Details of the Researcher

PHOTO

Sherif Mohamed Rashad
Section
Graduate School of Biomedical Engineering
Job title
Associate Professor
Degree

  • PhD (Tohoku University)

  • MD (Alexandria University, Egypt)

Profile

My research lies at the interface of RNA biology, translational regulation, neuroscience, and cancer biology. I investigate how changes in the RNA epitranscriptome and protein synthesis shape cellular adaptation, vulnerability, and fate under physiological and pathological stress. My work particularly focuses on transfer RNA modifications, tRNA-derived RNAs, codon-dependent translation, ribosome dynamics and collisions, and transcript isoform remodeling. By combining molecular and cellular models with RNA sequencing, ribosome profiling, tRNA sequencing and modifications analysis, long-read sequencing, and integrative computational analysis, I aim to uncover regulatory mechanisms that cannot be resolved at the level of gene expression alone. These approaches are applied primarily to cerebral ischemia and neurological disorders, glioma, and cellular responses to oxidative and mitochondrial stress. Ultimately, my goal is to translate fundamental discoveries in RNA and translation biology into biomarkers, therapeutic targets, and new strategies for treating neurological diseases and cancer.

 

 

Research History 6

  • 2023/04 - Present
    Tohoku University　Graduate School of Biomedical Engineering　Associate Professor

  • 2018/04 - 2023/03
    Tohoku University　Department of Neurosurgery, Graduate school of medicine　Assistant professor

  • 2022/02 - 2023/02
    Massachusetts Institute of Technology　Department of Biological Engineering　Visiting Professor

  • 2014/10 - 2018/03
    Tohoku University　Department of Neurosurgery, Graduate school of medicine　PhD student

  • 2011/01 - 2014/09
    Alexandria University, Egypt　Department of Neurosurgery, Graduate school of medicine　Neurosurgical Resident doctor

  • 2025/09 -
    Masaryk University　Department of Anatomy, Faculty of Medicine　Visiting Professor

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Education 3

  • Tohoku University Graduate school of medicine　Neurosurgery　PhD course

    2014/10 - 2018/03

  • Alexandria University school of medicine　Neurosurgery　Master's course

    2010/10 - 2014/03

  • Alexandria University school of medicine　MBcch

    2001/09 - 2008/10

Research Interests 13

  • oxidative stress

  • neuron

  • Cell Death

  • Glioma

  • Epitranscriptome

  • tRNA

  • apoptosis

  • Moyamoya disease

  • computational flow dynamics

  • stem cell therapy

  • sphingosine-1-phosphate

  • brain aneurysm

  • Stroke

Research Areas 7

  • Life sciences / Systems genomics /

  • Life sciences / Tumor biology /

  • Life sciences / Cell biology /

  • Life sciences / Neurosurgery /

  • Life sciences / Molecular biology /

  • Life sciences / Neuroanatomy and physiology /

  • Life sciences / Neuroscience - general /

Papers 55

  1. Long read multi-omics sequencing reveals DNA-to-RNA evolutionary remodeling trajectories of recurrent astrocytoma

    Sherif Rashad, Daisuke Ando, Shota Yamashita, Yoshiteru Shimoda, Masayuki Kanamori, Hidenori Endo, Kuniyasu Niizuma

    2026/07/14

    DOI： 10.64898/2026.07.12.738108 　

  2. G/C-ending and synonymous codon bias define functional translational programs that shape human tissue and cancer proteomes Peer-reviewed

    Sherif Rashad, Kuniyasu Niizuma

    NAR Genomics and Bioinformatics　2026/03/27

    DOI： 10.1093/nargab/lqag033 　

  3. Context-specific Angiogenin-mediated tRNA fragments (tDRs) biogenesis shapes the mitochondrial stress response Peer-reviewed

    Shadi Al-Mesitef, Daisuke Ando, Tomoya Saigasaki, Yuki Sakaguchi, Shunya Akagi, Abdulrahman Mousa, Sherif Rashad, Kuniyasu Niizuma

    Redox Biology　2026/03

    DOI： 10.1016/j.redox.2026.104038 　

  4. 脳虚血時のエピ転写および翻訳調節異常のマルチオミクス解析(Multi-omics Analysis of Epitranscriptional and Translational Dysregulation During Cerebral Ischemia.)

    Rashad Sherif, 北村 佑樹, 池之内 初, 安藤 大祐, 新妻 邦泰

    脳循環代謝　37　(1)　73-73　2025/10

    Publisher: (一社)日本脳循環代謝学会

    ISSN： 0915-9401

    eISSN： 2188-7519

  5. Multi-omics Analysis of Epitranscriptional and Translational Dysregulation During Cerebral Ischemia.(タイトル和訳中)

    Rashad Sherif, 北村 佑樹, 池之内 初, 安藤 大祐, 新妻 邦泰

    脳循環代謝　37　(1)　73-73　2025/10

    Publisher: (一社)日本脳循環代謝学会

    ISSN： 0915-9401

    eISSN： 2188-7519

  6. Optimized tDR Sequencing Reveals Diversity and Heterogeneity in tRNA-Derived Fragment Landscapes in Mouse Tissues Peer-reviewed

    Daisuke Ando, Sherif Rashad, Kuniyasu Niizuma

    International Journal of Molecular Sciences　2025/09/09

    DOI： 10.3390/ijms26188772 　

  7. Ischemic stroke induces staged translational remodeling in mouse cortex independent from transcriptional responses

    Sherif Rashad, Yuki Kitamura, Tomohito Nagai, Daisuke Ando, Abdulrahman Mousa, Hajime Ikenouchi, Hidenori Endo, Kuniyasu Niizuma

    2025/08/16

    DOI： 10.1101/2025.08.15.670488 　

  8. Queuosine tRNA Modification: Connecting the Microbiome to the Translatome. International-journal Peer-reviewed

    Sherif Rashad

    BioEssays : news and reviews in molecular, cellular and developmental biology　47　(2)　e202400213　2025/02

    DOI： 10.1002/bies.202400213 　

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    Transfer RNA (tRNA) modifications play an important role in regulating mRNA translation at the codon level. tRNA modifications can influence codon selection and optimality, thus shifting translation toward specific sets of mRNAs in a dynamic manner. Queuosine (Q) is a tRNA modification occurring at the wobble position. In eukaryotes, queuosine is synthesized by the tRNA-guanine trans-glycosylase (TGT) complex, which incorporates the nucleobase queuine (or Qbase) into guanine of the GUN anticodons. Queuine is sourced from gut bacteria and dietary intake. Q was recently shown to be critical for cellular responses to oxidative and mitochondrial stresses, as well as its potential role in neurodegenerative diseases and brain health. These unique features of Q provide an interesting insight into the regulation of mRNA translation by gut bacteria, and the potential health implications. In this review, Q biology is examined in the light of recent literature and nearly 4 decades of research. Q's role in neuropsychiatric diseases and cancer is highlighted and discussed. Given the recent interest in Q, and the new findings, more research is needed to fully comprehend its biological function and disease relevance, especially in neurobiology.

  9. Transcriptome-wide alternative mRNA splicing analysis reveals post-transcriptional regulation of neuronal differentiation. International-journal Peer-reviewed

    Yuan Zhou, Sherif Rashad, Kuniyasu Niizuma

    The FEBS journal　2025/01/24

    DOI： 10.1111/febs.17408 　

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    Alternative splicing (AS) plays an important role in neuronal development, function, and disease. Efforts to analyze the transcriptome of AS in neurons on a wide scale are currently limited. We characterized the transcriptome-wide AS changes in SH-SY5Y neuronal differentiation model, which is widely used to study neuronal function and disorders. Our analysis revealed global changes in five AS programs that drive neuronal differentiation. Motif analysis revealed the contribution of RNA-binding proteins (RBPs) to the regulation of AS during neuronal development. We concentrated on the primary alternative splicing program that occurs during differentiation, specifically on events involving exon skipping (SE). Motif analysis revealed motifs for polypyrimidine tract-binding protein 1 (PTB) and ELAV-like RNA binding protein 1 (HuR/ELAVL1) to be the top enriched in SE events, and their protein levels were downregulated after differentiation. shRNA knockdown of either PTB and HuR was associated with enhanced neuronal differentiation and transcriptome-wide exon skipping events that drive the process of differentiation. At the level of gene expression, we observed only modest changes, indicating predominant post-transcriptional effects of PTB and HuR. We also observed that both RBPs altered cellular responses to oxidative stress, in line with the differentiated phenotype observed after either gene knockdown. Our work characterizes the AS changes in a widely used and important model of neuronal development and neuroscience research and reveals intricate post-transcriptional regulation of neuronal differentiation.

