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1,013 results on '"Arai, Ken"'

5. Impact of small dense low-density lipoprotein cholesterol and triglyceride-rich lipoproteins on plaque rupture with ST-segment elevation myocardial infarction

Author

Arai, Taito, Sekimoto, Teruo, Koba, Shinji, Mori, Hiroyoshi, Matsukawa, Naoki, Sakai, Rikuo, Yokota, Yuya, Sato, Shunya, Tanaka, Hideaki, Masaki, Ryota, Oishi, Yosuke, Ogura, Kunihiro, Arai, Ken, Nomura, Kosuke, Sakai, Koshiro, Tsujita, Hiroaki, Kondo, Seita, Tsukamoto, Shigeto, Suzuki, Hiroshi, and Shinke, Toshiro

Published
2022
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6. Impact of small dense low-density lipoprotein cholesterol on cholesterol crystals in patients with acute coronary syndrome: An optical coherence tomography study

Author

Sekimoto, Teruo, Koba, Shinji, Mori, Hiroyoshi, Arai, Taito, Matsukawa, Naoki, Sakai, Rikuo, Yokota, Yuya, Sato, Shunya, Tanaka, Hideaki, Masaki, Ryota, Oishi, Yosuke, Ogura, Kunihiro, Arai, Ken, Nomura, Kosuke, Sakai, Koshiro, Tsujita, Hiroaki, Kondo, Seita, Tsukamoto, Shigeto, Matsumoto, Hidenari, Suzuki, Hiroshi, and Shinke, Toshiro

Published
2022
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9. Transcriptomic Profiles of AKAP12 Deficiency in Mouse Corpus Callosum.

Author

Hoshino, Tomonori, Takase, Hajime, Ishikawa, Hidehiro, Hamanaka, Gen, Kimura, Shintaro, Fukuda, Norito, Park, Ji Hyun, Nakajima, Hiroki, Shirakawa, Hisashi, Shindo, Akihiro, Kim, Kyu-Won, H Gelman, Irwin, Lok, Josephine, and Arai, Ken

Subjects
CORPUS callosum, CENTRAL nervous system, GENE expression, SCAFFOLD proteins, CEREBRAL cortex, BLOOD-brain barrier
Abstract

A-kinase anchor protein 12 (AKAP12), a scaffold protein, has been implicated in the central nervous system, including blood-brain barrier (BBB) function. Although its expression level in the corpus callosum is higher than in other brain regions, such as the cerebral cortex, the role of AKAP12 in the corpus callosum remains unclear. In this study, we investigate the impact of AKAP12 deficiency by transcriptome analysis using RNA-sequencing (RNA-seq) on the corpus callosum of AKAP12 knockout (KO) mice. We observed minimal changes, with only 13 genes showing differential expression, including Akap12 itself. Notably, Klf2 and Sgk1, genes potentially involved in BBB function, were downregulated in AKAP12 KO mice and expressed in vascular cells similar to Akap12. These changes in gene expression may affect important biological pathways that may be associated with neurological disorders. Our findings provide an additional data set for future research on the role of AKAP12 in the central nervous system. [ABSTRACT FROM AUTHOR]

Published
2024
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12. Proceedings from the Albert Charitable Trust Inaugural Workshop on white matter and cognition in aging

Author

Sorond, Farzaneh A., Whitehead, Shawn, Arai, Ken, Arnold, Douglas, Carmichael, S. Thomas, De Carli, Charles, Duering, Marco, Fornage, Myriam, Flores-Obando, Rafael E., Graff-Radford, Jonathan, Hamel, Edith, Hess, David C., Ihara, Massafumi, Jensen, Majken K., Markus, Hugh S., Montagne, Axel, Rosenberg, Gary, Shih, Andy Y., Smith, Eric E., Thiel, Alex, Tse, Kai Hei, Wilcock, Donna, and Barone, Frank

Published
2020
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16. Transcriptomic Profiling Reveals Neuroinflammation in the Corpus Callosum of a Transgenic Mouse Model of Alzheimer's Disease.

