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153. Site-specific demethylation and normal chromatin structure of the human dihydrofolate reductase gene promoter after transfection into CHO cells

Author

Shimada, T, Inokuchi, K, and Nienhuis, A W

Abstract

The effect of in vitro methylation on the function and chromatin structure of the human dihydrofolate reductase (DHFR) promoter linked to the DHFR coding sequences (minigene) was studied after DNA-mediated gene transfer into DHFR- CHO cells. Methylation of HhaI sites reduced the transforming frequency to about 10% of control, whereas methylation of HpaII sites had a less significant effect. The integrated genes were demethylated at specific sites in the promoter sequence, namely, HpaII sites around -57 base pairs from the major start site for transcription and HhaI sites around +9, +24, or both. All other HpaII or HhaI sites in the DHFR coding region or in the plasmid sequences remained consistently methylated. The DHFR minigene, after methylation with HhaI methylase, was also introduced without selection by cotransfection with pSV2neo and selection for neor clones in G418. Preferential demethylation of the same sites was observed even without selection for the DHFR+ phenotype. Analysis of the chromatin structure of the integrated minigene revealed characteristic proximal and distal hypersensitive regions of the promoter, as previously observed in human cells. Correctly initiated DHFR mRNA was detected in all of the transformants studied. These results suggest that formation of the characteristic chromatin structure is an intrinsic property of the DHFR promoter sequence and that demethylation of specific sites accompanies gene expression.

Published
1987
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156. Domains involved in osmoregulation of the ompF gene in Escherichia coli

Author

Inokuchi, K, Itoh, M, and Mizushima, S

Abstract

Expression of the ompF gene, which is under the control of the OmpR protein, is regulated by the osmolarity of the medium. To study the mechanism of osmoregulation, plasmids carrying two different types of chimeric genes were constructed. In one type, the coding region of the ompF gene was linked to the trp promoter (trpPO) preceding ompF, and in the other type the ompF upstream region, mostly composed of the region for regulation by OmpR and the promoter region, was linked to the lacZ gene by protein fusion. Expression of beta-galactosidase by the lacZ chimeric gene was OmpR dependent and osmoregulated as sensitively as that of the intact ompF gene. In the ompR20 background the direction of osmoregulation was opposite that of normal osmoregulation, as was the direction of osmoregulation of the intact ompF gene. Osmoregulation was also observed with trpPO-ompF chimeric genes. However, the regulation was not as sensitive to the osmolarity of the medium as was regulation of the intact ompF gene and was independent of OmpR. These results suggest that OmpR-dependent osmoregulation played a primary role in the osmoregulation of ompF expression and that ompR-independent osmoregulation most likely did not play a crucial role. Studies with a series of trpPO-ompF chimeric genes also suggest that the untranslated leader region, about 100 base pairs in length, between the transcription initiation site and the initiation codon was not required for osmoregulation.

Published
1985
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157. Mutation causing reverse osmoregulation of synthesis of OmpF, a major outer membrane protein of Escherichia coli

Author

Nara, F, Inokuchi, K, Matsuyama, S, and Mizushima, S

Abstract

Supplementation of growth media with high concentrations of substances like sucrose results in the induction of OmpC synthesis and the suppression of OmpF synthesis. We isolated a novel mutant in which OmpF synthesis is in the opposite direction from normal osmoregulation. By transductional mapping, the mutation was localized at 75 min between malA and aroB on the Escherichia coli chromosome map where the ompR-envZ region is. The mutation was suppressed by a plasmid carrying the ompR gene but not by a plasmid carrying the envZ gene alone. The mutation also resulted in the almost complete suppression of OmpC synthesis. However, the remaining OmpC synthesis was osmoregulated normally. Based on these observations, the mechanism of osmoregulation of OmpF-OmpC synthesis is discussed.

Published
1984
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158. Promoter exchange between ompF and ompC, genes for osmoregulated major outer membrane proteins of Escherichia coli K-12

Author

Matsuyama, S, Inokuchi, K, and Mizushima, S

Abstract

Expression of the ompF and ompC genes coding for major outer membrane proteins OmpF and OmpC is regulated in opposite directions by medium osmolarity. Chimera genes were constructed by a reciprocal exchange of the promoter-signal sequence region between the two genes. The chimera gene construction was designed so that the proteins synthesized by these genes were essentially the same as the OmpC and OmpF proteins. Studies with the chimera genes demonstrated that the osmoregulation of the OmpF-OmpC synthesis was promoter dependent. They also showed that cells grew normally even when the osmoregulation took place in opposite directions. The effects of the ompR2 and envZ mutations, which suppress ompC and ompF expression, respectively, also became reversed. The reduced expression was still subject to the promoter-controlled osmoregulation. Based on these observations, the mechanism of regulation of the ompF-ompC gene expression and its physiological importance are discussed.

