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Article ; Online: Intra-bronchial migration of peritoneal catheter of lumboperitoneal shunt

Takashi Kawahara / Masakazu Yanagi / Hirofumi Hirano / Kazunori Arita

Surgical Neurology International, Vol 6, Iss 1, Pp 167-

2015 Volume 167

Abstract: Background: A rare case of intra-bronchial migration of peritoneal catheter of lumboperitoneal (LP) shunt was treated under the bronchoscopic and fluoroscopic observation. Case Description: A 71-year-old man, who underwent LP shunt installation due to ... ...

Abstract	Background: A rare case of intra-bronchial migration of peritoneal catheter of lumboperitoneal (LP) shunt was treated under the bronchoscopic and fluoroscopic observation. Case Description: A 71-year-old man, who underwent LP shunt installation due to idiopathic normal pressure hydrocephalus a year before, presented with history of high fever and sputum production. Roentgenography and computed tomography of the chest revealed migration of distal end of the peritoneal catheter into the left main bronchus. Migrated catheter was gently extracted through the abdominal wound incision under the bronchoscopic and fluoroscopic observation. Contrast material infused into the catheter did not spread into the pleural cavity. The patient was free of the symptoms within 2 postoperative weeks. Moreover, he underwent the ventriculo-peritoneal shunt surgery 1-month later. Conclusion: This is the first case of the migration of peritoneal catheter of LP shunt into the main bronchus.
Keywords	Bronchial migration ; contrast medium injection ; lumboperitoneal shunt ; Medicine ; R ; Surgery ; RD1-811 ; Internal medicine ; RC31-1245 ; Neurosciences. Biological psychiatry. Neuropsychiatry ; RC321-571 ; Neurology. Diseases of the nervous system ; RC346-429
Publishing date	2015-01-01T00:00:00Z
Publisher	Medknow Publications
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Use of the guidewire for repositioning displaced spinal catheter during lumboperitoneal shunt placement

Takashi Kawahara / Tatsuki Oyoshi / Masamichi Atsuchi / Koji Takasaki / Kazunori Arita

Surgical Neurology International, Vol 7, Iss 1, Pp 63-

2016 Volume 63

Abstract: Background : During lumboperitoneal shunt operation, we may inadvertently pull and displace the spinal catheter after the catheter placement into the spinal canal. The authors introduce an easy and efficient technique for repositioning a prolapsed ... ...

Abstract	Background : During lumboperitoneal shunt operation, we may inadvertently pull and displace the spinal catheter after the catheter placement into the spinal canal. The authors introduce an easy and efficient technique for repositioning a prolapsed catheter into correct place. Methods: After the confirmation of cerebrospinal fluid outflow from the end of the catheter, a guidewire for angiogram was gently inserted into the catheter until its tip reached the end of the catheter. The guidewire-inserted catheter was able to be pushed back manually and adequately placed in the spinal canal under the fluoroscope guidance. Results: Three patients underwent repositioning using this "rescue wire technique" without complications. Conclusion: This "rescue wire technique" is useful for repositioning of the displaced catheter into the spinal canal.
Keywords	Guidewire ; lumboperitoneal shunt ; spinal catheter ; Medicine ; R ; Surgery ; RD1-811 ; Internal medicine ; RC31-1245 ; Neurosciences. Biological psychiatry. Neuropsychiatry ; RC321-571 ; Neurology. Diseases of the nervous system ; RC346-429
Language	English
Publishing date	2016-01-01T00:00:00Z
Publisher	Medknow Publications
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Initiating an epilepsy surgery program with limited resources in Indonesia

Muhamad Thohar Arifin / Ryosuke Hanaya / Yuriz Bakhtiar / Aris Catur Bintoro / Koji Iida / Kaoru Kurisu / Kazunori Arita / Jacob Bunyamin / Rofat Askoro / Surya Pratama Brilliantika / Novita Ikbar Khairunnisa / Zainal Muttaqin

Scientific Reports, Vol 11, Iss 1, Pp 1-

2021 Volume 11

Abstract: Abstract To share the experiences of organizing the epilepsy surgery program in Indonesia. This study was divided into two periods based on the presurgical evaluation method: the first period (1999–2004), when interictal electroencephalogram (EEG) and ... ...