  10. Decoding Codon Bias: The Role of tRNA Modifications in Tissue-Specific Translation. International-journal Peer-reviewed

    Daisuke Ando, Sherif Rashad, Thomas J Begley, Hidenori Endo, Masashi Aoki, Peter C Dedon, Kuniyasu Niizuma

    International journal of molecular sciences　26　(2)　2025/01/15

    DOI： 10.3390/ijms26020706 　

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    The tRNA epitranscriptome has been recognized as an important player in mRNA translation regulation. Our knowledge of the role of the tRNA epitranscriptome in fine-tuning translation via codon decoding at tissue or cell levels remains incomplete. We analyzed tRNA expression and modifications as well as codon optimality across seven mouse tissues. Our analysis revealed distinct enrichment patterns of tRNA modifications in different tissues. Queuosine (Q) tRNA modification was most enriched in the brain compared to other tissues, while mitochondrial tRNA modifications and tRNA expression were highest in the heart. Using this observation, we synthesized, and delivered in vivo, codon-mutated EGFP for Q-codons, where the C-ending Q-codons were replaced with U-ending codons. The protein levels of mutant EGFP were downregulated in liver, which is poor in Q, while in brain EGFP, levels did not change. These data show that understanding tRNA modification enrichments across tissues is not only essential for understanding codon decoding and bias but can also be utilized for optimizing gene and mRNA therapeutics to be more tissue-, cell-, or condition-specific.

  11. Metabolism Meets Translation: Dietary and Metabolic Influences on tRNA Modifications and Codon Biased Translation. International-journal Invited Peer-reviewed

    Sherif Rashad, Aseel Marahleh

    Wiley interdisciplinary reviews. RNA　16　(2)　e70011　2025

    DOI： 10.1002/wrna.70011 　

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    Transfer RNA (tRNA) is not merely a passive carrier of amino acids, but an active regulator of mRNA translation controlling codon bias and optimality. The synthesis of various tRNA modifications is regulated by many "writer" enzymes, which utilize substrates from metabolic pathways or dietary sources. Metabolic and bioenergetic pathways, such as one-carbon (1C) metabolism and the tricarboxylic acid (TCA) cycle produce essential substrates for tRNA modifications synthesis, such as S-Adenosyl methionine (SAM), sulfur species, and α-ketoglutarate (α-KG). The activity of these metabolic pathways can directly impact codon decoding and translation via regulating tRNA modifications levels. In this review, we discuss the complex interactions between diet, metabolism, tRNA modifications, and mRNA translation. We discuss how nutrient availability, bioenergetics, and intermediates of metabolic pathways, modulate the tRNA modification landscape to fine-tune protein synthesis. Moreover, we highlight how dysregulation of these metabolic-tRNA interactions contributes to disease pathogenesis, including cancer, metabolic disorders, and neurodegenerative diseases. We also discuss the new emerging field of GlycoRNA biology drawing parallels from glycobiology and metabolic diseases to guide future directions in this area. Throughout our discussion, we highlight the links between specific modifications, their metabolic/dietary precursors, and various diseases, emphasizing the importance of a metabolism-centric tRNA view in understanding many pathologies. Future research should focus on uncovering the interplay between metabolism and tRNA in specific cellular and disease contexts. Addressing these gaps will guide new research into novel disease interventions.

  12. Dynamic mRNA Stability Buffer Transcriptional Activation During Neuronal Differentiation and Is Regulated by SAMD4A. International-journal Peer-reviewed

    Yuan Zhou, Sherif Rashad, Daisuke Ando, Yuki Kobayashi, Teiji Tominaga, Kuniyasu Niizuma

    Journal of cellular physiology　2024/11/08

    DOI： 10.1002/jcp.31477 　

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    Neurons are exceptionally sensitive to oxidative stress, which is the basis for many neurodegenerative disease pathophysiologies. The posttranscriptional basis for neuronal differentiation and behavior is not well characterized. The steady-state levels of mRNA are outcomes of an interplay between RNA transcription and decay. However, the correlation between mRNA transcription, translation, and stability remains elusive. We utilized a SH-SY5Y-based neural differentiation model that is widely used to study neurodegenerative diseases. After neuronal differentiation, we observed enhanced sensitivity of mature neurons to mitochondrial stresses and ferroptosis induction. We employed a newly developed simplified mRNA stability profiling technique to explore the role of mRNA stability in SH-SY5Y neuronal differentiation model. Transcriptome-wide mRNA stability analysis revealed neural-specific RNA stability kinetics. Our analysis revealed that mRNA stability could either exert the buffering effect on gene products or change in the same direction as transcription. Importantly, we observed that changes in mRNA stability corrected over or under transcription of mRNAs to maintain mRNA translation dynamics. Furthermore, we conducted integrative analysis of our mRNA stability data set, and a published CRISPR-i screen focused on neuronal oxidative stress responses. Our analysis unveiled novel neuronal stress response genes that were not evident at the transcriptional or translational levels. SEPHS2 emerged as an important neuronal stress regulator based on this integrative analysis. Motif analysis unveiled SAMD4A as a major regulator of the dynamic changes in mRNA stability observed during differentiation. Knockdown of SAMD4A impaired neuronal differentiation and influenced the response to oxidative stress. Mechanistically, SAMD4A was found to alter the stability of several mRNAs. The novel insights into the interplay between mRNA stability and cellular behaviors provide a foundation for understanding neurodevelopmental processes and neurodegenerative disorders and highlight dynamic mRNA stability as an important layer of gene expression.

  13. Intravenous administration of muse cells improves cerebral ischemia outcome via immunomodulation in the spleen. International-journal Peer-reviewed

    Yuya Kato, Daiki Aburakawa, Ryosuke Tashiro, Yuan Zhou, Sherif Rashad, Hidenori Endo, Teiji Tominaga, Kuniyasu Niizuma

    Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism　271678X241290363　2024/10/13

    DOI： 10.1177/0271678X241290363 　

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    Ischemic stroke is a leading cause of disability and death globally. Stem cell therapies are emerging as a frontier for enhancing post-stroke recovery, with Muse cells-a subclass of pluripotent stem cells-demonstrating considerable promise. Muse cells are notable not only for their potential in cell replacement but also for their role in modulating immune responses following cerebral infarction. In the present study, we administered Muse cells intravenously to mice after inducing a stroke via distal middle cerebral artery occlusion. We evaluated motor outcomes, splenocyte populations, cytokine profiles, and gene expression 2 weeks after inducing stroke. Additionally, comparisons were drawn between outcomes in splenectomized mice and those receiving adoptive splenocyte transfer to discern the specific influence of the spleen on treatment efficacy. Our findings revealed that Muse cell therapy facilitates motor recovery, an effect that is compromised in the absence of the spleen. Spleens in treated mice exhibited a shift in neutrophil counts, increased cytokine activity, and a notable uptick in the expression of genes related to protein folding. These insights affirm the potential therapeutic effect of Muse cells in post-stroke treatment strategies, with their efficacy attributed, at least in part, to immunomodulatory pathways involving the spleen.

  14. High-throughput fluorescence lifetime imaging flow cytometry. International-journal Peer-reviewed

    Hiroshi Kanno, Kotaro Hiramatsu, Hideharu Mikami, Atsushi Nakayashiki, Shota Yamashita, Arata Nagai, Kohki Okabe, Fan Li, Fei Yin, Keita Tominaga, Omer Faruk Bicer, Ryohei Noma, Bahareh Kiani, Olga Efa, Martin Büscher, Tetsuichi Wazawa, Masahiro Sonoshita, Hirofumi Shintaku, Takeharu Nagai, Sigurd Braun, Jessica P Houston, Sherif Rashad, Kuniyasu Niizuma, Keisuke Goda

    Nature communications　15　(1)　7376-7376　2024/09/04

    DOI： 10.1038/s41467-024-51125-y 　

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    Flow cytometry is a vital tool in biomedical research and laboratory medicine. However, its accuracy is often compromised by undesired fluctuations in fluorescence intensity. While fluorescence lifetime imaging microscopy (FLIM) bypasses this challenge as fluorescence lifetime remains unaffected by such fluctuations, the full integration of FLIM into flow cytometry has yet to be demonstrated due to speed limitations. Here we overcome the speed limitations in FLIM, thereby enabling high-throughput FLIM flow cytometry at a high rate of over 10,000 cells per second. This is made possible by using dual intensity-modulated continuous-wave beam arrays with complementary modulation frequency pairs for fluorophore excitation and acquiring fluorescence lifetime images of rapidly flowing cells. Moreover, our FLIM system distinguishes subpopulations in male rat glioma and captures dynamic changes in the cell nucleus induced by an anti-cancer drug. FLIM flow cytometry significantly enhances cellular analysis capabilities, providing detailed insights into cellular functions, interactions, and environments.