Published
1984
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159. Novel members of the Vesl/Homer family of PDZ proteins that bind metabotropic glutamate receptors.

Author

Kato, A, Ozawa, F, Saitoh, Y, Fukazawa, Y, Sugiyama, H, and Inokuchi, K

Abstract

Vesl-1S (186 amino acids, also called Homer) is a protein containing EVH1- and PDZ-like domains whose expression in the hippocampus is regulated during long term potentiation (LTP), one form of synaptic plasticity thought to underlie memory formation (Kato, A., Ozawa, F., Saitoh, Y., Hirai, K., and Inokuchi, K. (1997) FEBS Lett. 412, 183-189; Brakeman, P. R., Lanahan, A. A., O'Brien, R., Roche, K., Barnes, C. A., Huganir, R. L., and Worley, P. F. (1997) Nature 386, 284-288). Here we report additional members of the Vesl/Homer family of proteins, Vesl-1L and Vesl-2. Vesl-1L (366 amino acids), a splicing variant of Vesl-1S, shares N-terminal 175 amino acids with Vesl-1S and contains additional amino acids at the C terminus. Vesl-2 (354 amino acids) was highly related to Vesl-1L in that both contain EVH1- and PDZ-like domains at the N terminus (86% conservation) and an MCC (mutated in colorectal cancer)-like domain and a leucine zipper at the C terminus. In contrast to vesl-1S, we observed no changes in the levels of vesl-1L and vesl-2 mRNAs during dentate gyrus LTP. All these proteins interacted with metabotropic glutamate receptors (mGluR1 and mGluR5) as well as several hippocampal proteins in vitro. Vesl-1L and Vesl-2, but not Vesl-1S, interacted with each other through the C-terminal portion that was absent in Vesl-1S. Vesl-1L and Vesl-2 may mediate clustering of mGluRs at synaptic junctions. We propose that Vesl-1S may be involved in the structural changes that occur at metabotropic glutamatergic synapses during the maintenance phase of LTP by modulating the redistribution of synaptic components.

Published
1998

160. Mutation causing overproduction of outer membrane protein OmpF and suppression of OmpC synthesis in Escherichia coli

Author

Koga-Ban, Y, Mutoh, N, Inokuchi, K, and Mizushima, S

Abstract

A novel mutation affecting the synthesis of major outer membrane proteins OmpF and OmpC in Escherichia coli K-12 is described. The mutation resulted in overproduction of the OmpF protein with concomitant suppression of OmpC synthesis. This mutation, designated as ompFp100, was mapped at 21 min on the E. coli chromosome map with the gene order aroA-aspC-ompF4-ompFp100-asnS-pyrD. This mutation was cis-dominant to the expression of the ompF gene. In addition, the direction of the mRNA transcription of the ompF gene was from asnS to aspC. These results strongly indicate that ompFp100 is a promoter mutation of the ompF gene. Introduction of an ompF mutation, which causes the disappearance of the OmpF protein, into strains carrying the ompFp100 mutation resulted in the reappearance of the OmpC protein in the outer membrane. Addition of a high concentration of sucrose to the medium, which suppresses the OmpF synthesis and stimulates the OmpC synthesis in the wild-type strain, resulted in the reappearance of the OmpC protein in the ompFp100 mutant with concomitant suppression of the overproduction of the OmpF protein. These results suggest that suppression of OmpC synthesis in the ompFp100 mutant is due to overproduction of the OmpF protein.

Published
1983
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161. Cytophotometric DNA Analysis of Superficial and Advanced Carcinoma of the Esophagus

Author

Hidenobu Kai, Masayuki Kitamura, Y. Koga, Yasuyuki Okudaira, K. Sugimachi, Inokuchi K, and Hiroyuki Kuwano

Subjects
medicine.medical_specialty, business.industry, Esophageal cancer, medicine.disease, Advanced carcinoma, Lesion, medicine.anatomical_structure, Medicine, Radiology, Biopsy material, Esophagus, medicine.symptom, business, Lymph node
Abstract

With the conventional methods of diagnosis of esophageal cancer, it is very difficult to know preoperatively whether or not the lesion is accompanied by lymph node involvement, which aggravates the prognosis. However, if a technique were available making it feasible to acquire information regarding the malignant potential from biopsy material, this would certainly help us to prescribe adequate treatment and assess the prognosis.