Abstract	Abstract To share the experiences of organizing the epilepsy surgery program in Indonesia. This study was divided into two periods based on the presurgical evaluation method: the first period (1999–2004), when interictal electroencephalogram (EEG) and magnetic resonance imaging (MRI) were used mainly for confirmation, and the second period (2005–2017), when long-term non-invasive and invasive video-EEG was involved in the evaluation. Long-term outcomes were recorded up to December 2019 based on the Engel scale. All 65 surgical recruits in the first period possessed temporal lobe epilepsy (TLE), while 524 patients were treated in the second period. In the first period, 76.8%, 16.1%, and 7.1% of patients with TLE achieved Classes I, II, and III, respectively, and in the second period, 89.4%, 5.5%, and 4.9% achieved Classes I, II, and III, respectively, alongside Class IV, at 0.3%. The overall median survival times for patients with focal impaired awareness seizures (FIAS), focal to bilateral tonic–clonic seizures and generalized tonic–clonic seizures were 9, 11 and 11 years (95% CI: 8.170–9.830, 10.170–11.830, and 7.265–14.735), respectively, with p = 0.04. The utilization of stringent and selective criteria to reserve surgeries is important for a successful epilepsy program with limited resources.
Keywords	Medicine ; R ; Science ; Q
Subject code	616
Language	English
Publishing date	2021-03-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: 1,5-Anhydro-D-fructose Protects against Rotenone-Induced Neuronal Damage In Vitro through Mitochondrial Biogenesis

Yuki Kasamo / Kiyoshi Kikuchi / Munekazu Yamakuchi / Shotaro Otsuka / Seiya Takada / Yuki Kambe / Takashi Ito / Ko-ichi Kawahara / Kazunori Arita / Koji Yoshimoto / Ikuro Maruyama

International Journal of Molecular Sciences, Vol 22, Iss 9941, p

2021 Volume 9941

Abstract: Mitochondrial functional abnormalities or quantitative decreases are considered to be one of the most plausible pathogenic mechanisms of Parkinson’s disease (PD). Thus, mitochondrial complex inhibitors are often used for the development of experimental ... ...

Abstract	Mitochondrial functional abnormalities or quantitative decreases are considered to be one of the most plausible pathogenic mechanisms of Parkinson’s disease (PD). Thus, mitochondrial complex inhibitors are often used for the development of experimental PD. In this study, we used rotenone to create in vitro cell models of PD, then used these models to investigate the effects of 1,5-anhydro-D-fructose (1,5-AF), a monosaccharide with protective effects against a range of cytotoxic substances. Subsequently, we investigated the possible mechanisms of these protective effects in PC12 cells. The protection of 1,5-AF against rotenone-induced cytotoxicity was confirmed by increased cell viability and longer dendritic lengths in PC12 and primary neuronal cells. Furthermore, in rotenone-treated PC12 cells, 1,5-AF upregulated peroxisome proliferator-activated receptor-γ coactivator 1α (PGC-1α) expression and enhanced its deacetylation, while increasing AMP-activated protein kinase (AMPK) phosphorylation. 1,5-AF treatment also increased mitochondrial activity in these cells. Moreover, PGC-1α silencing inhibited the cytoprotective and mitochondrial biogenic effects of 1,5-AF in PC12 cells. Therefore, 1,5-AF may activate PGC-1α through AMPK activation, thus leading to mitochondrial biogenic and cytoprotective effects. Together, our results suggest that 1,5-AF has therapeutic potential for development as a treatment for PD.
Keywords	1,5-AF ; 1,5-AG ; metformin ; Parkinson’s disease ; parkinsonism ; AMPK ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	610
Language	English
Publishing date	2021-09-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Involvement of orexin neurons in fasting- and central adenosine-induced hypothermia

Takahiro Futatsuki / Akira Yamashita / Khairunnisa Novita Ikbar / Akihiro Yamanaka / Kazunori Arita / Yasuyuki Kakihana / Tomoyuki Kuwaki

Scientific Reports, Vol 8, Iss 1, Pp 1-

2018 Volume 11

Abstract: Abstract We examined whether orexin neurons might play a protective role against fasting- and adenosine-induced hypothermia. We first measured body temperature (BT) in orexin neuron-ablated (ORX-AB) mice and wild-type (WT) controls during 24 hours of ... ...

