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1. Stroke genetics informs drug discovery and risk prediction across ancestries

Author

Mishra, A, Malik, R., Hachiya, T., Jürgenson, T., Namba, S., Posner, D.C., Kamanu, F.K., Koido, M., Grand, Q. Le, Shi, M., He, Y., Georgakis, M.K., Caro, I., Krebs, K., Liaw, Y.C., Vaura, F.C., Lin, K., Winsvold, B.S., Srinivasasainagendra, V., Parodi, L., Bae, H.J., Chauhan, G., Chong, M.R., Tomppo, L., Akinyemi, R., Roshchupkin, G.V., Habib, N., Jee, Y.H., Thomassen, J.Q., Abedi, V., Cárcel-Márquez, J., Nygaard, M., Leonard, H.L., Yang, C., Yonova-Doing, E., Knol, M.J., Lewis, A.J., Judy, R.L., Ago, T., Amouyel, P., Armstrong, N.D., Bakker, M.K., Bartz, T.M., Bennett, D.A., Bis, J.C., Bordes, C., Børte, S., Cain, A., Ridker, P.M., Cho, K., Chen, Z., Cruchaga, C., Cole, J.W., Jager, P.L., Cid, R. de, Endres, M., Ferreira, L.E., Geerlings, M.I., Gasca, N.C., Gudnason, V., Hata, J., He, J., Heath, A.K., Ho, Y.L., Havulinna, A.S., Hopewell, J.C., Hyacinth, H.I., Inouye, M., Jacob, M.A., Jeon, C.E., Jern, C., Kamouchi, M., Keene, K.L., Kitazono, T., Kittner, S.J., Konuma, T., Kumar, A., Lacaze, P., Launer, L.J., Lee, K.J., Lepik, K., Li, J, Li, L, Manichaikul, A., Markus, H.S., Marston, N.A., Meitinger, T., Mitchell, B.D., Montellano, F.A., Morisaki, T., Mosley, T.H., Nalls, M.A., Nordestgaard, B.G., O'Donnell, M.J., Okada, Y., Onland-Moret, N.C., Ovbiagele, B., Peters, A., Psaty, B.M., Rich, S.S., Tuladhar, A.M., Leeuw, F.E. de, Dichgans, M., Debette, S., Mishra, A, Malik, R., Hachiya, T., Jürgenson, T., Namba, S., Posner, D.C., Kamanu, F.K., Koido, M., Grand, Q. Le, Shi, M., He, Y., Georgakis, M.K., Caro, I., Krebs, K., Liaw, Y.C., Vaura, F.C., Lin, K., Winsvold, B.S., Srinivasasainagendra, V., Parodi, L., Bae, H.J., Chauhan, G., Chong, M.R., Tomppo, L., Akinyemi, R., Roshchupkin, G.V., Habib, N., Jee, Y.H., Thomassen, J.Q., Abedi, V., Cárcel-Márquez, J., Nygaard, M., Leonard, H.L., Yang, C., Yonova-Doing, E., Knol, M.J., Lewis, A.J., Judy, R.L., Ago, T., Amouyel, P., Armstrong, N.D., Bakker, M.K., Bartz, T.M., Bennett, D.A., Bis, J.C., Bordes, C., Børte, S., Cain, A., Ridker, P.M., Cho, K., Chen, Z., Cruchaga, C., Cole, J.W., Jager, P.L., Cid, R. de, Endres, M., Ferreira, L.E., Geerlings, M.I., Gasca, N.C., Gudnason, V., Hata, J., He, J., Heath, A.K., Ho, Y.L., Havulinna, A.S., Hopewell, J.C., Hyacinth, H.I., Inouye, M., Jacob, M.A., Jeon, C.E., Jern, C., Kamouchi, M., Keene, K.L., Kitazono, T., Kittner, S.J., Konuma, T., Kumar, A., Lacaze, P., Launer, L.J., Lee, K.J., Lepik, K., Li, J, Li, L, Manichaikul, A., Markus, H.S., Marston, N.A., Meitinger, T., Mitchell, B.D., Montellano, F.A., Morisaki, T., Mosley, T.H., Nalls, M.A., Nordestgaard, B.G., O'Donnell, M.J., Okada, Y., Onland-Moret, N.C., Ovbiagele, B., Peters, A., Psaty, B.M., Rich, S.S., Tuladhar, A.M., Leeuw, F.E. de, Dichgans, M., and Debette, S.