Published
1988

168. Effects of radiotherapy and of differences in the extent of surgery for early breast cancer on local recurrence and 15-year survival: an overview of the randomised trials

Author

Abe, O., Abe, R., Enomoto, K., Kikuchi, K., Koyama, H., Masuda, H., Nomura, Y., Sakai, K., Sugimachi, K., Tominaga, T., Uchino, J., Yoshida, M., Haybittle, J. L., Davies, C., Harvey, V. J., Holdaway, T. M., Kay, R. G., Mason, B. H., Forbes, J. F., Wilcken, N., Gnant, M., Jakesz, R., Ploner, M., Yosef, H. M. A., Focan, C., Lobelle, J. P., Peek, U., Oates, G. D., Powell, J., Durand, M., Mauriac, L., Di Leo, A., Dolci, S., Piccart, M. J., Masood, M. B., Parker, D., Price, J. J., Hupperets, P. S. G. J., Jackson, S., Ragaz, J., Berry, D., Broadwater, G., Cirrincione, C., Muss, H., Norton, L., Weiss, R. B., Abu-Zahra, H. T., Portnoj, S. M., Baum, M., Cuzick, J., Houghton, J., Riley, D., Mansel, R. E., Gordon, N. H., Davis, H. L., Beatrice, A., Mihura, J., Naja, A., Lehingue, Y., Romestaing, P., Dubois, J. B., Delozier, T., Mace Lesec'h, J., Rambert, P., Petruzelka, L., Pribylova, O., Owen, J. R., Harbeck, N., Jänicke, F., Meisner, C., Meier, P., Howell, A., Ribeiro, G. C., Swindell, R., Burrett, J., Clarke, M., Collins, R., Darby, S., Elphinstone, P., Evans, V., Godwin, J., Gray, R., Harwood, C., Hicks, C., Jackson, D., James, S., Mackinnon, E., Mcgale, P., Mchugh, T., Mead, G., Morris, P., Oulds, J., Peto, R., Taylor, C., Wang, Y., Albano, J., De Oliveira, C. F., Gervásio, H., Gordilho, J., Johansen, H., Mouridsen, H. T., Gelman, R. S., Harris, J. R., Henderson, I. C., Shapiro, C. L., Christiansen, P., Ejlertsen, B., Møller, S., Overgaard, M., Carstensen, B., Palshof, T., Trampisch, H. J., Dalesio, O., De Vries, E. G. E., Rodenhuis, S., Van Tinteren, H., Comis, R. L., Davidson, N. E., Robert, N., Sledge, G., Tormey, D. C., Wood, W., Cameron, D., Chetty, U., Forrest, P., Jack, W., Rossbach, J., Klijn, J. G. M., Treurniet-Donker, A. D., Van Putten, W. L. J., Costa, A., Veronesi, U., Bartelink, H., Duchateau, L., Legrand, C., Sylvester, R., Van Der Hage, J. A., Van De Velde, C. J. H., Cunningham, M. P., Catalano, R., Creech, R. H., Bonneterre, J., Fargeot, P., Fumoleau, P., Kerbrat, P., Namer, M., Jonat, W., Kaufmann, M., Schumacher, M., Von Minckwitz, G., Bastert, G., Rauschecker, H., Sauer, R., Sauerbrei, W., Schauer, A., De Schryver, A., Vakaet, L., Belfiglio, M., Nicolucci, A., Pellegrini, F., Sacco, M., Valentini, M., Mcardle, C. S., Smith, D. C., Galligioni, E., Boccardo, F., Rubagotti, A., Dent, D. M., Gudgeon, C. A., Hacking, A., Erazo, A., Medina, J. Y., Izuo, M., Morishita, Y., Takei, H., Fentiman, I. S., Hayward, J. L., Rubens, R. D., Skilton, D., Scheurlen, H., Von Fournier, D., Dafni, U., Fountzilas, G., Klefstrom, P., Blomqvist, C., Saarto, T., Margreiter, R., Asselain, B., Salmon, R. J., Vilcoq, J. R., Arriagada, R., Hill, C., Laplanche, A., M. G., Lê, Spielmann, M., Bruzzi, P., Montanaro, E., Rosso, R., Sertoli, M. R., Venturini, M., Amadori, D., Benraadt, J., Kooi, M., Van De Velde, A. O., Van