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2. Aberrant CHCHD2-associated mitochondriopathy in Kii ALS/PDC astrocytes

Author

Leventoux, Nicolas, Morimoto, Satoru, Ishikawa, Mitsuru, Nakamura, Shiho, Ozawa, Fumiko, Kobayashi, Reona, Watanabe, Hirotaka, Supakul, Sopak, Okamoto, Satoshi, Zhou, Zhi, Kobayashi, Hiroya, Kato, Chris, Hirokawa, Yoshifumi, Aiba, Ikuko, Takahashi, Shinichi, Shibata, Shinsuke, Takao, Masaki, Yoshida, Mari, Endo, Fumito, Yamanaka, Koji, Kokubo, Yasumasa, and Okano, Hideyuki

Published
2024
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3. Intravenous glibenclamide for cerebral oedema after large hemispheric stroke (CHARM): a phase 3, double-blind, placebo-controlled, randomised trial

Author

Abraham, Michael, Acosta, Indrani, Agostoni, Elio Clemente, Aguera Morales, Eduardo, Akaike, Yuji, Ale Bark, Samir, Alexandrov, Andrei, Altschul, Dorothea, Arenillas Lara, Juan Francisco, Arias Rivas, Susana, Arnold, Marcel, Asimos, Andrew, Bar, Michal, Barlinn, Kristian, Beccia, Mario, Benesch, Curtis, Bereczki, Daniel, Berk, Julie, Berkeley, Jennifer, Berrouschot, Joerg, Bettermann, Kerstin, Bevers, Matthew, Bösel, Julian, Bogdanov, Enver, Bonato, Sara, Bornstein, Natan, Boutwell, Christine, Bowling, Susana, Brown, Helen, Bruno, Askiel, Burgin, William, Bustamante, Rafael, Cabral Moro, Carla Heloísa, Cao, Wenfeng, Carandang, Raphael, Cardona Portela, Pedro, Castro, Pedro, Cativo, Maria, Cereda, Carlo, Cerejo, Russell, Chang, Chiung-Chih, Cheng, Roger, Chin, Masaki, Ching, Marilou, Christensen, Hanne, Chung, Lee, Clark, Jonie, Clark, Wayne, Cloud, Geoffrey, Cogez, Julien, Comi, Giancarlo, Cordato, Dennis, Coull, Bruce, Cronin, Carolyn, Csanyi, Attila, Cullis, Paul, Czeisler, Barry, Dangayach, Neha, Datta, Mohit, Debouverie, Marc, Demchuk, Andrew, Denier, Christian, Desfontaines, Philippe, Devlin, Thomas, Dhar, Rajat, Diomedi, Marina, Dioszeghy, Peter, Diringer, Michael, Dixit, Anand, Dong, Qiang, Eichel, Roni, Elliott, Jamie, Fan, Dongsheng, Fernandez Sanchez, Victoria Eugenia, Ferro, José Manuel, Finocchi, Cinzia, Foreman, Brandon, Fortea Cabo, Gerardo, Freire Goncalves, Antonio, Fukuyama, Kozo, Gamero Garcia, Miguel Angel, Garcia Esperon, Carlos, Geng, Deqin, Ghoshal, Shivani, Gomes, Joao, Gordon, Errol, Guillon, Benoit, Hagihara, Yasushi, Hallevi, Hen, Halse, Omid, Han, Moon-Ku, Hargis, Mitch, Harnof, Sagi, Harsany, Michal, Hasegawa, Yasuhiro, Hassan, Ameer, Hayasaka, Michihiro, He, Jincai, Hemelsoet, Dimitri, Henon, Hilde, Herzig, Roman, Hill, Michael, Hinduja, Archana, Hirano, Teruyuki, Horev, Anat, Howell, Bradley, Hu, Xingyue, Huang, David, Hwang, Yangha, Ifergane, Gal, Isayev, Yevgeniy, Ito, Yasuhiro, Iversen, Helle, Jatuzis, Dalius, Jeng, Jiann-Shing, Jeon, Sang-Beom, Jeong, Jin-Heon, Ji, Qiuhong, Kahles, Timo, Kallmuenzer, Bernd, Kaneko, Chikako, Kanzawa, Takao, Kasner, Scott, Kawabata, Masayuki, Kelly, Adam, Kerrigan, Deborah, Keshary, Sanjeev, Khanna, Anna, Kidjemet-Piskac, Spomenka, Kidwell, Chelsea, Kim, Minjee, Kimura, Kazumi, Kimura, Naoto, Kin, Shigenari, Kirmani, Jawad, Kitazawa, Kazuo, Kleinig, Timothy, Koehrmann, Martin, Koga, Masatoshi, Kollmar, Rainer, Konno, Hiromu, Krause, Martin, Kuga, Yoshihiro, Kullman, Dimitri, Kurka, Natalia, Lago Martin, Aida, Latorre, Julius (Gene), LeDoux, David, Leal