92 results on '"Hano H"'
Search Results
2. Development and study of the multi pixel photon counter
- Author
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Gomi, S., Hano, H., Iijima, T., Itoh, S., Kawagoe, K., Kim, S.H., Kubota, T., Maeda, T., Matsumura, T., Mazuka, Y., Miyabayashi, K., Miyata, H., Murakami, T., Nakadaira, T., Nakaya, T., Otono, H., Sano, E., Shinkawa, T., Sudo, Y., Takeshita, T., Taguchi, M., Tsubokawa, T., Uozumi, S., Yamaoka, M., Yamazaki, H., Yokoyama, M., Yoshimura, K., and Yoshioka, T.
- Published
- 2007
- Full Text
- View/download PDF
3. SAFETY EVALUATION OF SUPERHEATED PERFLUOROCARBON NANODROPLETS FOR NOVEL NEUROLOGICAL THERAPY: O31
- Author
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Shimizu, J., Endoh, R., Fukuda, T., Inagaki, T., Hano, H., Asami, R., Kawabata, K.-I., Yokoyama, M., and Furuhata, H.
- Published
- 2011
4. Immunohistochemical ETS-related gene detection in a Japanese prostate cancer cohort: Diagnostic use in Japanese prostate cancer patients
- Author
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Furusato, B, van Leenders, Arno, Trapman, Jan, Kimura, T, Egawa, S, Takahashi, H, Furusato, M, Visakorpi, T, Hano, H, and Pathology
- Subjects
genetic structures ,SDG 3 - Good Health and Well-being ,sense organs ,urologic and male genital diseases ,eye diseases - Abstract
Chromosomal rearrangements that result in high expression levels of the ETS-related gene (ERG) present in approximately 50% of prostate cancer (PCa) patients, making this one of the most common oncogenic alterations in PCa. However, ERG overexpression at the protein level has not been rigorously evaluated in Japanese PCa patients. In this study, we evaluated ERG expression using antibody-based detection in 230 prostate specimens in a Japanese PCa cohort. Overall, we identified 20.1% ERG-positive PCa cases. ERG was not detected in benign glands. The specificity of ERG staining for detecting PCa was almost 100%; all of the ERG-positive samples were also diagnosed as PCa. The expression level of the ERG protein correlated with clinicopathological variables, including grade (P = 0.038), stage (P = 0.005), and metastatic status (P = 0.014). No correlation was observed with age (P = 0.196) or with preoperative prostate-specific antigen level (P = 0.322). Although the frequency of ERG-positive cases in Japanese PCa patients (20.1%) was lower than that reported in a PCa cohort in Western countries (approximately 50%), our study demonstrates that the clinical utility of ERG detection at the protein level can serve as an ancillary tool for diagnosing PCa in the Japanese population.
- Published
- 2011
5. Structures and crystal chemistry of the double perovskites Ba2LnB′O6 (Ln=lanthanide and B′=Nb, Ta):. Part II-Temperature dependence of the structures of Ba2LnB′O6
- Author
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Saines, P, Spencer, JR, Kennedy, B, Kubota, Y, Minakata, C, Hano, H, Kato, K, and Takata, M
- Abstract
The structures of eight members of the series of double perovskites of the type Ba2LnB′O6 (Ln=La3+-Sm3+ and Y3+ and B′=Nb5+ and Ta5+) were examined both above and below room temperature using synchrotron X-ray powder diffraction. The La3+ and Pr3+ containing compounds had an intermediate rhombohedral phase whereas the other tantalates and niobates studied have a tetragonal intermediate. This difference in symmetry appears to be a consequence of the larger size of the La3+ and Pr3+ cations compared to the other lanthanides. The temperature range over which the intermediate symmetry is stable is reduced in those compounds near the point where the preferred intermediate symmetry changes from tetragonal to rhombohedral. In such compounds the transition to the cubic phase involves higher order terms in the Landau expression. This suggests that in this region the stability of the two intermediate phases is similar. © 2007 Elsevier Inc. All rights reserved.
- Published
- 2007
6. Spermatogenesis in aged rats after prenatal 3,3′,4,4′,5-pentachlorobiphenyl exposure
- Author
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WAKUI, S, primary, TAKAGI, F, additional, MUTO, T, additional, YOKOO, K, additional, HIRONO, S, additional, KOBAYASHI, Y, additional, SHIROTA, K, additional, AKAHORI, F, additional, SUZUKI, Y, additional, and HANO, H, additional
- Published
- 2007
- Full Text
- View/download PDF
7. Development of Multi-Pixel Photon Counters
- Author
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Gomi, S., primary, Taguchi, M., additional, Hano, H., additional, Itoh, S., additional, Kubota, T., additional, Maeda, T., additional, Mazuka, Y., additional, Otono, H., additional, Sano, E., additional, Sudo, Y., additional, Tsubokawa, T., additional, Yamaoka, M., additional, Yamazaki, H., additional, Uozumi, S., additional, Yoshioka, T., additional, lijima, T., additional, Kawagoe, K., additional, Kim, S. H., additional, Matsumura, T., additional, Miyabayashi, K., additional, Murakami, T., additional, Nakadaira, T., additional, Nakaya, T., additional, Shinkawa, T., additional, Takeshita, T., additional, Yokoyama, M., additional, and Yoshimura, K., additional
- Published
- 2006
- Full Text
- View/download PDF
8. Hidden particle production at the ILC
- Author
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Itoh, H., Ikematsu, K., Fujii, K., Hano, H., Okada, N., and Tamaki Yoshioka
9. Detector concepts
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Aarons, G., Abe, T., Abernathy, J., Ablikim, M., Abramowicz, H., Adey, D., Adloff, C., Adolphsen, C., Afanaciev, K., Agapov, I., Ahn, J. -K, Aihara, H., Akemoto, M., Del Carmenalabau, M., Albert, J., Albrecht, H., Albrecht, M., Alesini, D., Alexander, G., Alexander, J., Allison, W., Amann, J., Amirikas, R., An, Q., Anami, S., Ananthanarayan, B., Anderson, T., Andricek, L., Anduze, M., Anerella, M., Anfimov, N., Angal-Kalinin, D., Antipov, S., Antoine, C., Aoki, M., Aoza, A., Aplin, S., Appleby, R., Arai, Y., Araki, S., Arkan, T., Arnold, N., Arnold, R., Arnowitt, R., Artru, X., Arya, K., Aryshev, A., Asakawa, E., Asiri, F., Asner, D., Atac, M., Atoian, G., Attié, D., Augustin, J. -E, Augustine, D. B., Ayres, B., Aziz, T., Baars, D., Badaud, F., Baddams, N., Bagger, J., Bai, S., Bailey, D., Bailey, I. R., Baker, D., Balalykin, N. I., Balbuena, J. P., Baldy, J. -L, Ball, M., Ballestrero, A., Ballin, J., Baltay, C., Bambade, P., Ban, S., Band, H., Bane, K., Banerjee, B., Barbanotti, S., Barbareschi, D., Barbaro-Galtieri, A., Barber, D. P., Barbi, M., Bardin, D. Y., Barish, B., Barklow, T. L., Barlow, R., Barnes, V. E., Barone, M., Bartels, C., Bartsch, V., Basu, R., Battaglia, M., Batygin, Y., Baudot, J., Baur, U., Baynham, D. E., Beard, C., Bebek, C., Bechtle, P., Becker, U. J., Bedeschi, F., Bedjidian, M., Behera, P., Behnke, T., Bellantoni, L., Bellerive, A., Bellomo, P., Bentson, L. D., Benyamna, M., Bergauer, T., Berger, E., Bergholz, M., Beri, S., Berndt, M., Bernreuther, W., Bertolini, A., Besancon, M., Besson, A., Beteille, A., Bettoni, S., Beyer, M., Bhandari, R. K., Bharadwaj, V., Bhatnagar, V., Bhattacharya, S., Bhattacharyya, G., Bhattacherjee, B., Bhuyan, R., Bi, X. -J, Biagini, M., Bialowons, W., Biebel, O., Bieler, T., Bierwagen, J., Birch, A., Bisset, M., Biswal, S. S., Blackmore, V., Blair, G., Blanchard, G., Blazey, G., Blue, A., Blümlein, J., Boffo, C., Bohn, C., Boiko, V. I., Boisvert, V., Bondarchuk, E. N., Boni, R., Bonvicini, G., Boogert, S., Boonekamp, M., Boorman, G., Borras, K., Bortoletto, D., Bosco, A., Bosio, C., Bosland, P., Bosotti, A., Boudry, V., Boumediene, D. -E, Bouquet, B., Bourov, S., Bowden, G., Bower, G., Boyarski, A., Bozovic-Jelisavcic, I., Bozzi, C., Brachmann, A., Bradshaw, T. W., Brandt, A., Brasser, H. P., Brau, B., Brau, J. E., Breidenbach, M., Bricker, S., Brient, J. -C, Brock, I., Brodsky, S., Brooksby, C., Broome, T. A., Brown, D., Brownell, J. H., Bruchon, M., Brueck, H., Brummitt, A. J., Brun, N., Buchholz, P., Budagov, Y. A., Bulgheroni, A., Bulyak, E., Bungau, A., Bürger, J., Burke, D., Burkhart, C., Burrows, P., Burt, G., Burton, D., Büsser, K., Butler, J., Butterworth, J., Buzulutskov, A., Cabruja, E., Caccia, M., Cai, Y., Calcaterra, A., Caliier, S., Camporesi, T., Cao, J. -J, Cao, J. S., Capatina, O., Cappellini, C., Carcagno, R., Carena, M., Carloganu, C., Carosi, R., Carr, F. S., Carrion, F., Carter, H. F., Carter, J., Carwardine, J., Cassel, R., Cassell, R., Cavallari, G., Cavallo, E., Cembranos, J. A. R., Chakraborty, D., Chandez, F., Charles, M., Chase, B., Chattopadhyay, S., Chauveau, J., Chefdeville, M., Chehab, R., Chel, S., Chelkov, G., Chen, C., Chen, H. S., Chen, H. B., Chen, J. E., Chen, S. Y., Chen, S., Chen, X., Chen, Y. B., Cheng, J., Chevallier, M., Chi, Y. L., Chickering, W., Cho, G. -C, Cho, M. -H, Choi, J. -H, Choi, J. B., Choi, S. Y., Choi, Y. -I, Choudhary, B., Choudhury, D., Choudhury, S. R., Christian, D., Christian, G., Christophe, G., Chung, J. -H, Church, M., Ciborowski, J., Cihangir, S., Ciovati, G., Clarke, C., Clarke, D. G., Clarke, J. A., Clements, E., Coca, C., Coe, P., Cogan, J., Colas, P., Collard, C., Colledani, C., Combaret, C., Comerma, A., Compton, C., Constance, B., Conway, J., Cook, E., Cooke, P., Cooper, W., Corcoran, S., Cornat, R., Corner, L., Gil, E. C., Corvin, W. C., Ramusino, A. C., Cowan, R., Crawford, C., Cremaldi, L. M., Crittenden, J. A., Cussans, D., Cvach, J., Da Silva, W., Khah, H. D., Dabrowski, A., Dabrowski, W., Dadoun, O., Dai, J. P., Dainton, J., Daly, C., Damerell, C., Danilov, M., Daniluk, W., Daram, S., Datta, A., Dauncey, P., David, J., Davier, M., Davies, K. P., Dawson, S., Boer, W., Curtis, S., Groot, N., La Taille, C., Lira, A., Roeck, A., Sangro, R., Santis, S., Deacon, L., Deandrea, A., Klaus Dehmelt, Delagnes, E., Delahaye, J. -P, Delebecque, P., Delerue, N., Delferriere, O., Demarteau, M., Deng, Z., Denisov, Yu N., Densham, C. J., Desch, K., Deshpande, N., Devanz, G., Devetak, E., Dexter, A., Di