start-ver=1.4
cd-journal=joma
no-vol=101
cd-vols=
no-issue=3-4
article-no=
start-page=414
end-page=422
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1989
dt-pub=198904
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=第108回 岡山外科会
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=西本詮
kn-aut-sei=西本
kn-aut-mei=詮
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=101
cd-vols=
no-issue=3-4
article-no=
start-page=403
end-page=413
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1989
dt-pub=198904
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=第107回 岡山外科会
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=竹馬浩
kn-aut-sei=竹馬
kn-aut-mei=浩
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=101
cd-vols=
no-issue=3-4
article-no=
start-page=395
end-page=402
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1989
dt-pub=198904
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=第106回 岡山外科会
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=西本詮
kn-aut-sei=西本
kn-aut-mei=詮
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=101
cd-vols=
no-issue=3-4
article-no=
start-page=387
end-page=394
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1989
dt-pub=198904
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=The influence of HCO(3) -induced and CO(2) -induced pH changes on the action of non-depolarizing muscle relaxants in rats
kn-title=代謝性酸・塩基平衡の変化ならびに呼吸性酸・塩基平衡の変化が非脱分極性筋弛緩薬の作用に及ぼす影響に関する研究
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The influences of HCO(3)-induced and CO(2)-induced pH changes on the action of nondepolarizing muscle relaxants (MRs) were investigated using a rat phrenic nervehemidiaphragm preparation. Changes in pH were induced by varying HCO(3) concentration of the modified Krebs' solution (mK') or by varying the CO(2) concentration in the gas aerating the mK'. Changes in [Ca(++)] and [Mg(++)], associated with changes in HCO(3) concentration, were measured and corrected. A change in HCO(3) from 50mM to 13.5mM or a change in CO(2) from 2.5% to 9%, augmented the partial neromuscular blockade produced by d-Tc or vecuronium (p<0.01), while inhibiting that produced by metocurine or pancuronium (p<0.01). A change in HCO(3) from 13.5mM to 50mM or a change in CO(2) from 9% to 2.5%, inhibited the partial neuromuscular blockade produced by d-Tc or vecuronium (p<0.01), while augmenting that produced by metocurine or pancuronium (p<0.01). These findings suggest that the HCO(3)-induced and CO(2)-induced pH changes have a similar influence on the action of MRs. A difference exists between mono- and bisquaternary MRs with regard to their response to pH changes.
en-copyright=
kn-copyright=

en-aut-name=NaganoOsamu
en-aut-sei=Nagano
en-aut-mei=Osamu
kn-aut-name=長野修
kn-aut-sei=長野
kn-aut-mei=修
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部麻酔・蘇生学教室
en-keyword=非脱分極性筋弛緩薬
kn-keyword=非脱分極性筋弛緩薬
en-keyword=代謝性pH変化
kn-keyword=代謝性pH変化
en-keyword=呼吸性pH変化
kn-keyword=呼吸性pH変化
en-keyword=筋弛緩作用
kn-keyword=筋弛緩作用
END

start-ver=1.4
cd-journal=joma
no-vol=101
cd-vols=
no-issue=3-4
article-no=
start-page=379
end-page=385
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1989
dt-pub=198904
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Daily changes of lung guanidino compounds in rats in acute renal failure
kn-title=急性腎不全ラットにおける肺内グアニジノ化合物の経日的変化に関する実験的研究
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Renal failure causes various metabolic disorders, especially increases of uremic toxins. Of the uremic toxins, guanidino compounds have a main role in uremia. Although lung injury is often complicated by renal failure, the role of guanidino compounds in lung injury is obscure. I have studied the changes in guanidino compounds in the lung of rat with ischemic acute renal failure. Guanidino compounds increased the first day after ischemia, but methylguanidine, which is the most toxic guanidino compound, showed a delayed increase in the lung. These results suggest the de novo synthesis of methylguanidine in the lung. A guanidinogram may by useful to judge changes in guanidino compounds.
en-copyright=
kn-copyright=