Abstract

Item does not contain fulltext, Previous genome-wide association studies (GWASs) of stroke - the second leading cause of death worldwide - were conducted predominantly in populations of European ancestry(1,2). Here, in cross-ancestry GWAS meta-analyses of 110,182 patients who have had a stroke (five ancestries, 33% non-European) and 1,503,898 control individuals, we identify association signals for stroke and its subtypes at 89 (61 new) independent loci: 60 in primary inverse-variance-weighted analyses and 29 in secondary meta-regression and multitrait analyses. On the basis of internal cross-ancestry validation and an independent follow-up in 89,084 additional cases of stroke (30% non-European) and 1,013,843 control individuals, 87% of the primary stroke risk loci and 60% of the secondary stroke risk loci were replicated (P < 0.05). Effect sizes were highly correlated across ancestries. Cross-ancestry fine-mapping, in silico mutagenesis analysis(3), and transcriptome-wide and proteome-wide association analyses revealed putative causal genes (such as SH3PXD2A and FURIN) and variants (such as at GRK5 and NOS3). Using a three-pronged approach(4), we provide genetic evidence for putative drug effects, highlighting F11, KLKB1, PROC, GP1BA, LAMC2 and VCAM1 as possible targets, with drugs already under investigation for stroke for F11 and PROC. A polygenic score integrating cross-ancestry and ancestry-specific stroke GWASs with vascular-risk factor GWASs (integrative polygenic scores) strongly predicted ischaemic stroke in populations of European, East Asian and African ancestry(5). Stroke genetic risk scores were predictive of ischaemic stroke independent of clinical risk factors in 52,600 clinical-trial participants with cardiometabolic disease. Our results provide insights to inform biology, reveal potential drug targets and derive genetic risk prediction tools across ancestries.