Author

Takase, Hajime, Hamanaka, Gen, Hoshino, Tomonori, Ohtomo, Ryo, Guo, Shuzhen, Mandeville, Emiri T., Lo, Eng H., and Arai, Ken

Subjects
CORPUS callosum, ALZHEIMER'S disease, TRANSGENIC mice, LABORATORY mice, NEUROINFLAMMATION, AGENESIS of corpus callosum, VASCULAR dementia
Abstract

Background: Alzheimer's disease (AD) is a widespread neurodegenerative disorder characterized by progressive cognitive decline, affecting a significant portion of the aging population. While the cerebral cortex and hippocampus have been the primary focus of AD research, accumulating evidence suggests that white matter lesions in the brain, particularly in the corpus callosum, play an important role in the pathogenesis of the disease. Objective: This study aims to investigate the gene expression changes in the corpus callosum of 5xFAD transgenic mice, a widely used AD mouse model. Methods: We conducted behavioral tests for spatial learning and memory in 5xFAD transgenic mice and performed RNA sequencing analyses on the corpus callosum to examine transcriptomic changes. Results: Our results show cognitive decline and demyelination in the corpus callosum of 5xFAD transgenic mice. Transcriptomic analysis reveals a predominance of upregulated genes in AD mice, particularly those associated with immune cells, including microglia. Conversely, downregulation of genes related to chaperone function and clock genes such as Per1, Per2, and Cry1 is also observed. Conclusions: This study suggests that activation of neuroinflammation, disruption of chaperone function, and circadian dysfunction are involved in the pathogenesis of white matter lesions in AD. The findings provide insights into potential therapeutic targets and highlight the importance of addressing white matter pathology and circadian dysfunction in AD treatment strategies. [ABSTRACT FROM AUTHOR]

Published
2024
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26. Myelination‐ and migration‐associated genes are downregulated after phagocytosis in cultured oligodendrocyte precursor cells.

Author

Hamanaka, Gen, Hernández, Iván Coto, Takase, Hajime, Ishikawa, Hidehiro, Benboujja, Fouzi, Kimura, Shintaro, Fukuda, Norito, Guo, Shuzhen, Lok, Josephine, Lo, Eng H., and Arai, Ken

Subjects
PHAGOCYTOSIS, MYELIN proteins, NEUROGLIA, CENTRAL nervous system, AMYLOID plaque, CORPUS callosum
Abstract

In the central nervous system, microglia are responsible for removing infectious agents, damaged/dead cells, and amyloid plaques by phagocytosis. Other cell types, such as astrocytes, are also recently recognized to show phagocytotic activity under some conditions. Oligodendrocyte precursor cells (OPCs), which belong to the same glial cell family as microglia and astrocytes, may have similar functions. However, it remains largely unknown whether OPCs exhibit phagocytic activity against foreign materials like microglia. To answer this question, we examined the phagocytosis activity of OPCs using primary rat OPC cultures. Since innate phagocytosis activity could trigger cell death pathways, we also investigated whether participating in phagocytosis activity may lead to OPC cell death. Our data shows that cultured OPCs phagocytosed myelin‐debris‐rich lysates prepared from rat corpus callosum, without progressing to cell death. In contrast to OPCs, mature oligodendrocytes did not show phagocytotic activity against the bait. OPCs also exhibited phagocytosis towards lysates of rat brain cortex and cell membrane debris from cultured astrocytes, but the percentage of OPCs that phagocytosed beta‐amyloid was much lower than the myelin debris. We then conducted RNA‐seq experiments to examine the transcriptome profile of OPC cultures and found that myelination‐ and migration‐associated genes were downregulated 24 h after phagocytosis. On the other hand, there were a few upregulated genes in OPCs 24 h after phagocytosis. These data confirm that OPCs play a role in debris removal and suggest that OPCs may remain in a quiescent state after phagocytosis. [ABSTRACT FROM AUTHOR]

Published
2023
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27. A brief overview of a mouse model of cerebral hypoperfusion by bilateral carotid artery stenosis.