en-aut-name=KosogabeYoshinori
en-aut-sei=Kosogabe
en-aut-mei=Yoshinori
kn-aut-name=香曽我部義則
kn-aut-sei=香曽我部
kn-aut-mei=義則
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部麻酔・蘇生学教室
en-keyword=急性腎不全
kn-keyword=急性腎不全
en-keyword=グアニジノ化合物
kn-keyword=グアニジノ化合物
en-keyword=メチルグアニジン
kn-keyword=メチルグアニジン
END

start-ver=1.4
cd-journal=joma
no-vol=101
cd-vols=
no-issue=3-4
article-no=
start-page=371
end-page=377
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1989
dt-pub=198904
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Metabolic changes of hepatic and renal guanidino compounds by inhalation of halothane in rats
kn-title=ハロセンによる肝腎グアニジノ化合物代謝の変動に関する実験的研究
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=A metabolic relationship between the liver and kidney exists in combination with the urea cycle. In patients with acute renal or hepatic insufficiency, certain variations among several guanidino compounds are relevant to the condition of the liver or kidney. An experimental model of rats exposed to inhaled halothane was evaluated for metabolic changes in the liver and kidney by measuring guanidino compound levels using high performance liquid chromatography. As a result, no significant difference in serum ornithine carbamoyltransferase (OCT) activities were observed among all groups. In the liver, concentrations of creatine (CR) and guanidinobutyric acid (GBA) were significantly elevated immediately after inhalation of halothane without any accompanying changes in guanidinoacetic acid (GAA) and argnine (ARG). In the kidney, ARG and GAA were significantly decreased without any accompanying changes in CR and GBA. No significant difference in serum GC levels was observed among the groups. The inhalation of halothane appers to change the concentrations of GAA, ARG and CR in the liver and kidney. It also appers that inhalation of halothane caused GBA to appear in the blood, indicating a possible association of halothane with hepatotoxicity.
en-copyright=
kn-copyright=

en-aut-name=KitauraMichio
en-aut-sei=Kitaura
en-aut-mei=Michio
kn-aut-name=北浦道夫
kn-aut-sei=北浦
kn-aut-mei=道夫
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部麻酔・蘇生学教室
en-keyword=ハロセン
kn-keyword=ハロセン
en-keyword=尿素回路
kn-keyword=尿素回路
en-keyword=アルギニン
kn-keyword=アルギニン
en-keyword=肝腎代謝
kn-keyword=肝腎代謝
END

start-ver=1.4
cd-journal=joma
no-vol=101
cd-vols=
no-issue=3-4
article-no=
start-page=363
end-page=369
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1989
dt-pub=198904
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=An experimental study of nitrogen metabolism in acute hepatic failure (Changes in guanidinoacetic acid level and kidney glycine amidinotransferase activity)
kn-title=急性肝不全時の窒素代謝に関する基礎的研究―クアニジノ酢酸および腎グリシンアミヂノトランスフェラーゼ活性の変動―
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=It was reported that serum guanidinoacetic acid (GAA) levels are elevated in acute hapatic failure. To explore the mechanism of this GAA level change, the activities of kidney glycine amidinotransferase (GAT) and liver GAA-methyltransferase (GAA-MT) were measured in experimental rat models of acute hepatic failure. GAA is synthesized by the former enzyme and catabolized by the latter enzyme. In the early stage, kidney GAT activity was increased (P<0.1) but the serum GAA level remained normal. In the late stage, liver GAA-MT activity was decreased (P<0.01) and serum GAA level was increased. From this result, it is concluded that GAA synthesis is increased in acute hepatic failure and that serum GAA level is increased when liver is severely damaged.
en-copyright=
kn-copyright=