Benedetto, V., Diéguez, Á, Diener, R., Dinh, N. D., Dixit, M., Dixit, S., Djouadi, A., Dolezal, Z., Dollan, R., Dong, D., Dong, H. Y., Dorfan, J., Dorokhov, A., Doucas, G., Downing, R., Doyle, E., Doziere, G., Drago, A., Dragt, A., Drake, G., Drásal, Z., Dreiner, H., Drell, P., Driouichi, C., Drozhdin, A., Drugakov, V., Du, S., Dugan, G., Duginov, V., Dulinski, W., Dulucq, F., Dutta, S., Dwivedi, J., Dychkant, A., Dzahini, D., Eckerlin, G., Edwards, H., Ehrenfeld, W., Ehrlichman, M., Ehrlichmann, H., Eigen, G., Elagin, A., Elementi, L., Eliasson, P., Ellis, J., Ellwood, G., Elsen, E., Emery, L., Enami, K., Endo, K., Enomoto, A., Eozénou, F., Erbacher, R., Erickson, R., Eyser, K. O., Fadeyev, V., Fang, S. X., Fant, K., Fasso, A., Giannelli, M. F., Fehlberg, J., Feld, L., Feng, J. L., Ferguson, J., Fernandez-Garcia, M., Fernandez-Hernando, J. L., Fiala, P., Fieguth, T., Finch, A., Finocchiaro, G., Fischer, P., Fisher, P., Fisk, H. E., Fitton, M. D., Fleck, I., Fleischer, M., Fleury, J., Flood, K., Foley, M., Ford, R., Fortin, D., Foster, B., Fourches, N., Francis, K., Frey, A., Frey, R., Friedsam, H., Frisch, J., Frishman, A., Fuerst, J., Fujii, K., Fujimoto, J., Fukuda, M., Fukuda, S., Funahashi, Y., Funk, W., Furletova, J., Furukawa, K., Furuta, F., Fusayasu, T., Fuster, J., Gadow, K., Gaede, F., Gaglione, R., Gai, W., Gajewski, J., Galik, R., Galkin, A., Galkin, V., Gallin-Martel, L., Gannaway, F., Gao, J. S., Gao, J., Gao, Y., Garbincius, P., Garcia-Tabares, L., Garren, L., Garrido, L., Garutti, E., Garvey, T., Garwin, E., Gascón, D., Gastal, M., Gatto, C., Gatto, R., Gay, P., Ge, L., Ge, M. Q., Ge, R., Geiser, A., Gellrich, A., Genat, J. -F, Geng, Z. Q., Gentile, S., Gerbick, S., Gerig, R., Ghosh, D. K., Ghosh, K., Gibbons, L., Giganon, A., Gillespie, A., Gillman, T., Ginzburg, I., Giomataris, I., Giunta, M., Gladkikh, P., Gluza, J., Godbole, R., Godfrey, S., Goldhaber, G., Goldstein, J., Gollin, G. D., Gonzalez-Sanchez, F. J., Goodrick, M., Gornushkin, Y., Gostkin, M., Gottschalk, E., Goudket, P., Eschrich, I. G., Gournaris, F., Graciani, R., Graf, N., Grah, C., Grancagnolo, F., Grandjean, D., Grannis, P., Grassellino, A., Graugés, E., Gray, S., Green, M., Greenhalgh, J., Greenshaw, T., Grefe, C., Gregor, I. -M, Grenier, G., Grimes, M., Grimm, T., Gris, P., Grivaz, J. -F, Groll, M., Gronberg, J., Grondin, D., Groom, D., Gross, E., Grunewald, M., Grupen, C., Grzelak, G., Gu, J., Gu, Y. -T, Guchait, M., Guiducci, S., Guler, A. M., Guler, H., Gulmez, E., Gunion, J., Guo, Z. Y., Gurtu, A., Ha, H. B., Haas, T., Haase, A., Haba, N., Haber, H., Haensel, S., Hagge, L., Hagura, H., Hajdu, C., Haller, G., Haller, J., Hallermann, L., Halyo, V., Hamaguchi, K., Hammond, L., Han, L., Han, T., Hand, L., Handu, V. K., Hano, H., Hansen, C., Hansen, J. D., Hansen, J. B., Hara, K., Harder, K., Hartin, A., Hartung, W., Hast, C., Hauptman, J., Hauschild, M., Hauviller, C., Havranek, M., Hawkes, C., Hawkings, R., Hayano, H., Hazumi, M., He, A., He, H. J., Hearty, C., Heath, H., Hebbeker, T., Hedberg, V., Hedin, D., Heifets, S., Heinemeyer, S., Heini, S., Helebrant, C., Helms, R., Heltsley, B., Henrot-Versille, S., Henschel, H., Hensel, C., Hermel, R., Herms, A., Herten, G., Hesselbach, S., Heuer, R. -D, Heusch, C. A., Hewett, J., Higashi, N., Higashi, T., Higashi, Y., Higo, T., Hildreth, M. D., Hiller, K., Hillert, S., Hillier, S. J., Himel, T., Himmi, A., Hinchliffe, I., Hioki, Z., Hirano, K., Hirose, T., Hisamatsu, H., Hisano, J., Hlaing, C. T., Hock, K. M., Hoeferkamp, M., Hohlfeld, M., Honda, Y., Hong, J., Hong, T. M., Honma, H., Horii, Y., Horvath, D., Hosoyama, K., Hostachy, J. -Y, Hou, M., Hou, W. -S, Howell, D., Hronek, M., Hsiung, Y. B., Hu, B., Hu, T., Huang, J. -Y, Huang, T. M., Huang, W. H., Huedem, E., Huggard, P., Hugonie, C., Hu-Guo, C., Huitu, K., Hwang, Y., Idzik, M., Ignatenko, A., Ignatov, F., Ikeda, H., Ikematsu, K., Ilicheva, T., Imbault, D., Imhof, A., Incagli, M., Ingbir, R., Inoue, H., Inoue, Y., Introzzi, G., Ioakeimidi, K., Ishihara, S., Ishikawa, A., Ishikawa, T., Issakov, V., Ito, K., Ivanov, V. V., Ivanov, V., Ivanyushenkov, Y., Iwasaki, M., Iwashita, Y., Jackson, D., Jackson, F., Jacobsen, B., Jaganathan, R., Jamison, S., Janssen, M. E., Jaramillo-Echeverria, R., Jaros, J., Jauffret, C., Jawale, S. B., Jeans, D., Jedziniak, R., Jeffery, B., Jehanno, D., Jenner, L. J., Jensen, C., Jensen, D. R., Jiang, H., Jiang, X. M., Jimbo, M., Jin, S., Jobe, R. K., Johnson, A., Johnson, E., Johnson, M., Johnston, M., Joireman, P., Jokic, S., Jones, J., Jones, R. M., Jongewaard, E., Jönsson, L., Joshi, G., Joshi, S. C., Jung, J. -Y, Junk, T., Juste, A., Kado, M., Kadyk, J., Käfer, D., Kako, E., Kalavase, P., Kalinin, A., Kalinowski, J., Kamitani, T., Kamiya, Y., Kamoshita, J. -I, Kananov, S., Kanaya, K., Kanazawa, K. -I, Kanemura, S., Kang, H. -S, Kang, W., Kanjial, D., Kapusta, F., Karataev, P., Karchin, P. E., Karlen, D., Karyotakis, Y., Kashikhin, V., Kashiwagi, S., Kasley, P., Katagiri, H., Kato, T., Kato, Y., Katzy, J., Kaukher, A., Kaur, M., Kawagoe, K., Kawamura, H., Kazakov, S., Kekelidze, V. D., Keller, L., Kelley, M., Kelly, M., Kennedy, K., Kephart, R., Keung, J., Khainovski, O., Khan, S. A., Khare, P., Khovansky, N., Kiesling, C., Kikuchi, M., Kilian, W., Killenberg, M., Kim, D., Kim, E. S., Kim, E. -J, Kim, G., Kim, H., Kim, H. -C, Kim, J., Kim, K. -J, Kim, K. S., Kim, P., Kim, S., Kim, S. -H, Kim, S. K., Kim, T. J., Kim, Y., Kim, Y. -K, Kimmitt, M., Kirby, R., Kircher, F., Kisielewska, D., Kittel, O., Klanner, R., Klebaner, A. L., Kleinwort, C., Klimkovich, T., Klinkby, E., Kluth, S., Knecht, M., Kneisel, P., Ko, I. S., Ko, K., Kobayashi, M., Kobayashi, N., Kobel, M., Koch, M., Kodys, P., Koetz, U., Kohrs, R., Kojima, Y., Kolanoski, H., Kolodziej, K., Kolomensky, Y. G., Komamiya, S., Kong, X. C., Konigsberg, J., Korbel, V., Koscielniak, S., Kostromin, S., Kowalewski, R., Kraml, S., Krammer, M., Krasnykh, A., Krautscheid, T., Krawczyk, M., Krebs, H. J., Krempetz, K., Kribs, G., Krishnagopal, S., Kriske, R., Kronfeld, A., Kroseberg, J., Kruchonak, U., Kruecker, D., Krüger, H., Krumpa, N. A., Krumshtein, Z., Kuang, Y. P., Kubo, K., Kuchler, V., Kudoh, N., Kulis, S., Kumada, M., Kumar, A., Kume, T., Kundu, A., Kurevlev, G., Kurihara, Y., Kuriki, M., Kuroda, S., Kuroiwa, H., Kurokawa, S. -I, Kusano, T., Kush, P. K., Kutschke, R., Kuznetsova, E., Kvasnicka, P., Kwon, Y., Labarga, L., Lacasta, C., Lackey, S., Lackowski, T. W., Lafaye, R., Lafferty, G., Lagorio, E., Laktineh, I., Lal, S., Laloum, M., Lam, B., Lancaster, M., Lander, R., Lange, W., Langenfeld, U., Langeveld, W., Larbalestier, D., Larsen, R., Lastovicka, T., Lastovicka-Medin, G., Latina, A., Latour, E., Laurent, L., Le, B. N., Le, D. N., Le Diberder, F., Le Dû, P., Lebbolo, H., Lebrun, P., Lecoq, J., Lee, S. -W, Lehner, F., Leibfritz, J., Lenkszus, F., Lesiak, T., Levy, A., Lewandowski, J., Leyh, G., Li, C., Li, C. S., Li, C. H., Li, D. Z., Li, G., Li, J., Li, S. P., Li, W. M., Li, W., Li, X. P., Li, X. -Q, Li, Y., Li, Z., Li, Z. Q., Liang, J. T., Liao, Y., Lilje, L., Lima, J. G., Lintern, A. J., Lipton, R., List, B., List, J., Liu, C., Liu, J. F., Liu, K. X., Liu, L. Q., Liu, S. Z., Liu, S. G., Liu, S., Liu, W., Liu, W. B., Liu, Y. P., Liu, Y. D., Lockyer, N., Logan, H. E., Logatchev, P. V., Lohmann, W., Lohse, T., Lola, S., Lopez-Virto, A., Loveridge, P., Lozano, M., Lu, C. -D, Lu, C., Lu, G. -L, Lu, W. H., Lubatti, H., Lucotte, A., Lundberg, B., Lundin, T., Luo, M., Luong, M., Luth, V., Lutz, B., Lutz, P., Lux, T., Luzniak, P., Lyapin, A., Lykken, J., Lynch, C., Ma, L., Ma, Q., Ma, W. -G, Macfarlane, D., Maciel, A., Macleod, A., Macnair, D., Mader, W., Magill, S., Magnan, A. -M, Maiheu, B., Maity, M., Majchrzak, M., Majumder, G., Makarov, R., Makowski, D., Malaescu, B., Mallik, C., Mallik, U., Malton, S., Malyshev, O. B., Malysheva, L. I., Mammosser, J., Mamta, Mamuzic, J., Manen, S., Manghisoni, M., Manly, S., Marcellini, F., Marcisovsky, M., Markiewicz, T. W., Marks, S., Marone, A., Marti, F., Martin, J. -P, Martin, V., Martin-Chassard, G., Martinez, M., Martinez-Rivero, C., Martsch, D., Martyn, H. -U, Maruyama, T., Masuzawa, M., Mathez, H., Matsuda, T., Matsumoto, H., Matsumoto, S., Matsumoto, T., Matsunaga, H., Mättig, P., Mattison, T., Mavromanolakis, G., Mawatari, K., Mazzacane, A., Mcbride, P., Mccormick, D., Mccormick, J., Mcdonald, K. T., Mcgee, M., Mcintosh, P., Mckee, B., Mcpherson, R. A., Meidlinger, M., Meier, K., Mele, B., Meller, B., Melzer-Pellmann, I. -A, Mendez, H., Mercer, A., Merkin, M., Meshkov, I. N., Messner, R., Metcalfe, J., Meyer, C., Meyer, H., Meyer, J., Meyer, N., Meyners, N., Michelato, P., Michizono, S., Mihalcea, D., Mihara, S., Mihara, T., Mikami, Y., Mikhailichenko, A. A., Milardi, C., Miller, D. J., Miller, O., Miller, R. J., Milstene, C., Mimashi, T., Minashvili, I., Miquel, R., Mishra, S., Mitaroff, W., Mitchell, C., Miura, T., Miyamoto, A., Miyata, H., Mjörnmark, U., Mnich, J., Moenig, K., Moffeit, K., Mokhov, N., Molloy, S., Monaco, L., Monasterio, P. R., Montanari, A., Moon, S. I., Moortgat-Pick, G. A., Freitas, P. M., Morel, F., Moretti, S., Morgunov, V., Mori, T., Morin, L., Morisseau, F., Morita, Y., Morozov, N., Morozumi, Y., Morse, W., Moser, H. -G, Moultaka, G., Mtingwa, S., Mudrinic, M., Mueller, A., Mueller, W., Muennich, A., Muhlleitner, M. M., Mukherjee, B., Mukhopadhyaya, B., Müller, T., Munro, M., Murayama, H., Muto, T., Myneni, G. R., Nabhiraj, P. Y., Nagaitsev, S., Nagamine, T., Nagano, A., Naito, T., Nakai, H., Nakajima, H., Nakamura, I., Nakamura, T., Nakanishi, T., Nakao, K., Nakao, N., Nakayoshi, K., Nam, S., Namito, Y., Namkung, W., Nantista, C., Napoly, O., Narain, M., Naroska, B., Nauenberg, U., Nayyar, R., Neal, H., Nelson, C., Nelson, J., Nelson, T., Nemecek, S., Neubauer, M., Neuffer, D., Newman, M. Q., Nezhevenko, O., Ng, C. -K, Nguyen, A. K., Nguyen, M., Thi, H. V. N., Niebuhr, C., Niehoff, J., Niezurawski, P., Nishitani, T., Nitoh, O., Noguchi, S., Nomerotski, A., Noonan, J., Norbeck, E., Nosochkov, Y., Notz, D., Nowak, G., Nowak, H., Noy, M., Nozaki, M., Nyffeler, A., Nygren, D., Oddone, P., O, J., Oh, J. -S, Oh, S. 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I., Strologas, J., Strom, D., Strube, J., Stupakov, G., Su, D., Sudo, Y., Suehara, T., Suehiro, T., Suetsugu, Y., Sugahara, R., Sugimoto, Y., Sugiyama, A., Suh, J. S., Sukovic, G., Sun, H., Sun, S., Sun, W., Sun, Y., Suszycki, L., Sutcliffe, P., Suthar, R. L., Suwada, T., Suzuki, A., Suzuki, C., Suzuki, S., Suzuki, T., Swent, R., Swientek, K., Swinson, C., Syresin, E., Szleper, M., Tadday, A., Takahashi, R., Takahashi, T., Takano, M., Takasaki, F., Takeda, S., Takenaka, T., Takeshita, T., Takubo, Y., Tanaka, M., Tang, C. X., Taniguchi, T., Tantawi, S., Tapprogge, S., Tartaglia, M. A., Tassielli, G. F., Tauchi, T., Tavian, L., Tawara, H., Taylor, G., Telnov, A. V., Telnov, V., Tenenbaum, P., Teodorescu, E., Terashima, A., Terracciano, G., Terunuma, N., Teubner, T., Teuscher, R., Theilacker, J., Thomson, M., Tice, J., Tigner, M., Timmermans, J., Titov, M., Toge, N., Tokareva, N. A., Tollefson, K., Tomasek, L., Tomovic, S., Tompkins, J., Tonutti, M., Topkar, A., Toprek, D., Toral, F., Torrence, E., Traversi, G., Trimpl, M., Tripathi, S. M., Trischuk, W., Trodden, M., Trubnikov, G. V., Tschirhart, R., Tskhadadze, E., Tsuchiya, K., Tsukamoto, T., Tsunemi, A., Tucker, R., Turchetta, R., Tyndel, M., Uekusa, N., Ueno, K., Umemori, K., Ummenhofer, M., Underwood, D., Uozumi, S., Urakawa, J., Urban, J., Uriot, D., Urner, D., Ushakov, A., Usher, T., Uzunyan, S., Vachon, B., Valerio, L., Valin, I., Valishev, A., Vamra, R., Graaf, H., Kooten, R., Zandbergen, G., Vanel, J. -C, Variola, A., Varner, G., Velasco, M., Velte, U., Velthuis, J., Vempati, S. K., Venturini, M., Vescovi, C., Videau, H., Vila, I., Vincent, P., Virey, J. -M, Visentin, B., Viti, M., Vo, T. C., Vogel, A., Vogt, H., Toerne, E., Vorozhtsov, S. B., Vos, M., Votava, M., Vrba, V., Wackeroth, D., Wagner, A., Wagner, C. E. M., Wagner, S., Wake, M., Walczak, R., Walker, N. 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M., Zhou, F., Zhou, S., Zhu, S. H., Zhu, X. W., Zhukov, V., Zimmermann, F., Ziolkowski, M., Zisman, M. S., Zomer, F., Zong, Z. G., Zorba, O., and Zutshi, V.