Published
2022

2. Stroke genetics informs drug discovery and risk prediction across ancestries (vol 611, pg 115, 2022)

Author

Mishra, A, Malik, R, Hachiya, T, Jurgenson, T, Namba, S, Posner, DC, Kamanu, FK, Koido, M, Le Grand, Q, Shi, M, He, Y, Georgakis, MK, Caro, I, Krebs, K, Liaw, Y-C, Vaura, FC, Lin, K, Winsvold, BS, Srinivasasainagendra, V, Parodi, L, Bae, H-J, Chauhan, G, Chong, MR, Tomppo, L, Akinyemi, R, Roshchupkin, GV, Habib, N, Jee, YH, Thomassen, JQ, Abedi, V, Carcel-Marquez, J, Nygaard, M, Leonard, HL, Yang, C, Yonova-Doing, E, Knol, MJ, Lewis, AJ, Judy, RL, Ago, T, Amouyel, P, Armstrong, ND, Bakker, MK, Bartz, TM, Bennett, DA, Bis, JC, Bordes, C, Borte, S, Cain, A, Ridker, PM, Cho, K, Chen, Z, Cruchaga, C, Cole, JW, de Jager, PL, de Cid, R, Endres, M, Ferreira, LE, Geerlings, MI, Gasca, NC, Gudnason, V, Hata, J, He, J, Heath, AK, Ho, Y-L, Havulinna, AS, Hopewell, JC, Hyacinth, IH, Inouye, M, Jacob, MA, Jeon, CE, Jern, C, Kamouchi, M, Keene, KL, Kitazono, T, Kittner, SJ, Konuma, T, Kumar, A, Lacaze, P, Launer, LJ, Lee, K-J, Lepik, K, Li, J, Li, L, Manichaikul, A, Markus, HS, Marston, NA, Meitinger, T, Mitchell, BD, Montellano, FA, Morisaki, T, Mosley, TH, Nalls, MA, Nordestgaard, BG, O'Donnell, MJ, Okada, Y, Onland-Moret, NC, Ovbiagele, B, Peters, A, Psaty, BM, Rich, SS, Rosand, J, Sabatine, MS, Sacco, RL, Saleheen, D, Sandset, EC, Salomaa, V, Sargurupremraj, M, Sasaki, M, Satizabal, CL, Schmidt, CO, Shimizu, A, Smith, NL, Sloane, KL, Sutoh, Y, Sun, YV, Tanno, K, Tiedt, S, Tatlisumak, T, Torres-Aguila, NP, Tiwari, HK, Tregouet, D-A, Trompet, S, Tuladhar, AM, Tybjaerg-Hansen, A, van Vugt, M, Vibo, R, Verma, SS, Wiggins, KL, Wennberg, P, Woo, D, Wilson, PWF, Xu, H, Yang, Q, Yoon, K, Millwood, IY, Gieger, C, Ninomiya, T, Grabe, HJ, Jukema, JW, Rissanen, IL, Strbian, D, Kim, YJ, Chen, P-H, Mayerhofer, E, Howson, JMM, Irvin, MR, Adams, H, Wassertheil-Smoller, S, Christensen, K, Ikram, MA, Rundek, T, Worrall, BB, Lathrop, GM, Riaz, M, Simonsick, EM, Korv, J, Franca, PHC, Zand, R, Prasad, K, Frikke-Schmidt, R, de Leeuw, F-E, Liman, T, Haeusler, KG, Ruigrok, YM, Heuschmann, PU, Longstreth, WT, Jung, KJ, Bastarache, L, Pare, G, Damrauer, SM, Chasman, DI, Rotter, JI, Anderson, CD, Zwart, J-A, Niiranen, TJ, Fornage, M, Liaw, Y-P, Seshadri, S, Fernandez-Cadenas, I, Walters, RG, Ruff, CT, Owolabi, MO, Huffman, JE, Milani, L, Kamatani, Y, Dichgans, M, Debette, S, Mishra, A, Malik, R, Hachiya, T, Jurgenson, T, Namba, S, Posner, DC, Kamanu, FK, Koido, M, Le Grand, Q, Shi, M, He, Y, Georgakis, MK, Caro, I, Krebs, K, Liaw, Y-C, Vaura, FC, Lin, K, Winsvold, BS, Srinivasasainagendra, V, Parodi, L, Bae, H-J, Chauhan, G, Chong, MR, Tomppo, L, Akinyemi, R, Roshchupkin, GV, Habib, N, Jee, YH, Thomassen, JQ, Abedi, V, Carcel-Marquez, J, Nygaard, M, Leonard, HL, Yang, C, Yonova-Doing, E, Knol, MJ, Lewis, AJ, Judy, RL, Ago, T, Amouyel, P, Armstrong, ND, Bakker, MK, Bartz, TM, Bennett, DA, Bis, JC, Bordes, C, Borte, S, Cain, A, Ridker, PM, Cho, K, Chen, Z, Cruchaga, C, Cole, JW, de Jager, PL, de Cid, R, Endres, M, Ferreira, LE, Geerlings, MI, Gasca, NC, Gudnason, V, Hata, J, He, J, Heath, AK, Ho, Y-L, Havulinna, AS, Hopewell, JC, Hyacinth, IH, Inouye, M, Jacob, MA, Jeon, CE, Jern, C, Kamouchi, M, Keene, KL, Kitazono, T, Kittner, SJ, Konuma, T, Kumar, A, Lacaze, P, Launer, LJ, Lee, K-J, Lepik, K, Li, J, Li, L, Manichaikul, A, Markus, HS, Marston, NA, Meitinger, T, Mitchell, BD, Montellano, FA, Morisaki, T, Mosley, TH, Nalls, MA, Nordestgaard, BG, O'Donnell, MJ, Okada, Y, Onland-Moret, NC, Ovbiagele, B, Peters, A, Psaty, BM, Rich, SS, Rosand, J, Sabatine, MS, Sacco, RL, Saleheen, D, Sandset, EC, Salomaa, V, Sargurupremraj, M, Sasaki, M, Satizabal, CL, Schmidt, CO, Shimizu, A, Smith, NL, Sloane, KL, Sutoh, Y, Sun, YV, Tanno, K, Tiedt, S, Tatlisumak, T, Torres-Aguila, NP, Tiwari, HK, Tregouet, D-A, Trompet, S, Tuladhar, AM, Tybjaerg-Hansen, A, van Vugt, M, Vibo, R, Verma, SS, Wiggins, KL, Wennberg, P, Woo, D, Wilson, PWF, Xu, H, Yang, Q, Yoon, K, Millwood, IY, Gieger, C, Ninomiya, T, Grabe, HJ, Jukema, JW, Rissanen, IL, Strbian, D, Kim, YJ, Chen, P-H, Mayerhofer, E, Howson, JMM, Irvin, MR, Adams, H, Wassertheil-Smoller, S, Christensen, K, Ikram, MA, Rundek, T, Worrall, BB, Lathrop, GM, Riaz, M, Simonsick, EM, Korv, J, Franca, PHC, Zand, R, Prasad, K, Frikke-Schmidt, R, de Leeuw, F-E, Liman, T, Haeusler, KG, Ruigrok, YM, Heuschmann, PU, Longstreth, WT, Jung, KJ, Bastarache, L, Pare, G, Damrauer, SM, Chasman, DI, Rotter, JI, Anderson, CD, Zwart, J-A, Niiranen, TJ, Fornage, M, Liaw, Y-P, Seshadri, S, Fernandez-Cadenas, I, Walters, RG, Ruff, CT, Owolabi, MO, Huffman, JE, Milani, L, Kamatani, Y, Dichgans, M, and Debette, S