en-aut-name=KabutanKoji
en-aut-sei=Kabutan
en-aut-mei=Koji
kn-aut-name=株丹浩二
kn-aut-sei=株丹
kn-aut-mei=浩二
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部麻酔・蘇生学教室
en-keyword=急性肝不全
kn-keyword=急性肝不全
en-keyword=グアニジノ酢酸
kn-keyword=グアニジノ酢酸
en-keyword=グリシンアミヂノトランスフェラーゼ
kn-keyword=グリシンアミヂノトランスフェラーゼ
END

start-ver=1.4
cd-journal=joma
no-vol=101
cd-vols=
no-issue=3-4
article-no=
start-page=327
end-page=345
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1989
dt-pub=198904
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Correlation of EEG analysis and Parkinsonism
kn-title=パーキンソニズムの頭皮上と深部脳波の相関分析
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Scalp and depth EEG were obtained during thalamotomy in 19 Parkinsonian patients, and a correlation analysis was performed to demonstrate additional information. 1) The decrease in mean frequency of alpha and increase in theta activity constituted a characteristic feature in Parkinsonism. The degree of these findings was closely related to the progression of the disease. 2) Simultaneous recordings in the thalamus and the scalp tended to show approximate spectral values in mild cases, but demonstrated some differences as the disease progressed. 3) Comparison of scalp and thalamic recordings revealed the existence of coincident and independent alpha activities in each area. 4) Cross-correlation analysis of the scalp EEG revealed that there were some progessive changes in phase relationships, including advance of activities from the front and delay of from the occiput with phase shifts over 90°. 5) Travelling waves were also found in the depth EEG, and the direction was from the thalamus to the cortex in some cases, but reversed in others. The phase shifts of alpha activities between the scalp and the thalamus were from 10° to 90°. From these values, the conduction velocity of the spreading alpha were from 2.4m/s to 21.6m/s.
en-copyright=
kn-copyright=

en-aut-name=TanigawaMasahiro
en-aut-sei=Tanigawa
en-aut-mei=Masahiro
kn-aut-name=谷川雅洋
kn-aut-sei=谷川
kn-aut-mei=雅洋
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部脳神経外科学教室
en-keyword=Parkinsonism
kn-keyword=Parkinsonism
en-keyword=Depth EEG
kn-keyword=Depth EEG
en-keyword=Alpha activity Correlation analysis
kn-keyword=Alpha activity Correlation analysis
en-keyword=Travelling wave
kn-keyword=Travelling wave
END

start-ver=1.4
cd-journal=joma
no-vol=101
cd-vols=
no-issue=3-4
article-no=
start-page=315
end-page=325
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1989
dt-pub=198904
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Modification of intracellular uptake and killing effect of Adriamycin (ADR) by cepharanthine on ADR resistant Ehrlich ascites tumor cells
kn-title=Ehrlich腹水癌細胞の薬剤耐性細胞における温熱によるAdriamycinの効果増強とその修飾
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Adriamycin (ADR) is a well known anticancer agent which is frequently used alone or combination with other anticancer agents. An ADR-resistant cell line derived from Ehrlich ascites tumor cells (EATC) was established in our laboratory. In this report, differences between wild EATC and ADR resistant EATC were studied. The intracellular ADR uptake increased at a temperature (41.0°C) that had a little effect on the viability of wild EATC. The intracellular ADR uptake of ADR-resistant EATC also increased at elevated temperature (41.0°C). However, ADR resistant EATC had an enhanced acquired capacity that increased the efflux of intracellular ADR. Cepharanthine (CP), 1mcg/ml, inhibited the efflux of intracellular ADR and maintained the retention of ADR at high levels in cells from both cell lines, so the killing effects were enhanced with a combination ADR and CP. From these results, the mechanisms of resistance to ADR may be discussed. The killing effects of ADR depend on intracellular ADR uptake, retention and maintenance. Hyperthermic treatment accelerates the influx of ADR. In addition, CP suppresses the efflux of intracellular ADR, and increased markedly the cytotoxic effect of ADR on ADR resistant EATC. The combination of ADR, CP and hyperthermia may be effective and useful therapy to overcome ADR-resistant cancer cells.
en-copyright=
kn-copyright=