Abstract	Abstract We examined whether orexin neurons might play a protective role against fasting- and adenosine-induced hypothermia. We first measured body temperature (BT) in orexin neuron-ablated (ORX-AB) mice and wild-type (WT) controls during 24 hours of fasting. As expected, the magnitude of BT drop and the length of time suffering from hypothermia were greater in ORX-AB mice than in WT mice. Orexin neurons were active just before onset of hypothermia and during the recovery period as revealed by calcium imaging in vivo using G-CaMP. We next examined adenosine-induced hypothermia via an intracerebroventricular administration of an adenosine A1 receptor agonist, N6-cyclohexyladenosine (CHA), which induced hypothermia in both ORX-AB and WT mice. The dose of CHA required to initiate a hypothermic response in ORX-AB mice was more than 10 times larger than the dose for WT mice. Once hypothermia was established, the recovery was seemingly slower in ORX-AB mice. Activation of orexin neurons during the recovery phase was confirmed by immunohistochemistry for c-Fos. We propose that orexin neurons play dual roles (enhancer in the induction phase and compensator during the recovery phase) in adenosine-induced hypothermia and a protective/compensatory role in fasting-induced hypothermia.
Keywords	Medicine ; R ; Science ; Q
Subject code	572
Language	English
Publishing date	2018-02-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Correction to

Takaya Iwasaki / Noriko Tsumura / Tanio Ito / Kazunori Arita / Makoto Matsubara / Hiroshi Sato / Eiji Kurashimo / Naoshi Hirata / Susumu Abe / Katsuya Noda / Akira Fujiwara / Shinsuke Kikuchi / Kazuko Suzuki

Earth, Planets and Space, Vol 72, Iss 1, Pp 1-

Structural heterogeneity in and around the fold-and-thrust belt of the Hidaka Collision zone, Hokkaido, Japan and its relationship to the aftershock activity of the 2018 Hokkaido Eastern Iburi Earthquake

2020 Volume 1

Abstract: In the original publication of this article (Iwasaki et al. 2019), the author name ‘Matsubara Makoto’ in author list is not correct. The correct name should be ‘Makoto Matsubara’. ...

Abstract	In the original publication of this article (Iwasaki et al. 2019), the author name ‘Matsubara Makoto’ in author list is not correct. The correct name should be ‘Makoto Matsubara’.
Keywords	Geography. Anthropology. Recreation ; G ; Geodesy ; QB275-343 ; Geology ; QE1-996.5
Language	English
Publishing date	2020-03-01T00:00:00Z
Publisher	SpringerOpen
Document type	Article ; Online
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Article ; Online: Structural heterogeneity in and around the fold-and-thrust belt of the Hidaka Collision zone, Hokkaido, Japan and its relationship to the aftershock activity of the 2018 Hokkaido Eastern Iburi Earthquake

Takaya Iwasaki / Noriko Tsumura / Tanio Ito / Kazunori Arita / Matsubara Makoto / Hiroshi Sato / Eiji Kurashimo / Naoshi Hirata / Susumu Abe / Katsuya Noda / Akira Fujiwara / Shinsuke Kikuchi / Kazuko Suzuki

Earth, Planets and Space, Vol 71, Iss 1, Pp 1-

2019 Volume 19

Abstract: Abstract The Hokkaido Eastern Iburi Earthquake (M = 6.7) occurred on Sep. 6, 2018 in the southern part of Central Hokkaido, Japan. Since Paleogene, this region has experienced the dextral oblique transpression between the Eurasia and North American ( ... ...

Abstract	Abstract The Hokkaido Eastern Iburi Earthquake (M = 6.7) occurred on Sep. 6, 2018 in the southern part of Central Hokkaido, Japan. Since Paleogene, this region has experienced the dextral oblique transpression between the Eurasia and North American (Okhotsk) Plates and the subsequent collision between the Northeast Japan Arc and the Kuril Arc due to the oblique subduction of the Pacific Plate. This earthquake occurred beneath the foreland fold-and-thrust belt of the Hidaka Collision zone developed by the collision process, and is characterized by its deep focal depth (~ 37 km) and complicated rupture process. The reanalyses of controlled source seismic data collected in the 1998–2000 Hokkaido Transect Project revealed the detailed structure beneath the fold-and-thrust belt, and its relationship with the aftershock activity of this earthquake. Our reflection processing using the CRS/MDRS stacking method imaged for the first time the lower crust and uppermost mantle structures of the Northeast Japan Arc underthrust beneath a thick (~ 5–10 km) sedimentary package of the fold-and-thrust belt. Based on the analysis of the refraction/wide-angle reflection data, the total thickness of this Northeast Japan Arc crust is only 16–22 km. The Moho is at depths of 26–28 km in the source region of the Hokkaido Eastern Iburi Earthquake. Our hypocenter determination using a 3D structure model shows that most of the aftershocks are distributed in a depth range of 7–45 km with steep geometry facing to the east. The seismic activity is quite low within the thick sediments of the fold–thrust belt, from which we find no indication on the relationship of this event with the shallow (< 10–15 km) and rather flat active faults developed in the fold-and-thrust belt. On the other hand, a number of aftershocks are distributed below the Moho. This high activity may be caused by the cold crust delaminated from the Kuril Arc side by the arc–arc collision, which prevents the thermal circulation and cools the forearc uppermost mantle to generate an environment more favorable for brittle fracture.
Keywords	The Hokkaido Eastern Iburi Earthquake ; Hokkaido ; Arc–arc collision ; Fold-and-thrust belt ; Seismic structure ; Controlled source seismic experiments ; Geography. Anthropology. Recreation ; G ; Geodesy ; QB275-343 ; Geology ; QE1-996.5
Subject code	550
Language	English
Publishing date	2019-09-01T00:00:00Z
Publisher	SpringerOpen
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Clinical significance of ABCA2' a possible molecular marker for oligodendrogliomas.

