Search

Your search keyword '"Tamano S"' showing total 244 results
Start Over Author "Tamano S"
244 results on '"Tamano S"'

1. P2.09-23 A Multicentre, Real-World Observational Study of First-Line Osimertinib and Post Progression Patterns in EGFR Positive NSCLC (Reiwa Study)

Author

Watanabe, K., primary, Hosomi, Y., additional, Naoki, K., additional, Kato, T., additional, Tsukita, Y., additional, Matsumoto, H., additional, Yoh, K., additional, Fujisaka, Y., additional, Takahashi, S., additional, Takata, S., additional, Usui, K., additional, Kishi, K., additional, Naka, G., additional, Tamano, S., additional, Uemura, K., additional, and Kunitoh, H., additional

Published
2023
Full Text
View/download PDF

9. Characterization of the diffusion properties of different gadolinium-based MRI contrast agents after ultrasound induced blood–brain barrier permeabilization

Author

Fowlkes, B, Ghanouni, P, Sanghvi, N, Coussios, C, Lyon, Pc, Gray, M, Mannaris, C, Victor, Mds, Stride, E, Cleveland, R, Carlisle, R, Feng, W, Middleton, M, Gleeson, F, Aubry, J, Pauly, Kb, Moonen, C, Vortman, J, Sharabi, S, Daniels, D, Last, D, Guez, D, Levy, Y, Volovick, A, Grinfeld, J, Rachmilevich, I, Amar, T, Zibly, Z, Mardor, Y, Harnof, S, Plaksin, M, Weissler, Y, Shoham, S, Kimmel, E, Naor, O, Farah, N, Paeng, D, Zhiyuan, X, Snell, J, Quigg, Ah, Eames, M, Jin, C, Everstine, Ac, Sheehan, Jp, Lopes, Bs, Kassell, N, Looi, T, Khokhlova, V, Mougenot, C, Hynynen, K, Drake, J, Slayton, M, Amodei, Rc, Compton, K, Mcnelly, A, Latt, D, Kearney, J, Melodelima, D, Dupre, A, Chen, Y, Perol, D, Vincenot, J, Chapelon, J, Rivoire, M, Guo, W, Ren, G, Shen, G, Neidrauer, M, Zubkov, L, Weingarten, Ms, Margolis, Dj, Lewin, Pa, Mcdannold, N, Sutton, J, Vykhodtseva, N, Livingstone, M, Kobus, T, Zhang, Y, Schwartz, M, Huang, Y, Lipsman, N, Jain, J, Chapman, M, Sankar, T, Lozano, A, Yeung, R, Damianou, C, Papadopoulos, N, Brokman, O, Zadicario, E, Brenner, O, Castel, D, Shih-Ying, W, Grondin, J, Zheng, W, Heidmann, M, Karakatsani, Me, Sánchez, Cjs, Ferrera, V, Konofagou, Ee, Yiannakou, M, Cho, H, Lee, H, Han, M, Choi, J, Lee, T, Ahn, S, Chang, Y, Park, J, Ellens, N, Partanen, A, Farahani, K, Airan, R, Carpentier, A, Canney, M, Vignot, A, Lafon, C, Delattre, J, Idbaih, A, Odéen, H, Bolster, B, Jeong, Ek, Parker, Dl, Gaur, P, Feng, X, Fielden, S, Meyer, C, Werner, B, Grissom, W, Marx, M, Weber, H, Taviani, V, Hargreaves, B, Tanaka, J, Kikuchi, K, Ishijima, A, Azuma, T, Minamihata, K, Yamaguchi, S, Nagamune, T, Sakuma, I, Takagi, S, Santin, Md, Marsac, L, Maimbourg, G, Monfort, M, Larrat, B, François, C, Lehéricy, S, Tanter, M, Samiotaki, G, Wang, S, Acosta, C, Feinberg, Er, Kovacs, Zi, Tsang-Wei, T, Papadakis, Gz, Reid, Wc, Hammoud, Da, Frank, Ja, Kim, S, Jikaria, N, Bresler, M, Qureshi, F, Xia, J, Tsui, P, Liu, H, Plata, Jc, Sveinsson, B, Salgaonkar, Va, Adams, M, Diederich, C, Ozhinsky, E, Bucknor, Md, Rieke, V, Mikhail, A, Severance, L, Negussie, Ah, Wood, B, de Greef, M, Schubert, G, Ries, M, Poorman, Me, Dockery, M, Chaplin, V, Dudzinski, So, Spears, R, Caskey, C, Giorgio, T, Costa, Mm, Papaevangelou, E, Shah, A, Rivens, I, Box, C, Bamber, J, ter Haar, G, Burks, Sr, Nagle, M, Nguyen, B, Milo, B, Nhan