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Author Nishimiya, Yusuke| Konuma, Toshimitsu| Tasaka, Ken| Sendo, Toshiaki|
Published Date 2012-08-01
Publication Title 岡山医学会雑誌
Volume volume124
Issue issue2
Content Type Journal Article
Author Nishii, Nobuhiro|
Published Date 2012-08-01
Publication Title 岡山医学会雑誌
Volume volume124
Issue issue2
Content Type Journal Article
Author Kataoka, Yuko| Fukushima, Kunihiro| Sugaya, Akiko| Nishizaki, Kazunori|
Published Date 2012-08-01
Publication Title 岡山医学会雑誌
Volume volume124
Issue issue2
Content Type Journal Article
Author Kimura, Yuji| Iwakawa, Kazuhide| Nishie, Manabu| Inagaki, Masaru| Iwagaki, Hiromi|
Published Date 2012-08-01
Publication Title 岡山医学会雑誌
Volume volume124
Issue issue2
Content Type Journal Article
Author Tanabe, Shunsuke| Shirakawa, Yasuhiro| Maeda, Naoaki| Ohara, Toshiaki| Noma, Kazuhiro| Sakurama, Kazufumi| Yanai, Hiroyuki| Yamatsuji, Tomoki| Naomoto, Yoshio| Fujiwara, Toshiyoshi|
Published Date 2012-08-01
Publication Title 岡山医学会雑誌
Volume volume124
Issue issue2
Content Type Journal Article
Author Ma, Shaobo|
Published Date 2012-08-01
Publication Title 岡山医学会雑誌
Volume volume124
Issue issue2
Content Type Journal Article
Author Nakao, Miyuki|
Published Date 2012-08-01
Publication Title 岡山医学会雑誌
Volume volume124
Issue issue2
Content Type Journal Article
Author Yagi, Takahito|
Published Date 2012-08-01
Publication Title 岡山医学会雑誌
Volume volume124
Issue issue2
Content Type Journal Article
Author Doihara, Hiroyoshi|
Published Date 2012-08-01
Publication Title 岡山医学会雑誌
Volume volume124
Issue issue2
Content Type Journal Article
Author Hayashi, Keiichiro| Ohmori, Iori| Matsui, Hideki|
Published Date 2012-08-01
Publication Title 岡山医学会雑誌
Volume volume124
Issue issue2
Content Type Journal Article
Author Wang, Feifei| Yasuhara, Takao| Kameda, Masahiro| Date, Isao|
Published Date 2012-08-01
Publication Title 岡山医学会雑誌
Volume volume124
Issue issue2
Content Type Journal Article
Author Sasaki, Tsuyoshi| Tazawa, Hiroshi| Hasei, Jo| Kunisada, Toshiyuki| Yoshida, Aki| Hashimoto, Yuuri| Yano, Shuya| Yoshida, Ryosuke| Uno, Futoshi| Kagawa, Shunsuke| Morimoto, Yuki| Urata, Yasuo| Fujiwara, Toshiyoshi| Ozaki, Toshifumi|
Published Date 2012-08-01
Publication Title 岡山医学会雑誌
Volume volume124
Issue issue2
Content Type Journal Article
Author Fujimura, Atsushi| Tomizawa, Kazuhito| Matsui, Hideki|
Published Date 2012-08-01
Publication Title 岡山医学会雑誌
Volume volume124
Issue issue2
Content Type Journal Article
Author Nagai, Yusuke|
Published Date 2012-02
Publication Title Biomaterials
Volume volume33
Issue issue4
Content Type Journal Article
JaLCDOI 10.18926/AMO/48569
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
JaLCDOI 10.18926/AMO/48567
FullText URL 66_3_271.pdf
Author Lee, Shin-Wha| Kim, Yong-Man| Kim, Moon-Bo| Kim, Dae-Yeon| Kim, Jong-Hyeok| Nam, Joo-Hyun| Kim, Young-Tak|
Abstract The choice of chemotherapeutic drugs to treat patients with epithelial ovarian cancer has not depended on individual patient characteristics. We have investigated the correlation between in vitro chemosensitivity, as determined by the histoculture drug response assay (HDRA), and clinical responses in epithelial ovarian cancer. Fresh tissue samples were obtained from 79 patients with epithelial ovarian cancer. The sensitivity of these samples to 11 chemotherapeutic agents was tested using the HDRA method according to established methods, and we analyzed the results retrospectively. HDRA showed that they were more chemosensitive to carboplatin, topotecan and belotecan, with inhibition rates of 49.2%, 44.7%, and 39.7%, respectively, than to cisplatin, the traditional drug of choice in epithelial ovarian cancer. Among the 37 patients with FIGO stage Ⅲ/Ⅳ serous adenocarcinoma who were receiving carboplatin combined with paclitaxel, those with carboplatin-sensitive samples on HDRA had a significantly longer median disease-free interval than patients with carboplatin- resistant samples (23.2 vs. 13.8 months, p<0.05), but median overall survival did not differ significantly (60.4 vs. 37.3 months, p=0.621). In conclusion, this study indicates that HDRA could provide useful information for designing individual treatment strategies in patients with epithelial ovarian cancer.