Soichi, Obara / Masanori, Nakata / Hideo, Takeshima / Kazunori, Arita / Nobuya, Inagaki / Jun-ichi, Kuratsu

Neurosurgery

2007 Volume 60, Issue 4, Page(s) 707–14; discussion 714

Abstract: Objective: ABCA2 is a member of the adenosine triphosphate-binding cassette transporter superfamily and is proposed to exert critical functions in the transmembrane transport of endogenous lipids such as myelin. It is expressed predominantly in the ... ...

Abstract	Objective: ABCA2 is a member of the adenosine triphosphate-binding cassette transporter superfamily and is proposed to exert critical functions in the transmembrane transport of endogenous lipids such as myelin. It is expressed predominantly in the cytoplasm of oligodendrocytes and Schwann cells, the myelin-forming cells in the brain and peripheral nerves. Recently, it has been shown that it may be a useful marker for the cellular characterization of vestibular schwannomas. Methods: To determine whether or not ABCA2 can distinguish oligodendrogliomas from astrocytic tumors, the authors investigated the expression of ABCA2 in a panel of 55 glioma tissues (13 oligodendrogliomas, nine anaplastic oligodendrogliomas, 12 anaplastic astrocytomas, and 21 glioblastomas) using real-time reverse-transcriptase polymerase chain reaction analysis, immunoblot analysis, and immunohistochemistry analysis. The authors also compared the expression of Olig2, a recently identified marker for oligodendroglioma. Results: The relative expression level of ABCA2 messenger ribonucleic acid determined by real-time quantitative polymerase chain reaction is significantly higher (by a factor of five) in oligodendroglioma than in anaplastic astrocytoma or glioblastoma. It was moderately increased in anaplastic oligodendrogliomas. In immunohistochemical analysis, ABCA2 exhibited remarkable immunopositivity in 11 out of 13 oligodendrogliomas showing a granular pattern in the cytoplasm of tumor cells. However, ABCA2 was completely negative in most anaplastic astrocytomas (75%) and glioblastomas (76%). Anaplastic oligodendroglioma showed an intermediate pattern: strongly positive in two out of nine samples and negative in seven out of nine samples. However, Olig2 was strongly positive in most anaplastic astrocytomas (83%) and glioblastomas (71%). Although there was no difference in the detection of oligodendroglial tumors, the specificity (negative in astrocytic tumor) was significantly higher in ABCA2 than in Olig2. Conclusion: These lines of evidence suggest that ABCA2 could be a molecular marker for oligodendroglioma.
MeSH term(s)	ATP-Binding Cassette Transporters/metabolism ; Biomarkers, Tumor/metabolism ; Brain Neoplasms/diagnosis ; Brain Neoplasms/metabolism ; Feasibility Studies ; Humans ; Neoplasm Proteins/metabolism ; Oligodendroglioma/metabolism
Chemical Substances	ABCA2 protein, human ; Biomarkers, Tumor ; Neoplasm Proteins
Language	English
Publishing date	2007-04
Publishing country	United States
Document type	Journal Article
ZDB-ID	135446-2
ISSN	1524-4040 ; 0148-396X
ISSN (online)	1524-4040
ISSN	0148-396X
DOI	10.1227/01.NEU.0000255395.15657.06
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: National trends in the outcomes of subarachnoid haemorrhage and the prognostic influence of stroke centre capability in Japan

