JaLCDOI | 10.18926/AMO/48569 |
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FullText URL | 66_3_285.pdf |
Author | Mizobuchi, Satoshi| Matsuoka, Yoshikazu| Obata, Norihiko| Kaku, Ryuji| Itano, Yoshitaro| Tomotsuka, Naoto| Taniguchi, Arata| Nishie, Hiroyuki| Kanzaki, Hirotaka| Ouchida, Mamoru| Morita, Kiyoshi| |
Abstract | Perioperative beta-blocker administration has recently been recommended for patients undergoing cardiac or other surgery due to the beneficial cardiovascular effects of these agents. In addition, some studies have reported that perioperatively administered beta-blockers also have analgesic effects. In this study, to investigate the antinociceptive effects and the analgesic profile of landiolol, we examined the effects of intrathecal landiolol administration on nociceptive pain behavior and c-fos mRNA expression (a neural marker of pain) in the spinal cord using a rat formalin model. We found that pain-related behavior was inhibited by intrathecal landiolol administration. Moreover, the increase in c-fos mRNA expression on the formalin-injected side was less pronounced in rats administered landiolol than in saline administered controls. Thus, intrathecal administration of landiolol exhibited antinociceptive effects. Further investigation of the antinociceptive mechanism of landiolol is required. |
Keywords | beta-blocker landiolol formalin pain behavior c-fos |
Amo Type | Original Article |
Publication Title | Acta Medica Okayama |
Published Date | 2012-06 |
Volume | volume66 |
Issue | issue3 |
Publisher | Okayama University Medical School |
Start Page | 285 |
End Page | 289 |
ISSN | 0386-300X |
NCID | AA00508441 |
Content Type | Journal Article |
language | English |
Copyright Holders | CopyrightⒸ 2012 by Okayama University Medical School |
File Version | publisher |
Refereed | True |
PubMed ID | 22729110 |
Web of Science KeyUT | 000305669700013 |
Author | Nishie, Hiroyuki| Mizobuchi, Satoshi| Matsusaki, Takashi| Miyake, Asako| Kaku, Ryuji| Ishikawa, Shinichi| Sato, Kenji| Matsumi, Masaki| Kiyoshi, Morita| |
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Published Date | 2007-05-01 |
Publication Title | 岡山医学会雑誌 |
Volume | volume119 |
Issue | issue1 |
Content Type | Journal Article |
Author | Mizobuchi, Satoshi| |
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Published Date | 1994-10 |
Publication Title | 岡山医学会雑誌 |
Volume | volume106 |
Issue | issue9-10 |
Content Type | Journal Article |
JaLCDOI | 10.18926/AMO/54808 |
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FullText URL | 70_6_455.pdf |
Author | Tanino, Masaaki| Kobayashi, Motomu| Sasaki, Toshihiro| Takata, Ken| Takeda, Yoshimasa| Mizobuchi, Satoshi| Morita, Kiyoshi| Nagai, Taku| Morimatsu, Hiroshi| |
Abstract | Postoperative cognitive dysfunction (POCD) occurs in nearly one-third of patients after non-cardiac surgery. Many animal behavior studies have investigated the effect of general anesthesia on cognitive function. However, there have been no studies examining the effects on working memory specifically, with a focus on the retention of working memory. We demonstrate here that isoflurane anesthesia induces deficits in the retention of spatial working memory in rats, as revealed by an increase in isoflurane-induced across-phase errors in the delayed spatial win-shift (SWSh) task with a 30-min delay in an 8-arm radial arm maze on post-anesthesia days (PADs) 1,2,4, and 10. A post-hoc analysis revealed a significant increase in across-phase errors on PAD 1 and recovery on PAD 10 in the isoflurane group. In contrast, within-phase errors independent of the retention of working memory were unaffected by isoflurane. These results demonstrate that isoflurane anesthesia transiently impairs the retention of spatial working memory in rats. |
Keywords | postoperative cognitive dysfunction isoflurane spatial working memory retention delayed spatial win-shift task |
Amo Type | Original Article |
Publication Title | Acta Medica Okayama |
Published Date | 2016-12 |
Volume | volume70 |
Issue | issue6 |
Publisher | Okayama University Medical School |
Start Page | 455 |
End Page | 460 |
ISSN | 0386-300X |
NCID | AA00508441 |
Content Type | Journal Article |
language | English |
Copyright Holders | CopyrightⒸ 2016 by Okayama University Medical School |
File Version | publisher |
Refereed | True |
PubMed ID | 28003670 |
JaLCDOI | 10.18926/AMO/46627 |
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FullText URL | 65_3_163.pdf |