10. P-361 Significance of the CD5 positive B cells in chronic hepatitis C
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Tsuno, S, Zeniya, M, Ishikawa, T, Hokari, A, Ookawa, Y, Okuaki, Y, Hara, M, Sakaguchi, M, Aizawa, Y, Itsubo, M, Hano, H, and Toda, G
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- 1995
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11. Growth hormone is involved in GATA1 gene expression via STAT5B in human erythroleukemia and monocytic cell lines.
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Mitsutani M, Yokoyama M, Hano H, Morita A, Matsushita M, Tagami T, and Moriyama K
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GATAs are a family of transcription factors consisting of six members. Particularly, GATA1 and GATA2 have been reported to promote the development of erythrocytes, megakaryocytes, eosinophils, and mast cells. However, little information is available on the extracellular ligands that promote GATA1 expression. We evaluated whether growth hormone (GH) is an extracellular stimulator that participates in the signal transduction of GATAs, focusing on GATA1 expression in hematopoietic cell lineages. We used a reporter assay, RT-PCR, real-time quantitative PCR, and western blotting to evaluate GH-induced expression of GATA1 and GATA2 in the human erythroleukemic cell line K562 and the non-erythroid cell line U937. GATA1 expression in these hematopoietic cell lines increased at the transcriptional and protein levels in the presence of GH, and was inhibited by a STAT5 specific inhibitor. Cells transfected with activated STAT5B showed increased expression of GATA1. We identified functional STAT5B consensus sequences as binding site-158 bp from the transcription starting site in the GATA1 promoter region. These results suggest that GH directly induces GATA1 expression via GHR/JAK/STAT5 and is related to hematopoietic cell proliferation., Competing Interests: Declaration of competing interest The authors declare no conflict of interest., (Copyright © 2024 Elsevier Inc. All rights reserved.)
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- 2024
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12. Power of Light: Raman Spectroscopy and Machine Learning for the Detection of Lung Cancer.
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Hano H, Lawrie CH, Suarez B, Paredes Lario A, Elejoste Echeverría I, Gómez Mediavilla J, Crespo Cruz MI, Lopez E, and Seifert A
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Lung cancer is the leading cause of cancer-related deaths worldwide, emphasizing the urgent need for reliable and efficient diagnostic methods. Conventional approaches often involve invasive procedures and can be time-consuming and costly, thereby delaying the effective treatment. The current study explores the potential of Raman spectroscopy, as a promising noninvasive technique, by analyzing human blood plasma samples from lung cancer patients and healthy controls. In a benchmark study, 16 machine learning models were evaluated by employing four strategies: the combination of dimensionality reduction with classifiers; application of feature selection prior to classification; stand-alone classifiers; and a unified predictive model. The models showed different performances due to the inherent complexity of the data, achieving accuracies from 0.77 to 0.85 and areas under the curve for receiver operating characteristics from 0.85 to 0.94. Hybrid methods incorporating dimensionality reduction and feature selection algorithms present the highest figures of merit. Nevertheless, all machine learning models deliver creditable scores and demonstrate that Raman spectroscopy represents a powerful method for future in vitro diagnostics of lung cancer., Competing Interests: The authors declare no competing financial interest., (© 2024 The Authors. Published by American Chemical Society.)
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- 2024
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13. Intratracheal administration of cross-linked water-soluble acrylic acid polymer is associated with inducible bronchi-related lymphoid tissue formation and allergic inflammation.
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Kido T, Sugaya C, Hano H, Yanagisawa H, and Suka M
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- Male, Rats, Animals, Polymers, Rats, Inbred F344, Lymphoid Tissue, Bronchi pathology, Lung pathology, Inflammation pathology, Transforming Growth Factor beta, Collagen, Pulmonary Fibrosis pathology, Acrylates
- Abstract
In a Japanese chemical factory, lung diseases such as pneumoconiosis have been reported among workers handling cross-linked water-soluble acrylic acid polymers (CWAAP). Our previous study reported that a single intratracheal administration of CWAAP induces acute inflammation and fibrosis. In this study, we investigated the effects of multiple intratracheal administrations of CWAAP on inflammatory responses and pulmonary fibrosis along with inducible bronchus-associated lymphoid tissues (iBALT) formation, which is involved in allergic inflammation. Male F344 rats (190-200 g) received single or multiple intratracheal administrations of phosphate-buffered saline (PBS) or CWAAP. To assess inflammatory responses and pulmonary fibrosis, immunohistochemical and histological staining was performed. CD68, CD163, CD169, TGF-β, and collagen I positive cells/areas in the lungs of the CWAAP-group rats were significantly increased than those in the PBS group. Furthermore, the number of iBALT structures, CD4 + T cells, along with CD19, PAX5, IL-4, GATA-3, T-bet, and IgE-positive cells in the terminal bronchioles and blood vessels of the lungs were significantly increased in the CWAAP group. Moreover, pulmonary fibrosis, iBALT formation, and levels of specific IgG were significantly increased in rats who received multiple intratracheal administrations of CWAAP compared to those with single intratracheal administration. Multiple intratracheal administrations of CWAAP potentiated the classical fibrotic pathway (M2 macrophage-TGF-β-collagen I) more potently than single intratracheal administration. Furthermore, it was possible that iBALT was formed around terminal bronchioles and blood vessels and the number of immune cells was increased, resulting in enhanced allergic inflammation and pulmonary fibrosis., (© 2023 John Wiley & Sons Ltd.)
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- 2024
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14. Growth hormone directly stimulates GATA2 expression.
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Mitsutani M, Matsushita M, Yokoyama M, Morita A, Hano H, Fujikawa T, Tagami T, and Moriyama K
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- Mice, Animals, STAT5 Transcription Factor genetics, STAT5 Transcription Factor metabolism, Janus Kinases metabolism, Signal Transduction, STAT Transcription Factors metabolism, Milk Proteins, Growth Hormone metabolism, Human Growth Hormone metabolism
- Abstract
Objective: GATA2 is a key transcription factor involved in the differentiation and determination of thyrotrophs and gonadotrophs in pituitary and hematopoietic development. However, studies on the upstream ligands of the GATA2 signal transduction pathway have been limited. To identify upstream ligands, we examined growth hormone (GH) as a plausible stimulator., Design: We evaluated GH-induced GATA2 expression in murine TtT/GF thyrotrophic pituitary tumor cells and its direct impact on the GHR/JAK/STAT5 pathway using a combination of a reporter assay, real-time quantitative polymerase chain reaction, and western blotting., Results: GATA2 expression increased with activated STAT5B in a dose-dependent manner and was inhibited by a STAT5 specific inhibitor. Moreover, we found functional STAT5B binding site consensus sequences at -359 bp in the GATA2 promoter region., Conclusion: These findings suggest that GH directly stimulates GATA2 via the GHR/JAK/STAT pathway and participates in various developmental phenomena mediated by GATA2., Competing Interests: Declaration of competing interest None., (Copyright © 2024 Elsevier Ltd. All rights reserved.)
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- 2024
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15. Laparoscopic Groin Hernia Repair Using the Totally Extraperitoneal Approach: A Retrospective Study and Our Experience.
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Harvitkar RU, Gattupalli GB, Al-Hano H, Al-Kharouf KF, and Joshi A
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Background Recently, laparoscopic totally extraperitoneal (TEP) inguinal hernia repair has been considered one of the most effective and widely performed techniques for repairing inguinal hernias by avoiding entry into the peritoneal cavity. Its indications have evolved and expanded to almost encompass the entire range of groin hernias. This retrospective study aims to determine the outcomes and postoperative complications in patients undergoing TEP inguinal hernia repair performed by a single surgeon for groin hernias at a single center. Methodology We retrospectively evaluated the prospectively collected data of 900 patients who underwent elective TEP repair over 18 years at a single center performed by a single surgeon from April 2004 to February 2023. Patients were evaluated for age, sex, type of hernia, time taken for surgery, open from laparoscopy, intra and postoperative complications, hospital stay, and days taken to resume regular activity. Results The mean age of the 900 patients was 59 years (range = 21-83 years). The mean age of males and females was 59 and 56 years, respectively. The mean operative time was 40 and 55 minutes for a unilateral and bilateral hernia, respectively. In total, 369 (41%) patients had a right-sided groin hernia, 382 (42%) patients had a left-sided groin hernia, and 149 (16.5%) patients had bilateral groin hernias. A total of 121 (13%) patients had occult hernias, and 17 patients underwent concurrent TEP and transurethral resection of the prostate. Of the 900 patients, 20 (2.2%) had a recurrent hernia after a previous open inguinal hernia repair. Seven (0.8%) patients had a recurrence of hernias post-TEP and subsequently underwent open inguinal hernia repair. Seven (0.7%) patients needed conversion from TEP to the transabdominal pre-peritoneal approach. Only minor complications were noted intra and postoperatively. The average time of hospitalization was 24 hours. The time to resume normal activities was five (±1) days. Conclusions Our experience suggests that TEP repair with mesh fixation is a safe and effective procedure with a marginal recurrence rate. Apart from the obvious cosmetic benefits of minimal tissue invasion, a significant advantage of TEP is the visualization of the contralateral groin along with the surgical repair of a hernia, if required, in the same sitting and without the insertion of any extra trocars., Competing Interests: The authors have declared that no competing interests exist., (Copyright © 2023, Harvitkar et al.)
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- 2023
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16. Hepatocellular adenoma, approximately half and predominantly inflammatory subtype, in 38 Japanese patients with several differences in age, gender, and clinical background factors from Western populations.
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Izu A, Sugitani M, Kinukawa N, Matsumura H, Ogawa M, Moriyama M, Yamazaki S, Takayama T, Hano H, Yao T, Kanda H, Suzuki K, Hayashi S, Ariizumi S, Yamamoto M, Morishita Y, Matsumoto K, Nakamura N, and Nakano M
- Abstract
Aim: Hepatocellular adenoma (HCA) has a lower prevalence in Japan than in Western countries and HCA subtypes have been reported for only a few Japanese patients. We analyzed HCA subtype data 38 patients from 23 hospitals in Japan in order to examine character and difference between Western countries., Methods: To confirm HCA and to analyze subtypes, we performed immunohistochemical examinations., Results: Thirty-eight cases were found to have HCA without cirrhosis. The male/female ratio was 18/20. Ages ranged from 15 to 79 (average, 43.2) years. Male and elder patients are not rare, furthermore, most of elder patients are male. Glycogen storage disease, past history of medicament use, hepatitis B virus surface antigen-positivity, antihepatitis C virus -positivity, diabetes mellitus, obesity, lipid metabolism disorder and alcoholism were present in of 6, 8, 1, 1, 6, 6, 4, and 6 cases, respectively. As to HCA subtypes, HNF1alpha-inactivated HCA, beta-catenin activated HCA (b-HCA), inflammatory HCA (IHCA) and unclassified HCA (U-HCA) accounted for nine (23.7%), four (10.5%), 17 (44.7%) and eight (21.1%) cases, respectively. Two cases showed coexistence of HCA and hepatocellular carcinoma (HCC) at surgery, and another had HCC which had been detected 23 years after HCA diagnosis. The HCA subtype of one of the former cases was U-HCA, while the remaining two had b-HCA and U-HCA., Conclusions: In Japanese HCA cases, the proportions of U-HCA, male and elder cases were slightly higher than in Western countries, and most of elder patients were male. IHCA was however common regardless of race, and was assumed to be the predominant subtype of HCA., (© 2020 The Japan Society of Hepatology.)
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- 2021
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17. Single intratracheal administration of cross-linked water-soluble acrylic acid polymer causes acute alveolo-interstitial inflammation and the subsequent fibrotic formation possibly via the TGF-β1 pathway in the lung of rats.