Keywords chemosensitivity carboplatin HDRA (histoculture drug response assay) epithelial ovarian cancer
Amo Type Original Article
Publication Title Acta Medica Okayama
Published Date 2012-06
Volume volume66
Issue issue3
Publisher Okayama University Medical School
Start Page 271
End Page 277
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 22729108
Web of Science KeyUT 000305669700011
JaLCDOI 10.18926/AMO/48566
FullText URL 66_3_263.pdf
Author Sasaki, Takanori| Kuroda, Masahiro| Katashima, Kazunori| Ashida, Masakazu| Matsuzaki, Hidenobu| Asaumi, Junichi| Murakami, Jun| Ohno, Seiichiro| Kato, Hirokazu| Kanazawa, Susumu|
Abstract The roles of cell density, extracellular space, intracellular factors, and apoptosis induced by the molecularly targeted drug rituximab on the apparent diffusion coefficient (ADC) values were investigated using bio-phantoms. In these bio-phantoms, Ramos cells (a human Burkittセs lymphoma cell line) were encapsulated in gellan gum. The ADC values decreased linearly with the increase in cell density, and declined steeply when the extracellular space became less than 4 μm. The analysis of ADC values after destruction of the cellular membrane by sonication indicated that approximately 65% of the ADC values of normal cells originate from the cell structures made of membranes and that the remaining 35% originate from intracellular components. Microparticles, defined as particles smaller than the normal cells, increased in number after rituximab treatments, migrated to the extracellular space and significantly decreased the ADC values of bio-phantoms during apoptosis. An in vitro study using bio-phantoms was conducted to quantitatively clarify the roles of cellular factors and of extracellular space in determining the ADC values yielded by tumor cells and the mechanism by which apoptosis changes those values.
Keywords apparent diffusion coefficient value cell density extracellular space bio-phantom
Amo Type Original Article
Publication Title Acta Medica Okayama
Published Date 2012-06
Volume volume66
Issue issue3
Publisher Okayama University Medical School
Start Page 263
End Page 270
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 22729107
Web of Science KeyUT 000305669700010
JaLCDOI 10.18926/AMO/48565
FullText URL 66_3_253.pdf
Author Zhang, Kai| Yamamoto, Yumiko| Suzuki, Tomonori| Yokota, Kenji| Ma, Shaobo| Nengah Dwi Fatmawati, Ni| Oguma, Keiji|
Abstract Cultured Clostridium botulinum strains produce progenitor toxins designated as 12S, 16S, and 19S toxins. The 12S toxin consists of a neurotoxin (NTX, 7S) and a non-toxic non-hemagglutinin (NTNH). The 16S and 19S toxins are formed by conjugation of the 12S toxin with hemagglutinin (HA), and the 19S toxin is a dimer of the 16S toxin. Type A cultures produce all 3 of these progenitor toxins, while type E produces only the 12S toxin. The 7S toxin is cleaved into heavy (H) and light (L) chains by a protease(s) in some strains, and the H chain has 2 domains, the N-terminus (Hn) and C-terminus (Hc). It has been reported that type A toxins bind to the intestinal cells or cultured cells via either HA or Hc. In this study, we investigated the binding of type A and E toxins to Caco-2 cells using Western blot analysis. Both the type E 7S and 12S toxins bound to the cells, with the 7S toxin binding more strongly, whereas, in the type A strain, only the 16S/19S toxins showed obvious binding. Pre-incubation of the type E 7S toxin with IgG against recombinant type E Hc significantly inhibited the 7S toxin binding, indicating that Hc might be a main binding domain of the type E toxin.