Dongen, J. A., Vermorken, J. B., Castiglione, M., Cavalli, F., Coates, A., Collins, J., Forbes, J., Gelber, R. D., Goldhirsch, A., Lindtner, J., Price, K. N., Rudenstam, C. M., Senn, H. J., Bliss, J. M., Chilvers, C. E. D., Coombes, R. C., Hall, E., Marty, M., Borovik, R., Brufman, G., Hayat, H., Robinson, E., Wigler, N., Bonadonna, G., Camerini, T., De Palo, G., Del Vecchio, M., Formelli, F., Valagussa, P., Martoni, A., Pannuti, F., Cocconi, G., Colozza, A., Camisa, R., Aogi, K., Takashima, S., Ikeda, T., Inokuchi, K., Sawa, K., Sonoo, H., Korzeniowski, S., Skolyszewski, J., Ogawa, M., Yamashita, J., Bonte, J., Christiaens, R., Paridaens, R., Van Den Bogaert, W., Martin, P., Geniez, ROMAIN SYLVAIN JEAN, Hakes, T., Hudis, C. A., Wittes, R., Giokas, G., Kondylis, D., Lissaios, B., De La Huerta, R., Sainz, M. G., Altemus, R., Cowan, K., Danforth, D., Lichter, A., Lippman, M., O'Shaughnessy, J., Pierce, L. J., Steinberg, S., Venzon, D., Zujewski, J. A., Paradiso, A., De Lena, M., Schittulli, F., Myles, J. D., Pater, J. L., Pritchard, K. I., Whelan, T., Anderson, S., Bass, G., Brown, A., Bryant, J., Costantino, J., Dignam, J., Fisher, B., Redmond, C., Wieand, S., Wolmark, N., Jackson, I. M., Palmer, M. K., Ingle, J. N., Suman, V. J., Bengtsson, N. O., Jonsson, H., Larsson, L. G., Lythgoe, J. P., Kissin, M., Erikstein, B., Hannisdal, E., Jacobsen, A. B., Varhaug, J. E., Gundersen, S., Hauer-Jensen, M., Høst, H., Nissen-Meyer, R., Blamey, R. W., Mitchell, A. K., Morgan, D. A. L., Robertson, J. F. R., Di Palma, M., Mathé, G., Misset, J. L., Clark, R. M., Levine, M., Morimoto, K., Takatsuka, Y., Crossley, E., Harris, A., Talbot, D., Taylor, M., Di Blasio, B., Ivanov, V., Semiglazov, V., Brockschmidt, J., Cooper, M. R., Ueo, H., Falkson, C. I., A'Hern, R., Ashley, S., Powles, T. J., Smith, I. E., Yarnold, J. R., Gazet, J. C., Corcoran, N., Deshpande, N., Di Martino, L., Douglas, P., Lindtner, A., Notter, G., Bryant, A. J. S., Ewing, G. H., Firth, L. A., Krushen-Kosloski, J. L., Foster, L., George, W. D., Stewart, H. J., Stroner, P., Malmström, P., Möller, T. R., Rydén, S., Tengrup, I., Tennvall-Nittby, L., Carstenssen, J., Dufmats, M., Hatschek, T., Nordenskjöld, B., Söderberg, M., Carpenter, J. T., Albain, K., Crowley, J., Green, S., Martino, S., Osborne, C. K., Ravdin, P. M., Glas, U., Johansson, U., Rutqvist, L. E., Singnomklao, T., Wallgren, A., Maibach, R., Thürlimann, B., Brenner, H., Hercbergs, A., Yoshimoto, M., Deboer, G., Paterson, A. H. G., Meakin, J. W., Panzarella, T., Shan, Y., Shao, Y. F., Wang, X., Zhao, D. B., Chen, Z. M., Pan, H. C., Bahi, J., Reid, M., Spittle, M., Deutsch, G. P., Senanayake, F., Kwong, D. L. W., Bianco, A. R., Carlomagno, C., De Laurentiis, M., De Placido, S., Buzdar, A. U., Smith, T., Bergh, J., Holmberg, L., Liljegren, G., Nilsson, J., Seifert, M., Sevelda, P., Zielinsky, C. C., Buchanan, R. B., Cross, M., Royle, G. T., Dunn, J. A., Hills, R. K., Lee, M., Morrison, J. M., Spooner, D., Litton, A., Chlebowski, R. T., Caffier, H., Clarke, M, Collins, R, Darby, S, Davies, C, Elphinstone, P, Evans, E, Godwin, J, Gray, R, Hicks, C, James, S, MacKinnon, E, McGale, P, McHugh, T, Peto, R, Taylor, C, and Wang, Y