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Suka M, Kido T, Yoshioka W, Hachisuka E, Okoshi H, Yamauchi T, Hano H, Okano T, Yokoyama M, and Yanagisawa H
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- Acrylates administration & dosage, Animals, Cross-Linking Reagents administration & dosage, Inflammation chemically induced, Inflammation metabolism, Inflammation pathology, Lung drug effects, Lung metabolism, Lung pathology, Male, Polymers administration & dosage, Pulmonary Alveoli drug effects, Pulmonary Alveoli pathology, Pulmonary Fibrosis chemically induced, Pulmonary Fibrosis pathology, Rats, Rats, Inbred F344, Signal Transduction drug effects, Signal Transduction physiology, Trachea drug effects, Trachea metabolism, Trachea pathology, Acrylates toxicity, Cross-Linking Reagents toxicity, Polymers toxicity, Pulmonary Alveoli metabolism, Pulmonary Fibrosis metabolism, Transforming Growth Factor beta1 metabolism
- Abstract
In a Japanese chemical factory, a lung disease like pneumoconiosis appeared at a high rate among workers handling cross-linked water-soluble acrylic acid polymer (CWAAP). To our knowledge, no such case was known in the world until very recently. The present study was designed to elucidate the effect of single intratracheal CWAAP instillation on the lung of rats. The CWAAP group had a significant increase in relative lung weight accompanied by a significant elevation in the number of total cells, total protein concentrations, and myeloperoxidase concentrations in bronchoalveolar lavage fluid when compared to the control group. The histopathological study revealed acute lung inflammation with the destruction of alveoli. The factors promoting fibrosis, macrophages, TGF-β1, collagen and fibronectin vs. the factors suppressing fibrosis, matrix metalloproteinases were more powerfully driven in the CWAAP group, resultantly leading to fibrotic formation. In turn, we examined if acute lung inflammation and the subsequent fibrotic formation seen in the CWAAP group appeared in the other water-soluble polymer groups. Their histopathological findings were observed only in the polyacrylic acid sodium (PAAS), a monomer of CWAAP, group. The degree of inflammation and fibrogenesis was stronger in the CWAAP group than in the PAAS group. In conclusion, the present study demonstrated the induction of acute lung inflammation and the subsequent fibrotic formation by single intratracheal CWAAP instillation. The structural features of CWAAP that contains many carboxyl groups and cross-linked chains may be responsible for enhanced inflammation and fibrogenesis in the lung., (Copyright © 2020. Published by Elsevier B.V.)
- Published
- 2021
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18. Histological and biochemical evaluation of transforming growth factor-β activation and its clinical significance in patients with chronic liver disease.
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Yokoyama H, Masaki T, Inoue I, Nakamura M, Mezaki Y, Saeki C, Oikawa T, Saruta M, Takahashi H, Ikegami M, Hano H, Ikejima K, Kojima S, and Matsuura T
- Abstract
Transforming growth factor-β (TGF-β) is a key driver for liver fibrogenesis. TGF-β must be activated in order to function. Plasma kallikrein (PLK) is a TGF-β activator that cleaves the latency-associated protein (LAP) between arginine
58 and lysine59 residues and releases active TGF-β from the latent TGF-β-LAP complex. Thus, the generation of two LAP degradation products, ending at arginine58 (R58 /LAP-DPs) and beginning from lysine59 (L59 /LAP-DPs), reflects PLK-dependent TGF-β activation. However, the significance and details of TGF-β activation in patients with chronic liver disease (CLD) remain uncertain. We herein examined the PLK-dependent TGF-β activation in patients by detecting R58 and L59 /LAP-DPs. A total of 234 patients with CLD were included in this study. Liver biopsy specimens were used for immunostaining to detect R58 /LAP-DPs, while plasma samples were subjected to an enzyme-linked immunosorbent assay to measure the L59 /LAP-DP concentration. R58 /LAP-DP was robustly expressed in and around the sinusoidal cells before the development of the fibrous regions. The R58 /LAP-DP expression at fibrosis stage 1 was higher than at any other stages, and the relationship between the plasma L59 /LAP-DP level and the stage of fibrosis also showed a similar trend. The abundance of plasma L59 /LAP-DP showed no correlation with the levels of direct serum biomarkers of liver fibrosis; however, its changes during interferon-based therapy for chronic hepatitis C were significantly associated with virological responses. Our results suggest that PLK-dependent TGF-β activation occurs in the early stages of fibrosis and that its unique surrogate markers, R58 and L59 /LAP-DPs, are useful for monitoring the clinical course of CLD.- Published
- 2019
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19. Hepatocellular adenoma in a woman who was undergoing testosterone treatment for gender identity disorder.
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Kato K, Abe H, Hanawa N, Fukuzawa J, Matsuo R, Yonezawa T, Itoh S, Sato Y, Ika M, Shimizu S, Endo S, Hano H, Izu A, Sugitani M, and Tsubota A
- Subjects
- Adult, Carcinoma, Hepatocellular classification, Carcinoma, Hepatocellular diagnosis, Carcinoma, Hepatocellular surgery, Female, Humans, Liver Neoplasms classification, Liver Neoplasms diagnosis, Liver Neoplasms surgery, Neoplasms, Multiple Primary classification, Neoplasms, Multiple Primary diagnosis, Neoplasms, Multiple Primary surgery, Testosterone adverse effects, Androgens adverse effects, Carcinoma, Hepatocellular chemically induced, Gender Identity, Liver Neoplasms chemically induced, Neoplasms, Multiple Primary chemically induced, Testosterone analogs & derivatives
- Abstract
A 32-year-old Japanese woman was admitted to our hospital for the diagnosis and treatment of multiple liver tumors. She had been receiving 125 mg testosterone enanthate every 2 weeks following female-to-male gender identity disorder (GID) diagnosis at 20 years of age. Ultrasonography, computed tomography, and magnetic resonance imaging showed 11 hepatic nodular tumors with a maximum diameter of 28 mm. Liver tumors with hepatocellular adenoma (HCA) were diagnosed with needle biopsy. Segmentectomy of the left lateral lobe including two lesions, subsegmentectomy of S6 including two lesions, enucleation of each tumor in S5 and S7, and open surgical radiofrequency ablation for each tumor in S4 and S7 were performed. Immunohistochemical specimens showed that the tumor cells were diffusely and strongly positive for glutamine synthetase and that the nuclei were ectopically positive for β-catenin. Thus, the tumors were diagnosed as β-catenin-activated HCA (b-HCA). Transcatheter arterial chemoembolization plus subsequent radiofrequency ablation was performed for the 3 residual lesions in S4 and S8. Although testosterone enanthate was being continued for GID, no recurrence was observed until at least 22 months after the intensive treatments. HCA development in such patients receiving testosterone should be closely monitored using image inspection.
- Published
- 2018
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20. Folliculin Regulates Osteoclastogenesis Through Metabolic Regulation.
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Baba M, Endoh M, Ma W, Toyama H, Hirayama A, Nishikawa K, Takubo K, Hano H, Hasumi H, Umemoto T, Hashimoto M, Irie N, Esumi C, Kataoka M, Nakagata N, Soga T, Yao M, Kamba T, Minami T, Ishii M, and Suda T
- Subjects
- Animals, Basic Helix-Loop-Helix Leucine Zipper Transcription Factors metabolism, Bone Marrow pathology, Mice, Mice, Knockout, Organelle Biogenesis, Osteoclasts pathology, Osteoporosis metabolism, Osteoporosis pathology, Oxidative Phosphorylation, Purines metabolism, RAW 264.7 Cells, Signal Transduction, Transcription Factors metabolism, Up-Regulation, Osteoclasts metabolism, Osteogenesis, Proto-Oncogene Proteins metabolism, Tumor Suppressor Proteins metabolism
- Abstract
Osteoclast differentiation is a dynamic differentiation process, which is accompanied by dramatic changes in metabolic status as well as in gene expression. Recent findings have revealed an essential connection between metabolic reprogramming and dynamic gene expression changes during osteoclast differentiation. However, the upstream regulatory mechanisms that drive these metabolic changes in osteoclastogenesis remain to be elucidated. Here, we demonstrate that induced deletion of a tumor suppressor gene, Folliculin (Flcn), in mouse osteoclast precursors causes severe osteoporosis in 3 weeks through excess osteoclastogenesis. Flcn-deficient osteoclast precursors reveal cell autonomous accelerated osteoclastogenesis with increased sensitivity to receptor activator of NF-κB ligand (RANKL). We demonstrate that Flcn regulates oxidative phosphorylation and purine metabolism through suppression of nuclear localization of the transcription factor Tfe3, thereby inhibiting expression of its target gene Pgc1. Metabolome studies revealed that Flcn-deficient osteoclast precursors exhibit significant augmentation of oxidative phosphorylation and nucleotide production, resulting in an enhanced purinergic signaling loop that is composed of controlled ATP release and autocrine/paracrine purinergic receptor stimulation. Inhibition of this purinergic signaling loop efficiently blocks accelerated osteoclastogenesis in Flcn-deficient osteoclast precursors. Here, we demonstrate an essential and novel role of the Flcn-Tfe3-Pgc1 axis in osteoclastogenesis through the metabolic reprogramming of oxidative phosphorylation and purine metabolism. © 2018 The Authors Journal of Bone and Mineral Research published by Wiley Periodicals, Inc. on behalf of American Society for Bone and Mineral Research (ASBMR)., (© 2018 The Authors Journal of Bone and Mineral Research published by Wiley Periodicals, Inc. on behalf of American Society for Bone and Mineral Research (ASBMR).)
- Published
- 2018
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21. Serum Wisteria floribunda agglutinin-positive Mac-2 binding protein more reliably distinguishes liver fibrosis stages in non-alcoholic fatty liver disease than serum Mac-2 binding protein.
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Atsukawa M, Tsubota A, Okubo T, Arai T, Nakagawa A, Itokawa N, Kondo C, Kato K, Hatori T, Hano H, Oikawa T, Emoto N, Abe M, Kage M, and Iwakiri K
- Abstract
Aim: Serum Mac-2 binding protein (M2BP) and Wisteria floribunda agglutinin-positive Mac-2 binding protein (WFA
+ -M2BP) are used to estimate the liver fibrosis stage in chronic liver diseases. However, few head-to-head studies have been carried out to compare the two biomarkers in non-alcoholic fatty liver disease (NAFLD)., Methods: Serum M2BP and WFA+ -M2BP levels were compared against clinical characteristics and liver histological manifestations in the same samples collected from 213 biopsy-proven NAFLD patients., Results: Median levels (range) of M2BP and WFA+ -M2BP were 1.58 (0.70-7.75) pg/mL and 0.85 (0.22-11.32) cut-off index (COI), respectively. Fibrosis stages 1, 2, 3, and 4 were determined in 136, 37, 17, and 23 patients, respectively. Median levels of both biomarkers increased stepwise with fibrosis progression. The M2BP and WFA+ -M2BP levels showed a significant positive correlation (r = 0.643, P = 2.91 × 10-26 ), but a marked discrepancy between both biomarkers was noted in five stage 4 and three stage 1 patients, who had high WFA+ -M2BP but relatively low M2BP levels. Most of these outliers had findings suggestive of more advanced fibrosis. For diagnosing any fibrosis severity, WFA+ -M2BP had greater area under the receiver operating characteristic curve (AUC) and predictive accuracy than M2BP. Among eight fibrosis markers/indices, WFA+ -M2BP yielded the second highest AUC (0.832) and the highest predictive accuracy (82.2%) to diagnose cirrhosis. In addition, WFA+ -M2BP showed the second highest predictive accuracy to diagnose severe fibrosis (78.4%) and significant fibrosis (76.1%)., Conclusion: This head-to-head comparison suggests that WFA+ -M2BP is superior to M2BP for distinguishing liver fibrosis stages in NAFLD patients. A marked discrepancy between the two biomarkers may be indicative of advanced NAFLD (UMIN000023286)., (© 2017 The Japan Society of Hepatology.)- Published
- 2018
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22. Fluoride potentiates tubulointerstitial nephropathy caused by unilateral ureteral obstruction.
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Kido T, Tsunoda M, Sugaya C, Hano H, and Yanagisawa H
- Subjects
- Actins genetics, Actins metabolism, Animals, Dose-Response Relationship, Drug, Fluorides blood, Kidney drug effects, Kidney physiopathology, Macrophages cytology, Macrophages drug effects, Male, Myofibroblasts cytology, Myofibroblasts drug effects, Organ Size drug effects, Rats, Rats, Sprague-Dawley, Transforming Growth Factor beta1 genetics, Transforming Growth Factor beta1 metabolism, Fluorides toxicity, Kidney Diseases pathology, Ureteral Obstruction pathology
- Abstract
The contamination of ground water by fluoride has been reported worldwide. Most fluoride (approximately 70%) is filtered by the kidneys; humans or experimental animals with renal damage therefore may be more affected by fluoride exposure than those with normal kidney function. Tubulointerstitial fibrosis, which involves macrophage-promoted extracellular matrix production and myofibroblast migration, can be induced in rats by unilateral ureteral obstruction (UUO). We examined the effects of fluoride exposure on tubulointerstitial fibrosis in the obstructed kidney of UUO rats. The left ureters of 6-week-old male rats were ligated using silk sutures. Fluoride was then administered for 2 weeks at doses of 0, 75, and 150ppm in the drinking water. Real-time polymerase chain reaction was performed to analyze transforming growth factor beta 1 (TGF-β
1 ) transcription; histological and immunohistochemical staining were used to identify positive areas within the renal cortex and staining-positive cells by image analysis. Significant increases were observed in the obstructed kidneys of UUO rats exposed to 150ppm fluoride (compared to 0ppm) for areas or number of cells that stained with Masson trichrome or with antibodies against collagen type I, alpha-smooth muscle actin (α-SMA, a myofibroblast marker), ED1, ED2, and ED3 (macrophage markers), and TGF-β1 . Taken together, these observations suggested that fluoride exacerbates tuburointerstitial nephropathy resulting from UUO, and that this effect occurs via activation of the M2 macrophage-TGF-β1-fibroblast/myofibroblast-collagen synthesis pathway., (Copyright © 2017 Elsevier B.V. All rights reserved.)- Published
- 2017
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23. Tissue thrombin is associated with the pathogenesis of dilated cardiomyopathy.