en-aut-name=KashitaniNaoko
en-aut-sei=Kashitani
en-aut-mei=Naoko
kn-aut-name=柏谷尚子
kn-aut-sei=柏谷
kn-aut-mei=尚子
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部放射線医学教室
en-keyword=Ehrlich腹水癌細胞
kn-keyword=Ehrlich腹水癌細胞
en-keyword=Adriamycin
kn-keyword=Adriamycin
en-keyword=Hyperthermia
kn-keyword=Hyperthermia
en-keyword=Multidrug resistance
kn-keyword=Multidrug resistance
en-keyword=Flow cytometry
kn-keyword=Flow cytometry
END

start-ver=1.4
cd-journal=joma
no-vol=101
cd-vols=
no-issue=3-4
article-no=
start-page=303
end-page=314
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1989
dt-pub=198904
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Modification by hyperthermia and cepharanthine of the Killing effect of adriamycin on NIH 3T3 cells
kn-title=Adriamycinの殺細胞効果の加温およびCepharanthineによる修飾
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The cytotoxic effect of anticancer agents depends markedly on the intracellular uptake of the anticancer drug; its maintenance is increased by accelerating the intracellular uptake of anticancer agent and inchbiting. Using with flow-cytometry, we demonstrated that the intracellular uptake of adriamycin (ADM) is increased by hyperthermia, and that cepharanthine (CEP) and Verapamil inhibit its retention. We investigated the cytotoxic effect of the combination of ADR, CEP and hyperthermia, using a NIH3T3 cell line. The cytotoxic effect of ADR is increased by hyperthermia; its effect is acquired at a lower temperature which has no cytotoxic effect alone. With the conbination of CEP, ADR and hyperthermia, the cytotoxic effect is further increased. The synergism is increased by the elevation of temperature and a long of exposure time of CEP. The increase of the intracellular accumulation anticanceragent is important to overcome multidrugresistance, a phenomenon which has that attracted agreat deal of attention.
en-copyright=
kn-copyright=

en-aut-name=MizutaAkifumi
en-aut-sei=Mizuta
en-aut-mei=Akifumi
kn-aut-name=水田昭文
kn-aut-sei=水田
kn-aut-mei=昭文
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部放射線医学教室
en-keyword=Adriamycin
kn-keyword=Adriamycin
en-keyword=cepharantine
kn-keyword=cepharantine
en-keyword=加温
kn-keyword=加温
en-keyword=殺細胞効果
kn-keyword=殺細胞効果
END

start-ver=1.4
cd-journal=joma
no-vol=101
cd-vols=
no-issue=3-4
article-no=
start-page=295
end-page=302
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1989
dt-pub=198904
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Improvement of head magnetic resonance image quality
kn-title=頭部MRI像の画質改善について
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The purpose of this study is to present a method of boundary enhancement algorithms for magnetic resonance images using a V-filter and clinical applications. By iterated V-filtering, the signal-to-noise ratio can be increased with preservation of edge sharpness. This is due to the relationship of the signal-to-noise ratio to the mean-to-variance ratio. These techniques were applied to clinical cases using MRI in the evaluation of the brain tumor. The boundaries of the brain tumor and the edematous region were precisely extracted.
en-copyright=
kn-copyright=

en-aut-name=KanzakiNoriko
en-aut-sei=Kanzaki
en-aut-mei=Noriko
kn-aut-name=神崎典子
kn-aut-sei=神崎
kn-aut-mei=典子
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部放射線医学教室
en-keyword=V-filter
kn-keyword=V-filter
en-keyword=MRI
kn-keyword=MRI
en-keyword=Boundary enhancement
kn-keyword=Boundary enhancement
en-keyword=Edematous region
kn-keyword=Edematous region
END