  15. Translational response to mitochondrial stresses is orchestrated by tRNA modifications. International-journal

    Sherif Rashad, Shadi Al-Mesitef, Abdulrahman Mousa, Yuan Zhou, Daisuke Ando, Guangxin Sun, Tomoko Fukuuchi, Yuko Iwasaki, Jingdong Xiang, Shane R Byrne, Jingjing Sun, Masamitsu Maekawa, Daisuke Saigusa, Thomas J Begley, Peter C Dedon, Kuniyasu Niizuma

    bioRxiv : the preprint server for biology　2024/02/14

    DOI： 10.1101/2024.02.14.580389 　

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    Mitochondrial stress and dysfunction play important roles in many pathologies. However, how cells respond to mitochondrial stress is not fully understood. Here, we examined the translational response to electron transport chain (ETC) inhibition and arsenite induced mitochondrial stresses. Our analysis revealed that during mitochondrial stress, tRNA modifications (namely f5C, hm5C, queuosine and its derivatives, and mcm5U) dynamically change to fine tune codon decoding, usage, and optimality. These changes in codon optimality drive the translation of many pathways and gene sets, such as the ATF4 pathway and selenoproteins, involved in the cellular response to mitochondrial stress. We further examined several of these modifications using targeted approaches. ALKBH1 knockout (KO) abrogated f5C and hm5C levels and led to mitochondrial dysfunction, reduced proliferation, and impacted mRNA translation rates. Our analysis revealed that tRNA queuosine (tRNA-Q) is a master regulator of the mitochondrial stress response. KO of QTRT1 or QTRT2, the enzymes responsible for tRNA-Q synthesis, led to mitochondrial dysfunction, translational dysregulation, and metabolic alterations in mitochondria-related pathways, without altering cellular proliferation. In addition, our analysis revealed that tRNA-Q loss led to a domino effect on various tRNA modifications. Some of these changes could be explained by metabolic profiling. Our analysis also revealed that utilizing serum deprivation or alteration with Queuine supplementation to study tRNA-Q or stress response can introduce various confounding factors by altering many other tRNA modifications. In summary, our data show that tRNA modifications are master regulators of the mitochondrial stress response by driving changes in codon decoding.

  16. Codon usage and mRNA stability are translational determinants of cellular response to canonical ferroptosis inducers Peer-reviewed

    Sherif Rashad, Shane R Byrne, Daisuke Saigusa, Jingdong Xiang, Yuan Zhou, Liyin Zhang, Thomas J Begley, Teiji Tominaga, Kuniyasu Niizuma

    Neuroscience　2022/08

    Publisher: Elsevier BV

    DOI： 10.1016/j.neuroscience.2022.08.009 　

    ISSN： 0306-4522

  17. RNF213 loss of function reshapes vascular transcriptome and spliceosome leading to disrupted angiogenesis and aggravated vascular inflammatory responses. International-journal Peer-reviewed

    Liyin Zhang, Sherif Rashad, Yuan Zhou, Kuniyasu Niizuma, Teiji Tominaga

    Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism　42　(11)　271678X221110679-2122　2022/06/25

    DOI： 10.1177/0271678X221110679 　

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    RNF213 gene mutations are the cause behind Moyamoya disease, a rare cerebrovascular occlusive disease. However, the function of RNF213 in the vascular system and the impact of its loss of function are not yet comprehended. To understand RNF23 function, we performed gene knockdown (KD) in vascular cells and performed various phenotypical analysis as well as extensive transcriptome and epitranscriptome profiling. Our data revealed that RNF213 KD led to disrupted angiogenesis in HUVEC, in part due to downregulation of DNA replication and proliferation pathways. Furthermore, HUVEC cells became sensitive to LPS induced inflammation after RNF213 KD, leading to retarded cell migration and enhanced macrophage transmigration. This was evident at the level of transcriptome as well. Interestingly, RNF213 led to extensive changes in mRNA splicing that were not previously reported. In vascular smooth muscle cells (vSMCs), RNF213 KD led to alteration in cytoskeletal organization, contractility, and vSMCs function related pathways. Finally, RNF213 KD disrupted endothelial-to-vSMCs communication in co-culture models. Overall, our results indicate that RNF213 KD sensitizes endothelial cells to inflammation, leading to altered angiogenesis. Our results shed the light on the important links between RNF213 mutations and inflammatory/immune inducers of MMD and on the unexplored role of epitranscriptome in MMD.

  18. Non-Kolmogorov turbulence in carotid artery stenosis and the impact of carotid stenting on near-wall turbulence

    Khalid M. Saqr, Kiyomitsu Kano, Sherif Rashad, Kuniyasu Niizuma, Yasuhiko Kaku, Toru Iwama, Teiji Tominaga

    AIP Advances　12　(1)　015124-015124　2022/01/01

    Publisher: {AIP} Publishing

    DOI： 10.1063/5.0076271 　

  19. Dysregulation of Rnf 213 gene contributes to T cell response via antigen uptake, processing, and presentation. International-journal Peer-reviewed

    Ryosuke Tashiro, Kuniyasu Niizuma, Jun Kasamatsu, Yuko Okuyama, Sherif Rashad, Atsuo Kikuchi, Miki Fujimura, Shigeo Kure, Naoto Ishii, Teiji Tominaga

    Journal of cellular physiology　236　(11)　7554-7564　2021/05/10

    DOI： 10.1002/jcp.30396 　

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    Growing evidence suggest the association between Moyamoya disease (MMD) and immune systems, such as antigen presenting cells in particular. Rnf213 gene, a susceptibility gene for MMD, is highly expressed in immune tissues, however, its function remains unclear. In addition, the physiological role of RNF213 gene polymorphism c.14576G > A (rs112735431), susceptibility variant for MMD, is also poorly understood. By studying Rnf213-knockout (Rnf213-KO) mice with deletion of largest exon32 and Rnf213-knockin (Rnf213-KI) mice with insertion of single-nucleotide polymorphism corresponding to c.14576G > A mutation in MMD patients, we aimed to investigate the role of RNF213 in dendritic cell development, and antigen processing and presentation. First, we found a high level of Rnf213 gene expression in conventional DCs and monocytes. Second, flow cytometric and confocal microscopic analysis revealed ovalbumin protein-pulsed Rnf213-KO and Rnf213-KI DCs showed impaired antigen uptake, proteolysis and reduced numbers of endosomes and lysosomes, and thereby failed to activate and proliferate antigen-specific T cells efficiently. In addition, Rnf213-KI DCs showed a similar phenotype to that of Rnf213-KO BMDCs. In conclusion, our findings suggest the critical role of RNF213 in antigen uptake, processing and presentation.

  20. The cell and stress-specific canonical and noncanonical tRNA cleavage. International-journal Peer-reviewed

    Sherif Rashad, Teiji Tominaga, Kuniyasu Niizuma

    Journal of cellular physiology　236　(5)　3710-3724　2021/05

    DOI： 10.1002/jcp.30107 　

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    Following stress, transfer RNA (tRNA) is cleaved to generate tRNA halves (tiRNAs). These tiRNAs have been shown to repress protein translation. Angiogenin was considered the main enzyme that cleaves tRNA at its anticodon to generate 35-45 nucleotide long tiRNA halves, however, the recent reports indicate the presence of angiogenin-independent cleavage. We previously observed tRNA cleavage pattern occurring away from the anticodon site. To explore this noncanonical cleavage, we analyze tRNA cleavage patterns in rat model of ischemia-reperfusion and in two rat cell lines. In vivo mitochondrial tRNAs were prone to this noncanonical cleavage pattern. In vitro, however, cytosolic and mitochondrial tRNAs could be cleaved noncanonically. Our results show an important regulatory role of mitochondrial stress in angiogenin-mediated tRNA cleavage. Neither angiogenin nor RNH1 appear to regulate the noncanonical tRNA cleavage. Finally, we verified our previous findings of the role of Alkbh1 in regulating tRNA cleavage and its impact on noncanonical tRNA cleavage.

  21. Physiologic blood flow is turbulent. International-journal Peer-reviewed

    Khalid M Saqr, Simon Tupin, Sherif Rashad, Toshiki Endo, Kuniyasu Niizuma, Teiji Tominaga, Makoto Ohta

    Scientific reports　10　(1)　15492-15492　2020/09/23

    DOI： 10.1038/s41598-020-72309-8 　

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    Contemporary paradigm of peripheral and intracranial vascular hemodynamics considers physiologic blood flow to be laminar. Transition to turbulence is considered as a driving factor for numerous diseases such as atherosclerosis, stenosis and aneurysm. Recently, turbulent flow patterns were detected in intracranial aneurysm at Reynolds number below 400 both in vitro and in silico. Blood flow is multiharmonic with considerable frequency spectra and its transition to turbulence cannot be characterized by the current transition theory of monoharmonic pulsatile flow. Thus, we decided to explore the origins of such long-standing assumption of physiologic blood flow laminarity. Here, we hypothesize that the inherited dynamics of blood flow in main arteries dictate the existence of turbulence in physiologic conditions. To illustrate our hypothesis, we have used methods and tools from chaos theory, hydrodynamic stability theory and fluid dynamics to explore the existence of turbulence in physiologic blood flow. Our investigation shows that blood flow, both as described by the Navier-Stokes equation and in vivo, exhibits three major characteristics of turbulence. Womersley's exact solution of the Navier-Stokes equation has been used with the flow waveforms from HaeMod database, to offer reproducible evidence for our findings, as well as evidence from Doppler ultrasound measurements from healthy volunteers who are some of the authors. We evidently show that physiologic blood flow is: (1) sensitive to initial conditions, (2) in global hydrodynamic instability and (3) undergoes kinetic energy cascade of non-Kolmogorov type. We propose a novel modification of the theory of vascular hemodynamics that calls for rethinking the hemodynamic-biologic links that govern physiologic and pathologic processes.