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Ito K, Hongo K, Date T, Ikegami M, Hano H, Owada M, Morimoto S, Kashiwagi Y, Katoh D, Yoshino T, Yoshii A, Kimura H, Nagoshi T, Kajimura I, Kusakari Y, Akaike T, Minamisawa S, Ogawa K, Minai K, Ogawa T, Kawai M, Yajima J, Matsuo S, Yamane T, Taniguchi I, Morimoto S, and Yoshimura M
- Subjects
- Animals, Antithrombins therapeutic use, Cardiomyopathy, Dilated pathology, Case-Control Studies, Dabigatran therapeutic use, Disease Models, Animal, Humans, Mice, Cardiomyopathy, Dilated etiology, Cardiomyopathy, Dilated metabolism, Thrombin metabolism
- Abstract
Background: Thrombin is a serine protease known to be the final product of the coagulation cascade. However, thrombin plays other physiological roles in processes such as gastric contractions and vessel wound healing, and a state of coagulability is increased in patients with dilated cardiomyopathy (DCM). In this study, we investigate the role of thrombin in the pathogenesis of DCM. The purpose of this study is to clarify the role of thrombin in the pathogenesis of DCM and investigate the possibility of treatment against DCM by thrombin inhibition., Methods: We investigated the expression of thrombin in the left ventricles of five patients with DCM who underwent the Batista operation and four patients without heart disease. Furthermore, we investigated the involvement of thrombin in the development of DCM using knock-in mice with a deletion mutation of cardiac troponin T that causes human DCM (∆K210 knock-in mouse) (B6;129-Tnnt2
tm2Mmto ) and assessed the effects of a direct thrombin inhibitor, dabigatran on ∆K210 knock-in mice using echocardiographic examinations, the Kaplan-Meier method and Western blotting., Results: The immunohistochemical analysis showed a strong thrombin expression in the DCM patients compared to the patients without heart disease. In immunohistochemical analysis, a strong thrombin expression was observed in the heart tissues analysis in the ∆K210 knock-in mice. Dabigatran administration significantly improved fractional shortening according to the echocardiographic examination and the survival outcomes in ∆K210 knock-in mice., Conclusion: Tissue thrombin is involved in the pathogenesis of DCM and thrombin inhibition can be beneficial for the treatment of DCM., (Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.)- Published
- 2017
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24. Histological reassessment of the role of bridging fibrosis in the angioarchitectural features associated with lobular distortion of the liver in chronic viral hepatitis.
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Hano H, Takasaki S, Endo Y, Harada T, Komine K, and Koike Y
- Abstract
Aim: To reassess the role of bridging fibrosis in the lobular distortion of the liver from an angioarchitectural aspect., Methods: Two tissue samples obtained from surgically resected livers with chronic hepatitis and one obtained from an autopsy case with chronic hepatitis were used for the three-dimensional observation of angioarchitecture by histological reconstruction., Results: Samples showed bridging fibrosis with various degrees of severity, without cirrhotic changes. Two different types of portal-portal bridging fibrosis were found. In our samples, the type that developed in the bifurcation region of the portal tracts was more common than the type observed between the distal portions originating from different parent portal tracts. The angioarchitecture tended to be generally maintained in these lesions. Concerning portal-central bridging fibrosis, two types were observed. One type developed in the lesion with partial paucity of the third-step portal branches in the portal tract at a relatively early stage of chronic hepatitis. The other type developed in an advanced lesion with a complete loss of the normal angioarchitecture of the parenchymal portion of the portal veins. The former was likely developed after large-scale necrosis, such as bridging necrosis, while the latter was presumed to be attributable to portal vein damage associated with long standing chronic inflammation., Conclusion: As has been previously noted regarding lobular angioarchitecture, portal-central bridging fibrosis clearly affects the lobular structure of the liver more than portal-portal bridging fibrosis. Therefore, portal vein damage may be a critical event in the eventual distortion of the lobular structure., (© 2015 The Japan Society of Hepatology.)
- Published
- 2016
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25. Prognostic significance of receptor for advanced glycation end products expression in hepatocellular carcinoma after hepatectomy.
- Author
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Ito R, Ishii Y, Wakiyama S, Shiba H, Fujioka S, Misawa T, Ishida Y, Hano H, and Yanaga K
- Subjects
- Adult, Aged, Aged, 80 and over, Biomarkers, Tumor metabolism, Down-Regulation, Female, Humans, Kaplan-Meier Estimate, Male, Middle Aged, Multivariate Analysis, Predictive Value of Tests, Prognosis, Receptor for Advanced Glycation End Products, Carcinoma, Hepatocellular metabolism, Carcinoma, Hepatocellular mortality, Carcinoma, Hepatocellular surgery, Hepatectomy mortality, Liver Neoplasms metabolism, Liver Neoplasms mortality, Liver Neoplasms surgery, Receptors, Immunologic metabolism
- Abstract
Background: The receptor for advanced glycation end products (RAGE) is recognized to be responsible for cancer progression in several human cancers. In this study, we investigated the clinical impact of RAGE expression in patients with hepatocellular carcinoma (HCC) after hepatectomy., Materials and Methods: Sixty-five consecutive patients who underwent initial hepatectomy for HCC were investigated. The relationships between immunohistochemical expression of RAGE and clinicopathologic features, clinical outcome (overall survival [OS], and disease-free survival [DFS]) were evaluated., Results: The cytoplasmic expression of RAGE in HCC cells was observed in 46 patients (70.8%) and correlated with histologic grade (poorly differentiated versus moderately differentiated HCC, P = 0.021). Five-year OS in RAGE-positive and RAGE-negative groups were 72% and 94%, respectively, whereas 5-y DFS were 29% and 55%, respectively. There were significant differences between OS and DFS (P = 0.018 and 0.031, respectively). Multivariate analysis indicated that RAGE was an independent predictor for both OS and DFS (P = 0.048 and 0.032, respectively)., Conclusions: Our data suggest for the first time a positive correlation between RAGE expression and poor therapeutic outcome. Furthermore, RAGE downregulation may provide a novel therapeutic target for HCC., (Copyright © 2014 Elsevier Inc. All rights reserved.)
- Published
- 2014
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26. Hepatic stellate cells that coexpress LRAT and CRBP-1 partially contribute to portal fibrogenesis in patients with human viral hepatitis.
- Author
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Nagatsuma K, Hano H, Murakami K, Shindo D, Matsumoto Y, Mitobe J, Tanaka K, Saito M, Maehashi H, Owada M, Ikegami M, Tsubota A, Ohkusa T, Aizawa Y, Takagi I, Tajiri H, and Matsuura T
- Subjects
- Acyltransferases immunology, Adult, Aged, Aged, 80 and over, Female, Fibrosis etiology, Fibrosis metabolism, Hepatitis complications, Hepatitis metabolism, Humans, Immunohistochemistry, Male, Microscopy, Fluorescence, Middle Aged, Retinol-Binding Proteins, Cellular immunology, Vitamin A metabolism, Acyltransferases metabolism, Fibrosis pathology, Hepatic Stellate Cells metabolism, Hepatitis physiopathology, Portal Vein pathology, Retinol-Binding Proteins, Cellular metabolism
- Abstract
Background & Aims: Precisely what type of cells mainly contributes to portal fibrosis, especially in chronic viral hepatitis, such as hepatic stellate cells (HSCs) in the parenchyma or myofibroblasts in the portal area, still remains unclear. It is necessary to clarify the characteristics of cells that contribute to portal fibrosis in order to determine the mechanism of portal fibrogenesis and to develop a therapeutic target for portal fibrosis. This study was undertaken to examine whether LRAT+/CRBP-1+ HSCs contribute to portal fibrosis on viral hepatitis., Methods: Antibodies to lecithin:retinol acyltransferase (LRAT), cellular retinol-binding protein-1 (CRBP-1) and widely ascertained antibodies to HSCs (alpha-smooth muscle actin, neurotrophin-3) and endothelial cells (CD31) were used for immunohistochemical studies to assess the distribution of cells that contribute to the development of portal fibrosis with the aid of fluorescence microscopy. A quantitative analysis of LRAT+/CRBP-1+ HSCs was performed., Results: The number of LRAT+/CRBP-1+ HSCs was increased in fibrotic liver in comparison with normal liver in the portal area and fibrous septa. The number of double positive cells was less than 20% of all cells/field in maximum., Conclusion: This study provides evidence that functional HSCs coexpressing both LRAT and CRBP-1 that continue to maintain the ability to store vitamin A contribute in part to the development of portal fibrogenesis in addition to parenchymal fibrogenesis in patients with viral hepatitis., (© 2013 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)
- Published
- 2014
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27. Predictors of success at six-month follow-up at a public smoking cessation clinic in South Korea.
- Author
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Bhang SY, Choi SW, Ahn JH, Kim K, Kim H, and Park HK
- Subjects
- Adult, Aged, Aged, 80 and over, Employment statistics & numerical data, Female, Follow-Up Studies, Humans, Insurance, Health statistics & numerical data, Kaplan-Meier Estimate, Male, Middle Aged, Republic of Korea epidemiology, Sex Factors, Smoking epidemiology, Treatment Outcome, Young Adult, Smoking Cessation statistics & numerical data
- Abstract
Introduction: Our objective was to identify the factors related to returning to smoking by analyzing data obtained from a smoking cessation clinic., Methods: We analyzed data from 2,089 subjects (age 44.0 ± 12.9 years) who started a smoking cessation program between 16 July 2007 and 31 December 2008 in a community health center in the city of Ulsan. We analyzed demographic information and clinical variables using Kaplan-Meier survival analysis and calculated the hazard ratio for returning to smoking., Results: Mean abstinence time differed according to the following factors: sex, past attempts to quit, employment status, type of health insurance, CO levels, results from Fagerstrom test for nicotine dependence (FTND), number of cigarettes smoked daily, use of a nicotine replacement, and number of contacts in the program. Using multivariate analysis, we identified negative relationships between treatment intensity and hazard ratio for the following: visits ≤4 (Exp(B) = 3.752, P < 0.001, reference: 5 visits ≤), telephone contacts ≤5 (Exp(B) = 10.528, P < 0.001, reference: 6 calls ≤) and SMS ≤ 20 (Exp(B) = 3.821, P < 0.001 in 0-10 group; Exp(B) = 1.407, P = 0.003 for the 11-20 group; reference: 21 messages ≤)., Discussion: Type of insurance, baseline CO, FTND level, and intensity of smoking cessation intervention positively affects outcomes in a smoking cessation clinic. A cost-effectiveness study on the intensity of interventions in smoking cessation clinics is needed., (Copyright © 2012 Wiley Publishing Asia Pty Ltd.)
- Published
- 2013
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28. In the non-cirrhotic stage of nonalcoholic steatohepatitis, angioarchitecture of portal veins and lobular architecture are maintained.
- Author
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Hano H, Takasaki S, Kobayashi H, Koyama T, Lu T, and Nagatsuma K
- Subjects
- Adult, Female, Humans, Image Interpretation, Computer-Assisted, Male, Middle Aged, Fatty Liver pathology, Liver pathology, Portal Vein pathology
- Abstract
The morphogenesis of lobular restructuring to liver cirrhosis in nonalcoholic steatohepatitis (NASH) is yet to be clearly understood. Therefore, we observed tissue samples from three biopsies and one autopsy with NASH in the non-cirrhotic stage three-dimensionally to elucidate the evolution of fibrosis and the changes of angioarchitecture. Histologic reconstructions revealed that pericellular fibrosis developed around the central vein in the early stage and gradually progressed to arch-shaped band-like fibrosis connecting the central veins in the neighboring lobules. In contrast, the basic angioarchitecture of the portal vein in the portal tracts tended to be preserved in the non-cirrhotic stage, although the portal vein architecture was slightly altered as the portal tract underwent gradual fibrous expansion. In addition, a striking development of arteries originating from the portal tract was found in the fibrotic area around the central and sublobular veins. In summary, while central-central bridging fibrosis and ectopic arterial development were conspicuous, the lobular architecture was maintained relatively well in the non-cirrhotic stage of NASH because of only mildly damaged angioarchitecture of the portal veins. The process of lobular restructuring in NASH is considered to be different from that in chronic viral hepatitis in the non-cirrhotic stage.
- Published
- 2013
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29. Apoptosis inhibitor of macrophage (AIM) expression in alveolar macrophages in COPD.
- Author
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Kojima J, Araya J, Hara H, Ito S, Takasaka N, Kobayashi K, Fujii S, Tsurushige C, Numata T, Ishikawa T, Shimizu K, Kawaishi M, Saito K, Kamiya N, Hirano J, Odaka M, Morikawa T, Hano H, Arai S, Miyazaki T, Kaneko Y, Nakayama K, and Kuwano K
- Subjects
- Aged, Antigens, CD biosynthesis, Antigens, CD genetics, Antigens, Differentiation, T-Lymphocyte biosynthesis, Antigens, Differentiation, T-Lymphocyte genetics, Apoptosis Regulatory Proteins genetics, Bronchoalveolar Lavage Fluid, Cells, Cultured, Female, HEK293 Cells, Humans, Lectins, C-Type biosynthesis, Lectins, C-Type genetics, Macrophages, Alveolar pathology, Male, Middle Aged, Pulmonary Disease, Chronic Obstructive genetics, Pulmonary Disease, Chronic Obstructive pathology, U937 Cells, Apoptosis Regulatory Proteins biosynthesis, Gene Expression Regulation, Macrophages, Alveolar metabolism, Pulmonary Disease, Chronic Obstructive metabolism
- Abstract
Background: Marked accumulation of alveolar macrophages (AM) conferred by apoptosis resistance has been implicated in pathogenesis of chronic obstructive pulmonary disease (COPD). Apoptosis inhibitor of macrophage (AIM), has been shown to be produced by mature tissue macrophages and AIM demonstrates anti-apoptotic property against multiple apoptosis-inducing stimuli. Accordingly, we attempt to determine if AIM is expressed in AM and whether AIM is involved in the regulation of apoptosis in the setting of cigarette smoke extract (CSE) exposure., Methods: Immunohistochemical evaluations of AIM were performed. Immunostaining was assessed by counting total and positively staining AM numbers in each case (n = 5 in control, n = 5 in non-COPD smoker, n = 5 in COPD). AM were isolated from bronchoalveolar lavage fluid (BALF). The changes of AIM expression levels in response to CSE exposure in AM were evaluated. Knock-down of anti-apoptotic Bcl-xL was mediated by siRNA transfection. U937 monocyte-macrophage cell line was used to explore the anti-apoptotic properties of AIM., Results: The numbers of AM and AIM-positive AM were significantly increased in COPD lungs. AIM expression was demonstrated at both mRNA and protein levels in isolated AM, which was enhanced in response to CSE exposure. AIM significantly increased Bcl-xL expression levels in AM and Bcl-xL was involved in a part of anti-apoptotic mechanisms of AIM in U937 cells in the setting of CSE exposure., Conclusions: These results suggest that AIM expression in association with cigarette smoking may be involved in accumulation of AM in COPD.