Author | Arai, Minako| Takata, Ken| Takeda, Yoshimasa| Mizobuchi, Satoshi| Morita, Kiyoshi| |
Abstract | The mechanism of oxygen toxicity for central nervous system and hyperbaric oxygen (HBO) seizure has not been clarified. Noradrenergic cells in the brain may contribute to HBO seizure. In this study, we defined the activation of noradrenergic cells during HBO exposure by c-fos immunohistochemistry. Electroencephalogram electrodes were pre-implanted in all animals under general anesthesia. In HBO seizure animals, HBO was induced with 5 atm of 100% oxygen until manifestation of general tonic convulsion. HBO non-seizure animals were exposed to 25 min of HBO. Control animals were put in the chamber for 120 min without pressurization. All animals were processed for c-fos immunohistochemical staining. All animals in the HBO seizure group showed electrical discharge on EEG. In the immunohistochemistry, c-fos was increased in the A1, A2 and A6 cells of the HBO seizure group, and in the A2 and A6 cells of the HBO non-seizure group, yet was extremely low in all three cell types in the control group. These results suggest the participation of noradrenaline in HBO seizure, which can be explained by the early excitement of A1 cells due to their higher sensitivity to high blood pressure, hyperoxia, or by the post-seizure activation of all noradrenergic cells. |
Keywords | hyperbaric oxygen seizure noradrenergic cells immunohistochemistry |
Amo Type | Original Article |
Publication Title | Acta Medica Okayama |
Published Date | 2011-06 |
Volume | volume65 |
Issue | issue3 |
Publisher | Okayama University Medical School |
Start Page | 163 |
End Page | 168 |
ISSN | 0386-300X |
NCID | AA00508441 |
Content Type | Journal Article |
language | English |
Copyright Holders | CopyrightⒸ 2011 by Okayama University Medical School |
File Version | publisher |
Refereed | True |
PubMed ID | 21709713 |
Web of Science KeyUT | 000292017500002 |
JaLCDOI | 10.18926/AMO/46628 |
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FullText URL | 65_3_169.pdf |
Author | Takeda, Masanori| Nagasaka, Takeshi| Dong-Sheng, Sun| Nishie, Hiroyuki| Oka, Tetsuhiro| Yamada, Eiji| Mori, Yoshiko| Shigeyasu, Kunitoshi| Morikawa, Tatsuya| Mizobuchi, Satoshi| Fujiwara, Toshiyoshi| |
Abstract | Secreted frizzled-related protein 2, (SFRP2) is a Wnt inhibitor whose promoter CpGs were recently found to be methylated at high frequency in colorectal cancers (CRCs). We hypothesized that the pattern of SFRP2 methylation may differ throughout the promoter during progressive tumorigenesis. Using combined bisulfite restriction analysis (COBRA), two methylation-sensitive regions (Regions A and B) of the SFRP2 promoter were investigated in 569 specimens of colorectal tissue:222 CRCs, 103 adenomatous polyps (APs), 208 normal colonic mucosa from CRC patients (N-Cs), and 36 normal colonic mucosa from subjects with no evidence of colorectal neoplasia at colonoscopy (N-Ns). Extensive (including both Regions A and B) and partial (either Region A or B) SFRP2 methylation levels were found in 61.7% and 24.8% of CRCs, 8.7% and 37.9% of APs, 3.9% and 39.9% of N-Cs, and 0% and 30.6% of N-Ns, respectively. Extensive methylation of the SFRP2 promoter was present primarily in CRCs, while partial methylation was common in APs. Whereas APs with the KRAS mutant showed no correlation to any pattern of SFRP2 methylation, extensive methylation of the SFRP2 promoter was significantly associated with KRAS mutant CRCs (p<.0001), suggesting that genetic alteration in the RAS-RAF pathway might precede the spread of CpG methylation through the SFRP2 promoter, which is observed in over 60% of advanced colorectal tumors. |
Keywords | BRAF/KRAS mutations promoter methylation colorectal cancer |
Amo Type | Original Article |
Publication Title | Acta Medica Okayama |
Published Date | 2011-06 |
Volume | volume65 |
Issue | issue3 |
Publisher | Okayama University Medical School |
Start Page | 169 |
End Page | 177 |
ISSN | 0386-300X |
NCID | AA00508441 |
Content Type | Journal Article |
language | English |
Copyright Holders | CopyrightⒸ 2011 by Okayama University Medical School |
File Version | publisher |
Refereed | True |
PubMed ID | 21709714 |
Web of Science KeyUT | 000292017500003 |
Author | Mizobuchi, Satoshi| |
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Published Date | 1994-09-30 |
Publication Title | |
Content Type | Thesis or Dissertation |