Satoshi Suzuki / Kenji Yamamoto / Hiroaki Tanaka / Hiroshi Ozawa / Yuji Okamoto / Tatsuya Abe / Hidenori Suzuki / Akiko Kada / Shigeki Nishino / Nobuyuki Sakai / Kunihiro Nishimura / Tomoyoshi Oikawa / Takanari Kitazono / Hiroshi Tanaka / Daisuke Onozuka / Akihito Hagihara / Hiroshi Ooyama / Akira Watanabe / Shinichi Yoshimura /

Toru Iwama / Hiroki Sato / Satoshi Ushikoshi / Kiyohiro Houkin / Nobuhiro Mikuni / Naoyuki Nakao / Michio Nakamura / Nanako Tamiya / Naofumi Isono / Koji Iihara / Yutaka Yamaguchi / Kuniaki Ogasawara / Osamu Onodera / Yusaku Nakamura / Naoki Hayashi / Akira Takada / Hiroyuki Arai / Masayuki Ezura / Akio Hyodo / Shigeru Miyachi / Susumu Miyamoto / Yuji Matsumaru / Ichiro Nakahara / Tomoaki Terada / Kazunari Yoshida / Ai Kurogi / Ataru Nishimura / Yoshiaki Shiokawa / Koichi Arimura / Kaoru Kurisu / Fusao Ikawa / Kenji Ohata / Kyoichi Nomura / Nobuhito Saito / Hiroaki Fujiwara / Susumu Suzuki / Masanori Isobe / Soshiro Ogata / Takeshi Matsuoka / Junichiro Satomi / Takashi Matsumoto / Hiroyuki Nakase / Yasunari Niimi / Manabu Kinoshita / Mamoru Murakami / Masaaki Uno / Junichi Iida / Takashi Matsuoka / Tatsuya Sasaki / Shinichi Wakabayashi / Hiroki Toda / Hideki Sakai / Hajime Ohta / Osamu Yamamura / Hideyuki Ohnishi / Hiroko Oyama / Junichi Ono / Izumi Nagata / Hiroharu Kataoka / Ryota Kurogi / Hajime Arai / Atsuo Yoshino / Tsuyoshi Ohta / Hiroshi Sugimori / Hidehiro Hirabayashi / Hiroyuki Masaoka / Satoshi Yamamoto / Hideki Murakami / Kazuhiko Nozaki / Hiroyuki Matsumoto / Yuichiro Tanaka / Takahisa Mori / Keizo Yasui / Akira Takahashi / Ichiro Suzuki / Sachio Suzuki / TAKASHI YOSHIDA / Masanori Morimoto / Tetsuya Ueba / Hiromu Hadeishi / Masaki Chin / Michihiro Kohno / Hitoshi Fukuda / Toru Nishi / Kazunari Koga / Toshihiko Wakabayashi / Hiroki Ohkuma / Kazuhiro Hongo / Hiroshi Nakane / Kazumi Nitta / Satoshi Utsuki / Toshihiko Iuchi / Nice Ren / Hidefuku Gi / Kensuke Kawai / Masayuki Ishihara / Eiji Kohmura / Yoshihiro Nishiura / Kazutaka Yatsushiro / Kensaku Yoshida / Atsushi Tominaga / Masayuki Sumida / Hidenori Yoshida / Atsushi Sato / Takashi Inoue / Hiroaki Shimizu / Eiichiro Kamatsuka / Makoto Ichinose / Naoya Takeda / Tsuyoshi Inoue / Hidekazu Takahashi / Satoshi Kuroda / Toshiaki Osato / Nobutaka Horie / Isao Date / Yoichiro Hashimoto / Haruhiko Hoshino / Takafumi Shimogawa / Koji Yoshimoto / Teiji Tominaga / Isao Sasaki / Kazuo Kitazawa / Minoru Saitoh / Hitoshi Saito / Minoru Asahi / Makoto Goda / Atsuhito Takemura / Masaaki Shibukawa / Isao Fuwa / Saburo Watanabe / Seiko Kataoka / Koji Takasaki / Kouji Shiga / Kensuke Hayashida / Ryunosuke Uranishi / Chiaki Ito / Kenji Wakui / Takashi Saegusa / Isao Kitahara / Yasushi Ejima / Satoru Hayashi / Kazuyoshi Hattori / Shinji Okita / Toshikazu Ichihashi / Tsugumichi Ichioka / Shinichi Shirakami / Teruo Kimura / Tomonori Kobayashi / Kanehisa Kohno / Kazunori Yamanaka / Akira Morooka / Nozomi Mori / Hideo Kunimine / Masahiro Satoh / Syougo Imae / Hirochiyo Wada / Masanori Kabuto / Katsuyuki Hirakawa / Isao Inoue / Kiyoshi Kazekawa / Masani Nonaka / Kouzou Fukuyama / Shigenari Kin / Kiyoshi Saito / Yoichi Watanabe / Tadashi Arisawa / Kou Takahashi / Tetsuya Tanigawara / Junki Ito / Kei Hisada / Makoto Takeda / Jun Niwa / Mikio Nishiya / Shuji Hayashi / Ichiro Fujishima / Teiji Nakayama / Yoshihiko Watanabe / Koichirou Matsukado / Takamichi Yuguchi / Tadahisa Shono / Hiroyuki