- Published
- 2013
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30. Atypical Leydig cell hyperplasia in adult rats with low T and high LH induced by prenatal Di(n-butyl) phthalate exposure.
- Author
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Wakui S, Takahashi H, Mutou T, Shirai M, Jutabha P, Anzai N, Wempe MF, Kansaku N, Hano H, Inomata T, and Endou H
- Subjects
- Animals, Female, Histocytochemistry, Hyperplasia chemically induced, Hyperplasia pathology, Male, Pregnancy, Rats, Rats, Sprague-Dawley, Testis chemistry, Testis drug effects, Testis pathology, Dibutyl Phthalate toxicity, Leydig Cells drug effects, Leydig Cells pathology, Luteinizing Hormone blood, Prenatal Exposure Delayed Effects chemically induced, Prenatal Exposure Delayed Effects pathology, Testosterone metabolism
- Abstract
The present study describes atypical Leydig cell (LC) hyperplasia in 20-week-old Sprague-Dawley rats with low testosterone and high luteinizing hormone levels after prenatal administration of 100 mg/kg/day di(n-butyl) phthalate on days 12 to 21 postconception. Light microscopy revealed LC hyperplasia surrounded by severely degenerated seminiferous tubules. Aggregated LCs had large ovoid nuclei with nucleoli and abundant eosinophilic cytoplasm. Immunohistochemical analysis showed expression of proliferating cell nuclear antigen and vimentin in many hyperplastic LCs. Electron microscopy revealed atypical nuclei, abundant free ribosomes, stripped rough endoplasmic reticulum, intermediate-size filaments, elongated cytoplasmic filopodia, atypical tight junctions, and cilia formations, but smooth endoplasmic reticulum was scarcely observed.
- Published
- 2013
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31. Insufficient autophagy in idiopathic pulmonary fibrosis.
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Araya J, Kojima J, Takasaka N, Ito S, Fujii S, Hara H, Yanagisawa H, Kobayashi K, Tsurushige C, Kawaishi M, Kamiya N, Hirano J, Odaka M, Morikawa T, Nishimura SL, Kawabata Y, Hano H, Nakayama K, and Kuwano K
- Subjects
- Adaptor Proteins, Signal Transducing biosynthesis, Cell Differentiation physiology, Cellular Senescence physiology, Endoplasmic Reticulum Stress physiology, Epithelial Cells pathology, Epithelial Cells physiology, Humans, Myofibroblasts cytology, Sequestosome-1 Protein, Tunicamycin pharmacology, Ubiquitin biosynthesis, Autophagy, Idiopathic Pulmonary Fibrosis physiopathology
- Abstract
Autophagy, a process that helps maintain homeostatic balance between the synthesis, degradation, and recycling of organelles and proteins to meet metabolic demands, plays an important regulatory role in cellular senescence and differentiation. Here we examine the regulatory role of autophagy in idiopathic pulmonary fibrosis (IPF) pathogenesis. We test the hypothesis that epithelial cell senescence and myofibroblast differentiation are consequences of insufficient autophagy. Using biochemical evaluation of in vitro models, we find that autophagy inhibition is sufficient to induce acceleration of epithelial cell senescence and myofibroblast differentiation in lung fibroblasts. Immunohistochemical evaluation of human IPF biospecimens reveals that epithelial cells show increased cellular senescence, and both overlaying epithelial cells and fibroblasts in fibroblastic foci (FF) express both ubiquitinated proteins and p62. These findings suggest that insufficient autophagy is an underlying mechanism of both accelerated cellular senescence and myofibroblast differentiation in a cell-type-specific manner and is a promising clue for understanding the pathogenesis of IPF.
- Published
- 2013
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32. Male Sprague-Dawley rats exposed to in utero di(n-butyl) phthalate: dose dependent and age-related morphological changes in Leydig cell smooth endoplasmic reticulum.
- Author
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Shirai M, Wakui S, Wempe MF, Mutou T, Oyama N, Motohashi M, Takahashi H, Kansaku N, Asari M, Hano H, and Endou H
- Subjects
- Age Factors, Animals, Body Weight drug effects, Dibutyl Phthalate administration & dosage, Dose-Response Relationship, Drug, Endoplasmic Reticulum, Smooth metabolism, Endoplasmic Reticulum, Smooth pathology, Female, Leydig Cells metabolism, Leydig Cells pathology, Luteinizing Hormone metabolism, Male, Maternal Exposure, Pregnancy, Prenatal Exposure Delayed Effects metabolism, Prenatal Exposure Delayed Effects pathology, Rats, Rats, Sprague-Dawley, Testis drug effects, Testis metabolism, Dibutyl Phthalate toxicity, Endoplasmic Reticulum, Smooth drug effects, Leydig Cells drug effects, Prenatal Exposure Delayed Effects chemically induced, Testosterone metabolism
- Abstract
When 100 mg/kg/day of di(n-butyl) phthalate (DBP) was intragastrically administered to pregnant Sprague-Dawley rats throughout gestation days 12 to 21, the male pups had similar body weights with no apparent physical differences (e.g., litter size, sex ratio) compared to that of the vehicle group. However, prominent age-related morphological alterations in the smooth endoplasmic reticulum (sER) of testicular Leydig cells (LCs) were observed once these animals reached puberty. At weeks 5 to 7, the abundant sER with non-dilated cisternae was distributed in LCs. Subsequently, although the number of LCs significantly increased, the amount of sER was significantly decreased at 9 to 14 weeks of age and had disappeared at 17 weeks. In contrast, the number of LCs and the amount of sER in LCs of the lower dose groups (10, 30, and 50 mg/kg/day) were similar to those of the vehicle group. Further, serum testosterone levels in the 100 mg/kg dose group were significantly lower during 5 to 17 weeks of age. While their luteinizing hormone (LH) level was significantly lower at 5 to 7 weeks of age, it became significantly higher during 9 to 17 weeks. The amount of sER in LCs decreased with age with the increase in LCs proliferation and serum LH levels in rat exposed in utero to DBP in a dose-dependent manner.
- Published
- 2013
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33. A stand-alone mesoporous crystal structure model from in situ X-ray diffraction: nitrogen adsorption on 3D cagelike mesoporous silica SBA-16.
- Author
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Miyasaka K, Hano H, Kubota Y, Lin Y, Ryoo R, Takata M, Kitagawa S, Neimark AV, and Terasaki O
- Subjects
- Adsorption, Models, Molecular, Porosity, Powder Diffraction, Surface Properties, X-Ray Diffraction, Nitrogen chemistry, Silicon Dioxide chemistry
- Abstract
We present a modeling scheme to analyze cagelike silica mesoporous crystals based on in situ X-ray diffraction (XRD) data collected during gas adsorption-desorption (physisorption) processes. Nitrogen physisorption on a silica mesoporous crystal of SBA-16 was directly monitored by using synchrotron in situ powder XRD measurements conducted at SPring-8. SBA-16 is a well-ordered mesoporous silica in which three-dimensional interconnected cagelike primary mesopores are located at the body-centered cubic lattice points. In addition, the surrounding silica matrix contains random microporous and mesoporous intrawall porosities that are significantly influential to the diffusion properties, and thus important to be quantified for this media. The in situ XRD data exhibits seven Bragg reflections throughout the measurements, and the present method allows one to obtain the maximal and stand-alone information about the pore structure (for example, the mesopore size, the matrix density, the intrawall porosity, and pore surface roughness) together with the nitrogen film evolution in the primary mesopores and the intrawall pore-filling in the silica matrix. We furthermore observe a macroscopic amount of nitrogen adsorbed assuming the density of the fluid, and confirm that the XRD "isotherm" recalculated from the analysis result is consistent with the conventional nitrogen isotherm on a semi-quantitative level; however, these results suggest that the intrawall pores would have a greater contribution to the adsorption than considered based on the conventional isotherm analyses. The present method is readily extendable to any ordered mesopores wrapped by the wall matrix containing a certain intrawall porosity., (Copyright © 2012 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.)
- Published
- 2012
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34. Involvement of creatine kinase B in cigarette smoke-induced bronchial epithelial cell senescence.
- Author
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Hara H, Araya J, Takasaka N, Fujii S, Kojima J, Yumino Y, Shimizu K, Ishikawa T, Numata T, Kawaishi M, Saito K, Hirano J, Odaka M, Morikawa T, Hano H, Nakayama K, and Kuwano K
- Subjects
- Bronchi enzymology, Bronchi immunology, Bronchi pathology, Cells, Cultured, Creatine Kinase, BB Form antagonists & inhibitors, Creatine Kinase, BB Form genetics, Cyclin B1 metabolism, Down-Regulation, Enzyme-Linked Immunosorbent Assay, Epithelial Cells enzymology, Epithelial Cells immunology, Epithelial Cells pathology, Humans, Immunohistochemistry, Interleukin-8 metabolism, Oxidative Stress drug effects, Protease Inhibitors pharmacology, Proteasome Endopeptidase Complex metabolism, Proteasome Inhibitors, Protein Carbonylation drug effects, Protein Kinase Inhibitors pharmacology, RNA Interference, Signal Transduction drug effects, Ubiquitination, beta-Galactosidase metabolism, Bronchi drug effects, Cellular Senescence drug effects, Creatine Kinase, BB Form metabolism, Epithelial Cells drug effects, Smoke adverse effects, Smoking adverse effects
- Abstract
Cigarette smoke induces damage to proteins and organelles by oxidative stress, resulting in accelerated epithelial cell senescence in the lung, which is implicated in chronic obstructive pulmonary disease (COPD) pathogenesis. Although the detailed molecular mechanisms are not fully understood, cellular energy status is one of the most crucial determinants for cell senescence. Creatine kinase (CK) is a constitutive enzyme, playing regulatory roles in energy homeostasis of cells. Among two isozymes, brain-type CK (CKB) is the predominant CK in lung tissue. In this study, we investigated the role of CKB in cigarette smoke extract (CSE)-induced cellular senescence in human bronchial epithelial cells (HBECs). Primary HBECs and Beas2B cells were used. Protein carbonylation was evaluated as a marker of oxidative protein damage. Cellular senescence was evaluated by senescence-associated β-galactosidase staining. CKB inhibition was examined by small interfering RNA and cyclocreatine. Secretion of IL-8, a hallmark of senescence-associated secretary phenotype, was measured by ELISA. CKB expression levels were reduced in HBECs from patients with COPD compared with that of HBECs from nonsmokers. CSE induced carbonylation of CKB and subsequently decreased CKB protein levels, which was reversed by a proteasome inhibitor. CKB inhibition alone induced cell senescence, and further enhanced CSE-induced cell senescence and IL-8 secretion. CSE-induced oxidation of CKB is a trigger for proteasomal degradation. Concomitant loss of enzymatic activity regulating energy homeostasis may lead to the acceleration of bronchial epithelial cell senescence, which is implicated in the pathogenesis of COPD.
- Published
- 2012
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35. Alcohol and cognition in the elderly: a review.
- Author
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Kim JW, Lee DY, Lee BC, Jung MH, Kim H, Choi YS, and Choi IG
- Abstract
Consumption of large amounts of alcohol is known to have negative effects, but consumption in smaller amounts may be protective. The effect of alcohol may be greater in the elderly than in younger adults, particularly with regard to cognition. However, the drinking pattern that will provide optimal protection against dementia and cognitive decline in the elderly has not been systematically investigated. The present paper is a critical review of research on the effect of alcohol on cognitive function and dementia in the elderly. Studies published from 1971 to 2011 related to alcohol and cognition in the elderly were reviewed using a PubMed search. Alcohol may have both a neurotoxic and neuroprotective effect. Longitudinal and brain imaging studies in the elderly show that excessive alcohol consumption may increase the risk of cognitive dysfunction and dementia, but low to moderate alcohol intake may protect against cognitive decline and dementia and provide cardiovascular benefits. Evidence suggesting that low to moderate alcohol consumption in the elderly protects against cognitive decline and dementia exists; however, because of varying methodology and a lack of standardized definitions, these findings should be interpreted with caution. It is important to conduct more, well-designed studies to identify the alcohol drinking pattern that will optimally protect the elderly against cognitive decline and dementia.
- Published
- 2012
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36. Organizing pneumonia complicated by cyst and pneumothorax formation.