start-ver=1.4
cd-journal=joma
no-vol=101
cd-vols=
no-issue=3-4
article-no=
start-page=285
end-page=293
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1989
dt-pub=198904
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Analysis of cellular oncogenes in human bone and soft tissue tumors
kn-title=ヒト骨・軟部腫瘍組織における癌遺伝子の解析
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The amplification and rearrangement of five cellular oncogenes (c-myc, c-K-ras, c-fos, c-raf-1, and N-myc) were studied by Southern hybridization in fourteen human bone and soft tissue tumors obtained at surgery. Amplification of c-myc was detected in the two of four osteosarcomas and one of two malignant fibrous histiocytomas. The c-myc genes in these tissues were amplified 4- to 8-fold in comparision with the placenta DNA. One of these osteosarcomas had 16- to 32-fold amplification of c-raf-1 gene without rearrangement. The clinical course of osteosarcoma and malignant fibrous histiocytoma with the amplified c-myc or c-raf-1 gene showed a rapid malignant progress with lung or bone metastasis. There appears to be a correlation between clinical prognosis and oncogene amplification.
en-copyright=
kn-copyright=

en-aut-name=SumiiHiroshi
en-aut-sei=Sumii
en-aut-mei=Hiroshi
kn-aut-name=住居広士
kn-aut-sei=住居
kn-aut-mei=広士
aut-affil-num=1
ORCID=

en-aut-name=InoueHajime
en-aut-sei=Inoue
en-aut-mei=Hajime
kn-aut-name=井上一
kn-aut-sei=井上
kn-aut-mei=一
aut-affil-num=2
ORCID=

en-aut-name=ItoShiro
en-aut-sei=Ito
en-aut-mei=Shiro
kn-aut-name=伊藤士郎
kn-aut-sei=伊藤
kn-aut-mei=士郎
aut-affil-num=3
ORCID=

en-aut-name=TanabeGozo
en-aut-sei=Tanabe
en-aut-mei=Gozo
kn-aut-name=田辺剛造
kn-aut-sei=田辺
kn-aut-mei=剛造
aut-affil-num=4
ORCID=

en-aut-name=TakechiHideo
en-aut-sei=Takechi
en-aut-mei=Hideo
kn-aut-name=武智秀夫
kn-aut-sei=武智
kn-aut-mei=秀夫
aut-affil-num=5
ORCID=

en-aut-name=IkedaShogo
en-aut-sei=Ikeda
en-aut-mei=Shogo
kn-aut-name=池田正五
kn-aut-sei=池田
kn-aut-mei=正五
aut-affil-num=6
ORCID=

en-aut-name=OdaTakuzo
en-aut-sei=Oda
en-aut-mei=Takuzo
kn-aut-name=小田琢三
kn-aut-sei=小田
kn-aut-mei=琢三
aut-affil-num=7
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部整形外科学教室

affil-num=2
en-affil=
kn-affil=岡山大学医学部整形外科学教室

affil-num=3
en-affil=
kn-affil=岡山大学医学部整形外科学教室

affil-num=4
en-affil=
kn-affil=岡山大学医学部整形外科学教室

affil-num=5
en-affil=
kn-affil=吉備高原医療リハビリテーションセンター

affil-num=6
en-affil=
kn-affil=岡山大学医学部癌源研究施設生化学部門

affil-num=7
en-affil=
kn-affil=岡山大学医学部癌源研究施設生化学部門
en-keyword=Oncogene
kn-keyword=Oncogene
en-keyword=Gene amplification
kn-keyword=Gene amplification
en-keyword=c-myc
kn-keyword=c-myc
en-keyword=c-raf-1
kn-keyword=c-raf-1
en-keyword=Osteosarcoma
kn-keyword=Osteosarcoma
en-keyword=MFH
kn-keyword=MFH
END