Loureiro, Jose, Lebedeva, Anna, Lee, Tsong-Hai, Leker, Ronen, Lemmens, Robin, Li, Yansheng, Lioutas, Vasileious-Arsenios, Liu, Chunfeng, Liu, Liping, Liu, Wei, Liu, Yaling, Longoni, Marco, Lopez, George, Lord, Aaron, Lu, Zuneng, Machida, Akira, Magoni, Mauro, Malik, Maheen, Marcheselli, Simona, Marques Pontes Neto, Octávio, Martin, Jerry, Martino, Stephen, Martins Maia Carvalho, Fernanda, Masjuan Vallejo, Jaime, Matijosaitis, Vaidas, Mayer, Stephan, McGrade, Harold, Mehta, Sanal, Melmed, Kara, Melnikova, Elena, Messe, Steven, Meyer, Brett, Miller, Chad, Minnerup, Jens, Mittal, Shilpi, Molina Cateriano, Carlos, Moniche Alvarez, Francisco, Moroi, Junta, Moulin, Thierry, Muir, Keith, Murase, Satoru, Murialdo, Alessandra, Muscat, Paul, Nagy, Ferenc, Nakagawa, Kazuma, Nakagawa, Koshi, Nakano, Shin, Naval, Neeraj, Nencini, Patrizia, Ng, Kwan, Niesen, Wolf-Dirk, Nomura, Sadahiro, Olds, Karin, Olga, Samoshkina, Ota, Shinzo, Ouriques Martins, Sheila Cristina, Ovary, Csaba, Panczel, Gyula, Peretz, Shlomi, Perry, Richard, Petersen, Nils, Phan, Thanh, Pinho e Melo, Teresa, Poisson, Sharon, Poljakovic, Zdravka, Pulido, Angel, Radai, Ferenc, Ramiro, Joanna Isabelle I., Ramos-Estebanez, Ciro, Ratcliff, Jonathan, Renati, Swetha, Richard, Sébastien, Rincon, Fred, Rippee, Michael, Rocha, Marcelo, Rodrigues, Miguel, Rodriguez Campello, Ana, Roh, David, Roje Bedekovic, Marina, Roquer Gonzalez, Jaime, Roriz Cruz, Matheus, Roriz, José Mário, Roshkovskaya, Ludmila, Roveri, Luisa, Ruano, Luis, Rubio Borrego, Francisco, Ruuskanen, Jori, Rybinnik, Igor, Sabet, Arman, Sakai, Nobuyuki, Sampaio Silva, Gisele, Santo, Gustavo, Sarwal, Aarti, Sato, Kenichi, Sato, Kota, Sattin, Justin, Schaefer, Jan-Hendrik, Schneider, Hauke, Serena Leal, Joaquin, Shah, Ruchir, Shah, Shreyansh, Sharma, Kartavya, Shepherd, Starane, Shi, Fudong, Shimoe, Yutaka, Shuaib, Ashfaq, Sibon, Igor, Silliman, Scott, Skorna, Miroslav, Snider, Samuel, Soda, Hassan, Sprigg, Nikola, Stetkarova, Ivana, Strbian, Daniel, Streib, Christopher, Stretz, Hanns Christoph, Sugimori, Hiroshi, Sundararajan, Sophia, Sung, Pi-Shan, Sztriha, Laszlo, Takahashi, Shinichi, Takizawa, Katsumi, Takizawa, Shunya, Tang, Sung-Chun, Tassi, Rosanna, Tayal, Ashis, Tedim Cruz, Vitor, Telman, Gregory, Temes, Richard, Terry, John, Tian, Xiangyang, Timchenko, Ludmila, Timsit, Serge, Tirschwell, David, Tokunaga, Koji, Tomek, Ales, Toni, Danilo, Torbey, Michel, Ueda, Masayuki, Uriel, Eitan, Valverde Moyano, Roberto, Vandermeeren, Yves, Vannier, Stéphane, Vargas, Alejandro, Vecsei, Laszlo, Veltkamp, Roland, Venkatasubramanian, Chitra, Viana Baptista, Miguel, Vilionskis, Aleksandras, Vohanka, Stanislav, Voznyuk, Igor, Wang, Furong, Wang, Guoping, Wang, Ning, Warburton, Elizabeth, Waters, Michael, Wen, Guoqiang, Wendell, Linda, Werring, David, Wienecke, Troels, Wijeratne, Tissa, Wilson, Laura, Witt, John, Wu, Jin, Xiong, Yingqiong, Xu, En, Xu, Jindong, Yamano, Yoshihisa, Yan, Fuling, Yang, Yi, Yi, Fei, Youn, Teddy, Zachariah, George, Zafar, Sahar, Zaidi, Syed, Zammit, Christopher, Zeng, Jinsheng, Zhang, Guilian, Zhang, Meng, Zini, Andrea, Zinke, Jan, Zurasky, John, Sheth, Kevin N, Albers, Gregory W, Saver, Jeffrey L, Campbell, Bruce C V, Molyneaux, Bradley J, Hinson, H E, Cordonnier, Charlotte, Steiner, Thorsten, Toyoda, Kazunori, Wintermark, Max, Littauer, Ross, Collins, Jessica, Lucas, Nisha, Nogueira, Raul G, Simard, J Marc, Wald, Michael, Dawson, Kate, and Kimberly, W Taylor