Published
2022

3. Publisher Correction: Stroke genetics informs drug discovery and risk prediction across ancestries (Nature, (2022), 611, 7934, (115-123), 10.1038/s41586-022-05165-3)

Author

Mishra, A, Malik, R, Hachiya, T, Jürgenson, T, Namba, S, Posner, DC, Kamanu, FK, Koido, M, Le Grand, Q, Shi, M, He, Y, Georgakis, MK, Caro, I, Krebs, K, Liaw, YC, Vaura, FC, Lin, K, Winsvold, BS, Srinivasasainagendra, V, Parodi, L, Bae, HJ, Chauhan, G, Chong, MR, Tomppo, L, Akinyemi, R, Roshchupkin, GV, Habib, N, Jee, YH, Thomassen, JQ, Abedi, V, Cárcel-Márquez, J, Nygaard, M, Leonard, HL, Yang, C, Yonova-Doing, E, Knol, MJ, Lewis, AJ, Judy, RL, Ago, T, Amouyel, P, Armstrong, ND, Bakker, MK, Bartz, TM, Bennett, DA, Bis, JC, Bordes, C, Børte, S, Cain, A, Ridker, PM, Cho, K, Chen, Z, Cruchaga, C, Cole, JW, de Jager, PL, de Cid, R, Endres, M, Ferreira, LE, Geerlings, MI, Gasca, NC, Gudnason, V, Hata, J, He, J, Heath, AK, Ho, YL, Havulinna, AS, Hopewell, JC, Hyacinth, HI, Inouye, M, Jacob, MA, Jeon, CE, Jern, C, Kamouchi, M, Keene, KL, Kitazono, T, Kittner, SJ, Konuma, T, Kumar, A, Lacaze, P, Launer, LJ, Lee, KJ, Lepik, K, Li, J, Li, L, Manichaikul, A, Markus, HS, Marston, NA, Meitinger, T, Mitchell, BD, Montellano, FA, Morisaki, T, Mosley, TH, Nalls, MA, Nordestgaard, BG, O’Donnell, MJ, Okada, Y, Onland-Moret, NC, Ovbiagele, B, Peters, A, Psaty, BM, Rich, SS, Mishra, A, Malik, R, Hachiya, T, Jürgenson, T, Namba, S, Posner, DC, Kamanu, FK, Koido, M, Le Grand, Q, Shi, M, He, Y, Georgakis, MK, Caro, I, Krebs, K, Liaw, YC, Vaura, FC, Lin, K, Winsvold, BS, Srinivasasainagendra, V, Parodi, L, Bae, HJ, Chauhan, G, Chong, MR, Tomppo, L, Akinyemi, R, Roshchupkin, GV, Habib, N, Jee, YH, Thomassen, JQ, Abedi, V, Cárcel-Márquez, J, Nygaard, M, Leonard, HL, Yang, C, Yonova-Doing, E, Knol, MJ, Lewis, AJ, Judy, RL, Ago, T, Amouyel, P, Armstrong, ND, Bakker, MK, Bartz, TM, Bennett, DA, Bis, JC, Bordes, C, Børte, S, Cain, A, Ridker, PM, Cho, K, Chen, Z, Cruchaga, C, Cole, JW, de Jager, PL, de Cid, R, Endres, M, Ferreira, LE, Geerlings, MI, Gasca, NC, Gudnason, V, Hata, J, He, J, Heath, AK, Ho, YL, Havulinna, AS, Hopewell, JC, Hyacinth, HI, Inouye, M, Jacob, MA, Jeon, CE, Jern, C, Kamouchi, M, Keene, KL, Kitazono, T, Kittner, SJ, Konuma, T, Kumar, A, Lacaze, P, Launer, LJ, Lee, KJ, Lepik, K, Li, J, Li, L, Manichaikul, A, Markus, HS, Marston, NA, Meitinger, T, Mitchell, BD, Montellano, FA, Morisaki, T, Mosley, TH, Nalls, MA, Nordestgaard, BG, O’Donnell, MJ, Okada, Y, Onland-Moret, NC, Ovbiagele, B, Peters, A, Psaty, BM, and Rich, SS

Abstract

In the version of this article initially published, the name of the PRECISE4Q Consortium was misspelled as “PRECISEQ” and has now been amended in the HTML and PDF versions of the article. Further, data in the first column of Supplementary Table 55 were mistakenly shifted and have been corrected in the file accompanying the HTML version of the article.