M., L, Song, S, Zhou, K, Nabi, G, Huang, Z, Ben-Ezra, S, Rosen, S, Mihcin, S, Strehlow, J, Karakitsios, I, Nhan, L, Schwenke, M, Demedts, D, Prentice, P, Haase, S, Preusser, T, Melzer, A, Mestas, J, Chettab, K, Gomez, Gs, Dumontet, C, Werle, B, Marquet, F, Bour, P, Vaillant, F, Amraoui, S, Dubois, R, Ritter, P, Haïssaguerre, M, Hocini, M, Bernus, O, Quesson, B, Livneh, A, Adam, D, Robin, J, Arnal, B, Fink, M, Pernot, M, Khokhlova, Td, Schade, Gr, Wang, Y, Kreider, W, Simon, J, Starr, F, Karzova, M, Maxwell, A, Bailey, Mr, Lundt, Je, Allen, Sp, Sukovich, Jr, Hall, T, Zhen, X, May, P, Lin, Dw, Constans, C, Deffieux, T, Park, E, Ahn, Yd, Kang, Sy, Park, D, Lee, Jy, Vidal-Jove, J, Perich, E, Ruiz, A, Jaen, A, Eres, N, del Castillo, Ma, Myers, R, Kwan, J, Coviello, C, Rowe, C, Crake, C, Finn, S, Jackson, E, Pouliopoulos, A, Caiqin, L, Tinguely, M, Tang, M, Garbin, V, Choi, Jj, Folkes, L, Stratford, M, Nwokeoha, S, Tong, L, Farr, N, D’Andrea, S, Gravelle, K, Chen, H, Lee, D, Hwang, Jh, Tardoski, S, Ngo, J, Gineyts, E, Roux, J, Clézardin, P, Conti, A, Magnin, R, Gerstenmayer, M, Lux, F, Tillement, O, Mériaux, S, Penna, Sd, Romani, Gl, Dumont, E, Sun, T, Power, C, Miller, E, Sapozhnikov, O, Tsysar, S, Yuldashev, Pv, Svet, V, Dongli, L, Pellegrino, A, Petrinic, N, Siviour, C, Jerusalem, A, Cunitz, Bw, Dunmire, B, Inserra, C, Guedra, M, Mauger, C, Gilles, B, Solovchuk, M, Sheu, Twh, Thiriet, M, Zhou, Y, Neufeld, E, Baumgartner, C, Payne, D, Kyriakou, A, Kuster, N, Xiao, X, Mcleod, H, Dillon, C, Payne, A, Khokhova, Va, Sinilshchikov, I, Andriyakhina, Y, Rybyanets, A, Shvetsova, N, Berkovich, A, Shvetsov, I, Shaw, Cj, Civale, J, Giussani, D, Lees, C, Ozenne, V, Toupin, S, Salgaonkar, V, Kaye, E, Monette, S, Maybody, M, Srimathveeravalli, G, Solomon, S, Gulati, A, Bezzi, M, Jenne, Jw, Lango, T, Müller, M, Sat, G, Tanner, C, Zangos, S, Günther, M, Dinh, Ah, Niaf, E, Bratan, F, Guillen, N, Souchon, R, Lartizien, C, Crouzet, S, Rouviere, O, Han, Y, Payen, T, Palermo, C, Sastra, S, Olive, K, van Breugel, Jm, van den Bosch, Ma, Fellah, B, Le Bihan, D, Hernandez-Garcia, L, Cain, Ca, Lyka, E, Elbes, D, Chunhui, L, Tamano, S, Jimbo, H, Yoshizawa, S, Fujiwara, K, Itani, K, Umemura, S, Stoianovici, D, Zaini, Z, Takagi, R, Zong, S, Watkins, R, Pascal-Tenorio, A, Jones, P, Butts-Pauly, K, Bouley, D, Lin, C, Hsieh, H, Wei, K, Garnier, C, Renault, G, Seifabadi, R, Wilson, E, Eranki, A, Kim, P, Lübke, D, Huber, P, Georgii, J, Dresky, Cv, Haller, J, Yarmolenko, P, Sharma, K, Celik, H, Guofeng, L, Qiu, W, Zheng, H, Tsai, M, Chu, P, Webb, T, Vyas, U, Walker, M, Zhong, J, Waspe, Ac, Hodaie, M, Yang, F, Huang, S, Zur, Y, Assif, B, Aurup, C, Kamimura, H, Carneiro, Aa, Rothlübbers, S, Schwaab, J, Houston, G, Azhari, H, Weiss, N, Sosna, J, Goldberg, Sn, Barrere, V, Jang, Kw, Lewis, B, Wang, X, Suomi, V, Edwards, D, Larrabee, Z, Hananel, A, Rafaely, B, Debbiny, Re, Dekel, Cz, Assa, M, Menikou, G, Mouratidis, P, Pineda-Pardo, Ja, de Pedro, Mda, Martinez, R, Hernandez, F, Casas, S, Oliver, C, Pastor, P, Vela, L, Obeso, J, Greillier, P, Zorgani, A, Catheline, S, Solovov, V, Vozdvizhenskiy, Mo, Orlov, Ae, Chueh-Hung, W, Sun, M, Shih, Tt, Chen, W, Prieur, F, Pillon, A, Cartron, V, Cebe, P, Chansard, N, Lafond, M, Seya, Pm, Bera, J, Boissenot, T, Fattal, E, Bordat, A, Chacun, H, Guetin, C, Tsapis, N, Maruyama, K, Unga, J, Suzuki, R, Fant, C, Rogez, B, Afadzi, M, Myhre, Of, Vea, S, Bjørkøy, A, Yemane, Pt, van Wamel, A, Berg, S, Hansen, R, Angelsen, B, and Davies, C