Published
2024
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8. Executive summary: Japanese pediatric guideline for the treatment and management of asthma (JPGL) 2020

Author

Committee members, Adachi, Yuichi, Takizawa, Takumi, Futamura, Masaki, Fujisawa, Takao, Yoshihara, Shigemi, Shimojo, Naoki, Iino, Akira, Ebisawa, Mothiro, Mochizuki, Hiroyuki, Ohya, Yukihiro, Katsunuma, Toshio, Kameda, Makoto, Inoue, Toshishige, Fukuie, Tatsuki, External committee members, Iwanaga, Takashi, Kuriyama, Mariko, Kuroki, Haruo, Sonobe, Mariko, Takase, Masato, Masuko, Ikuyo, Collaborators, Yamaide, Fumiya, Yoshida, Koichi, Nagakura, Kenichi, Hirai, Kota, Miyaji, Yumiko, Ito, Yasunori, Yagi, Hisako, Miura, Katsushi, Horino, Satoshi, Fukuda, Hironobu, Yoshida, Yukinori, Takahashi, Shinichi, Natsume, Osamu, Nagao, Mizuho, Yamada, Yoshiyuki, Members of systematic review team, Okafuji, Ikuo, Yamamoto-Hanada, Kiwako, Nakajima, Yoichi, Tanaka, Yuya, Suzuki, Shuichi, Sato, Kotaro, Murai, Hiroki, Miura, Taro, Hiraguchi, Yukiko, Takaoka, Yuri, Manabe, Tetsuharu, Kuwabara, Yu, Akashi, Kenichi, Nishikido, Tomoki, Sugimoto, Mayumi, Maeda, Mayu, Kawamoto, Norio, Takahashi, Kyohei, Yamaide, Akiko, Wada, Takuya, Kitazawa, Hiroshi, Saito, Mayako, Executive Adviser, and Nishima, Sankei

Published
2022
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9. Spatial accuracy of dose delivery significantly impacts the planning target volume margin in linear accelerator-based intracranial stereotactic radiosurgery.