Published
2022

12. Sex Differences in the Survival of Patients Undergoing Maintenance Hemodialysis: A 10-year Outcome of the Q-Cohort Study

Author

Kitazono T, Torisu K, Taniguchi M, Hiyamuta H, Tsuruya K, Nakano T, Tsujikawa H, and Yamada S

Subjects
medicine.medical_specialty, Text mining, business.industry, Internal medicine, Medicine, Maintenance hemodialysis, business, Outcome (game theory), Cohort study
Abstract

Background: A survival advantage of women is observed in the general population. However, inconsistent findings have been reported regarding this advantage in patients undergoing maintenance hemodialysis. The aim of this study was to compare the risk of mortality, especially infection-related mortality, between male and female hemodialysis patients.Methods: A total of 3065 Japanese hemodialysis patients aged ≥18 years old were followed up for 10 years. Primary outcome was all-cause and infection-related mortality. The association between the sex and these outcomes were examined using Cox proportional hazards models.Results: During the median follow-up of 8.8 years, 1498 patients died of any cause, and 387 died of infection. Compared with men, the multivariable-adjusted HRs (95% CIs) for all-cause and infection-related mortality in women were 0.51 (0.45–0.58) and 0.36 (0.27–0.47), respectively. This association remained significant even when the propensity score-matching or inverse probability of treatment weighting adjustment methods were employed. Furthermore, even when the non-infection-related mortality was considered a competing risk, the infection-related mortality rate in women was still significantly lower than that in men.Conclusions: A female survival advantage over men is observed in Japanese patients undergoing maintenance hemodialysis.

Published
2021

19. Long-term outcomes of Japan-specific dosage of rivaroxaban in high-risk patients with non-valvular atrial fibrillation: analysis from the XAPASS

Author

Ikeda, T, primary, Ogawa, S, additional, Kitazono, T, additional, Nakagawara, J, additional, Minematsu, K, additional, Miyamoto, S, additional, Murakawa, Y, additional, Iwashiro, S, additional, Hayashi, Y, additional, Okayama, Y, additional, Sunaya, T, additional, Sato, S, additional, and Yamanaka, S, additional

Published
2020
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20. P752 A nationwide survey of chronic enteropathy associated with SLCO2A1 gene in Japan

Author

Umeno, J, primary, Fuyuno, Y, additional, Torisu, T, additional, Hirano, A, additional, Esaki, M, additional, Yanai, S, additional, Ohmiya, N, additional, Hisamatsu, T, additional, Watanabe, K, additional, Hosoe, N, additional, Ogata, H, additional, Hirai, F, additional, Hisabe, T, additional, Matsui, T, additional, Yao, T, additional, Kitazono, T, additional, and Matsumoto, T, additional

Published
2020
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21. P732 The clinical efficacy and safety of indigo naturalis in induction & maintenance therapy for moderate-to-severe ulcerative colitis: A single-centre prospective uncontrolled open-label study

Author

Matsuno, Y, primary, Hirano, A, additional, Torisu, T, additional, Fuyuno, Y, additional, Okamoto, Y, additional, Shin, F, additional, Tomohiko, M, additional, Umeno, J, additional, Hirakawa, Y, additional, Esaki, M, additional, and Kitazono, T, additional

Published
2020
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23. Polymorphism in the sorbin and SH3-domain-containing-1 (SORBS1) gene and the risk of brain infarction in the Japanese population: the Fukuoka Stroke Registry and the Hisayama study

Author

Hagiwara, N., Kitazono, T., Kamouchi, M., Kuroda, J., Ago, T., Hata, J., Ninomiya, T., Ooboshi, H., Kumai, Y., Yoshimura, S., Tamaki, K., Fujii, K., Nagao, T., Okada, Y., Toyoda, K., Nakane, H., Sugimori, H., Yamashita, Y., Wakugawa, Y., Kubo, M., Tanizaki, Y., Kiyohara, Y., Ibayashi, S., and Iida, M.

Published
2008

27. Global Outcome Assessment Life-long after stroke in young adults initiative-the GOAL initiative: study protocol and rationale of a multicentre retrospective individual patient data meta-analysis