Subjects
medicine.medical_specialty, Time Factors, medicine.medical_treatment, Breast Neoplasms, Rate ratio, Breast Conservation Treatment, Disease-Free Survival, Breast cancer, Cause of Death, Breast-conserving surgery, Medicine, Humans, Lung cancer, Aged, Probability, Randomized Controlled Trials as Topic, business.industry, Female, Middle Aged, Neoplasm Recurrence, Local, Medicine (all), General Medicine, medicine.disease, Surgery, Radiation therapy, Unilateral Breast Neoplasms, Neoplasm Recurrence, Local, business, Mastectomy
Abstract

Background In early breast cancer, variations in local treatment that substantially affect the risk of locoregional recurrence could also affect long-term breast cancer mortality. To examine this relationship, collaborative meta-analyses were undertaken, based on individual patient data, of the relevant randomised trials that began by 1995. Methods Information was available on 42 000 women in 78 randomised treatment comparisons (radiotherapy vs no radiotherapy, 23 500; more vs less surgery, 9300; more surgery vs radiotherapy, 9300). 24 types of local treatment comparison were identified. To help relate the effect on local (ie, locoregional) recurrence to that on breast cancer mortality, these were grouped according to whether or not the 5-year local recurrence risk exceeded 10% (10%, 25 000 women). Findings About three-quarters of the eventual local recurrence risk occurred during the first 5 years. In the comparisons that involved little (10%) differences, however, 5-year local recurrence risks were 7% active versus 26% control (absolute reduction 19%), and 15-year breast cancer mortality risks were 44·6% versus 49·5% (absolute reduction 5·0%, SE 0·8, 2p These 25 000 women included 7300 with breast-conserving surgery (BCS) in trials of radiotherapy (generally just to the conserved breast), with 5-year local recurrence risks (mainly in the conserved breast, as most had axillary clearance and node-negative disease) 7% versus 26% (reduction 19%), and 15-year breast cancer mortality risks 30·5% versus 35·9% (reduction 5·4%, SE 1·7, 2p=0·0002; overall mortality reduction 5·3%, SE 1·8, 2p=0·005). They also included 8500 with mastectomy, axillary clearance, and node-positive disease in trials of radiotherapy (generally to the chest wall and regional lymph nodes), with similar absolute gains from radiotherapy; 5-year local recurrence risks (mainly at these sites) 6% versus 23% (reduction 17%), and 15-year breast cancer mortality risks 54·7% versus 60·1% (reduction 5·4%, SE 1·3, 2p=0·0002; overall mortality reduction 4·4%, SE 1·2, 2p=0·0009). Radiotherapy produced similar proportional reductions in local recurrence in all women (irrespective of age or tumour characteristics) and in all major trials of radiotherapy versus not (recent or older; with or without systemic therapy), so large absolute reductions in local recurrence were seen only if the control risk was large. To help assess the life-threatening side-effects of radiotherapy, the trials of radiotherapy versus not were combined with those of radiotherapy versus more surgery. There was, at least with some of the older radiotherapy regimens, a significant excess incidence of contralateral breast cancer (rate ratio 1·18, SE 0·06, 2p=0·002) and a significant excess of non-breast-cancer mortality in irradiated women (rate ratio 1·12, SE 0·04, 2p=0·001). Both were slight during the first 5 years, but continued after year 15. The excess mortality was mainly from heart disease (rate ratio 1·27, SE 0·07, 2p=0·0001) and lung cancer (rate ratio 1·78, SE 0·22, 2p=0·0004). Interpretation In these trials, avoidance of a local recurrence in the conserved breast after BCS and avoidance of a local recurrence elsewhere (eg, the chest wall or regional nodes) after mastectomy were of comparable relevance to 15-year breast cancer mortality. Differences in local treatment that substantially affect local recurrence rates would, in the hypothetical absence of any other causes of death, avoid about one breast cancer death over the next 15 years for every four local recurrences avoided, and should reduce 15-year overall mortality.

179. STAPLER FOR A-V ANASTOMOSIS

Author

Ivanovich, P., primary, Kahan, B., additional, Bergan, J., additional, Someya, S., additional, Ono, K., additional, and Inokuchi, K., additional

Published
1977
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186. Kanzo

Author

Inokuchi, K, primary and Kobayashi, M, additional

Published
1968
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187. Kanzo

Author

Kaito, I., primary, Tamai, Y., additional, Niakano, H., additional, Minakuchi, S., additional, Nakagawa, J., additional, Ito, K., additional, Fukase, M, additional, Sato, S., additional, Ito, S., additional, Sahara, H., additional, Arisue, T, additional, Imai, F., additional, Takahashi, T., additional, Inoue, J., additional, Maruyama, Y., additional, Hida, S., additional, Mori, Y., additional, Koshikawa, H., additional, Kawamura, T., additional, Yoda, S., additional, Yamasaki, S., additional, Arima, T., additional, Minakuchi, N., additional, Inoue, S., additional, Fukumoto, T., additional, Hirayama, C., additional, Koyama, K., additional, Sato, T., additional, Watanabe, K., additional, Kimura, S., additional, Kashimura, S., additional, Matsuo, Y., additional, Futagawa, S., additional, Sugiura, M., additional, Ichihara, S., additional, Nomura, M., additional, Hatano, S., additional, Shimokawa, Y., additional, Okuda, K., additional, Kaneto, A., additional, Inokuchi, K., additional, Kobayashi, M., additional, Ogawa, Y., additional, Motoki, T., additional, Kamisaka, K., additional, Harada, T., additional, Hidaka, M., additional, Takahara, A., additional, Nakamura, A., additional, Nakao, H., additional, Nakanishi, T., additional, Yochimi, A., additional, Hashimoto, S., additional, Miyata, M., additional, Fukuhara, Y., additional, Kurokawa, K., additional, Miki, T., additional, Nakamura, T., additional, Yamamoto, S., additional, Okumura, M., additional, Funakoshi, Y., additional, Nanka, K., additional, Okayama, M., additional, and Katsuki, S., additional