Author

Takahashi, Yuta, Oshika, Riki, Tachibana, Rie, Shirai, Katsuyuki, Asakura, Hiroshi, Miyazaki, Masayoshi, Sagawa, Tomohiro, Takahashi, Shinichi, Kuwae, Tsunekazu, Kojima, Hironori, Nishiyama, Shiro, Nemoto, Hikaru, Ishihara, Yoshitomo, Umeda, Mariko, Kijima, Kotaro, Kobayashi, Daisuke, Suzuki, Keiji, Nozawa, Yuki, Hoshida, Kento, and Kitagawa, Tomoki

Subjects
STEREOTACTIC radiosurgery, POLYMER colloids, DOSIMETERS, QUALITY assurance, X-rays, LINEAR accelerators
Abstract

The impact of three-dimensional (3D) dose delivery accuracy of C-arm linacs on the planning target volume (PTV) margin was evaluated for non-coplanar intracranial stereotactic radiosurgery (SRS). A multi-institutional 3D starshot test using beams from seven directions was conducted at 22 clinics using Varian and Elekta linacs with X-ray CT-based polymer gel dosimeters. Variability in dose delivery accuracy was observed, with the distance between the imaging isocenter and each beam exceeding 1 mm at one institution for Varian and nine institutions for Elekta. The calculated PTV margins for Varian and Elekta linacs that could cover the gross tumor volume with 95% probability at 95% of the institutions were 2.3 and 3.5 mm, respectively, in the superior–inferior direction. However, with multifactorial system management (i.e., high-accuracy 3D dose delivery with rigorous linac quality assurance, strict patient immobilization, and high intra-fractional positioning accuracy), these margins could be reduced to 1.0 mm and 1.5 mm, respectively. The findings indicate significant millimeter-level variability in 3D dose delivery accuracy among linacs installed in clinical settings. Thus, maximizing a linac's 3D dose delivery accuracy is essential to achieve the required PTV margin in intracranial SRS. [ABSTRACT FROM AUTHOR]

Published
2025
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10. Factors affecting early neurological deterioration after intravenous alteplase treatment for branch atheromatous disease.

Author

Mizuno, Satoko, Deguchi, Ichiro, Takahashi, Shinichi, Arai, Noriko, Nakagami, Toru, Kimura, Ryutaro, Oryu, Kiichiro, Watanabe, Kaito, Ueda, Sae, Fujiwara, Shinako, Kato, Yuji, Hayashi, Takeshi, and Suda, Satoshi

Subjects
SYSTOLIC blood pressure, CEREBRAL infarction, CLINICAL deterioration, STROKE, BLOOD pressure
Abstract

Background: Intravenous alteplase treatment is effective for acute cerebral infarction, irrespective of the stroke type. However, its value for branch atheromatous disease (BAD) remains unclear, and early neurological deterioration (END) can occur. Aim: To investigate factors affecting END after intravenous alteplase treatment in patients with acute BAD. Methods: This study included 40 consecutive patients diagnosed with cerebral infarction due to BAD in the lenticulostriate artery territory and treated with intravenous alteplase between April 2007 and March 2023. END was defined as an increase of ≥2 points in the total National Institutes of Health Stroke Scale score or ≥1 point in the motor items within 24 h post‐alteplase administration compared to the score at admission. Factors affecting END were retrospectively evaluated. Results: END was observed in 17 of the 40 patients (43%). The median time from the start of alteplase administration to the worsening of neurologic symptoms was 5 h. After intravenous alteplase treatment, the END group had a significantly lower 24‐h average systolic blood pressure (SBP, mean ± standard deviation mmHg) than the non‐END group (142.0 ± 15.2 vs. 149.4 ± 12.0, p < 0.001). The SBP at each time point (immediately before alteplase administration and every 2 h up to 24 h after alteplase administration) was significantly lower in the END than in the non‐END group at 2, 4, and 6 h after alteplase administration. Conclusions: When intravenous alteplase was administered for BAD, BP control after alteplase administration affected END. When alteplase is administered for BAD, it is important to control the blood pressure to maintain hemodynamics. [ABSTRACT FROM AUTHOR]

Published
2025
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11. Clinical Outcome of Intravenous Alteplase Treatment in Patients With Acute Mild Cerebral Infarction.