Author

Ekker, M.S., Jacob, M.A., Dongen, M.M.E. van, Aarnio, K., Annamalai, A., Arauz, A., Arnold, M., Barboza, M., Bolognese, M., Brouns, R., Chuluun, B., Chuluunbaatar, E., Dagvajantsan, B., Debette, S., Don, A., Enzinger, C., Ekizoglu, E., Fandler-Hofler, S., Fazekas, F., Fromm, A., Gattringer, T., Gulli, G., Hoffmann, M., Hora, T., Jern, C., Jood, K., Kamouchi, M., Kim, Y.S., Kitazono, T., Kittner, S., Kleinig, T., Klijn, K., Korv, J., Lee, T.H., Leys, D., Maaijwee, N., Martinez-Majander, N., Marto, J.P., Mehndiratta, M., Mifsud, V., Montanaro, V., Owolabi, M.O., Patel, V., Phillips, M., Piechowski-Iozwiak, B., Pikula, A., Ruiz-Sandoval, J.L., Sarnowski, B., Schreuder, F.H.B.M., Swartz, R., Tan, K.S., Tanne, D., Tatlisumak, T., Thijs, V., Tuladhar, A., Viana-Baptista, M., Vibo, R., Wu, T., Yesilot, N., Waje-Andreassen, U., Pezzini, A., Putaala, J., Leeuw, F.E. de, Ekker, M.S., Jacob, M.A., Dongen, M.M.E. van, Aarnio, K., Annamalai, A., Arauz, A., Arnold, M., Barboza, M., Bolognese, M., Brouns, R., Chuluun, B., Chuluunbaatar, E., Dagvajantsan, B., Debette, S., Don, A., Enzinger, C., Ekizoglu, E., Fandler-Hofler, S., Fazekas, F., Fromm, A., Gattringer, T., Gulli, G., Hoffmann, M., Hora, T., Jern, C., Jood, K., Kamouchi, M., Kim, Y.S., Kitazono, T., Kittner, S., Kleinig, T., Klijn, K., Korv, J., Lee, T.H., Leys, D., Maaijwee, N., Martinez-Majander, N., Marto, J.P., Mehndiratta, M., Mifsud, V., Montanaro, V., Owolabi, M.O., Patel, V., Phillips, M., Piechowski-Iozwiak, B., Pikula, A., Ruiz-Sandoval, J.L., Sarnowski, B., Schreuder, F.H.B.M., Swartz, R., Tan, K.S., Tanne, D., Tatlisumak, T., Thijs, V., Tuladhar, A., Viana-Baptista, M., Vibo, R., Wu, T., Yesilot, N., Waje-Andreassen, U., Pezzini, A., Putaala, J., and Leeuw, F.E. de

Abstract

Contains fulltext : 215629.pdf (publisher's version ) (Open Access), INTRODUCTION: Worldwide, 2 million patients aged 18-50 years suffer a stroke each year, and this number is increasing. Knowledge about global distribution of risk factors and aetiologies, and information about prognosis and optimal secondary prevention in young stroke patients are limited. This limits evidence-based treatment and hampers the provision of appropriate information regarding the causes of stroke, risk factors and prognosis of young stroke patients. METHODS AND ANALYSIS: The Global Outcome Assessment Life-long after stroke in young adults (GOAL) initiative aims to perform a global individual patient data meta-analysis with existing data from young stroke cohorts worldwide. All patients aged 18-50 years with ischaemic stroke or intracerebral haemorrhage will be included. Outcomes will be the distribution of stroke aetiology and (vascular) risk factors, functional outcome after stroke, risk of recurrent vascular events and death and finally the use of secondary prevention. Subgroup analyses will be made based on age, gender, aetiology, ethnicity and climate of residence. ETHICS AND DISSEMINATION: Ethical approval for the GOAL study has already been obtained from the Medical Review Ethics Committee region Arnhem-Nijmegen. Additionally and when necessary, approval will also be obtained from national or local institutional review boards in the participating centres. When needed, a standardised data transfer agreement will be provided for participating centres. We plan dissemination of our results in peer-reviewed international scientific journals and through conference presentations. We expect that the results of this unique study will lead to better understanding of worldwide differences in risk factors, causes and outcome of young stroke patients.

Published
2019

28. Global Outcome Assessment Life-long after stroke in young adults initiative-the GOAL initiative: study protocol and rationale of a multicentre retrospective individual patient data meta-analysis