Subjects
Settore FIS/07
Published
2017

33. Presence of a threshold for promoting effects of phenobarbital on diethylnitrosamine-induced hepatic foci in the rat.

Author

Kitano, M, Ichihara, T, Matsuda, T, Wanibuchi, H, Tamano, S, Hagiwara, A, Imaoka, S, Funae, Y, Shirai, T, and Fukushima, S

Abstract

The dose dependence of the hepatopromoting effects of phenobarbital (PB) was investigated in a rat liver medium-term bioassay (Ito test) to elucidate a practical threshold level. F344 rats were given a single i.p. injection of diethylnitrosamine (200 mg/kg body wt) and subjected to two-thirds partial hepatectomy at week 3. Commencing 2 weeks from the start, PB at doses of 0, 1, 2, 4, 7.5, 15 or 500 p.p.m. in experiment 1 and 0. 0.01, 0.1 or 0.5 p.p.m. in experiment 2 were fed to the rats for 6 weeks. Experiment 3 was conducted to confirm previous data using the same medium-term bioassay, with PB at doses of 0, 1, 2, 4, 7.5, 15, 30, 60, 125, 250 or 500 p.p.m. fed to the rats. All surviving animals were killed at week 8 in these experiments and their livers were immunohistochemically examined for expression of glutathione S-transferase placental form (GST-P). Quantitative values for GST-P-positive foci in the liver were increased dose dependently in rats given 60-500 p.p.m. PB. However, those for doses in the range 1-7.5 p.p.m. demonstrated a decrease as compared with the control group (0 p.p.m.), with significant differences observed for 1 and 2 p.p.m. The results for 15-30 and 0.01-0.5 p.p.m. were comparable with the control values. Examination of transforming growth factor-α (TGF-α)-positive foci also produced similar results to those for GST-P in experiment 1. Immunohistochemical staining of TGF-α and GST-P using serial liver sections demonstrated that the TGF-α-positive foci comprised a sub-population of the GST-P positive lesions, being 1/8-1/10th as common in livers of animals treated with PB. TGF-α-positive foci were almost always negative on immunostaining for TGF-β. Western blotting for proteins CYP2B1, 2C6 and 3A2 revealed a good correlation between changes in GST-P-positive foci and CYP3A2 protein expression. The finding of inhibition effects at low doses of PB confirms the presence of a threshold level for promoting effects by PB on liver carcinogenesis in rats. [ABSTRACT FROM PUBLISHER]

Published
1998
Full Text
View/download PDF

34. Carcinogenicity of antioxidants BHA, caffeic acid, sesamol, 4-methoxyphenol and catechol at low doses, either alone or in combination, and modulation of their effects in a rat medium-term multi-organ carcinogenesis model.