Author

Deguchi, Ichiro, Takahashi, Shinichi, Nakagami, Toru, Arai, Noriko, Kimura, Ryutaro, Oryu, Kiichiro, Kido, Syunsuke, Kato, Yuji, Hayashi, Takeshi, and Suda, Satoshi

Subjects
*TISSUE plasminogen activator, *INTERNAL carotid artery, *INTRACRANIAL hemorrhage, *TREATMENT effectiveness, *STROKE, *LACUNAR stroke, *CEREBRAL infarction
Abstract

ABSTRACT Background Aim Methods Results Conclusion The efficacy of intravenous alteplase therapy for acute cerebral infarction is well established, regardless of the ischemic stroke subtype. However, its effectiveness in patients with mild cerebral infarction remains controversial, raising concerns about the significance of the treatment.To retrospectively evaluate the efficacy of intravenous alteplase in patients with mild cerebral infarction and other factors affecting the outcome.A total of 527 patients received intravenous alteplase (0.6 mg/kg) at our hospital between October 2012 and March 2023. Of these, 118 patients with mild cerebral infarction (National Institutes of Health Stroke Scale [NIHSS] ≤ 5) who were treated with intravenous alteplase without mechanical thrombectomy were retrospectively evaluated for treatment efficacy and the factors affecting the efficacy.The modified Rankin scale (mRS) outcome at 90 days was good (mRS: 0–1) in 85 (72%) patients and poor (mRS: 2–5) in 33 (28%) patients. Branch atheromatous disease (BAD) and proximal anterior circulation large vessel occlusion (proximal LVO: internal carotid artery and M1 segment of middle cerebral artery) were observed more frequently in the poor outcome group than in the good outcome group. Multivariate analysis, adjusted for age and sex, identified BAD and proximal LVO as factors associated with poor outcomes after intravenous alteplase treatment for mild cerebral infarction. Symptomatic intracranial hemorrhage was observed in one patient with BAD.Most patients with mild cerebral infarction who were treated with intravenous alteplase alone had good outcomes. BAD and proximal LVO were other factors influencing poor outcomes. [ABSTRACT FROM AUTHOR]

Published
2024
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13. Five-Year Stroke Risk and Its Predictors in Asymptomatic Moyamoya Disease: Asymptomatic Moyamoya Registry (AMORE)

Author

Kuroda, Satoshi, Yamamoto, Shusuke, Funaki, Takeshi, Fujimura, Miki, Kataoka, Hiroharu, Hishikawa, Tomohito, Takahashi, Jun, Endo, Hidenori, Nariai, Tadashi, Osato, Toshiaki, Saito, Nobuhito, Sato, Norihiro, Hori, Emiko, Ito, Yoichi M., Miyamoto, Susumu, Inaji, Motoki, Morita, Kenichi, Maruyama, Daisuke, Nakagawara, Jyoji, Hashimura, Naoki, Hamano, Eika, Iihara, Koji, Hashimoto, Nobuo, Honjo, Kaori, Nakamura, Hirohiko, Kashiwazaki, Daina, Imai, Hideaki, Miyawaki, Satoru, Hongo, Hiroki, Yoshida, Kazumichi, Kikuchi, Takayuki, Mineharu, Yohei, Isozaki, Makoto, Kikuta, Kenichiro, Araki, Yoshio, Kanamori, Fumiaki, Date, Isao, Ono, Junichi, Machida, Toshio, Mase, Mitsuhito, Katano, Hiroyuki, Yamaguchi, Koji, Kawamata, Takakazu, Tominaga, Teiji, Uchino, Haruto, Tokairin, Kikutaro, Ito, Masaki, Houkin, Kiyohiro, Chida, Kohei, Ogasawara, Kuniaki, Nagata, Izumi, Horie, Nobutaka, Oka, Hidehiro, Kumabe, Toshihiro, Itoh, Yoshiaki, Abe, Takato, Oki, Koichi, Takahashi, Shinichi, and Suzuki, Norihiro

Published
2023
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20. De novo and rare mutations in the HSPA1L heat shock gene associated with inflammatory bowel disease

Author

Takahashi, Shinichi, Andreoletti, Gaia, Chen, Rui, Munehira, Yoichi, Batra, Akshay, Afzal, Nadeem A, Beattie, R Mark, Bernstein, Jonathan A, Ennis, Sarah, and Snyder, Michael