Published
1971
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192. General lectures (II)

Author

Karasawa, Y., primary, Ōnuma, H., additional, Suzuki, H., additional, Okazaki, T., additional, Yasui, A., additional, Murakami, T., additional, Furuya, K., additional, Ohtsuki, M., additional, Sata, H., additional, Kondo, T., additional, Takada, H., additional, Kawaguchi, K., additional, Sai, S., additional, Takeda, S., additional, Kitagawa, M., additional, Morooka, T., additional, Shiraishi, T., additional, Namiki, M., additional, Kawauchi, H., additional, Nakagawa, K., additional, Kuramata, H., additional, Yamaguchi, Y., additional, Kabakino, T., additional, Inokuchi, T., additional, Wakisaka, J., additional, Yamauchi, Y., additional, Debuchi, T., additional, Ogo, W., additional, Yamasaki, C., additional, Sigemori, M., additional, Hashimoto, K., additional, Shirozu, T., additional, Kaibara, N., additional, Inokuchi, K., additional, Soejima, K., additional, Hiyama, T., additional, Wakita, M., additional, Ikemoto, T., additional, Hayasaka, H., additional, Fukui, S., additional, Takeda, T., additional, Aoyama, N., additional, Takada, Y., additional, Saheki, Y., additional, Yoshida, Y., additional, Minagawa, K., additional, Okuyama, T., additional, Yamamitsu, S., additional, Konishi, Y., additional, Ishimatsu, N., additional, Murai, S., additional, Nukaga, A., additional, Toyama, S., additional, Watanabe, Y., additional, Mizushima, N., additional, Abe, M., additional, Maruyama, K., additional, Yoshino, K., additional, Suzuki, T., additional, Akisato, K., additional, Kitajima, M., additional, Tabata, T., additional, Hashimoto, M., additional, Tanaka, T., additional, Nakagawa, Y., additional, Ishii, Y., additional, Inoue, M., additional, Katayama, S., additional, Nakano, Y., additional, Fukuda, M., additional, Takaki, M., additional, Hyodo, H., additional, Kobayashi, J., additional, Nishikawa, H., additional, Morimoto, K., additional, Takagi, T., additional, Sako, S., additional, Tomoda, H., additional, Furusawa, M., additional, Sassa, R., additional, Unuma, T., additional, Iwase, T., additional, Yoshioka, T., additional, Kusakabe, M., additional, Iio, M., additional, Kobayashi, S., additional, Kizu, M., additional, Kasugai, T., additional, Yoshida, K., additional, Kembo, T., additional, Yoshida, T., additional, Suga, Y., additional, Suguro, T., additional, Kono, Y., additional, Mitsui, S., additional, Nagamachi, Y., additional, Nakamura, T., additional, Suto, H., additional, Higuchi, T., additional, Onai, M., additional, Isizuka, K., additional, Takei, A., additional, Simoda, M., additional, Sekiguchi, T., additional, Shichijo, K., additional, Akashi, Y., additional, Mori, K., additional, Ogasawara, K., additional, Tanaka, R., additional, Yoshikawa, K., additional, Takahashi, T., additional, Ogata, T., additional, Tanaka, S., additional, Seito, T., additional, Matsuda, H., additional, Imajo, T., additional, Moriyasu, K., additional, Takata, Y., additional, Kamei, H., additional, Murai, H., additional, Takemitsu, T., additional, Kanemitsu, T., additional, Ishii, M., additional, Imaizumi, M., additional, Inada, M., additional, Glass, G. B. J., additional, Ebata, K., additional, Yamanaka, N., additional, Watanabe, S., additional, Mori, H., additional, Tsukasa, S., additional, Sato, H., additional, Chuman, Y., additional, Nakahara, N., additional, Taniguchi, H., additional, Ehira, S., additional, Hori, M., additional, Irisa, T., additional, Yokoyama, H., additional, Kunieda, T., additional, Ogushi, Y., additional, Kawakami, K., additional, Kuroda, M., additional, Sasaki, D., additional, SŌma, S., additional, Yanagiya, S., additional, Munakata, A., additional, Matsunaga, F., additional, Abiko, M., additional, Ohuchi, H., additional, Tai, C., additional, Kawashima, T., additional, Oosawa, W., additional, Asakura, H., additional, Senba, H., additional, Hatayama, T., additional, Yukawa, K., additional, Konishi, T., additional, Miyata, M., additional, Shimazu, H., additional, Kinoshita, T., additional, Nukada, K., additional, Yamagishi, T