Author

Hirose, M, Takesada, Y, Tanaka, H, Tamano, S, Kato, T, and Shirai, T

Abstract

The carcinogenicity of low dietary levels of the antioxidants butylated hydroxyanisole (BHA), caffeic acid, sesamol, 4-methoxyphenol (4-MP) and catechol, known to target the forestomach or glandular stomach, were examined alone or in combination in a 2-year long-term experiment and their modifying effects assessed in a medium-term multiorgan model. In the carcinogenicity study, groups of 30-31 male F344 rats were treated with 0.1% 4-MP and 0.16% catechol either alone or in combination for up to 104 weeks and then killed. In the medium-term multi-organ model, groups of 10 to 15 male F344 rats were given diethylnitrosamine (DEN), N-methylnitrosourea (MNU), 1,2-dimethylhydrazine (DMH), N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN) and 2,2'-dihydroxy-di-n-propylnitrosamine (DHPN) for a total multiple initiation period of 4 weeks (DMBDD treatment). BHA, caffeic acid, sesamol and 4-MP, each at doses of 0.4% or 0.08%, and catechol at doses of 0.16% or 0.032% were administered in the diet either alone or in combination after completion of the initiation regimen. All surviving animals were killed at the end of week 28, and major organs were examined histopathologically. In the carcinogenicity study, slightly increased incidences of forestomach papillomas were found in the sesamol- (15.8%), caffeic acid (14.8%), catechol- (3%) and 4-MP- (11.5%) treated groups as compared with the basal diet (0%), and a significant increase was observed with the five antioxidants in combination (42.9%, P <0.001). In a medium-term multi-organ carcinogenesis model, incidences of forestomach papillomas and/or carcinomas were increased in each high dose group, but additive or synergistic effects were not found in the combination group. In the low dose case, the incidence of forestomach papillomas was significantly increased only in the combination group. With regard to other organs, the incidence of colon tumors was significantly decreased only in the high dose combination group. The results indicate that even at low dose levels phenolic compounds can exert additive/synergistic effect on carcinogenesis. [ABSTRACT FROM PUBLISHER]

Published
1998
Full Text
View/download PDF

35. Assessment of regional myocardial strain by a novel automated tracking system from digital image files

Author

Toyoda, T., Baba, H., Akasaka, T., Akiyama, M., Neishi, Y., Tomita, J., Sukmawan, R., Koyama, Y., Watanabe, N., Tamano, S., Shinomura, R., Komuro, I., and Yoshida, K.

Abstract

Myocardial strain imaging by Doppler tissue echocardiography is a useful method to quantify regional left ventricular function. However, this method has a problem of its Doppler angle dependency. We attempted to quantify myocardial strain by a newly developed automated tracking system from digital image files. In 6 anesthetized open-chest dogs, a pair of ultrasonic crystals was implanted at the inner site and outer site of the left ventricular wall to measure myocardial radial strain. B-mode echocardiographic images and trajectories of crystals were recorded simultaneously. Three conditions were examined by intravenous infusion of dobutamine. We used a pattern matching algorithm, which allowed us to track objects from one frame to the next. In 18 image sequences obtained in the 6 dogs, there was an excellent correlation in maximal myocardial strain between the two methods (r = 0.92, P < .0001). Thus, this system is a promising tool to provide automated quantification of regional myocardial strain.

Published
2004
Full Text
View/download PDF

36. Organ dependent enhancement of rat 3,2'-dimethyl-4-aminobiphenyl (DMAB) carcinogenesis by 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP): positive effects on the intestine but not the prostate.

Author

Imaida, K, Sano, M, Tamano, S, Asamoto, M, Ogawa, K, Futakuchi, M, and Shirai, T

Abstract

In order to evaluate tumor enhancing effects of the heterocyclic carcinogen, 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP), doses of 100 and 300 p.p.m. PhIP were given for 40 weeks to male F344 rats, which initially received 3,2'-dimethyl-4-aminobiphenyl (DMAB). DMAB shows a similar carcinogenic organ spectrum to that of PhIP, including the prostate and colon. PhIP alone at a dose of 300 p.p.m. resulted in the development of prostate and intestine cancers. Furthermore, among the DMAB-treated group, enhancement of intestinal carcinogenesis by 300 p.p.m. PhIP was observed. However, no prostate enhancement was demonstrated in the DMAB + PhIP group. Since PhIP-DNA adduct formation in the prostate epithelial cells in a satellite experiment was not affected by pre-treatment with DMAB, it is speculated that the contradictory findings between the intestine and prostate may be due to the specific biological effects of PhIP. Taking into account previous data, that PhIP clearly enhanced rat 1,2-dimethylhydrazine-initiated colon tumorigenesis, the potential of PhIP to enhance colon carcinogenesis may be initiator dependent.

Published
2001
Full Text
View/download PDF

41. Presence of a threshold for promoting effects of phenobarbital on diethylnitrosamine-induced hepatic foci in the rat

Author

Funae, Y., Fukushima, S., Shirai, T., Tamano, S., Hagiwara, A., Imaoka, S., Kitano, M., Ichihara, T., Matsuda, T., and Wanibuchi, H.