Subjects
Biological Sciences, Bioinformatics and Computational Biology, Genetics, Autoimmune Disease, Pediatric, Clinical Research, Crohn's Disease, Digestive Diseases, Inflammatory Bowel Disease, Human Genome, 2.1 Biological and endogenous factors, Aetiology, Oral and gastrointestinal, Adolescent, Amino Acid Sequence, Child, Colitis, Ulcerative, Exome, Female, HSP70 Heat-Shock Proteins, Humans, Male, Mutation, Missense, Pedigree, Sequence Alignment, Sequence Analysis, DNA, White People, Sequencing, Ulcerative colitis, Crohn's disease, Clinical Sciences
Abstract

BackgroundInflammatory bowel disease (IBD) is a chronic, relapsing inflammatory disease of the gastrointestinal tract which includes ulcerative colitis and Crohn's disease. Genetic risk factors for IBD are not well understood.MethodsWe performed a family-based whole exome sequencing (WES) analysis on a core family (Family A) to identify potential causal mutations and then analyzed exome data from a Caucasian pediatric cohort (136 patients and 106 controls) to validate the presence of mutations in the candidate gene, heat shock 70 kDa protein 1-like (HSPA1L). Biochemical assays of the de novo and rare (minor allele frequency, MAF  T; p.Ser277Leu) in HSPA1L. Through analysis of WES data of 136 patients, we identified five additional rare HSPA1L mutations (p.Gly77Ser, p.Leu172del, p.Thr267Ile, p.Ala268Thr, p.Glu558Asp) in six patients. In contrast, rare HSPA1L mutations were not observed in controls, and were significantly enriched in patients (P = 0.02). Interestingly, we did not find non-synonymous rare mutations in the HSP70 isoforms HSPA1A and HSPA1B. Biochemical assays revealed that all six rare HSPA1L variant proteins showed decreased chaperone activity in vitro. Moreover, three variants demonstrated dominant negative effects on HSPA1L and HSPA1A protein activity.ConclusionsOur results indicate that de novo and rare mutations in HSPA1L are associated with IBD and provide insights into the pathogenesis of IBD, and also expand our understanding of the roles of HSP70s in human disease.

Published
2017

21. High-Coverage Whole-Exome Sequencing Identifies Candidate Genes for Suicide in Victims with Major Depressive Disorder.

Author

Tombácz, Dóra, Maróti, Zoltán, Kalmár, Tibor, Csabai, Zsolt, Balázs, Zsolt, Takahashi, Shinichi, Palkovits, Miklós, Snyder, Michael, and Boldogkői, Zsolt

Subjects
Humans, DNA, Viral, Chromosome Mapping, Suicide, Depressive Disorder, Major, Microsatellite Repeats, Alleles, Exons, Models, Biological, Female, Male, Genes, X-Linked, Gene Regulatory Networks, Genetic Variation, Genetic Association Studies, DNA Copy Number Variations, Whole Exome Sequencing, Loss of Function Mutation, DNA, Viral, Depressive Disorder, Major, Genes, X-Linked, Models, Biological
Abstract

We carried out whole-exome ultra-high throughput sequencing in brain samples of suicide victims who had suffered from major depressive disorder and control subjects who had died from other causes. This study aimed to reveal the selective accumulation of rare variants in the coding and the UTR sequences within the genes of suicide victims. We also analysed the potential effect of STR and CNV variations, as well as the infection of the brain with neurovirulent viruses in this behavioural disorder. As a result, we have identified several candidate genes, among others three calcium channel genes that may potentially contribute to completed suicide. We also explored the potential implication of the TGF-β signalling pathway in the pathogenesis of suicidal behaviour. To our best knowledge, this is the first study that uses whole-exome sequencing for the investigation of suicide.

Published
2017

23. Multiple lines of evidence for disruption of nuclear lamina and nucleoporins in FUS amyotrophic lateral sclerosis.

Author

Okada, Kensuke, Ito, Daisuke, Morimoto, Satoru, Kato, Chris, Oguma, Yuki, Warita, Hitoshi, Suzuki, Naoki, Aoki, Masashi, Kuramoto, Junko, Kobayashi, Reona, Shinozaki, Munehisa, Ikawa, Masahito, Nakahara, Jin, Takahashi, Shinichi, Nishimoto, Yoshinori, Shibata, Shinsuke, and Okano, Hideyuki

Subjects
NUCLEAR pore complex, AMYOTROPHIC lateral sclerosis, MOTOR neurons, SPINAL cord, RNA sequencing
Abstract