  22. The stress specific impact of ALKBH1 on tRNA cleavage and tiRNA generation. International-journal Peer-reviewed

    Sherif Rashad, Xiaobo Han, Kanako Sato, Eikan Mishima, Takaaki Abe, Teiji Tominaga, Kuniyasu Niizuma

    RNA biology　1-12　2020/06/21

    DOI： 10.1080/15476286.2020.1779492 　

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    tiRNAs are small non-coding RNAs produced when tRNA is cleaved under stress. tRNA methylation modifications has emerged in recent years as important regulators for tRNA structural stability and sensitivity to cleavage and tiRNA generation during stress, however, the specificity and higher regulation of such a process is not fully understood. Alkbh1 is a m1A demethylase that leads to destabilization of tRNA and enhanced tRNA cleavage. We examined the impact of Alkbh1 targeting via gene knockdown or overexpression on B35 rat neuroblastoma cell line fate following stresses and on tRNA cleavage. We show that Alkbh1 impact on cell fate and tRNA cleavage is a stress specific process that is impacted by the demethylating capacity of the cellular stress in question. We also show that not all tRNAs are cleaved equally following Alkbh1 manipulation and stress, and that Alkbh1 KD fails to rescue tRNAs from cleavage following demethylating stresses. These findings shed a light on the specificity and higher regulation of tRNA cleavage and should act as a guide for future work exploring the utility of Alkbh1 as a therapeutic target for cancers or ischaemic insult.

  23. What does computational fluid dynamics tell us about intracranial aneurysms? A meta-analysis and critical review Peer-reviewed

    Khalid M Saqr, Sherif Rashad, Simon Tupin, Kuniyasu Niizuma, Tamer Hassan, Teiji Tominaga, Makoto Ohta

    Journal of Cerebral Blood Flow & Metabolism　271678X19854640　2020/05

    DOI： 10.1177/0271678X19854640 　

    ISSN： 0271-678X

  24. Metabolic basis of neuronal vulnerability to ischemia; an in vivo untargeted metabolomics approach. International-journal Peer-reviewed

    Sherif Rashad, Daisuke Saigusa, Takahiro Yamazaki, Yotaro Matsumoto, Yoshihisa Tomioka, Ritsumi Saito, Akira Uruno, Kuniyasu Niizuma, Masayuki Yamamoto, Teiji Tominaga

    Scientific reports　10　(1)　6507-6507　2020/04/16

    DOI： 10.1038/s41598-020-63483-w 　

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    Understanding the root causes of neuronal vulnerability to ischemia is paramount to the development of new therapies for stroke. Transient global cerebral ischemia (tGCI) leads to selective neuronal cell death in the CA1 sub-region of the hippocampus, while the neighboring CA3 sub-region is left largely intact. By studying factors pertaining to such selective vulnerability, we can develop therapies to enhance outcome after stroke. Using untargeted liquid chromatography-mass spectrometry, we analyzed temporal metabolomic changes in CA1 and CA3 hippocampal areas following tGCI in rats till the setting of neuronal apoptosis. 64 compounds in CA1 and 74 in CA3 were found to be enriched and statistically significant following tGCI. Pathway analysis showed that pyrimidine and purine metabolism pathways amongst several others to be enriched after tGCI in CA1 and CA3. Metabolomics analysis was able to capture very early changes following ischemia. We detected 6 metabolites to be upregulated and 6 to be downregulated 1 hour after tGCI in CA1 versus CA3. Several metabolites related to apoptosis and inflammation were differentially expressed in both regions after tGCI. We offer a new insight into the process of neuronal apoptosis, guided by metabolomic profiling that was not performed to such an extent previously.

  25. Author Correction: The hemodynamic complexities underlying transient ischemic attacks in early-stage Moyamoya disease: an exploratory CFD study. International-journal Peer-reviewed

    Sherif Rashad, Khalid M Saqr, Miki Fujimura, Kuniyasu Niizuma, Teiji Tominaga

    Scientific reports　10　(1)　6217-6217　2020/04/07

    DOI： 10.1038/s41598-020-62862-7 　

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    An amendment to this paper has been published and can be accessed via a link at the top of the paper.

  26. Stress Induced tRNA Halves (tiRNAs) as Biomarkers for Stroke and Stroke Therapy; Pre-clinical Study. International-journal Peer-reviewed

    Kanako Sato, Sherif Rashad, Kuniyasu Niizuma, Teiji Tominaga

    Neuroscience　2020/03/19

    DOI： 10.1016/j.neuroscience.2020.03.018 　

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    tiRNAs are small non-coding RNAs generated by angiogenin-mediated tRNA cleavage during cellular stress. Some tiRNAs were shown to be cytoprotective, while other reports indicate that the generation of tiRNAs is cytotoxic. We used rat model of focal cerebral ischemia-reperfusion (I/R) injury to study the generation and regulation of tiRNAs following in vivo I/R and the impact of neuroprotective therapy on their generation. tiRNAs were induced after I/R and Minocycline therapy reduced global tiRNA levels. Our results showed that tRNA cleavage is tRNA species specific, and neuroprotective treatment does not affect all tiRNA species. We also evaluated the temporal changes in several tRNA modifying enzymes and showed a correlation between their expression and tRNA cleavage. In conclusion, we show that tiRNAs can serve as biomarkers for stroke and stroke therapy, further adding them to the repertoire of tools that can be used to monitor and treat stroke.

  27. The hemodynamic complexities underlying transient ischemic attacks in early-stage Moyamoya disease: an exploratory CFD study. International-journal Peer-reviewed

    Sherif Rashad, Khalid M Saqr, Miki Fujimura, Kuniyasu Niizuma, Teiji Tominaga

    Scientific reports　10　(1)　3700-3700　2020/02/28

    DOI： 10.1038/s41598-020-60683-2 　

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    Moyamoya disease (MMD) is a rare cerebro-occlusive disease with unknown etiology that can cause both ischemic and hemorrhagic stroke. MMD is characterized by progressive stenosis of the terminal internal carotid artery (ICA) and development of basal brain collaterals. Early-stage MMD is known to cause hemodynamic insufficiency despite mild or moderate stenosis of the intracranial arteries, but the exact mechanism underlying this pathophysiological condition is undetermined. We used high-resolution Large Eddy Simulations to investigate multiple complex hemodynamic phenomena that led to cerebral ischemia in five patients with early-stage MMD. The effects of transitional flow, coherent flow structures and blood shear-thinning properties through regions of tortuous and stenosed arteries were explored and linked to symptomatology. It is evidently shown that in some cases complex vortex structures, such as Rankine-type vortices, redirects blood flow away from some arteries causing significant reduction in blood flow. Moreover, partial blood hammer (PBH) phenomenon was detected in some cases and led to significant hemodynamic insufficiency. PBH events were attributed to the interaction between shear-thinning properties, transitional flow structures and loss of upstream pressure-velocity phase lag. We clearly show that the hemodynamic complexities in early-stage MMD could induce ischemia and explain the non-responsiveness to antiplatelet therapy.

  28. Octacalcium phosphate collagen composite (OCP/Col) enhance bone regeneration in a rat model of skull defect with dural defect. International-journal Peer-reviewed

    Takashi Sasaki, Kuniyasu Niizuma, Atsushi Kanoke, Keiko Matsui, Shogo Ogita, Sherif Rashad, Tadashi Kawai, Mika Watanabe, Hidenori Endo, Tetsu Takahashi, Shinji Kamakura, Teiji Tominaga

    Heliyon　6　(2)　e03347　2020/02

    DOI： 10.1016/j.heliyon.2020.e03347 　

    More details Close

    Cranial bone defects are a major issue in the field of neurosurgery, and improper management of such defects can cause cosmetic issues as well as more serious infections and inflammation. Several strategies exist to manage these defects clinically, but most rely on synthetic materials that are prone to complications; thus, a bone regenerative approach would be superior. We tested a material (octacalcium phosphate collagen composite [OCP/Col]) that is known to enhance bone regeneration in a skull defect model in rats. Using a critical-sized rat skull defect model, OCP/Col was implanted in rats with an intact dura or with a partial defect of the dura. The results were compared with those in a no-treatment group over the course of 12 weeks using computed tomographic and histological analysis. OCP/Col enhanced bone regeneration, regardless of whether there was a defect of the dura. OCP/Col can be used to treat skull defects, even when the dura is injured or removed surgically, via bone regeneration with enhanced resorption of OCP/Col, thus limiting the risk of infection greatly.

  29. Epigenetic response of endothelial cells to different wall shear stress magnitudes: A report of new mechano-miRNAs. International-journal Peer-reviewed

    Sherif Rashad, Xiaobo Han, Khalid Saqr, Simon Tupin, Makoto Ohta, Kuniyasu Niizuma, Teiji Tominaga

    Journal of cellular physiology　2020/01/08

    DOI： 10.1002/jcp.29436 　

    More details Close

    Endothelial cells (ECs) respond to flow stress via a variety of mechanisms, leading to various intracellular responses that can modulate the vessel wall and lead to diseases if the flow is disturbed. Mechano-microRNAs (miRNAs) are a subset of miRNAs in the ECs that are flow responsive. Mechano-miRNAs were shown to be related to atherosclerosis pathophysiology, and a number of them were identified as pathologic. Here, we exposed human carotid ECs to different wall shear stresses (WSS), high and low, and evaluated the response of miRNAs by microarray and quantitative polymerase chain reaction analysis. We discovered five new mechano-miRNAs that were not reported in that context previously to the best of our knowledge. Moreover, functional pathway analysis revealed that under low WSS conditions, several pathways regulating apoptosis are affected. In addition, KLF2 and KLF4, known atheroprotective genes, were downregulated under low WSS and upregulated under high WSS. KLF2 and VCAM1, both angiogenic, were upregulated under high WSS. NOS3, which is vascular protective, was also upregulated with higher WSS. On the contrary, ICAM-1 and E-selectin, both atherogenic and proinflammatory, were upregulated with high WSS. Collectively, the epigenetic landscape with the gene expression analysis reveals that low WSS is associated with a proapoptotic state, while high WSS is associated with a proliferative and proinflammatory state.

