K
Koichi Hirata
Researcher at Sapporo Medical University
Publications - 735
Citations - 21379
Koichi Hirata is an academic researcher from Sapporo Medical University. The author has contributed to research in topics: Cancer & Breast cancer. The author has an hindex of 68, co-authored 717 publications receiving 18834 citations. Previous affiliations of Koichi Hirata include Showa University.
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Journal ArticleDOI
Tokyo Guidelines 2018: diagnostic criteria and severity grading of acute cholecystitis (with videos).
Masamichi Yokoe,Jiro Hata,Tadahiro Takada,Steven M. Strasberg,Horacio J. Asbun,Go Wakabayashi,Kazuto Kozaka,Itaru Endo,Daniel J. Deziel,Fumihiko Miura,Kohji Okamoto,Tsann Long Hwang,Wayne Shih Wei Huang,Chen Guo Ker,Miin Fu Chen,Ho-Seong Han,Yoo Seok Yoon,In Seok Choi,Dong Sup Yoon,Yoshinori Noguchi,Satoru Shikata,Tomohiko Ukai,Ryota Higuchi,Toshifumi Gabata,Yasuhisa Mori,Yukio Iwashita,Taizo Hibi,Palepu Jagannath,Eduard Jonas,Kui Hin Liau,Christos Dervenis,Dirk J. Gouma,Daniel Cherqui,Giulio Belli,O. James Garden,Mariano E Giménez,Eduardo de Santibañes,Kenji Suzuki,Akiko Umezawa,Avinash Supe,Henry A. Pitt,Harjit Singh,Angus C.W. Chan,Wan Yee Lau,Anthony Yuen Bun Teoh,Goro Honda,Atsushi Sugioka,Koji Asai,Harumi Gomi,Takao Itoi,Seiki Kiriyama,Masahiro Yoshida,Toshihiko Mayumi,Naoki Matsumura,Hiromi Tokumura,Seigo Kitano,Koichi Hirata,Kazuo Inui,Yoshinobu Sumiyama,Masakazu Yamamoto +59 more
TL;DR: Thorough literature search about diagnostic criteria for acute cholecystitis, new and strong evidence that had been released from 2013 to 2017 was not found with serious and important issues about using TG13 diagnostic criteria of acute CholecyStitis, and the TG13 severity grading has been validated in numerous studies.
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Carbohydrate mimicry between human ganglioside GM1 and Campylobacter jejuni lipooligosaccharide causes Guillain-Barre syndrome.
Nobuhiro Yuki,Keiichiro Susuki,Michiaki Koga,Yukihiro Nishimoto,Masaaki Odaka,Koichi Hirata,Kyoji Taguchi,Tadashi Miyatake,Koichi Furukawa,Tetsuji Kobata,Mitsunori Yamada +10 more
TL;DR: Results show that carbohydrate mimicry is an important cause of autoimmune neuropathy, and conclusive evidence is reported here.
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Tokyo Guidelines 2018: flowchart for the management of acute cholecystitis.
Kohji Okamoto,Kenji Suzuki,Tadahiro Takada,Steven M. Strasberg,Horacio J. Asbun,Itaru Endo,Yukio Iwashita,Taizo Hibi,Henry A. Pitt,Akiko Umezawa,Koji Asai,Ho-Seong Han,Tsann Long Hwang,Yasuhisa Mori,Yoo Seok Yoon,Wayne Shih Wei Huang,Giulio Belli,Christos Dervenis,Masamichi Yokoe,Seiki Kiriyama,Takao Itoi,Palepu Jagannath,O. James Garden,Fumihiko Miura,Masafumi Nakamura,Akihiko Horiguchi,Go Wakabayashi,Daniel Cherqui,Eduardo de Santibañes,Satoru Shikata,Yoshinori Noguchi,Tomohiko Ukai,Ryota Higuchi,Keita Wada,Goro Honda,Avinash Supe,Masahiro Yoshida,Toshihiko Mayumi,Dirk J. Gouma,Daniel J. Deziel,Kui Hin Liau,Miin Fu Chen,Kazunori Shibao,Keng Hao Liu,Cheng Hsi Su,Angus C.W. Chan,Dong Sup Yoon,In Seok Choi,Eduard Jonas,Xiao Ping Chen,Sheung Tat Fan,Chen Guo Ker,Mariano E Giménez,Seigo Kitano,Masafumi Inomata,Koichi Hirata,Kazuo Inui,Yoshinobu Sumiyama,Masakazu Yamamoto +58 more
TL;DR: In the Tokyo Guidelines 2018 (TG18) as discussed by the authors, the authors proposed a flowchart for the treatment of acute cholecystitis (AC) in advanced centers with specialized surgeons experienced in this procedure.
Journal ArticleDOI
Anti-GQ1b IgG antibody syndrome: clinical and immunological range
TL;DR: It was confirmed clinically that MFS, GBS, BBE, and acute ophthalmoparesis are closely related, forming a continuous range, and a common autoantibody (anti-GQ1b IgG) suggest that a common autoimmune mechanism functions in the pathogenesis of these illnesses.
Journal ArticleDOI
Anti-GM1 antibodies cause complement-mediated disruption of sodium channel clusters in peripheral motor nerve fibers.
Keiichiro Susuki,Matthew N. Rasband,Koujiro Tohyama,Katsura Koibuchi,Saori Okamoto,Kei Funakoshi,Koichi Hirata,Hiroko Baba,Nobuhiro Yuki +8 more
TL;DR: The findings support the idea that acute motor axonal neuropathy is a disease that specifically disrupts the nodes of Ranvier, and suggest that Nav channel alterations occur as a consequence of complement-mediated disruption of interactions between axons and Schwann cells.