Author

Ekker, MS, Jacob, MA, van Dongen, MME, Aarnio, K, Annamalai, AK, Arauz, A, Arnold, M, Barboza, MA, Bolognese, M, Brouns, R, Chuluun, B, Chuluunbaatar, E, Dagvajantsan, B, Debette, S, Don, A, Enzinger, C, Ekizoglu, E, Fandler-Hoefler, S, Fazekas, F, Fromm, A, Gattringer, T, Gulli, G, Hoffmann, M, Hora, TF, Jern, C, Jood, K, Kamouchi, M, Kim, YS, Kitazono, T, Kittner, SJ, Kleinig, TJ, Klijn, CJM, Korv, J, Lee, T-H, Leys, D, Maaijwee, NAM, Martinez-Majander, N, Marto, JP, Mehndiratta, MM, Mifsud, V, Montanaro, VV, Owolabi, MO, Patel, VB, Phillips, MC, Piechowski-Iozwiak, B, Pikula, A, Luis Ruiz-Sandoval, J, Sarnowski, B, Schreuder, FHBM, Swartz, RH, Tan, KS, Tanne, D, Tatlisumak, T, Thijs, V, Tuladhar, AM, Viana-Baptista, M, Vibo, R, Wu, TY, Yesilot, N, Waje-Andreassen, U, Pezzini, A, Putaala, J, de Leeuw, F-E, Ekker, MS, Jacob, MA, van Dongen, MME, Aarnio, K, Annamalai, AK, Arauz, A, Arnold, M, Barboza, MA, Bolognese, M, Brouns, R, Chuluun, B, Chuluunbaatar, E, Dagvajantsan, B, Debette, S, Don, A, Enzinger, C, Ekizoglu, E, Fandler-Hoefler, S, Fazekas, F, Fromm, A, Gattringer, T, Gulli, G, Hoffmann, M, Hora, TF, Jern, C, Jood, K, Kamouchi, M, Kim, YS, Kitazono, T, Kittner, SJ, Kleinig, TJ, Klijn, CJM, Korv, J, Lee, T-H, Leys, D, Maaijwee, NAM, Martinez-Majander, N, Marto, JP, Mehndiratta, MM, Mifsud, V, Montanaro, VV, Owolabi, MO, Patel, VB, Phillips, MC, Piechowski-Iozwiak, B, Pikula, A, Luis Ruiz-Sandoval, J, Sarnowski, B, Schreuder, FHBM, Swartz, RH, Tan, KS, Tanne, D, Tatlisumak, T, Thijs, V, Tuladhar, AM, Viana-Baptista, M, Vibo, R, Wu, TY, Yesilot, N, Waje-Andreassen, U, Pezzini, A, Putaala, J, and de Leeuw, F-E

Abstract

INTRODUCTION: Worldwide, 2 million patients aged 18-50 years suffer a stroke each year, and this number is increasing. Knowledge about global distribution of risk factors and aetiologies, and information about prognosis and optimal secondary prevention in young stroke patients are limited. This limits evidence-based treatment and hampers the provision of appropriate information regarding the causes of stroke, risk factors and prognosis of young stroke patients. METHODS AND ANALYSIS: The Global Outcome Assessment Life-long after stroke in young adults (GOAL) initiative aims to perform a global individual patient data meta-analysis with existing data from young stroke cohorts worldwide. All patients aged 18-50 years with ischaemic stroke or intracerebral haemorrhage will be included. Outcomes will be the distribution of stroke aetiology and (vascular) risk factors, functional outcome after stroke, risk of recurrent vascular events and death and finally the use of secondary prevention. Subgroup analyses will be made based on age, gender, aetiology, ethnicity and climate of residence. ETHICS AND DISSEMINATION: Ethical approval for the GOAL study has already been obtained from the Medical Review Ethics Committee region Arnhem-Nijmegen. Additionally and when necessary, approval will also be obtained from national or local institutional review boards in the participating centres. When needed, a standardised data transfer agreement will be provided for participating centres. We plan dissemination of our results in peer-reviewed international scientific journals and through conference presentations. We expect that the results of this unique study will lead to better understanding of worldwide differences in risk factors, causes and outcome of young stroke patients.

Published
2019

33. Both hypo‐ and hyperglycaemia are associated with increased fracture risk in Japanese people with type 2 diabetes: the Fukuoka Diabetes Registry.

Author

Komorita, Y., Iwase, M., Fujii, H., Ohkuma, T., Ide, H., Yoshinari, M., Oku, Y., Nakamura, U., and Kitazono, T.

Subjects
CONFIDENCE intervals, BONE fractures, GLYCOSYLATED hemoglobin, HYPERGLYCEMIA, HYPOGLYCEMIA, LONGITUDINAL method, MULTIVARIATE analysis, TYPE 2 diabetes, RISK assessment, POSTMENOPAUSE, DESCRIPTIVE statistics, DISEASE risk factors
Abstract