  30. tRNA cleavage: a new insight. International-journal Invited Peer-reviewed

    Sherif Rashad, Kuniyasu Niizuma, Teiji Tominaga

    Neural regeneration research　15　(1)　47-52　2020/01

    DOI： 10.4103/1673-5374.264447 　

    ISSN： 1673-5374

    More details Close

    Over the past decades, tRNA was found to be a rich hub of RNA modifications such as 1-methyladenosine and 5-methycytosine modifications and others, holding more than half of all modifications occurring in RNA molecules. Moreover, tRNA was discovered to be a source of various small noncoding RNA species, such as the stress induced angiogenin cleaved tRNA halves (tiRNA) or the miRNA like tRNA derived fragments. tRNA cleavage under stress was fist discovered in bacteria and later was found to be conserved across different species, including mammals. Under cellular stress conditions, tRNA undergoes conformational changes and angiogenin cleaves it into 3' and 5' halves. 5'tiRNA halves were shown to repress protein translations. tRNA cleavage is thought of to be a cytoprotective mechanism by which cells evade apoptosis, however some data hints to the opposite; that tiRNA are cytotoxic or at least related to apoptosis initiation. tRNA cleavage also was shown to be affected by tRNA modifications via different enzymes in the cytosol and mitochondria. In this review, we will highlight the biology of tRNA cleavage, show the evidence of it being cytoprotective or a marker of cell death and shed a light on its role in disease models and human diseases as well as possible future directions in this field of RNA research.

  31. A novel model of cerebral hyperperfusion with blood-brain barrier breakdown, white matter injury, and cognitive dysfunction. Peer-reviewed

    Mansour A, Rashad S, Niizuma K, Fujimura M, Tominaga T

    Journal of neurosurgery　1-13　2019/10

    DOI： 10.3171/2019.7.JNS19212 　

    ISSN： 0022-3085

  32. tiRNAs as a novel biomarker for cell damage assessment in in vitro ischemia-reperfusion model in rat neuronal PC12 cells Peer-reviewed

    Alaa Elkordy, Sherif Rashad, Heba Shehabeldeen, Eikan Mishima, Kuniyasu Niizuma, Takaaki Abe, Teiji Tominaga

    Brain Research　1714　8-17　2019/07

    Publisher: Elsevier {BV}

    DOI： 10.1016/j.brainres.2019.02.019 　

    ISSN： 0006-8993

  33. Neuroprotective effects of minocycline and progesterone on white matter injury after focal cerebral ischemia. Peer-reviewed

    Faheem H, Mansour A, Elkordy A, Rashad S, Shebl M, Madi M, Elwy S, Niizuma K, Tominaga T

    Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia　64　206-213　2019/04

    DOI： 10.1016/j.jocn.2019.04.012 　

    ISSN： 0967-5868

  34. Early BBB breakdown and subacute inflammasome activation and pyroptosis as a result of cerebral venous thrombosis Peer-reviewed

    Sherif Rashad, Kuniyasu Niizuma, Mika Sato-Maeda, Miki Fujimura, Ahmed Mansour, Hidenori Endo, Shuntaro Ikawa, Teiji Tominaga

    Brain Research　1699　54-68　2018/11

    Publisher: Elsevier {BV}

    DOI： 10.1016/j.brainres.2018.06.029 　

  35. ラット上矢静脈洞血栓症モデルにおける、脳血流変化の観察

    濱崎 亮, 新妻 邦泰, Rashad Sherif, 清水 宏明, 冨永 悌二

    脳循環代謝　30　(1)　114-114　2018/10

    Publisher: (一社)日本脳循環代謝学会

    ISSN： 0915-9401

    eISSN： 2188-7519

  36. A refined model of chronic cerebral hypoperfusion resulting in cognitive impairment and a low mortality rate in rats. International-journal Peer-reviewed

    Ahmed Mansour, Kuniyasu Niizuma, Sherif Rashad, Akira Sumiyoshi, Rie Ryoke, Hidenori Endo, Toshiki Endo, Kenichi Sato, Ryuta Kawashima, Teiji Tominaga

    Journal of neurosurgery　131　(3)　892-902　2018/09/07

    DOI： 10.3171/2018.3.JNS172274 　

    More details Close

    OBJECTIVE: The cognitive deficits of vascular dementia and the vasoocclusive state of moyamoya disease have often been mimicked with bilateral stenosis/occlusion of the common carotid artery (CCA) or internal carotid artery. However, the cerebral blood flow (CBF) declines abruptly in these models after ligation of the CCA, which differs from "chronic" cerebral hypoperfusion. While some modified but time-consuming techniques have used staged occlusion of both CCAs, others used microcoils for CCA stenosis, producing an adverse effect on the arterial endothelium. Thus, the authors developed a new chronic cerebral hypoperfusion (CCH) model with cognitive impairment and a low mortality rate in rats. METHODS: Male Sprague-Dawley rats were subjected to unilateral CCA occlusion and contralateral induction of CCA stenosis (modified CCA occlusion [mCCAO]) or a sham operation. Cortical regional CBF (rCBF) was measured using laser speckle flowmetry. Cognitive function was assessed using a Barnes circular maze (BCM). MRI studies were performed 4 weeks after the operation to evaluate cervical and intracranial arteries and parenchymal injury. Behavioral and histological studies were performed at 4 and 8 weeks after surgery. RESULTS: The mCCAO group revealed a gradual CBF reduction with a low mortality rate (2.3%). White matter degeneration was evident in the corpus callosum and corpus striatum. Although the cellular density declined in the hippocampus, MRI revealed no cerebral infarctions after mCCAO. Immunohistochemistry revealed upregulated inflammatory cells and angiogenesis in the hippocampus and cerebral cortex. Results of the BCM assessment indicated significant impairment in spatial learning and memory in the mCCAO group. Although some resolution of white matter injury was observed at 8 weeks, the animals still had cognitive impairment. CONCLUSIONS: The mCCAO is a straightforward method of producing a CCH model in rats. It is associated with a low mortality rate and could potentially be used to investigate vascular disease, moyamoya disease, and CCH. This model was verified for an extended time point of 8 weeks after surgery.

  37. Real-World Variability in the Prediction of Intracranial Aneurysm Wall Shear Stress: The 2015 International Aneurysm CFD Challenge. Peer-reviewed

    sherif rashad, h co-author

    Cardiovasc Eng Technol.　2018/09

  38. Intracellular S1P Levels Dictate Fate of Different Regions of the Hippocampus following Transient Global Cerebral Ischemia Peer-reviewed

    Sherif Rashad, Kuniyasu Niizuma, Daisuke Saigusa, Xiaobo Han, Mika Sato-Maeda, Ritsumi Saito, Akira Uruno, Miki Fujimura, Shuntaro Ikawa, Masayuki Yamamoto, Teiji Tominaga

    Neuroscience　384　(384)　188-202　2018/08/01

    Publisher: Elsevier Ltd

    DOI： 10.1016/j.neuroscience.2018.05.015 　

    ISSN： 1873-7544 0306-4522

  39. Surgery for spinal intramedullary tumors: technique, outcome and factors affecting resectability Peer-reviewed

    Rashad, S., Elwany, A., Farhoud, A.