Nishimura / Jyunya Hayashi / Keisuke Migita / Kazuhiro Yokoyama / Hirotoshi Ohtaka / Takata Hisashi / Takamitsu Uchizawa / Naoki Shinohara / Mitsunobu Kaijima / Junkoh Yamamoto / Yoshio Sakagami / Hideo Aihara / Takayuki Sakaki / Keishi Fujita / Sumio Kobayashi / Nobuaki Momozaki / Masahito Hara / Akazi Kazunori / Fumitaka Miya / Hisato Minamide / Shinichiro Kurokawa / Syuichi Ishikawa / Naohisa Miura / Shinya Noda / Shoji Mashiyama / Shinji Amano / Takayuki Sugawara / Yukihiko Shimizu / Keiichi Saito / Kazuyuki Miura / Akinori Yabuta / Tatumi Yamanome / Hiroshi Seto / Makoto Hasebe / Hikaru Mizobuchi / Junkoh Sasaki / Shin Tsuruoka / Keiichi Nishimaki / Katsumi Takizawa / Hitoshi Tsugu / Nozomi Suzuki / Takeshi Kohno / Shu Hasegawa / Ken Asakura / Masaki Miyatake / Hiromu Konno / Katsunobu Takenaka / Akira Ikeda / Keizou Yamamoto / Keigo Matsumoto / Satoshi Inoha / Masaki Morisige / Kunihiko Harada / Hirofumi Hiyama / Yasuaki Takeda / Taturou Mori / Takekazu Akiyama / Osamu Okuda / Kazuaki Awamori / Naoki Shirasaki / Kimihiro Yoshino / Atsushi Shindo / Kazuho Hirahara / Shunichi Tanaka / Teruaki Kawano / Kazunori Arita / Hiroaki Sawaura / Yoichi Uozumi / Masahiko Tanaka / Shunsuke Shiraga / Shuji Sato / Mitsutoshi Nakada / Kimihisa Kinoshita / Nakazawa Kazutomo / Yasuhiro Fujimoto / Kunikazu Yoshimura / Masaaki Iwase / Shinichi Yagi / Atsushi Tsuchiya / Junichi Harashina / Sadao Kaneko / Naoto Kuwayama / Junya Hayashi / Masayuki Sasou / Sotaro Higashi / Masakazu Kitahara / Sumio Suda / Amami Kato / Satoshi Magarisawa / Kenji Hashimoto / Hirotoshi Hamaguchi / Tomohiko Satou / Masaru Idei / Haruhisa Tsukamoto / Toshihiro Kumabe / Naoaki Sato / Yasuyuki Toba / Takashi Tominaga / Haruo Yamashita / Toyoaki Shinohara / Kazuyoshi Watanabe / Hidenori Endo / Kenjirou Hujiwara / Toshinori Hasegawa / Hisashi Nitta / Kuroyanagi Takayuki / Nobuhiko Mizutani / Akira Tsunoda / Fumio Suzuki / Tetsuya Morimoto / Takuya Kawai / Mitsuyuki Fujitsuka / Hiromasa Tsuiki / Junichi Kuratsu / Hidemichi Sasayama / Shigehiro Ohmori / Seiko Hasegawa / Kazuhiro Kikuchi / Motohiro Morioka / Masayuki Yokota / Nozomu Murai / Yasumasa Yamamoto / Nobuhito Mori / Minoru Kidooka / Hiroshi Tenjin / Yoshihiro Iwamoto / Hitonori Takaba / Sei Haga / Yoshinori Arai / Toshiyuki Tsukada / Hirohide Karasudani / Masakazu Suga / Kawamoto Yukihiko / Naoto Izumi / Youtarou Takeuchi / Motohiro Arai / Shinji Okumura / Hisashi Tanaka / Yasushi Shibata / Tetsuya Masaoka / Masahiko Kasai / Hitoshi Miyake / Osamu Hamasaki / Misao Nishikawa / Naohiko Kubo / Yosimasa Kinosita / Hiroyuki Kaidu / Tarou Komuro / Hiroaki Shigeta / Yoshikazu Kusano / Shigekazu Takeuchi / Takayuki Matsuo / Yoshiharu Tokunaga / Norimoto Nakahara / Nobukazu Hashimoto / Mitsuhito Mase / Junpei Yoshimoto / Jin Momoji / Kenji Kamiyama / Koji Oka / Hiromichi Koga / Kazuya Morimoto / Tsutomu Kadekaru / Naoki Tokumitsu / Yasuyuki Nagai / Hirokazu Tanno / Takato Kagawa / Masaaki Saiki / Kotaro Ogihara / Junichi Imamura / Katsuhiro Yamashita / Akira Nakamizo / Yoshinari Nakamura / Ei-Ichirou Urasaki / Noriyuki Suzaki / Chiaki Takahashi / Youichirou Namba / Kazuo Hashikawa / Tomonori Yamada / Kazuyuki Kuwayama / Keiichi Sakai / Katsuhiro Kuroda / Hideyuki Kurihara / Masayuki Miyazono / Kosuke Miyahara / Hideaki Takahashi / Akihiko Saito / Igarashi Michitoku / Mitsuo Kouno / Shiro Kobayashi / Shunichi Yoneda / Hiroshi Kusunoki / Hiroji Miyake / Toshio Yokoe / Tatsuya Nakamura / Takayuki Kubodera / Mitsuhiko Hokari / Yasunari Otawara / Cheho Park / Hidemitu Nakagawa / Souichi Obara / Haruki Takahashi / Masafumi Ohtaki / Atsuya Okubo / Katsuhiko Hayashi / Masahisa Kawakami / Yu Takeda / Akihiko Kaga / Ryoichi Hayashi / Koji Tokunaga / Hiroyuki Nakashima / Yasuyuki Miyoshi / Atusi Kimoto / Toshimitsu Uchihara / Tomoaki Nagamine / Masahiro Noha / Hiromichi Sadashima / Toshihiko Kinjo / Osamu Tao / Masayuki Nakajima / Akira Isoshima / Kouichi Kuramoto / Shigeru Daido / Yoshiyasu Iwai / Toshihiko Kuroiwa / Akatsuki Wakayama / Kohsuke Yamashita / Yasunobu Gotou / Kouich Iwatsuki / Yoshida Masahiro / Nobuaki Kobayasi / Yoshimasa Niiya / Syouji Mabuchi / Motohiro Takayama / Kazuo Yamamoto / Junta Moroi / Masato Sugitani / Akio Ookura / Naoko Fujimura / Osamu Nishizaki / Sumio Isimaru / Hiroshi Wanihuchi / Nobukuni Murakami / Hiroto Murata / Naoki Kitagawa / Katsuhiko Kono / Michiya Kubo / Masashi Nakatsukasa / Makoto Inaba / Hidetoshi Ooigawa / Atsuhiro Kojima / Takamitsu Fujimaki / Osamu Fukuda / Yoshikazu Nakajima / Kazuyuki Kouno / Takaaki Yoshida / Reizou Kanemaru / Yohei Kudoh / Toshitaka Nakamura / Masayoshi Takigami / Shogo Nishi / Rokuya Tanikawa / Seisaburo Sakamoto / Makio Kaminogo / Seiichiro Hoshi / Yoshinari Okumura / Shinichi Okabe / Haruhiko Sato / Shiro Miyata / Kotaro Tsumura / Hiroshi Karibe / Noriaki Watabe / Ryuji Nakamura / Norifumi Shimoeda / Tsutomu Hitotsumatsu / Tomoaki Kameda / Hiroshi Ishiguchi / Atsuo Shinoda / Masanobu Hokama / Akinori Yamamura / Takeshi Kondoh / Kenichi Murao / Takafumi Wataya / Seiji Fukazawa / Shinsuke Muraoka / Hirosuke Fujisawa / Tsuneo Shishido / Mayumi Mori / Arai Hiroaki / Shinjitsu Nishimura / Zenichiro Watanabe / Susumu Nakashima / Kazuhito Nakamura / Yukinari Kakizawa / Hiroki Takano / Norihito Shirakawa / Masahiro Kagawa / Eiichiro Mabuchi / Kazusige Maeno / Takayuki Koizumi / Warou Taki / Yusuke Nakagaki / Kazuyuki Tane / Hiromichi Ooishi / Katsuyuki Asaoka / Yoshinori Akiyama / Tadao Kawamura / Atumi Takenobu / Takehisa Tuji / Masami Shimoda / Mitsunori Matsumae / Shinji Noda / Koiti Moroki / Hirofumi Oka / Masahito Agawa / Hajimu Miyake / Masateru Katayama / Shinichi Numazawa / Taketoshi Maehara / Hiroyuki Jimbo / Satoshi Ihara / Koji Matuoka / Oikawa Akihiro / Takahiro Oota / Makoto Noguchi / Takakazu Kawamata / Youichi Hashimoto / Keiichirou Onitsuka / Masahiko Kitano / Jae-Hyun Son / Toru Masuoka / Naoki Koketsu / Keiichi Akatsuka / Masamichi Kurosaki / Miyamori Tadao / Hiroaki Hondo / Kazumasa Yamatani / Hirofumi Oyama / Junji Koyama / Ogura Koichiro / Shinji Yamamoto / Hitoshi Tabata / Kazuya Uemura / Kazuhiko Sato / Hideyuki Yoshida / Takafumi Nishizaki / Hiroshi Egami / Hideo Takeshima / Shogo Ishiuchi / Akira Matsumura / Hiroyuki Kinouchi / Susumu Mekaru / Mikihiko Takeshita / Hitoshi Ozawa / Kiichiro Zenke / Takeshi Matsuyama / Toshikazu Kuwata / Teruyuki Habu / Tomoyoshi Okumura / Seiya Takehara / Rei Kondo / Takashi Kumagai / Keiten So / Sunao Takemura / Sonoda Yukihiko / Manabu Urakawa / Yasuhiro Hamada / Michiyasu Suzuki / Mikito Uchida / Hidehito Koizumi / Masaru Yamada / Takashi Tsuruno / Gen Ishida / Ryouichi Masuda / Makoto Kimura / Shinichirou Ishihara / Masashi Morikawa / Hidetoshi Murata / Katsumi Sakata / Motohiro Nomura / Akihiro Nemoto / Sumio Endou / Nobuo Hirota / Kennji Itou / Hiroaki Minami / Yoshihumi Teramoto