., additional, Harada, K., additional, Nakano, S., additional, Sakai, T., additional, Shindo, K., additional, Fukushima, K., additional, Odagiri, S., additional, Tarao, K., additional, Saito, Y., additional, Ohara, K., additional, Sasaki, S., additional, Tomoda, T., additional, Kaneda, N., additional, Yamaguchi, H., additional, Hayashi, T., additional, Suzuki, J., additional, Kofune, Y., additional, Urase, A., additional, Yamagata, A., additional, Sugino, N., additional, Hatano, M., additional, Oshima, K., additional, Tanabe, T., additional, Ohto, M., additional, Okuda, K., additional, Mitani, E., additional, Yamamoto, S., additional, Kobayashi, K., additional, Ono, T., additional, Kamata, T., additional, Mohri, S., additional, Makiishi, H., additional, Kitano, A., additional, Tatumi, S., additional, Mizuno, S., additional, Tsumori, K., additional, Shimizu, T., additional, Nomatsu, K., additional, Hiratsuka, H., additional, Ichinose, M., additional, Morishita, T., additional, Morita, A., additional, Matsuzaki, S., additional, Oda, M., additional, Kamegaya, K., additional, Tuchiya, M., additional, Sambe, K., additional, Murakami, Y., additional, Machii, A., additional, Nitta, Y., additional, Aiso, Y., additional, Kitahara, N., additional, Sato, M., additional, Yoshizawa, Y., additional, Hishinuma, Y., additional, Nagasako, H., additional, Nao, Y., additional, Harada, H., additional, Mishima, K., additional, Yamagata, Y., additional, Mandai, M., additional, Kondo, Y., additional, Uchida, Y., additional, Takizawa, S., additional, Kinoshita, S., additional, Kurihara, T., additional, Sakumoto, K., additional, Okamoto, H., additional, Sakurai, S., additional, Ishitobi, S., additional, Tanaka, H., additional, Ishihara, K., additional, Kuno, N., additional, Aoki, I., additional, Horiguchi, Y., additional, Kitamura, K., additional, Miwa, M., additional, Okada, K., additional, Endo, Y., additional, Tatsuta, M., additional, Morii, T., additional, Okuda, S., additional, Tamura, H., additional, Fukuda, K., additional, Sato, K., additional, Koizumi, K., additional, Takebe, T., additional, Yamagata, S., additional, Noda, S., additional, Toda, Y., additional, Hayakawa, T., additional, Nakajima, S., additional, Hitokawa, S., additional, Sawabu, N., additional, Hirose, S., additional, Takada, A., additional, Takeuchi, J., additional, Kuniyasu, Y., additional, Kakehi, H., additional, Uchiyama, G., additional, Arimizu, N., additional, Kuroda, T., additional, Saishyo, H., additional, Takashima, T., additional, Shin, M., additional, Akashi, M., additional, Moriyama, T., additional, Uchimura, M., additional, Tsuchiya, R., additional, Kakizaki, G., additional, Noto, N., additional, Oizumi, T., additional, Soeno, T., additional, Maeta, T., additional, Saito, T., additional, Naito, S., additional, Shimizu, K., additional, Nakajima, T., additional, Tanaka, M., additional, Kin, T., additional, Sugiyama, S., additional, Takayama, H., additional, Tomono, T., additional, Kamijo, N., additional, Kimura, Y., additional, Matsuo, T., additional, Shimada, 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Published
1973
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194. Aspiration of intraspinal synovial cyst: recurrence after temporal improvement

Author

Imai, K., Nakamura, K., Inokuchi, K., and Oda, H.

Abstract

Abstract: Intraspinal synovial cyst primarily occurs in the lumbar spine and may cause back pain and compression nerve disturbance. Percutaneous aspiration has been recommended as an alternative to surgery in three cases. We report on two patients who improved after aspiration of gelatinous material and steroid injection but whose cyst recurred within a short period of time. There are reportedly two types of synovial cyst: One contains serosanguinous fluid and the other gelatinous fluid. These two types are indistinguishable on computed tomography or magnetic resonance imaging. The results of all patients whose aspirated material was gelantinous were unsuccessful, including our cases. Thus, the outcome may depend on the pathology of the cyst.