Author

Ishikawa, Hidehiro, Shindo, Akihiro, Mizutani, Akane, Tomimoto, Hidekazu, Lo, Eng H, and Arai, Ken

Abstract

Vascular cognitive impairment (VCI) refers to all forms of cognitive disorder related to cerebrovascular diseases, including vascular mild cognitive impairment, post-stroke dementia, multi-infarct dementia, subcortical ischemic vascular dementia (SIVD), and mixed dementia. Among the causes of VCI, more attention has been paid to SIVD because the causative cerebral small vessel pathologies are frequently observed in elderly people and because the gradual progression of cognitive decline often mimics Alzheimer's disease. In most cases, small vessel diseases are accompanied by cerebral hypoperfusion. In mice, prolonged cerebral hypoperfusion is induced by bilateral carotid artery stenosis (BCAS) with surgically implanted metal micro-coils. This cerebral hypoperfusion BCAS model was proposed as a SIVD mouse model in 2004, and the spreading use of this mouse SIVD model has provided novel data regarding cognitive dysfunction and histological/genetic changes by cerebral hypoperfusion. Oxidative stress, microvascular injury, excitotoxicity, blood-brain barrier dysfunction, and secondary inflammation may be the main mechanisms of brain damage due to prolonged cerebral hypoperfusion, and some potential therapeutic targets for SIVD have been proposed by using transgenic mice or clinically used drugs in BCAS studies. This review article overviews findings from the studies that used this hypoperfused-SIVD mouse model, which were published between 2004 and 2021. [ABSTRACT FROM AUTHOR]

Published
2023
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38. Dual effects of carbon monoxide on pericytes and neurogenesis in traumatic brain injury

Author

Choi, Yoon Kyung, Maki, Takakuni, Mandeville, Emiri T, Koh, Seong-Ho, Hayakawa, Kazuhide, Arai, Ken, Kim, Young-Myeong, Whalen, Michael J, Xing, Changhong, Wang, Xiaoying, Kim, Kyu-Won, and Lo, Eng H

Subjects
Carbon monoxide -- Health aspects, Neurogenesis -- Health aspects, Brain injuries -- Care and treatment, Biological sciences, Health
Abstract

Author(s): Yoon Kyung Choi (corresponding author) [1, 2]; Takakuni Maki [1, 2]; Emiri T Mandeville [1, 2]; Seong-Ho Koh [1, 2, 3]; Kazuhide Hayakawa [1, 2]; Ken Arai [1, 2]; [...]

Published
2016
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42. Impact of Native Coronary Artery Calcification on Lesion Outcome Following Drug-Coated Balloon Angioplasty for Treatment of In-Stent Restenosis

Author

NOMURA, Kosuke, AKUTSU, Yasushi, TSUJITA, Hiroaki, KONDO, Seita, SEKIMOTO, Teruo, SATO, Shunya, TANAKA, Hideaki, ARAI, Ken, OISHI, Yosuke, OGURA, Kunihiro, TSUKAMOTO, Shigeto, GOKAN, Toshihiko, TANISAWA, Hiroki, KANEKO, Kyoichi, KODAMA, Yusuke, MATSUMOTO, Hidenari, and SHINKE, Toshiro

Subjects
cardiovascular diseases
Abstract

This study aimed to clarify whether native coronary artery（CA） calcification before index percutaneous coronary intervention（PCI） has an impact on the effectiveness of drug-coated balloon（DCB） angioplasty for the treatment of in-stent restenosis（ISR）. 100consecutive patients with 166ISR lesions underwent quantitative coronary angiography（QCA） before and after index PCI and before and after DCB angioplasty for ISR. CA calcification before index PCI was assessed by angiography and results were analyzed to reveal the predictive values for target lesion revascularization（TLR） and major adverse cardiac events（MACE）. During 1.03±1.03years of follow-up, TLR occurred in 44lesions（26.5%） and MACE in 33 patients（33%）. On multivariate analysis, CA calcification before index PCI（p=0.016）, and % diameter of stenosis（%DS）≥73%（p=0.023） and minimal lumen diameter（MLD）

Published
2020

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