Advanced pathological and genetic approaches have revealed that mutations in fused in sarcoma/translated in liposarcoma (FUS/TLS), which is pivotal for DNA repair, alternative splicing, translation and RNA transport, cause familial amyotrophic lateral sclerosis (ALS). The generation of suitable animal models for ALS is essential for understanding its pathogenesis and developing therapies. Therefore, we used CRISPR-Cas9 to generate FUS -ALS mutation in the non-classical nuclear localization signal (NLS), H517D (mouse position: H509D) and genome-edited mice. Fus WT/H509D mice showed progressive motor impairment (accelerating rotarod and DigiGait system) with age, which was associated with the loss of motor neurons and disruption of the nuclear lamina and nucleoporins and DNA damage in spinal cord motor neurons. We confirmed the validity of our model by showing that nuclear lamina and nucleoporin disruption were observed in lower motor neurons differentiated from patient-derived human induced pluripotent stem cells (hiPSC-LMNs) with FUS -H517D and in the post-mortem spinal cord of patients with ALS. RNA sequence analysis revealed that most nuclear lamina and nucleoporin-linking genes were significantly decreased in FUS -H517D hiPSC-LMNs. This evidence suggests that disruption of the nuclear lamina and nucleoporins is crucial for ALS pathomechanisms. Combined with patient-derived hiPSC-LMNs and autopsy samples, this mouse model might provide a more reliable understanding of ALS pathogenesis and might aid in the development of therapeutic strategies. [ABSTRACT FROM AUTHOR]

Published
2024
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34. Study Profile of the Tsuruoka Metabolomics Cohort Study (TMCS)

Author

Harada, Sei, primary, Iida, Miho, additional, Miyagawa, Naoko, additional, Hirata, Aya, additional, Kuwabara, Kazuyo, additional, Matsumoto, Minako, additional, Okamura, Tomonori, additional, Edagawa, Shun, additional, Kawada, Yoko, additional, Miyake, Atsuko, additional, Toki, Ryota, additional, Akiyama, Miki, additional, Kawai, Atsuki, additional, Sugiyama, Daisuke, additional, Sato, Yasunori, additional, Takemura, Ryo, additional, Fukai, Kota, additional, Ishibashi, Yoshiki, additional, Kato, Suzuka, additional, Kurihara, Ayako, additional, Sata, Mizuki, additional, Shibuki, Takuma, additional, Takeuchi, Ayano, additional, Kohsaka, Shun, additional, Sawano, Mitsuaki, additional, Shoji, Satoshi, additional, Izawa, Yoshikane, additional, Katsumata, Masahiro, additional, Oki, Koichi, additional, Takahashi, Shinichi, additional, Takizawa, Tsubasa, additional, Maruya, Hiroshi, additional, Nishiwaki, Yuji, additional, Kawasaki, Ryo, additional, Hirayama, Akiyoshi, additional, Ishikawa, Takamasa, additional, Saito, Rintaro, additional, Sato, Asako, additional, Soga, Tomoyoshi, additional, Sugimoto, Masahiro, additional, Tomita, Masaru, additional, Komaki, Shohei, additional, Ohmomo, Hideki, additional, Ono, Kanako, additional, Otsuka-Yamasaki, Yayoi, additional, Shimizu, Atsushi, additional, Sutoh, Yoichi, additional, Hozawa, Atsushi, additional, Kinoshita, Kengo, additional, Koshiba, Seizo, additional, Kumada, Kazuki, additional, Ogishima, Soichi, additional, Sakurai-Yageta, Mika, additional, Tamiya, Gen, additional, and Takebayashi, Toru, additional

Published
2024
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45. From bench to bedside: US-Japan Collaborative Workshop on the NVU.