    Neurosurgical Review　41　(2)　503-511　2018/04

    DOI： 10.1007/s10143-017-0879-z 　

  40. Impact of bifurcation angle and inflow coefficient on the rupture risk of bifurcation type basilar artery tip aneurysms Peer-reviewed

    Sherif Rashad, Shin-Ichiro Sugiyama, Kuniyasu Niizuma, Kenichi Sato, Hidenori Endo, Shunsuke Omodaka, Yasushi Matsumoto, Miki Fujimura, Teiji Tominaga

    Journal of Neurosurgery　128　(3)　723-730　2018/03/01

    Publisher: American Association of Neurological Surgeons

    DOI： 10.3171/2016.10.JNS161695 　

    ISSN： 1933-0693 0022-3085

  41. 神経アポトーシスにおけるS1Pシグナル伝達 虚血性細胞死に対する抵抗性と脆弱性への関連(S1P signaling in neuronal apoptosis: links to resistance and vulnerability to ischemic cell death)

    Rashad Sherif, 新妻 邦泰, 三枝 大輔, 韓 笑波, 前田 美香, 藤村 幹, 井川 俊太郎, 冨永 悌二

    脳循環代謝　29　(1)　215-215　2017/11

    Publisher: (一社)日本脳循環代謝学会

    ISSN： 0915-9401

    eISSN： 2188-7519

  42. Transient Global Cerebral Ischemia Induces RNF213, a Moyamoya Disease Susceptibility Gene, in Vulnerable Neurons of the Rat Hippocampus CA1 Subregion and Ischemic Cortex Peer-reviewed

    Mika Sato-Maeda, Miki Fujimura, Sherif Rashad, Yuiko Morita-Fujimura, Kuniyasu Niizuma, Hiroyuki Sakata, Shuntaro Ikawa, Teiji Tominaga

    JOURNAL OF STROKE & CEREBROVASCULAR DISEASES　26　(9)　1904-1911　2017/09

    DOI： 10.1016/j.jstrokecerebrovasdis.2017.06.032 　

    ISSN： 1052-3057

    eISSN： 1532-8511

  43. Uneven cerebral hemodynamic change as a cause of neurological deterioration in the acute stage after direct revascularization for moyamoya disease: cerebral hyperperfusion and remote ischemia caused by the 'watershed shift' Peer-reviewed

    Xian-kun Tu, Miki Fujimura, Sherif Rashad, Shunji Mugikura, Hiroyuki Sakata, Kuniyasu Niizuma, Teiji Tominaga

    NEUROSURGICAL REVIEW　40　(3)　507-512　2017/07

    DOI： 10.1007/s10143-017-0845-9 　

    ISSN： 0344-5607

    eISSN： 1437-2320

  44. Stereotactic radiosurgery as a feasible treatment for intramedullary spinal arteriovenous malformations: a single-center observation Peer-reviewed

    Sherif Rashad, Toshiki Endo, Yoshihiro Ogawa, Kenichi Sato, Hidenori Endo, Yasushi Matsumoto, Akira Takahashi, Teiji Tominaga

    NEUROSURGICAL REVIEW　40　(2)　259-266　2017/04

    DOI： 10.1007/s10143-016-0758-z 　

    ISSN： 0344-5607

    eISSN： 1437-2320

  45. Impact of bifurcation angle and inflow coefficient on rupture risk of bifurcation type basilar artery top aneurysms Invited

    sherif rashad, First author

    Transactions of Japanese Society for Medical and Biological Engineering　55　(5)　412-412　2017

    Publisher: Japanese Society for Medical and Biological Engineering

    DOI： 10.11239/jsmbe.55Annual.412 　

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    <p>Risk factors for aneurysm rupture have been studied extensively in the past, with several factors showing significant correlations with rupture status. We analysed seventy-one basilar tip aneurysms were included in this study, 22 ruptured and 49 unruptured. Patient data (age and sex), morphometric factors (aneurysm maximum height and volume, aspect ratio, bifurcation angle, bottleneck ratio, and neck-parent artery ratio) and hemodynamic factors (inflow coefficient and wall shear stress) were compared between ruptured and unruptured groups, and statistically analyzed. Aspect ratio, bifurcation angle, bottleneck ratio, and inflow coefficient were significantly correlated with the rupture status on univariate analysis. Logistic regression analysis showed that aspect ratio and bifurcation angle were predictors of rupture. Bifurcation angle correlated inversely with inflow coefficient which in turn correlated directly with wall shear stress on Pearson's correlation coefficient Bifurcation angle and aspect ratio were independent predictors for aneurysm rupture.</p>

  46. Daughter Sac Formation Related to Blood Inflow Jet in an Intracranial Aneurysm Peer-reviewed

    Sin-ichiro Sugiyama, Hidenori Endo, Shunsuke Omodaka, Toshiki Endo, Kuniyasu Niizuma, Sherif Rashad, Toshio Nakayama, Kenichi Funamoto, Makoto Ohta, Teiji Tominaga

    WORLD NEUROSURGERY　96　396-402　2016/12

    DOI： 10.1016/j.wneu.2016.09.040 　

    ISSN： 1878-8750

    eISSN： 1878-8769

  47. Long-term follow-up of pediatric moyamoya disease treated by combined direct-indirect revascularization surgery: single institute experience with surgical and perioperative management Peer-reviewed

    Sherif Rashad, Miki Fujimura, Kuniyasu Niizuma, Hidenori Endo, Teiji Tominaga

    NEUROSURGICAL REVIEW　39　(4)　615-622　2016/10

    DOI： 10.1007/s10143-016-0734-7 　

    ISSN： 0344-5607

    eISSN： 1437-2320

  48. Blood Flow Into Basilar Tip Aneurysms: A Predictor for Recanalization After Coil Embolization Peer-reviewed

    Shin-ichiro Sugiyama, Kuniyasu Niizuma, Kenichi Sato, Sherif Rashad, Misaki Kohama, Hidenori Endo, Toshiki Endo, Yasushi Matsumoto, Makoto Ohta, Teiji Tominaga

    STROKE　47　(10)　2541-2547　2016/10

    DOI： 10.1161/STROKEAHA.116.013555 　

    ISSN： 0039-2499

    eISSN： 1524-4628

  49. Endovascular Modalities for the Treatment of Cavernous Sinus Arteriovenous Fistulas: A Single-Center Experience Peer-reviewed

    Tamer Hassan, Sherif Rashad, Waseem Aziz, Ahmed Sultan, Tamer Ibrahim

    JOURNAL OF STROKE & CEREBROVASCULAR DISEASES　24　(12)　2824-2838　2015/12

    DOI： 10.1016/j.jstrokecerebrovasdis.2015.08.016 　

    ISSN： 1052-3057

    eISSN： 1532-8511

  50. De Novo Giant Partially Thrombosed Aneurysm Complicating STA-MCA Bypass Site in 3 Years: Case Report with Review of the Literature Peer-reviewed

    Sherif Rashad, Tamer Hassan, Hiroaki Shimizu, Tamer Ibrahim, Ahmed Sultan, Bassma El-Sabaa

    Neurosurgery Quarterly　25　(3)　296-301　2015/08/19

    Publisher: Lippincott Williams and Wilkins

    DOI： 10.1097/WNQ.0000000000000046 　

    ISSN： 1534-4916 1050-6438

  51. Therapeutic Clip Occlusion of the Anterior Choroidal Artery Involved with Partially Thrombosed Fusiform Aneurysm: A Case Report Peer-reviewed

    Sherif Rashad, Hidenori Endo, Ahmed Elsayed Sultan, Hiroaki Shimizu, Miki Fujimura, Kenichi Sato, Yasushi Matsumoto, Teiji Tominaga

    JOURNAL OF STROKE & CEREBROVASCULAR DISEASES　24　(8)　E227-E230　2015/08

    DOI： 10.1016/j.jstrokecerebrovasdis.2015.04.024 　

    ISSN： 1052-3057

    eISSN： 1532-8511

  52. Management of spinal dural arterio-venous fistulas. Report of 12 cases and review of literature Peer-reviewed

    Sherif Rashad, Mohamed Abdel-Bary, Waseem Aziz, Tamer Hassan

    CLINICAL NEUROLOGY AND NEUROSURGERY　125　81-86　2014/10

    DOI： 10.1016/j.clineuro.2014.07.028 　

    ISSN： 0303-8467

    eISSN： 1872-6968

  53. Carotid artery occlusion for the treatment of symptomatic giant carotid aneurysms: a proposal of classification and surgical protocol Peer-reviewed

    Sherif Rashad, Tamer Hassan, Waseem Aziz, Ahmed Marei

    NEUROSURGICAL REVIEW　37　(3)　501-511　2014/07

    DOI： 10.1007/s10143-014-0533-y 　

    ISSN： 0344-5607

    eISSN： 1437-2320

  54. Near-fatal epistaxis from traumatic giant carotid artery pseudoaneurysm: A case report Peer-reviewed

    Rashad, S., Hassan, T., Eldawoody, H.F.

    Neurosurgery Quarterly　24　(1)　56-62　2014/02

    DOI： 10.1097/WNQ.0b013e31828cbed9 　

  55. Vein of Galen Aneurysmal Malformation Presented by Dementia and Impotence in an Adult: Case Report Peer-reviewed

    Sherif Rashad, Tamer Hassan

    NEUROSURGERY QUARTERLY　23　(2)　140-143　2013/05

    DOI： 10.1097/WNQ.0b013e31828c6f01 　

    ISSN： 1050-6438

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Misc. 7

  1. 外傷性脳損傷に対するMuse細胞治療の有効性の探索

    永井新, 永井新, 中屋敷諄, 中屋敷諄, 北村祐樹, 北村祐樹, 安藤大祐, RASHAD Sherif, RASHAD Sherif, 金森正之, 遠藤英徳, 新妻邦泰, 新妻邦泰, 新妻邦泰

    日本分子脳神経外科学会プログラム・抄録集　24th　2024

  2. Tissue-specific tRNA epitranscriptome adaptations fine-tune mRNA translation via influencing codon bias and optimality.

