilic airway inflammation after challenge with OVA plus LPS instead of IL-18 and endogenous IL-18 is known to be involved. In contrast, IL-18 does not facilitate these changes in mice possessing OVA-specific Th2 cells. Here, we investigated whether IL-18 is involved in the development of asthma in mice immunized and challenged with bacterial proteins. Upon intranasal exposure to protein A (SpA) derived from Staphylococcus aureus, mice immunized with SpA exhibited AHR and peribronchial eosinophilic inflammation if IFN- or IL-13 were present, respectively. The CD4+ T cells from draining lymph nodes (DLNs) of the SpA-immunized and -challenged mice produced a robust IFN- and IL-13 in response to immobilized anti-CD3 antibodies. Treatment with neutralizing anti-IL-18 antibodies prevented asthmatic inflammation concomitant with their impaired potential to express IFN- and IL-13. Furthermore, naive mice that received the CD4+ T cells from DLNs of SpA-immunized mice developed airway inflammation depending upon the presence of IL-18. Immunodeficient mice that received human PBMCs, which had been stimulated with SpA in vitro, developed dense peribronchial accumulation of human CD4+ T cells upon SpA challenge. Neutralizing anti-human IL-18 antibodies protected against this airway inflammation. These results suggest the importance of IL-18 for the development of asthmatic inflammation associated with airway exposure to bacterial proteins.

  Y Imai , S Kondoh , A Kouzmenko and S. Kato
 

The osteoprotective action of estrogen in women has drawn considerable attention because estrogen deficiency-induced osteoporosis became one of the most widely spread diseases in developed countries. In men, the significance of estrogen action for bone health maintenance is also apparent from the osteoporotic phenotype seen in male patients with genetically impaired estrogen signaling. Severe bone loss and high bone turnover, including typical osteofeatures seen in postmenopausal women, can also be recapitulated in rodents after ovariectomy. However, the expected osteoporotic phenotype is not observed in female mice deficient in estrogen receptor (ER)- or -β or both, even though the degenerative defects are clearly seen in other estrogen target tissues together with up-regulated levels of circulating testosterone. It has also been reported that estrogens may attenuate bone remodeling by cell autonomous suppressive effects on osteoblastogenesis and osteoclastogenesis. Hence, the effects of estrogens in bone appear to be complex, and the molecular role of bone estrogen receptors in osteoprotective estrogen action remains unclear. Instead, it has been proposed that estrogens indirectly control bone remodeling. For example, the enhanced production of cytokines under estrogen deficiency induces bone resorption through stimulation of osteoclastogenesis. However, the osteoporotic phenotype without systemic defects has been recapitulated in female (but not in male) mice by osteoclast-specific ablation of the ER, proving that bone cells represent direct targets for estrogen action. An aberrant accumulation of mature osteoclasts in these female mutants indicates that in females, the inhibitory action of estrogens on bone resorption is mediated by the osteoclastic ER through the shortened lifespan of osteoclasts.

 
 
 
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