Aim: The impact of glycaemic control on fracture risk is controversial, which may be due to the possible presence of hypoglycaemia. The aim of this study was to separately investigate the impacts of severe hypoglycaemia and poor glycaemic control on fracture risk in people with type 2 diabetes. Methods: Overall, 4706 Japanese participants (2755 men and 1951 postmenopausal women) with type 2 diabetes (mean age 66 years) were followed prospectively (a median of 5.3 years; follow‐up rate, 97.6%), and were stratified by severe hypoglycaemia status and glycaemic control. The primary outcome was fractures at any anatomic site. Results: Fractures occurred in 662 participants (249 men and 413 women). The age‐ and sex‐adjusted incidence rates (expressed per 1000 person‐years) were: 71.2 (multiple episodes of severe hypoglycaemia), 43.1 (one episode), 25.2 [HbA1c < 53 mmol/mol (< 7%) without severe hypoglycaemia], 28.7 [HbA1c 53 to < 64 mmol/mol (7% to < 8%) without severe hypoglycaemia], 27.7 [HbA1c 64 to < 75 mmol/mol (8% to < 9%) without severe hypoglycaemia] and 40.5 [HbA1c ≥ 75 mmol/mol (≥ 9%) without severe hypoglycaemia]. Multivariate‐adjusted hazard ratios (95% confidence intervals) for fractures were 2.24 (1.56, 3.21) in those with multiple episodes of severe hypoglycaemia, and 1.42 (1.04, 1.95) in those with HbA1c ≥ 75 mmol/mol (≥ 9%) without severe hypoglycaemia, compared with those with HbA1c < 53 mmol/mol (< 7%) without severe hypoglycaemia. Conclusions: Both severe hypoglycaemia and poor glycaemic control were significantly related to an increased risk of fracture in people with type 2 diabetes, although severe hypoglycaemia conferred a stronger risk. What's new?: Bone fractures are common among older persons with type 2 diabetes. The impact of glycaemic control on fracture risk is controversial, and may be confounded by the possible presence of hypoglycaemia.Severe hypoglycaemia and poor glycaemic control [HbA1c ≥ 75 mmol/mol (≥ 9%)] were separately related to an increased risk of fracture in people with type 2 diabetes. Recurrent severe hypoglycaemia was strongly associated with fracture risk.This study highlights the importance of glycaemic control to prevent fractures, not only via an HbA1c < 75 mmol/mol (< 9%) but also by avoidance of severe hypoglycaemia. [ABSTRACT FROM AUTHOR]

Published
2020
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37. Primary and secondary prevention of stroke and systemic embolism with rivaroxaban in patients with non-valvular atrial fibrillation (sub-analysis of the expand study)

Author

Uchiyama, S., primary, Hirotsugu, A., additional, Inoue, H., additional, Kitazono, T., additional, Shimizu, W., additional, Yamashita, T., additional, Ikeda, T., additional, Kamouchi, M., additional, Kaikita, K., additional, Fukuda, K., additional, Origasa, H., additional, and Shimokawa, H., additional

Published
2017
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47. Impact of eating rate on obesity and cardiovascular risk factors according to glucose tolerance status: the Fukuoka Diabetes Registry and the Hisayama Study

Author

Ohkuma, T., primary, Fujii, H., additional, Iwase, M., additional, Kikuchi, Y., additional, Ogata, S., additional, Idewaki, Y., additional, Ide, H., additional, Doi, Y., additional, Hirakawa, Y., additional, Mukai, N., additional, Ninomiya, T., additional, Uchida, K., additional, Nakamura, U., additional, Sasaki, S., additional, Kiyohara, Y., additional, and Kitazono, T., additional

Published
2012
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50. Dilatation of the basilar artery in response to selective activation of endothelin B receptors in vivo

Author

Kitazono T, Dd, Heistad, and Frank Faraci

Subjects
Male, Receptors, Endothelin, Endothelins, Indomethacin, Arginine, Nitroarginine, Peptides, Cyclic, Peptide Fragments, Rats, Rats, Sprague-Dawley, Vasodilation, NG-Nitroarginine Methyl Ester, Basilar Artery, Animals
Abstract

The objective of this study was to examine effects of activation of endothelin (ET) B receptors on tone of the basilar artery in vivo. By using a cranial window in anesthetized rats, we examined the effects of IRL 1620, a selective ETB receptor agonist, on diameter of the basilar artery. Under control conditions, diameter of the basilar artery was 214 +/- 6 microns (mean +/- S.E.). Topical application of IRL 1620 (10(-8) mol/l) for 4 min dilated the basilar artery by 30 +/- 4%. Marked desensitization of vasodilator responses was observed in response to a second application of IRL 1620, but not acetylcholine, which indicates a homologous nature of desensitization. REA/001, an ETA/ETB receptor antagonist, abolished IRL 1620-induced dilatation of the basilar artery. BQ 123, a selective ETA receptor antagonist, inhibited constriction in response to ET-1, but did not affect dilator responses of the basilar artery to IRL 1620. Both NG-nitro-L-arginine methyl ester and NG-nitro-L-arginine, inhibitors of nitric oxide synthase, produced marked inhibition of dilator responses of the basilar artery to IRL 1620 without inhibiting vasodilator responses to sodium nitroprusside. Indomethacin did not inhibit vasodilatation in response to IRL 1620. These findings suggest that activation of ETB receptors produces dilatation of the basilar artery in vivo. Dilator responses of the basilar artery to activation of ETB receptors are dependent on production of nitric oxide.

Published
1995

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