    安藤大祐, 安藤大祐, RASHAD Sherif, RASHAD Sherif, BEGLEY Thomas J, DEDON Peter C, 新妻邦泰, 新妻邦泰

    日本分子生物学会年会プログラム・要旨集(Web)　46th　2023

  3. The Impact of ALKBH1 on Glioma Prognosis: The Regulation of Mitochondrial Function and Stemness through tRNA Modification

    中屋敷諄, 中屋敷諄, RASHAD Sherif, RASHAD Sherif, 永井新, 永井新, MOUSA Abdulrahman, 安藤大祐, 冨永慶太, 冨永慶太, 山下将太, 山下将太, 遠藤英徳, 新妻邦泰, 新妻邦泰, 新妻邦泰

    日本分子生物学会年会プログラム・要旨集(Web)　46th　2023

  4. ラット静脈洞血栓症モデルにおける,脳血流変化の観察

    濱崎亮, 新妻邦泰, RASHAD Sherif, 高橋和孝, 清水宏明, 冨永悌二

    日本分子脳神経外科学会プログラム・抄録集　19th　2018

  5. ラット上矢静脈洞血栓症モデルにおける,脳血流変化の観察

    濱崎亮, 濱崎亮, 新妻邦泰, 新妻邦泰, RASHAD Sherif, 清水宏明, 冨永悌二

    脳循環代謝(Web)　30　(1)　2018

    ISSN： 2188-7519

  6. ラット虚血脳モデルを用いた,もやもや病疾患感受性遺伝子Rnf213の転写バリアント発現動態の解析

    前田美香, 藤村幹, RASHAD Sherif, 藤村(森田)維子, 新妻邦泰, 坂田洋之, 井川俊太郎, 冨永悌二

    日本分子脳神経外科学会プログラム・抄録集　17th　2016

  7. AVEC CFD2016

    安西眸, TUPIN Simon, 渡邉和浩, RASHAD Sherif, 太田信

    日本バイオレオロジー学会誌(Web)　30　(2)　2016

    ISSN： 2186-5663

Show all ︎Show first 5

Presentations 71

  1. Tracing glioma evolutionary trajectories using long-read sequencing reveals extensive transcriptome remodeling International-presentation Invited

    Sherif Rashad

    PacBio PRISM Fukuoka 2026　2026/05

  2. tRNA modifications and the regulation of codon decoding in cancer and neurological disorders International-presentation Invited

    Sherif Rashad

    Asia-Africa Research Exchange Symposium 2026　2026/01

  3. Long-read sequencing reveals evolutionary trajectories of recurrent gliomas

    Sherif Rashad

    26th Annual Meeting of the Japan Society of Molecular Neurosurgery　2026

  4. tRNA modifications and the regulation of codon decoding in neurological disorders International-presentation Invited

    Sherif Rashad

    Department of Anatomy, Faculty of Medicine, Masaryk University　2025/10/15

  5. tRNA modifications and the regulation of codon decoding in neurological disorders International-presentation Invited

    Sherif Rashad

    Department of Chemistry and Biochemistry Seminar, San Diego State University　2025/05/27

  6. tRNA modifications in oxidative stress and stroke pathology International-presentation Invited

    Sherif Rashad

    SFB RNA-DECO Seminar Series　2025/05/13

  7. tRNA biology in health and disease International-presentation Invited

    Sherif Rashad

    Universidad del Istmo　2025/02/27

  8. Multi-omics analysis of epitranscriptional and translational dysregulation during cerebral ischemia reveals a role for tRNA modifications

    Sherif Rashad

    48th Annual Meeting of the Molecular Biology Society of Japan (MBSJ 2025)　2025

  9. tRNA modifications: New frontiers in glioblastoma therapy International-presentation

    Sherif Rashad

    20th Meeting of the European Association of Neuro-Oncology (EANO 2025)　2025

  10. Ribosome collision is a targetable vulnerability in glioma International-presentation

    Sherif Rashad

    20th Meeting of the European Association of Neuro-Oncology (EANO 2025)　2025

  11. tRNA modifications drive glioma oncogenesis and are targets for therapy

    Sherif Rashad

    84th Annual Meeting of the Japanese Cancer Association　2025

  12. tRNA modifications drive glioma oncogenesis and are targets for therapy

    Sherif Rashad

    25th Annual Meeting of the Japan Society of Molecular Neurosurgery　2025

  13. Multi-omics analysis of epitranscriptional and translational dysregulation during cerebral ischemia

    Sherif Rashad

    25th Annual Meeting of the Japan Society of Molecular Neurosurgery　2025

  14. Ribosome collision is a targetable vulnerability in glioma International-presentation

    Sherif Rashad

    RNA 2025: 30th Annual Meeting of the RNA Society　2025

  15. Stem cell therapy in spinal cord injury: Myth vs. reality, the Japanese experience International-presentation Invited

    Sherif Rashad

    Pan Arab Spine Society Conference 2025　2025

  16. The tRNA epitranscriptome and its role in cancer International-presentation Invited

    Sherif Rashad

    Invited Seminar, China-Japan Friendship Hospital　2024/10/24

  17. tRNA modifications orchestrate the translational response to mitochondrial stress

    Sherif Rashad

    47th Annual Meeting of the Molecular Biology Society of Japan (MBSJ 2024)　2024

  18. Ribosome collision is a targetable vulnerability in glioma International-presentation

    Sherif Rashad

    Ribosome Meeting 2024 in Japan　2024

  19. Ribosome collision is a targetable vulnerability in glioma International-presentation

    Sherif Rashad

    Cell Symposium: Functional RNAs (2024)　2024

  20. The translational response to mitochondrial stress is orchestrated by tRNA modifications through altered codon usage and optimality International-presentation

    Sherif Rashad

    Cell Symposium: Functional RNAs (2024)　2024

  21. Temporal dynamics of mRNA translation and tRNA epitranscriptome dysregulation during stroke evolution in mice International-presentation

    Sherif Rashad

    29th International tRNA Conference (2024)　2024

  22. Multi-omics analysis of epitranscriptional and translational dysregulation during cerebral ischemia

    Sherif Rashad

    24th Annual Meeting of the Japan Society of Molecular Neurosurgery　2024

  23. Ribosome collision as a targetable vulnerability in glioma

    Sherif Rashad

    24th Annual Meeting of the Japan Society of Molecular Neurosurgery　2024

  24. tRNA modifications orchestrate the translational response to mitochondrial stress

    Sherif Rashad

    25th Annual Meeting of the RNA Society of Japan　2024

  25. The epitranscriptome: A new frontier in cancer therapy International-presentation Invited

    Sherif Rashad

    Abu Dhabi International Brain and Spine Surgery Congress (ADNEURO 2024)　2024

  26. Ribosome collision is a targetable vulnerability in glioma during ferroptosis exposure

    Sherif Rashad

    46th Annual Meeting of the Molecular Biology Society of Japan (MBSJ 2023)　2023

  27. tRNA queuosine modifications regulate the translational response to mitochondrial stress

    Sherif Rashad

    46th Annual Meeting of the Molecular Biology Society of Japan (MBSJ 2023)　2023

  28. SAMD4A regulates neuronal differentiation and sensitivity to oxidative stress by altering mRNA stability International-presentation

    Sherif Rashad

    Cell Bio 2023: Joint Meeting of the American Society for Cell Biology and the European Molecular Biology Organization　2023

  29. tRNA queuosine modifications regulate the translational response to mitochondrial stress International-presentation

    Sherif Rashad

    Cell Bio 2023: Joint Meeting of the American Society for Cell Biology and the European Molecular Biology Organization　2023

  30. Ribosome collision is a targetable vulnerability in glioma during ferroptosis exposure International-presentation

    Sherif Rashad

    Cell Bio 2023: Joint Meeting of the American Society for Cell Biology and the European Molecular Biology Organization　2023

  31. Neuronal sensitivity to oxidative stress is epi- and post-transcriptionally regulated

    Sherif Rashad

    66th Annual Meeting of the Japanese Society of Cerebral Blood Flow and Metabolism (BRAIN Japan 2023)　2023

  32. Identification of ribosome collision as a therapeutic vulnerability in glioma

    Sherif Rashad

    66th Annual Meeting of the Japanese Society of Cerebral Blood Flow and Metabolism (BRAIN Japan 2023)　2023

  33. Neuronal sensitivity to oxidative stress is an epitranscriptional consequence of neuronal differentiation

    Sherif Rashad

    24th Annual Meeting of the RNA Society of Japan　2023

  34. Integrated Transcriptomics, Post-Transcriptomics and Translatomics Reveals Level-Specific Regulation of Neuronal Differentiation. International-presentation

    Sherif Rashad

    RNA 2023: 28th Annual Meeting of the RNA Society　2023

  35. Translational regulation of mitochondrial stress response via the tRNA epitranscriptome International-presentation

    Sherif Rashad

    RNA 2023: 28th Annual Meeting of the RNA Society　2023

  36. Neuronal sensitivity to oxidative stress is epitranscriptionally programmed International-presentation

    Sherif Rashad

    29th Annual Conference of the Society for Redox Biology and Medicine (SfRBM 2022)　2022

  37. Codon usage and mRNA stability are translational determinants of the cellular response to canonical ferroptosis inducers International-presentation

    Sherif Rashad

    29th Annual Conference of the Society for Redox Biology and Medicine (SfRBM 2022)　2022

  38. RNF213 loss of function reshapes the vascular transcriptome and spliceosome

    Sherif Rashad

    65th Annual Meeting of the Japanese Society of Cerebral Blood Flow and Metabolism (BRAIN Japan 2022)　2022