- Author
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Kadota T, Shimizu K, Tsurushige C, Kawaishi M, Araya J, Nakayama K, Kuwano K, and Hano H
- Subjects
- Adrenal Cortex Hormones adverse effects, Adult, Cysts diagnosis, Humans, Lung Diseases diagnosis, Male, Pneumonia diagnosis, Pneumonia drug therapy, Pneumothorax diagnosis, Pneumothorax surgery, Thoracic Surgery, Video-Assisted, Tomography, X-Ray Computed, Cysts etiology, Lung Diseases etiology, Pneumonia complications, Pneumothorax etiology
- Abstract
We present a case of organizing pneumonia complicated by pneumothorax in association with cyst formation that developed during corticosteroid treatment. Although it has been reported that the check-valve mechanism is a plausible cause of cyst and pneumothorax formation in patients with organizing pneumonia, the details of the corresponding pathological changes that occur in air-trapping have not been elucidated. A pathological examination of lung specimens obtained with video-assisted thoracoscopic surgery suggested that granulation tissues plugging the bronchiole lumens might be a potential cause of the check-valve mechanism in this case. In this report, we also reviewed eight other cases of organizing pneumonia with pneumothorax or cyst formation.
- Published
- 2012
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37. Sertoli cells proliferate in adult rats with prenatal exposure to 3,3',4,4',5-pentachlorobiphenyl.
- Author
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Wakui S, Muto T, Suzuki Y, Takahashi H, and Hano H
- Subjects
- Animals, Female, Male, Microscopy, Electron, Mitosis drug effects, Polychlorinated Biphenyls administration & dosage, Pregnancy, Prenatal Exposure Delayed Effects, Proliferating Cell Nuclear Antigen metabolism, Rats, Rats, Sprague-Dawley, Sertoli Cells metabolism, Cell Proliferation drug effects, Estrogen Antagonists toxicity, Polychlorinated Biphenyls toxicity, Sertoli Cells drug effects
- Abstract
Sertoli cells play a critical role in spermatogenesis, and in adults, they are terminally differentiated with loss of proliferative activity. This study revealed Sertoli cell proliferation in 17-week-old Sprague-Dawley rats whose dams had been intragastrically administered 250 ng of 3,3',4,4',5-pentachlorobiphenyl/kg on days 13-19 postconception. Immunohistochemical evidence of proliferating cell nuclear antigen (PCNA) expression and electron microscope observation of mitotic figures confirmed the proliferation. Because the serum follicle stimulating hormone (FSH), luteinizing hormone (LH) and testosterone concentrations were similar to those of vehicle-treated rats, a direct endocrine cause for the observed effects was unlikely.
- Published
- 2012
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38. Histopathologically proven autoimmune pancreatitis mimicking neuroendocrine tumor or pancreatic cancer.
- Author
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Onda S, Okamoto T, Kanehira M, Fujioka S, Harada T, Hano H, Fukunaga M, and Yanaga K
- Abstract
Autoimmune pancreatitis (AIP) can be difficult to distinguish from pancreatic cancer. We report a case of histopathologically proven AIP mimicking neuroendocrine tumor (NET) or pancreatic cancer in a 53-year-old man. He was referred to our hospital for further evaluation of a pancreatic mass detected on ultrasonography at a medical check-up. Abdominal ultrasonography showed a 15-mm hypoechoic mass located in the pancreatic body. Computed tomography revealed a tumor without any contrast enhancement, and magnetic resonance imaging demonstrated the mass to be hyperintense on diffusion-weighted image. Endoscopic retrograde cholangiopancreatography revealed slight dilatation of a branch of the pancreatic duct without stricture of the main pancreatic duct. The common bile duct seemed intact. Under suspicion of a non-functioning NET or malignant neoplasm, laparotomy was performed. At laparotomy, an elastic firm and well-circumscribed mass was found suggestive of a non-functioning NET, thus enucleation was performed. Histopathologically, the lesion corresponded to AIP.
- Published
- 2012
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39. Hepatocyte nuclear factor 4A expression discriminates gastric involvement by metastatic breast carcinomas from primary gastric adenocarcinomas.
- Author
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Koyama T, Sekine S, Taniguchi H, Tsuda H, Ikegami M, Hano H, and Kushima R
- Subjects
- Adenocarcinoma secondary, Adult, Aged, Carcinoma, Lobular metabolism, Carcinoma, Lobular secondary, Carcinoma, Signet Ring Cell secondary, Female, Humans, Immunohistochemistry, Middle Aged, Retrospective Studies, Sensitivity and Specificity, Stomach Neoplasms metabolism, Stomach Neoplasms pathology, Adenocarcinoma metabolism, Biomarkers, Tumor metabolism, Breast Neoplasms pathology, Hepatocyte Nuclear Factor 4 biosynthesis, Stomach Neoplasms secondary
- Abstract
Breast carcinomas sometimes metastasize to the stomach, and the histopathologic distinction of such metastases from primary gastric adenocarcinomas is often difficult. We characterized the clinicopathologic features of 21 breast carcinomas that had metastasized to the stomach and examined the use of a panel of antibodies, including hepatocyte nuclear factor 4A, for distinguishing the metastases from primary gastric diffuse-type adenocarcinomas. Histologically, all the metastatic breast carcinomas showed a poorly differentiated and/or signet ring cell morphology. Although most metastatic breast and primary gastric carcinomas contained signet ring cell components, the cases that were predominantly or exclusively composed of univacuolated-type signet ring cells were limited to metastatic breast carcinomas. Immunohistochemically, hepatocyte nuclear factor 4A was expressed in all 33 primary gastric carcinomas that were examined but was never expressed in metastatic breast carcinomas. Previously reported markers for breast and gastric carcinomas also showed a high specificity, but their sensitivities were quite variable. Estrogen receptor α, progesterone receptor, mammaglobin, and gross cystic disease fluid protein 15 were expressed in 76%, 33%, 52%, and 62%, respectively, of the metastatic breast carcinomas, whereas none of the primary gastric carcinomas expressed these antigens. CDX2, MUC5AC, MUC6, and CK20 were expressed in 36%, 85%, 27%, and 55%, respectively, of the primary gastric carcinomas. All the metastatic breast carcinomas were negative for these antibodies except for 1 case that expressed MUC5AC. Overall, the use of immunohistochemistry efficiently discriminated metastatic breast carcinomas from primary gastric carcinomas. In particular, the present study identified hepatocyte nuclear factor 4A as an excellent marker for differentiating the 2 lesions.
- Published
- 2011
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40. Sex-associated difference in estrogen receptor β expression in N-methyl-N'-nitro-N-nitrosoguanidine-induced gastric cancers in rats.
- Author
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Wakui S, Motohashi M, Muto T, Takahashi H, Hano H, Jutabha P, Anzai N, Wempe MF, and Endou H
- Subjects
- Animals, Blotting, Western, Female, Male, Proliferating Cell Nuclear Antigen metabolism, Rats, Rats, Wistar, Real-Time Polymerase Chain Reaction, Reverse Transcriptase Polymerase Chain Reaction, Sex Factors, Estrogen Receptor beta metabolism, Methylnitronitrosoguanidine toxicity, Stomach Neoplasms chemically induced, Stomach Neoplasms metabolism
- Abstract
Epidemiologic studies indicate that the incidence of gastric cancer is higher in males than in females. Although the mechanisms mediating this difference are unclear, a role for estrogens has been proposed. We used Western blotting to evaluate the role of estrogen receptor (ER) subtypes ERα and ERβ and proliferating cell nuclear antigen (PCNA) in N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)-induced gastric carcinogenesis in Wistar rats; ERα and ERβ mRNA levels also were analyzed by quantitative real-time RT-PCR analysis. The incidence of gastric cancer was significantly higher in male than female rats. In both sexes, ERα expression was similar in MNNG-treated cancerous and noncancerous tissues and normal gastric tissue. However, ERβ expression in MNNG-treated cancerous and noncancerous tissues was significantly lower in male rats and higher in female rats than that in normal gastric tissue; MNNG-induced cancerous tissue showed the highest ERβ expression. PCNA expression in MNNG-treated cancerous tissues was higher than that in noncancerous tissues, and was higher in male rats than female rats. Western blotting results were consistent with the mRNA changes determined by quantitative real-time RT-PCR. The present study provides evidence of a sex-associated difference in ERβ and PCNA expression in MNNG-induced gastric cancers in Wistar rats.
- Published
- 2011
41. Immunohistochemical ETS-related gene detection in a Japanese prostate cancer cohort: diagnostic use in Japanese prostate cancer patients.
- Author
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Furusato B, van Leenders GJ, Trapman J, Kimura T, Egawa S, Takahashi H, Furusato M, Visakorpi T, and Hano H
- Subjects
- Adenocarcinoma metabolism, Adult, Aged, Aged, 80 and over, Biomarkers, Tumor metabolism, Cohort Studies, Humans, Immunoenzyme Techniques, Japan, Male, Middle Aged, Predictive Value of Tests, Prostatic Neoplasms metabolism, Transcriptional Regulator ERG, Adenocarcinoma secondary, Prostatic Neoplasms pathology, Trans-Activators metabolism
- Abstract
Chromosomal rearrangements that result in high expression levels of the ETS-related gene (ERG) present in approximately 50% of prostate cancer (PCa) patients, making this one of the most common oncogenic alterations in PCa. However, ERG overexpression at the protein level has not been rigorously evaluated in Japanese PCa patients. In this study, we evaluated ERG expression using antibody-based detection in 230 prostate specimens in a Japanese PCa cohort. Overall, we identified 20.1% ERG-positive PCa cases. ERG was not detected in benign glands. The specificity of ERG staining for detecting PCa was almost 100%; all of the ERG-positive samples were also diagnosed as PCa. The expression level of the ERG protein correlated with clinicopathological variables, including grade (P= 0.038), stage (P= 0.005), and metastatic status (P= 0.014). No correlation was observed with age (P= 0.196) or with preoperative prostate-specific antigen level (P= 0.322). Although the frequency of ERG-positive cases in Japanese PCa patients (20.1%) was lower than that reported in a PCa cohort in Western countries (approximately 50%), our study demonstrates that the clinical utility of ERG detection at the protein level can serve as an ancillary tool for diagnosing PCa in the Japanese population., (© 2011 The Authors. Pathology International © 2011 Japanese Society of Pathology and Blackwell Publishing Asia Pty Ltd.)
- Published
- 2011
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42. Cyclin D1/cdk4, estrogen receptors α and β, in N-methyl-N'-nitro-N-nitrosoguanidine-induced rat gastric carcinogenesis: immunohistochemical study.
- Author
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Motohashi M, Wakui S, Muto T, Suzuki Y, Shirai M, Takahashi H, and Hano H
- Subjects
- Adenocarcinoma chemically induced, Adenocarcinoma metabolism, Animals, Biomarkers, Tumor metabolism, Female, Gastric Mucosa drug effects, Gastric Mucosa metabolism, Gastric Mucosa pathology, Immunohistochemistry methods, Male, Rats, Rats, Wistar, Sex Factors, Stomach Neoplasms chemically induced, Stomach Neoplasms metabolism, Adenocarcinoma pathology, Carcinogens toxicity, Cyclin D1 metabolism, Cyclin-Dependent Kinase 4 metabolism, Estrogen Receptor alpha metabolism, Estrogen Receptor beta metabolism, Methylnitronitrosoguanidine toxicity, Stomach Neoplasms pathology
- Abstract
Hyperproliferative cell growth due to cyclin D1/cdk4, marker of cellular proliferation, is considered to be regulated by the expression of estrogen receptors (ERs). We investigated the immunohistochemical expression of cyclin D1/cdk4 and ERs in N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)-induced rat gastric carcinogenesis. The gastric cancer incidence and expression of cyclin D1/ckd4 in gastric carcinogenesis were significantly higher in males than females. Although the ERα expression index was similar in both sexes, the ERβ expression in preneoplastic hyperplastic lesions as well as gastric cancers was significantly higher in females than in males. The present study revealed a gender difference in MNNG-induced rat gastric carcinogenesis that seemed to involve the sex difference in cyclin D1/cdk4 expression, and ERβ expression became evident at the preneoplastic promotion stage in gastric carcinogenesis.
- Published
- 2011
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43. Transplantation of liver organoids in the omentum and kidney.
- Author
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Saito R, Ishii Y, Ito R, Nagatsuma K, Tanaka K, Saito M, Maehashi H, Nomoto H, Ohkawa K, Mano H, Aizawa M, Hano H, Yanaga K, and Matsuura T
- Subjects
- Animals, Bioreactors, Cell Line, Coculture Techniques, Gene Expression, Hepatocytes cytology, Kidney cytology, Mice, Mice, Inbred BALB C, Mice, Nude, Omentum cytology, Organoids metabolism, Tissue Scaffolds chemistry, Liver cytology, Organoids transplantation
- Abstract
Liver organoids were reconstructed by mouse-immortalized hepatocytes and nonparenchymal cells (sinusoidal endothelial cells and hepatic stellate cells) in a radial-flow bioreactor (RFB). A biodegradable apatite-fiber scaffold (AFS) was used as a scaffold packed in the RFB, which enables three-dimensional cell cultures. The organoids cocultured in the RFB showed a liver-like structure with high-density layers of hepatocytes and the formation of vessel-like structures. A liver organoid consisting of three cocultured cells was transplanted under the kidney capsule (kidney group) or into the omentum (omentum group) using BALB/c nude mice. Transplanted liver organoids survived in the kidney or omentum. The expression of mRNAs of albumin, connexin 26 and 32, hepatocyte nuclear factor 4α, and glucose-6-phosphatase was increased in both groups at 8 weeks after transplantation in comparison to the pretransplant status. Tyrosine aminotransferase appeared only in the omentum group. The results suggested that the functions of liver organoids differed depending on the transplanted site in the recipient animals., (© 2010, Copyright the Authors. Artificial Organs © 2010, International Center for Artificial Organs and Transplantation and Wiley Periodicals, Inc.)
- Published
- 2011
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44. Testicular spermiation failure in rats exposed prenatally to 3,3',4,4',5-pentachlorobiphenyl.