Keywords Clostridum botulinum neurotoxins Caco-2 binding Hc
Amo Type Original Article
Publication Title Acta Medica Okayama
Published Date 2012-06
Volume volume66
Issue issue3
Publisher Okayama University Medical School
Start Page 253
End Page 261
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 22729106
Web of Science KeyUT 000305669700009
Related Url http://ousar.lib.okayama-u.ac.jp/metadata/48451
JaLCDOI 10.18926/AMO/48564
FullText URL 66_3_245.pdf
Author Okada, Toshiaki| Takigawa, Nagio| Kishino, Daizo| Katayama, Hideki| Kuyama, Shouichi| Sato, Ken| Mimoto, Junko| Ueoka, Hiroshi| Tanimoto, Mitsune| Kiura, Katsuyuki|
Abstract Cisplatin is used to treat lung cancer;however, it is also a known carcinogen. Cyclooxygenase-2 (COX-2) inhibitors have been shown to prevent carcinogen-induced experimental tumors. We investigated the effect of a COX-2 inhibitor, celecoxib, on cisplatin-induced lung tumors. One hundred twenty 4-week-old A/J mice were divided into 6 groups:group 1, no treatment;group 2, low-dose celecoxib (150mg/kg);group 3, high-dose celecoxib (1,500mg/kg);group 4, cisplatin alone;group 5, cisplatin plus low-dose celecoxib;and group 6, cisplatin plus high-dose celecoxib. Mice in groups 4-6 were administered cisplatin (1.62mg/kg, i.p.) once a week for 10 weeks between 7 and 16 weeks of age. All mice were sacrificed at week 30. Tumor incidence was 15.8% in group 1, 25% in group 2, 26.3% in group 3, 60% in group 4, 50% in group 5, and 50% in group 6. Tumor multiplicity was 0.2, 0.3, 0.3, 1.3, 1.0, and 0.6 in groups 1-6, respectively. Tumor multiplicity in the cisplatin-treated mice was reduced by celecoxib treatment in a dose-dependent manner (p<0.05, group 4 vs. group 6). Celecoxib significantly reduced COX-2 expression in cisplatin-induced tumors (p<0.01, group 4 vs. group 6).
Keywords cisplatin non-small cell lung cancer celecoxib cyclooxygenase-2 chemoprevention
Amo Type Original Article
Publication Title Acta Medica Okayama
Published Date 2012-06
Volume volume66
Issue issue3
Publisher Okayama University Medical School
Start Page 245
End Page 251
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 22729105
Web of Science KeyUT 000305669700008
JaLCDOI 10.18926/AMO/48563
FullText URL 66_3_239.pdf
Author Sawa, Kiminari| Mizushima, Takaaki| Matsushita, Koki| Shirahige, Akinori| Ochi, Koji| Koide, Norio|
Abstract Plain abdominal radiography is a very basic examination and plays an important role in primary care. The objectives of this study were to clarify colon distributions on plain abdominal radiographs. Forty-three healthy volunteers underwent gastric fluoroscopy, and 2 hours later, plain abdominal radiography in the supine position. A region of interest (ROI) was defined uniformly on each X-ray image to divide the image into 600 zones. The area corresponding to the large bowel within the ROI was divided into 4 segments (ascending colon, transverse colon, descending colon, and sigmoid colon+rectum). The percentage of barium in each segment relative to the total volume of barium used was calculated to evaluate the percent ROI occupancy. The large bowel covered 76.7% of the entire ROI, with the percent duplication being 55%. The duplicated area corresponded to the transverse colon region. When the method proposed by Arhan et al. was used, the percentage of the colon actually present in each segment relative to that determined theoretically was 99.6% for the right colon segment, 92.2% for the left colon segment, and 92.2% for the sigmoid/rectal segment. However, in cases in which the transverse colon descended partially from the fifth lumbar vertebra, the percentage occupied by the sigmoid colon+rectum decreased to 57.2%. We applied a new large bowel segmentation method especially for patients with ptosis, by devising a line joining the lateral side of the right lesser pelvis and the lower ends of both sacroiliac joints.
Keywords large bowel segmentation plain abdominal radiograph classification method primary care
Amo Type Original Article
Publication Title Acta Medica Okayama
Published Date 2012-06
Volume volume66
Issue issue3
Publisher Okayama University Medical School
Start Page 239
End Page 244
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 22729104
Web of Science KeyUT 000305669700007
Related Url http://ousar.lib.okayama-u.ac.jp/metadata/48881