  39. Transcriptional and Epigenetic Regulation of Neuronal Differentiation and Function Reveals Key Epigenetic Phenomena

    Sherif Rashad

    44th Annual Meeting of the Molecular Biology Society of Japan (MBSJ 2021)　2021

  40. The hemodynamic complexities underlying transient ischemic attacks in early moyamoya disease: A CFD study

    Sherif Rashad

    35th Annual Meeting of the Japanese Society for Neuroendovascular Therapy (JSNET 2019)　2019

  41. The hemodynamic complexities underlying transient ischemic attacks in early moyamoya disease: A CFD study

    Sherif Rashad

    62nd Annual Meeting of the Japanese Society of Cerebral Blood Flow and Metabolism (BRAIN Japan 2019)　2019

  42. Metabolic basis of neuronal vulnerability to ischemia; an in vivo untargeted metabolomics approach

    Sherif Rashad

    62nd Annual Meeting of the Japanese Society of Cerebral Blood Flow and Metabolism (BRAIN Japan 2019)　2019

  43. Metabolic basis of neuronal vulnerability to ischemia; an in vivo untargeted metabolomics approach International-presentation

    Sherif Rashad

    BRAIN & BRAIN PET 2019 (ISCBFM Meeting)　2019

  44. S1P and S1P metabolizing enzymes influence neuronal fate in the hippocampus after transient global cerebral ischemia in rats International-presentation

    Sherif Rashad

    BRAIN & BRAIN PET 2019 (ISCBFM Meeting)　2019

  45. Blood-brain barrier breakdown, neuroinflammation, and widespread lipid disturbances evident with spectrometric imaging after cerebral venous thrombosis in rats International-presentation

    Sherif Rashad

    BRAIN & BRAIN PET 2019 (ISCBFM Meeting)　2019

  46. Blood-brain barrier breakdown, neuroinflammation, and widespread lipid disturbances caused by cerebral venous thrombosis in rats

    Sherif Rashad

    44th Annual Meeting of the Japan Stroke Society (STROKE 2019)　2019

  47. Blood-brain barrier breakdown, neuroinflammation, and widespread lipid disturbances caused by cerebral venous thrombosis in rats

    Sherif Rashad

    77th Annual Meeting of the Japan Neurosurgical Society (JNS 2018)　2018

  48. BBB breakdown, neuroinflammation and widespread lipid disturbances caused by CVT in rats

    sherif rashad

    JNS 2018 – The 77th annual meeting of the Japanese neurosurgical society.　2018

  49. Impact of bifurcation angle and inflow coefficient on rupture risk of bifurcation-type basilar artery tip aneurysms Invited

    Sherif Rashad

    56th Annual Meeting of the Japanese Society for Medical and Biological Engineering (JSMBE 2017)　2017

  50. Impact of bifurcation angle and inflow coefficient on rupture risk of bifurcation-type basilar artery tip aneurysms

    Sherif Rashad

    42nd Annual Meeting of the Japan Stroke Society (STROKE 2017)　2017

  51. Impact of bifurcation angle and inflow coefficient on rupture risk of bifurcation type basilar artery aneurysms Invited

    sherif rashad

    JSMBE56 - The 56th Annual Meeting of Japanese Society for Medical and Biological Engineering　2017

  52. Impact of bifurcation angle and inflow coefficient on rupture risk of bifurcation type basilar artery top aneurysms Invited

    sherif rashad

    The 42nd Japan stroke society meeting (Stroke 2017), Osaka, Japan.　2017

  53. Conformational changes of tRNA in the hippocampal CA1 subregion after transient global cerebral ischemia in rats: Roles in apoptosis and value as a stress marker

    Sherif Rashad

    59th Annual Meeting of the Japanese Society of Cerebral Blood Flow and Metabolism (BRAIN Japan 2016)　2016

  54. Conformational changes of tRNA in the hippocampal CA1 subregion after transient global cerebral ischemia in rats: Roles in apoptosis and value as a stress marker

    Sherif Rashad

    75th Annual Meeting of the Japan Neurosurgical Society (JNS 2016)　2016

  55. Bifurcation configuration as a criterion affecting rupture risk in basilar artery aneurysms International-presentation

    Sherif Rashad

    VII European Congress on Computational Methods in Applied Sciences and Engineering (ECCOMAS Congress 2016)　2016

  56. Conformational changes of tRNA in the hippocampal CA1 subregion after transient global cerebral ischemia in rats

    sherif rashad

    59th Japan cerebral blood flow and metabolism Society meeting (BRAIN Japan 2016), Tokoshima, Japan　2016

  57. Experimental model of chronic cerebral hypoperfusion in rats with gradual decreasement of cerebral blood flow and cognitive impairment

    sherif rashad (Co-presenter

    The 75th annual meeting of the Japanese neurosurgical society (JNS 2016), Fukouka, Japan　2016

  58. Conformational changes of tRNA in the hippocampal CA1 subregion after transient global cerebral ischemia in rats, roles in apoptosis and value as a stress marker

    sherif rashad

    The 75th annual meeting of the Japanese neurosurgical society (JNS 2016), Fukouka, Japan　2016

  59. Bifurcation configuration as a criterion affecting risk of aneurysm rupture in Basilar artery aneurysms International-presentation

    sherif rashad

    VII European Congress on Computational Methods in Applied Sciences and Engineering (ECCOMAS 2016), Crete, Greece　2016

  60. Determination of rupture status of MCA aneurysms using hemodynamic and geometric parameters. Invited

    Sherif Rashad

    31st Annual Meeting of the Japanese Society for Neuroendovascular Therapy (JSNET 2015)　2015

  61. Radiotherapy for intramedullary AVMs

    Sherif Rashad

    30th Annual Meeting of the Japanese Society for Spinal Surgery (JSSS 2015)　2015

  62. Proposed protocol for where to occlude a giant carotid aneurysm with mass effect International-presentation

    Sherif Rashad

    World Live Neurovascular Conference 2014 (WLNC 2014)　2014

  63. Proposed Protocol for "where" to Occlude Giant Carotid Aneurysm with Mass Effect International-presentation

    sherif rashad

    World Live neurovascular conference 2014 (WLNC 2014), Buenos Aires, Argentina　2014

  64. De novo giant partially thrombosed aneurysm complicating an STA-MCA bypass site after 3 years: Case report with review of the literature International-presentation

    Sherif Rashad

    15th WFNS World Congress of Neurological Surgery (WFNS 2013)　2013

  65. Vein of Galen aneurysmal malformation presenting with dementia and impotence in an adult: Case report International-presentation

    Sherif Rashad

    15th WFNS World Congress of Neurological Surgery (WFNS 2013)　2013

  66. Near-fatal epistaxis from a traumatic giant carotid artery pseudoaneurysm: Case report International-presentation

    Sherif Rashad

    15th WFNS World Congress of Neurological Surgery (WFNS 2013)　2013

  67. De-novo Giant Partially Thrombosed Aneurysm Complicating Sta-mca Bypass Site in 3 Years; Case Report with Review of the Literature International-presentation

    sherif rashad

    15th World Federation of neurological surgeons 2013 (WFNS 2013), Seoul, South Korea　2013

  68. Vein of Galen Aneurysmal Malformation Presented by Dementia and Impotence in an Adult; Case Report International-presentation

    sherif rashad

    15th World Federation of neurological surgeons 2013 (WFNS 2013), Seoul, South Korea　2013

  69. Near Fatal Epistaxis from Traumatic Giant Carotid Artery Pseudoaneurysm; Case Report International-presentation

    sherif rashad

    15th World Federation of neurological surgeons 2013 (WFNS 2013), Seoul, South Korea　2013

  70. Recurrent near fatal epistaxis after parent vessel ligation from traumatic carotid pseudoaneurysm: case report

    sherif rashad

    28th meeting of the Japanese society for neuroendovascular therapy 2012 (JSNET 2012), Sendai, Japan　2012/11

  71. Recurrent near-fatal epistaxis after parent vessel ligation for a traumatic carotid pseudoaneurysm: Case report

    Sherif Rashad

    28th Annual Meeting of the Japanese Society for Neuroendovascular Therapy (JSNET 2012)　2012

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Research Projects 4

  1. 肺癌の病態を規定するtRNA修飾異常と翻訳制御の解明

    渋谷 里紗, 野津田 泰嗣, Rashad Sherif

    Offer Organization: 日本学術振興会

    System: 科学研究費助成事業

    Category: 基盤研究(C)

    Institution: 東北大学

    2026/04/01 - 2030/03/31

  2. Elucidating the role of tRNA as a source of disruptive RNAs in aging

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research

    Category: Grant-in-Aid for Transformative Research Areas (A)

    Institution: Tohoku University

    2026/04/01 - 2028/03/31

  3. Contribution of transfer RNA modification to the pathogenesis of sensorineural hearing loss and olfactory dysfunction

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research

    Category: Grant-in-Aid for Scientific Research (C)

    Institution: Tohoku University

    2025/04/01 - 2028/03/31

  4. Elucidating the role of tRNA epitranscriptome in Glioma pathology and development of novel therapies

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research

    Category: Grant-in-Aid for Scientific Research (B)

    Institution: Tohoku University

    2023/04/01 - 2026/03/31