Published
1998
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195. STAPLER FOR AV ANASTOMOSIS

Author

Ivanovich, P., Kahan, B., Bergan, J., Someya, S., Ono, K., and Inokuchi, K.

Published
1977

196. Treatment of adult AML with t(6;11)(q27;q23) by allogeneic hematopoietic SCT in the first CR.

Author

Tamai, H., Yamaguchi, H., Takahashi, S., Tojo, A., Hamaguchi, H., Kobayashi, T., Akiyama, H., Sakamaki, H., Okumura, H., Nakao, Si, Arai, A., Miura, O., Tajika, K., Inokuchi, K., and Dan, K.

Subjects
LETTERS to the editor, ACUTE myeloid leukemia treatment
Abstract

A letter to the editor is presented in response to the article "Treatment of Adult AML With t(6;11)(q27;q23) by Allogeneic Hematopoietic SCT in the First CR" in the October 2008 issue.

Published
2008
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197. Treatment of relapsed acute myeloid leukemia with MLL/AF6 fusion after allogeneic hematopoietic stem cell transplantation with gemtuzumab ozogamicin with a long interval followed by donor lymphocyte infusion.

Author

Tamai, H., Shioi, Y., Yamaguchi, H., Okabe, M., Wakita, S., Mizuki, T., Nakayama, K., Inokuchi, K., Tajika, K., and Dan, K.

Subjects
LETTERS to the editor, MYELOID leukemia, ACUTE myeloid leukemia treatment, AMINOGLYCOSIDES, ANTINEOPLASTIC agents, THERAPEUTIC use of monoclonal antibodies, CANCER relapse, CHROMOSOME abnormalities, CHROMOSOMES, RED blood cell transfusion, HEMATOPOIETIC stem cell transplantation, HOMOGRAFTS, MONOCLONAL antibodies, ORGAN donors, PROTEINS, TIME, TOXINS, ACUTE myeloid leukemia, THERAPEUTICS
Abstract

A letter to the editor is presented in response to the article "Treatment of Relapsed Acute Myeloid Leukemia With MLL/AF6 Fusion After Allogeneic Hematopoietic Stem Cell Transplantation With Gemtuzumab Ozogamicin With a Long Interval Followed By Donor Lymphocyte Infusion," in the November 8, 2007 issue.

Published
2008
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199. Hippocampal function is not required for the precision of remote place memory

Author

Kitamura Takashi, Okubo-Suzuki Reiko, Takashima Noriko, Murayama Akiko, Hino Toshiaki, Nishizono Hirofumi, Kida Satoshi, and Inokuchi Kaoru

Subjects
Neurology. Diseases of the nervous system, RC346-429
Abstract

Abstract Background During permanent memory formation, recall of acquired place memories initially depends on the hippocampus and eventually become hippocampus-independent with time. It has been suggested that the quality of original place memories also transforms from a precise form to a less precise form with similar time course. The question arises of whether the quality of original place memories is determined by brain regions on which the memory depends. Results To directly test this idea, we introduced a new procedure: a non-associative place recognition memory test in mice. Combined with genetic and pharmacological approaches, our analyses revealed that place memory is precisely maintained for 28 days, although the recall of place memory shifts from hippocampus-dependent to hippocampus-independent with time. Moreover, the inactivation of the hippocampal function does not inhibit the precision of remote place memory. Conclusion These results indicate that the quality of place memories is not determined by brain regions on which the memory depends.

Published
2012
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200. LTP induction within a narrow critical period of immature stages enhances the survival of newly generated neurons in the adult rat dentate gyrus

Author

Kitamura Takashi, Saitoh Yoshito, Murayama Akiko, Sugiyama Hiroyuki, and Inokuchi Kaoru

Subjects
Neurology. Diseases of the nervous system, RC346-429
Abstract

Abstract Neurogenesis occurs in the adult hippocampus of various animal species. A substantial fraction of newly generated neurons die before they mature, and the survival rate of new neurons are regulated in an experience-dependent manner. Previous study showed that high-frequency stimulation (HFS) of perforant path fibers to the hippocampal dentate gyrus (DG) induces the long-term potentiation (LTP) in the DG, and enhances the survival of newly generated neurons in the DG. In this study, we addressed whether a time period exists during which the survival of new neurons is maximally sensitive to the HFS. We found that the enhancement of cell survival by HFS was exclusively restricted to the specific narrow period during immature stages of new neurons (7-10 days after birth). Furthermore, the pharmacological blockade of LTP induction suppressed the enhancement of cell survival by the HFS. These results suggest that the LTP induction within a narrow critical period of immature stages enhances the survival of newly generated neurons in rat DG.

Published
2010
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