Author

2023 US-Japan NVU Workshop Group, Borlongan, Cesario, Esposito, Elga, Corales, Laarni Grace, Hattori, Yorito, Hayashi, Yu, Ihara, Masafumi, Iliff, Jeffrey J., Kisler, Kassandra, Kitazume, Shinobu, Koizumi, Schuichi, Liu, Jialing, Maki, Takakuni, Onodera, Osamu, Saito, Satoshi, Sawamoto, Kazunobu, Sohya, Kazuhiro, Taguchi, Akihiko, Takahashi, Shinichi, and Tanaka, Kenji

Abstract

The joint workshop between U.S. and Japanese researchers, supported by The U.S.–Japan Brain Research Cooperative Program, convened in January 2023 at Keio University Mita campus in Tokyo, Japan. The workshop had a threefold objective. Firstly, it aimed to facilitate robust exchanges between U.S. and Japanese researchers engaged in Neurovascular Unit (NVU) research, enhancing the global network of scholars in the field. Secondly, it aimed to encourage the initiation of collaborative research projects, fostering interdisciplinary efforts and synergistic advancements in understanding the brain vascular physiology and central nervous system. Lastly, the workshop emphasized the nurturing of young researchers, recognizing their pivotal role in shaping the future of NVU research. Throughout the workshop, participants discussed fundamental aspects of the NVU, exploring its complex connections and vital functions. By sharing their expertise and insights, the workshop attendees sought to uncover novel approaches to mitigate the burden of neurological diseases for individuals worldwide. This report provides a summary of the presentations and discussions held during the workshop, showcasing the collective efforts and progress made by the participants. [ABSTRACT FROM AUTHOR]

Published
2024
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46. Cerebral Small Vessel Disease Burden for Bleeding Risk during Antithrombotic Therapy: Bleeding with Antithrombotic Therapy 2 Study.

Author

Tanaka, Kanta, Miwa, Kaori, Koga, Masatoshi, Yoshimura, Sohei, Kamiyama, Kenji, Yagita, Yoshiki, Nagakane, Yoshinari, Hoshino, Haruhiko, Terasaki, Tadashi, Okada, Yasushi, Yakushiji, Yusuke, Takahashi, Shinichi, Ueda, Toshihiro, Hasegawa, Yasuhiro, Shiozawa, Masayuki, Sasaki, Makoto, Kudo, Kohsuke, Tanaka, Jun, Nishihara, Masashi, and Yamaguchi, Yoshitaka

Subjects
CEREBRAL small vessel diseases, FIBRINOLYTIC agents, INTRACRANIAL hemorrhage, GASTROINTESTINAL hemorrhage, CEREBROVASCULAR disease
Abstract

Objective: This study was undertaken to determine the excess risk of antithrombotic‐related bleeding due to cerebral small vessel disease (SVD) burden. Methods: In this observational, prospective cohort study, patients with cerebrovascular or cardiovascular diseases taking oral antithrombotic agents were enrolled from 52 hospitals across Japan between 2016 and 2019. Baseline multimodal magnetic resonance imaging acquired under prespecified conditions was assessed by a central diagnostic radiology committee to calculate total SVD score. The primary outcome was major bleeding. Secondary outcomes included bleeding at each site and ischemic events. Results: Of the analyzed 5,250 patients (1,736 women; median age = 73 years, 9,933 patient‐years of follow‐up), antiplatelets and anticoagulants were administered at baseline in 3,948 and 1,565, respectively. Median SVD score was 2 (interquartile range = 1–3). Incidence rate of major bleeding was 0.39 (per 100 patinet‐years) in score 0, 0.56 in score 1, 0.91 in score 2, 1.35 in score 3, and 2.24 in score 4 (adjusted hazard ratio [aHR] for score 4 vs 0 = 5.47, 95% confidence interval [CI] = 2.26–13.23), that of intracranial hemorrhage was 0.11, 0.33, 0.58, 0.99, and 1.06, respectively (aHR = 9.29, 95% CI = 1.99–43.35), and that of ischemic event was 1.82, 2.27, 3.04, 3.91, and 4.07, respectively (aHR = 1.76, 95% CI = 1.08–2.86). In addition, extracranial major bleeding (aHR = 3.43, 95% CI = 1.13–10.38) and gastrointestinal bleeding (aHR = 2.54, 95% CI = 1.02–6.35) significantly increased in SVD score 4 compared to score 0. Interpretation: Total SVD score was predictive for intracranial hemorrhage and probably for extracranial bleeding, suggesting the broader clinical relevance of cerebral SVD as a marker for safe implementation of antithrombotic therapy. ANN NEUROL 2024;95:774–787 [ABSTRACT FROM AUTHOR]

Published
2024
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