Abstract

The dose dependence of the hepatopromoting effects of phenobarbital (PB) was investigated in a rat liver medium-term bioassay (Ito test) to elucidate a practical threshold level. F344 rats were given a single i.p. injection of diethylnitrosamine (200 mg/kg body wt) and subjected to two-thirds partial hepatectomy at week 3. Commencing 2 weeks from the start, PB at doses of 0, 1, 2, 4, 7.5, 15 or 500 p.p.m. in experiment 1 and 0. 0.01, 0.1 or 0.5 p.p.m. in experiment 2 were fed to the rats for 6 weeks. Experiment 3 was conducted to confirm previous data using the same medium-term bioassay, with PB at doses of 0, 1, 2, 4, 7.5, 15, 30, 60, 125, 250 or 500 p.p.m. fed to the rats. All surviving animals were killed at week 8 in these experiments and their livers were immunohistochemically examined for expression of glutathione S-transferase placental form (GST-P). Quantitative values for GST-P-positive foci in the liver were increased dose dependently in rats given 60-500 p.p.m. PB. However, those for doses in the range 1-7.5 p.p.m. demonstrated a decrease as compared with the control group (0 p.p.m.), with significant differences observed for 1 and 2 p.p.m. The results for 15-30 and 0.01-0.5 p.p.m. were comparable with the control values. Examination of transforming growth factor-α (TGF-α)-positive foci also produced similar results to those for GST-P in experiment 1. Immunohistochemical staining of TGF-α and GST-P using serial liver sections demonstrated that the TGF-α-positive foci comprised a sub-population of the GST-P positive lesions, being 1/8-1/10th as common in livers of animals treated with PB. TGF-α-positive foci were almost always negative on immunostaining for TGF-β. Western blotting for proteins CYP2B1, 2C6 and 3A2 revealed a good correlation between changes in GST-P-positive foci and CYP3A2 protein expression. The finding of inhibition effects at low doses of PB confirms the presence of a threshold level for promoting effects by PB on liver carcinogenesis in rats.

Published
1998

43. Histogenesis and the role of p53 and K-ras mutations in hepatocarcinogenesis by glyceryl trinitrate (nitroglycerin) in male F344 rats.

Author

Tamano, S, Ward, J M, Diwan, B A, Keefer, L K, Weghorst, C M, Calvert, R J, Henneman, J R, Ramljak, D, and Rice, J M

Abstract

Glyceryl trinitrate (GTN) was previously reported to induce hepatocellular carcinoma (HCC) in rats after prolonged feeding. The present experiments were undertaken to evaluate the histogenesis and molecular biology of these tumors and the possible role of nitric oxide (NO), a GTN metabolite, in their development. Male F344 rats received a single i.g. intubation of GTN (1.2 g/kg) at 6 weeks of age and/or a diet containing 1% GTN from 8 weeks of age until necropsy, i.e. for up to 78 weeks. Some animals were subjected to 2/3 partial hepatectomy (PH) at 9 weeks of age. Five sequential sacrifices (14, 32, 52, 78 and 84 weeks of age) were performed. No liver tumors developed in control rats or in rats that received GTN only by a single i.g. intubation, even when intubation was followed by PH. Preneoplastic foci, mainly of clear cell and mixed cell type (identified as positive for glutathione S-transferase placental form) were found from 14 weeks of age in rats receiving GTN in the diet. Focal eosinophilic areas (atypical foci) composed of atypical hepatocytes that often extended into the veins were observed beginning at 52 weeks of age. Some mixed hepatocholangiocellular adenomas and carcinomas arose in eosinophilic lesions. HCCs were seen beginning at 78 weeks of age, but only in rats receiving dietary GTN. Incidence of HCC in the latter animals was 50-75%. Most HCCs were well differentiated. The carcinogenic effect of GTN given in the diet was not affected by prior intubation of a large single dose followed by PH. No p53 mutations were found in 18 tumors but K-ras point mutations, all within codon 12, were found in 8/18 tumors, mostly those with cholangiocellular elements. These were first or second position G-->T transversions or second position G-->A transitions. While these mutation types have also been commonly seen in bacteria after NO-related DNA damage, the fact that tumors arose only on prolonged feeding of this potently bioactive agent at massive doses seems consistent with a more complex mechanism involving multiple (i.e. genetic and/or epigenetic) factors in carcinogenesis by GTN.

Published
1996
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results