BMJ Open, Vol 13, Iss

retrospective cohort study

2023 Volume 4

Abstract: Objectives To examine the national, 6-year trends in in-hospital clinical outcomes of patients with subarachnoid haemorrhage (SAH) who underwent clipping or coiling and the prognostic influence of temporal trends in the Comprehensive Stroke Center (CSC) ... ...

Abstract	Objectives To examine the national, 6-year trends in in-hospital clinical outcomes of patients with subarachnoid haemorrhage (SAH) who underwent clipping or coiling and the prognostic influence of temporal trends in the Comprehensive Stroke Center (CSC) capabilities on patient outcomes in Japan.Design Retrospective study.Setting Six hundred and thirty-one primary care institutions in Japan.Participants Forty-five thousand and eleven patients with SAH who were urgently hospitalised, identified using the J-ASPECT Diagnosis Procedure Combination database.Primary and secondary outcome measures Annual number of patients with SAH who remained untreated, or who received clipping or coiling, in-hospital mortality and poor functional outcomes (modified Rankin Scale: 3–6) at discharge. Each CSC was assessed using a validated scoring system (CSC score: 1–25 points).Results In the overall cohort, in-hospital mortality decreased (year for trend, OR (95% CI): 0.97 (0.96 to 0.99)), while the proportion of poor functional outcomes remained unchanged (1.00 (0.98 to 1.02)). The proportion of patients who underwent clipping gradually decreased from 46.6% to 38.5%, while that of those who received coiling and those left untreated gradually increased from 16.9% to 22.6% and 35.4% to 38%, respectively. In-hospital mortality of coiled (0.94 (0.89 to 0.98)) and untreated (0.93 (0.90 to 0.96)) patients decreased, whereas that of clipped patients remained stable. CSC score improvement was associated with increased use of coiling (per 1-point increase, 1.14 (1.08 to 1.20)) but not with short-term patient outcomes regardless of treatment modality.Conclusions The 6-year trends indicated lower in-hospital mortality for patients with SAH (attributable to better outcomes), increased use of coiling and multidisciplinary care for untreated patients. Further increasing CSC capabilities may improve overall outcomes, mainly by increasing the use of coiling. Additional studies are necessary to determine the effect of confounders such as aneurysm ...
Keywords	Medicine ; R
Subject code	150
Language	English
Publishing date	2023-04-01T00:00:00Z
Publisher	BMJ Publishing Group
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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