- Author
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Wakui S, Muto T, Motohashi M, Kobayashi Y, Suzuki Y, Takahashi H, and Hano H
- Subjects
- Animals, Female, Follicle Stimulating Hormone blood, Gestational Age, Luteinizing Hormone blood, Male, Pregnancy, Prenatal Exposure Delayed Effects blood, Prenatal Exposure Delayed Effects physiopathology, Rats, Rats, Sprague-Dawley, Testosterone blood, Environmental Pollutants toxicity, Maternal Exposure adverse effects, Polychlorinated Biphenyls toxicity, Prenatal Exposure Delayed Effects chemically induced, Spermatogenesis drug effects, Testis drug effects
- Abstract
Testicular spermatogenesis was studied in 7-, 10-, 13- and 17-week-old Sprague-Dawley rats whose dams had been administered intragastrically with 2.5, 25, or 250 ng of 3,3',4,4',5-pentachlorobiphenyl (PCB126) or vehicle on days 13-19 of gestation. The 250 ng groups among the 7-, 10- and 13-week-old offspring showed significant inhibition of mature spermatid release (spermiation), but 17-week-old offspring did not show this. These alterations were not observed in other PCB126 and vehicle groups, and no germ cell or Sertoli cell degeneration were observed in any group. Spermiation failure at puberty appeared in those rats born to dams exposed 250 ng/kg PCB126 on days 13-19 of gestation was reversible change that recovered at adulthood. Because the serum testosterone, luteinizing hormone and follicle-stimulating hormone concentrations were similar in the PCB126 and vehicle groups, a direct endocrine cause for the observed effects was unlikely.
- Published
- 2010
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45. IQGAP1 and vimentin are key regulator genes in naturally occurring hepatotumorigenesis induced by oxidative stress.
- Author
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Tsubota A, Matsumoto K, Mogushi K, Nariai K, Namiki Y, Hoshina S, Hano H, Tanaka H, Saito H, and Tada N
- Subjects
- Animals, Copper metabolism, Disease Models, Animal, Disease Progression, Gene Expression Profiling, Genetic Association Studies, Hepatolenticular Degeneration, Humans, Liver metabolism, Liver Neoplasms, Experimental etiology, Liver Neoplasms, Experimental metabolism, Male, Molecular Sequence Data, Oligonucleotide Array Sequence Analysis, Precancerous Conditions genetics, Precancerous Conditions metabolism, RNA, Messenger biosynthesis, RNA, Messenger genetics, Rats, Rats, Inbred LEC, Rats, Long-Evans, Reverse Transcriptase Polymerase Chain Reaction, Vimentin biosynthesis, Vimentin genetics, ras GTPase-Activating Proteins biosynthesis, ras GTPase-Activating Proteins genetics, Gene Regulatory Networks genetics, Liver Neoplasms, Experimental genetics, Oxidative Stress, Vimentin physiology, ras GTPase-Activating Proteins physiology
- Abstract
To identify key genes involved in the complex multistep process of hepatotumorigenesis, we reduced multivariate clinicopathological variables by using the Long-Evans Cinnamon rat, a model with naturally occurring and oxidative stress-induced hepatotumorigenesis. Gene expression patterns were analyzed serially by profiling liver tissues from rats of a naive status (4 weeks old), through to those with chronic hepatitis (26 and 39 weeks old) to tumor development (67 weeks old). Of 31 099 probe sets used for microarray analysis, 87 were identified as being upregulated in a stepwise manner during disease progression and tumor development. Quantitative real-time reverse transcription-polymerase chain reaction and statistical analyses verified that IQGAP1 and vimentin mRNA expression levels increased significantly throughout hepatotumorigenesis. A hierarchical clustering algorithm showed both genes clustered together and in the same cluster group. Immunohistochemical and western blot analyses showed similar increases in protein levels of IAGAP1 and vimentin. Finally, pathway analyses using text-mining technology with more comprehensive and recent gene-gene interaction data identified IQGAP1 and vimentin as important nodes in underlying gene regulatory networks. These findings enhance our understanding of the multistep hepatotumorigenesis and identification of target molecules for novel treatments.
- Published
- 2010
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46. Lecithin: retinol acyltransferase protein is distributed in both hepatic stellate cells and endothelial cells of normal rodent and human liver.
- Author
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Nagatsuma K, Hayashi Y, Hano H, Sagara H, Murakami K, Saito M, Masaki T, Lu T, Tanaka M, Enzan H, Aizawa Y, Tajiri H, and Matsuura T
- Subjects
- Acyltransferases genetics, Animals, Hepatic Stellate Cells ultrastructure, Humans, Immunohistochemistry, Mice, Mice, Inbred BALB C, Microscopy, Electron, Microscopy, Fluorescence, Rats, Rats, Sprague-Dawley, Acyltransferases metabolism, Biomarkers metabolism, Endothelial Cells metabolism, Hepatic Stellate Cells metabolism
- Abstract
Background: To determine the extent to which hepatic stellate cell (HSC) activation contributes to liver fibrosis, it was found necessary to develop an alternative structural and functional stellate cell marker for in situ studies. Although several HSC markers have been reported, none of those are associated with particular HSC functions., Aim: The present study was undertaken to examine whether lecithin:retinol acyltransferase (LRAT), the physiological retinol esterification enzyme of the liver, is a potential and relevant tissue marker for HSC., Methods: An antibody specific to mouse and human LRAT was prepared based on the amino acid sequences. Antibodies to LRAT were used for immunohistochemical studies to assess the distribution of LRAT-positive cells in the liver with the aid of fluorescence and immunogold electron microscopy., Results: LRAT-positive cells were found to be confined in the space of Disse, corresponding with the location of desmin-positive HSC in rodent liver, also in human liver. Interestingly, LRAT-positive staining was also observed along the liver sinusoidal endothelial lining. Furthermore, immune electron microscopic studies revealed that LRAT was mainly distributed in HSC within the rough-endoplasmic reticulum (RER) and multivesicular bodies, whereas LRAT staining within the endothelial cells was largely confined to the perinuclear area and to some extent to the RER., Conclusion: Evidence has been accumulated that LRAT might serve as an excellent alternative HSC marker for future structural and functional studies. Furthermore, the presence of LRAT in endothelial cells might suggest a currently unknown function of this enzyme in liver endothelial biology.
- Published
- 2009
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47. Sertoli-Leydig cell tumor of the testis in a Sprague-Dawley rat.
- Author
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Wakui S, Muto T, Kobayashi Y, Ishida K, Nakano M, Takahashi H, Suzuki Y, Furusato M, and Hano H
- Subjects
- Animals, Cell Nucleus ultrastructure, Cytoplasm ultrastructure, Male, Microscopy, Electron veterinary, Rats, Rats, Sprague-Dawley, Sertoli-Leydig Cell Tumor pathology, Testicular Neoplasms pathology, Rodent Diseases pathology, Sertoli-Leydig Cell Tumor veterinary, Testicular Neoplasms veterinary
- Abstract
A rare intratubular gonadal stromal tumor was present in the testis of a 7-wk-old male Sprague-Dawley rat. The tumor comprised an intratubular mixture of 2 types of tumor cells with intercellular junctions: the predominant tumor cells were consistent with a Sertoli cell origin, and cells comprising the minor population were situated on basolateral side of the tubuli, consistent with a Leydig cell origin. The neoplastic Sertoli cells had large pleomorphic nuclei and clear cytoplasm with many tubulovesicular cristae and free ribosomes, whereas the neoplastic Leydig cells showed relatively small pleomorphic nuclei, dark cytoplasm with rich smooth endoplasmic reticulum, numerous mitochondria, and lipid droplets. Occasionally, a few transitional type neoplastic cells were observed. The presence of a thick or multilayered basement membrane was confirmed except in tumor-infiltrative lesions. The present case was considered to be a testicular mixed tubular Sertoli-Leydig cell tumor in a Sprague-Dawley rat.
- Published
- 2008
48. Prediction of clinically insignificant prostate cancer by detection of allelic imbalance at 6q, 8p and 13q.
- Author
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Nakano M, Takahashi H, Shiraishi T, Lu T, Furusato M, Wakui S, and Hano H
- Subjects
- Aged, Allelic Imbalance, Humans, Male, Microsatellite Repeats, Middle Aged, Loss of Heterozygosity, Prostatic Neoplasms genetics, Prostatic Neoplasms pathology
- Abstract
The criterion tumor volume (TV) for clinically insignificant prostate cancer has been reported, but it differs from study to study: some have reported TV < 200 mm(3); others, < 500 mm(3). The aim of the present study was to distinguish clinically insignificant cancers from significant ones using molecular biological methods. A total of 184 microscopic cancers (MC) defined as limited within a 3 mm circle and 82 main tumor (MT) nodules were selected. Thirteen microsatellite loci at 6q22, 8p23.2-23, 13q14 and 13q33 were evaluated for loss of heterozygosity (LOH). MT were subgrouped as TV > or = 500 mm(3) or < 500 mm(3); TV > or = 200 mm(3) or < 200 mm(3); and TV < 200 mm(3), 200 mm(3) < or = TV < 500 mm(3) or TV > or = 500 mm(3); and frequencies of LOH were compared between these three groups. Frequencies of LOH at 6q16-21, 6q22, 8p23.1, 8p23.2, 13q14 were significantly lower in MC (1.0%, 2.7%, 1.9%, 1.1% and 5.4%) than in MT (30.9%, 40.4%, 12%, 8.7% and 20.6%), but no significant differences in LOH frequency were found within each of the three TV groups, between each cut-off. When insignificant tumor is defined as TV < 200 mm(3) or < 500 mm(3), it should include tumors with malignant potential equivalent to larger tumors. It is suggested that in order to identify insignificant tumor within a strict safety range, TV should be set lower.
- Published
- 2008
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49. Immunohistochemical analysis of reserve cell-like cells of ovarian müllerian mucinous/mixed epithelial borderline tumor.
- Author
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Hamada T, Kiyokawa T, Nomura K, and Hano H
- Subjects
- Adult, Aged, Biomarkers metabolism, Cell Differentiation, Cervix Uteri metabolism, Cervix Uteri pathology, Endometriosis metabolism, Endometriosis pathology, Epithelial Cells metabolism, Epithelial Cells pathology, Female, Humans, Immunohistochemistry, Keratin-17 metabolism, Keratins metabolism, Membrane Proteins metabolism, Middle Aged, Mixed Tumor, Mullerian metabolism, Mixed Tumor, Mullerian pathology, Neoplasms, Glandular and Epithelial metabolism, Neoplasms, Glandular and Epithelial pathology, Ovarian Neoplasms metabolism, Ovarian Neoplasms pathology
- Abstract
Ovarian mucinous borderline tumor of müllerian type (MMBT) and mixed epithelial borderline tumor of müllerian type (MEBT) are uncommon subtypes of ovarian surface epithelial tumors. Both are often associated with endometriosis, but their histogenesis is still debated. We have noticed occasional foci of subepithelial cuboidal cells resembling uterine cervical reserve cells (RCs) in MMBTs/MEBTs, which have not been documented in the literature to the best of our knowledge. This study was carried out to identify the presence of RC-like cells (RCLCs) in MMBTs/MEBTs and their immunohistochemical features in comparison to those of cervical RCs. We analyzed 10 consecutive cases of RC-like MMBTs/MEBTs, 6 of which were associated with endometriosis. Immunohistochemistry was performed for p63, cytokeratin 34BE12, cytokeratin 17 (CK17), and low-molecular cytokeratin CAM5.2. In 9 of 10 cases, RCLCs were appreciated in hematoxylin-eosin stain, although their amount in the tumor varied from case to case. Immunohistochemically, RCLCs were positive for p63 in 9 cases. They were positive for both 34BE12 and CK17 and were very weakly positive or negative for CAM5.2 in 8 cases. This immunohistochemical profile is similar to that seen in the cervical RCs. Reserve cell-like cells were also found in the foci of endometriosis coexisting with MMBTs/MEBTs in 1 of 5 cases examined. We draw attention to the existence of the RCLCs in MMBTs/MEBTs and in endometriosis. Their similarity to the cervical RCs may indicate their potential role as precursor cell that may subsequently differentiate into different müllerian cell types, thus merit further study.
- Published
- 2008
- Full Text
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50. Identification of minimal regions of deletion at 8p23.1-22 associated with metastasis of hepatocellular carcinoma.
- Author
-
Lu T and Hano H
- Subjects
- Adult, Aged, Aged, 80 and over, Carcinoma, Hepatocellular secondary, Female, Humans, Liver Neoplasms pathology, Male, Microsatellite Repeats, Middle Aged, Neoplasm Invasiveness genetics, Carcinoma, Hepatocellular genetics, Chromosome Deletion, Chromosomes, Human, Pair 8, Gene Expression Regulation, Neoplastic, Liver Neoplasms genetics, Loss of Heterozygosity
- Abstract
Aims/background: Loss of heterozygosity (LOH) at 8p is the most frequent chromosomal alteration in tumorigenesis of human cancers. However, the genetic change in metastasis of hepatocellular carcinoma (HCC) still has to be investigated., Methods: We used 16 microsatellite markers informative in Japanese patients, selected from among 61 published microsatellite markers at 8p23.2-21 to compare the frequency of LOH in primary tumours (Tps) and metastatic tumours (Tms) in a PCR-based analysis. Sixty-three informative cancerous lesions (26 were Tps, 37 were Tms) from 23 cases of HCC were used., Results: The frequency of LOH at 8p23.2-21 with at least one marker was 19% in Tps and 68% in Tms. Allelic loss at 8p23.2-21 was significantly more frequent in Tms than in Tps (P=0.0003). More specifically, the frequency of LOH at D8S262, D8S1819, D8S503, D8S1130, D8S552, D8S1109, and D8S261 in Tms was 36-60% respectively., Conclusions: In contrast, allelic loss at the same markers in Tp was only detected in 0-17% of the tumour respectively. The significant difference in the frequency of LOH at 8p between primary cancer and metastatic cancer in individual cases of HCC suggests LOH at 8p to be involved in the enhancement of tumour aggressiveness, especially during metastasis.
- Published
- 2007
- Full Text
- View/download PDF
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