研究者詳細

顔写真

シエリフ　モハツメド　ラシヤード
Sherif Mohamed Rashad
Sherif Mohamed Rashad
所属
大学院医工学研究科　生体再生医工学講座（神経再建医工学分野）
職名
准教授
学位

  • PhD （Tohoku University）

経歴 4

  • 2023年4月 ～ 継続中
    東北大学　大学院医工学研究科　准教授

  • 2018年4月 ～ 2023年3月
    Tohoku University　Department of Neurosurgery, Graduate school of medicine　Assistant professor

  • 2014年10月 ～ 2018年3月
    Tohoku University　Department of Neurosurgery, Graduate school of medicine　PhD student

  • 2011年1月 ～ 2014年9月
    Alexandria University, Egypt　Department of Neurosurgery, Graduate school of medicine　Neurosurgical Resident doctor

学歴 3

  • Tohoku University Graduate school of medicine　Neurosurgery　PhD course

    2014年10月 ～ 2018年3月

  • Alexandria University school of medicine　Neurosurgery　Master's course

    2010年10月 ～ 2014年3月

  • Alexandria University school of medicine　MBcch

    2001年9月 ～ 2008年10月

研究キーワード 13

  • oxidative stress

  • neuron

  • Cell Death

  • Glioma

  • Epitranscriptome

  • tRNA

  • apoptosis

  • Moyamoya disease

  • computational flow dynamics

  • stem cell therapy

  • sphingosine-1-phosphate

  • brain aneurysm

  • Stroke

研究分野 6

  • ライフサイエンス / 実験動物学 /

  • ライフサイエンス / 細胞生物学 /

  • ライフサイエンス / 脳神経外科学 /

  • ライフサイエンス / 分子生物学 /

  • ライフサイエンス / 神経形態学 /

  • ライフサイエンス / 神経科学一般 /

論文 58

  1. HuR Knockdown in MLO-Y4 Osteocyte-like Cells Elevates OPG Expression and Suppresses Osteoclastogenesis In Vitro

    Ziqiu Fan, Hideki Kitaura, Aseel Marahleh, Abdulrahman Mousa, Fumitoshi Ohori, Alexandru Craevschi, Sherif Rashad, Hiroyasu Kanetaka

    International Journal of Molecular Sciences　2025年12月31日

    DOI： 10.3390/ijms27010430 　

  2. Rewiring of RNA–protein coupling in osteocytes in response to hyperglycemic levels of glucose

    Aseel Marahleh, Sherif Rashad, Eisuke Kanao, Ziqiu Fan, Fumitoshi Ohori, Hideki Kitaura

    2025年12月25日

    DOI： 10.64898/2025.12.25.696466 　

  3. Third-nucleotide codon bias and synonymous codon bias define functional translational programs that shape human tissue and cancer proteomes

    Sherif Rashad, Kuniyasu Niizuma

    2025年11月3日

    DOI： 10.1101/2025.10.31.685942 　

  4. Optimized tDR Sequencing Reveals Diversity and Heterogeneity in tRNA-Derived Fragment Landscapes in Mouse Tissues 査読有り

    Daisuke Ando, Sherif Rashad, Kuniyasu Niizuma

    International Journal of Molecular Sciences　2025年9月9日

    DOI： 10.3390/ijms26188772 　

  5. Temporal dynamics of mRNA translation dysregulation and codon decoding during murine stroke evolution

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

    2025年8月16日

    DOI： 10.1101/2025.08.15.670488 　

  6. Transcriptome-Wide Analysis of HuR Function Identifies TXNIP-Mediated Redox Dysregulation in Osteocytes

    Ziqiu Fan, Aseel Marahleh, Hideki Kitaura, Jiayi Ren, Abdulrahman Mousa, Fumitoshi Ohori, Kuniyasu Niizuma, Sherif Rashad, Hiroyasu Kanetaka

    2025年8月8日

    DOI： 10.1101/2025.08.08.668956 　

  7. Selective Biogenesis and Structural Diversity Shape tRNA-Derived Fragment Landscapes across Mouse Organs

    Daisuke Ando, Sherif Rashad, Kuniyasu Niizuma

    2025年6月18日

    DOI： 10.1101/2025.06.18.660468 　

  8. Queuosine tRNA Modification: Connecting the Microbiome to the Translatome. 国際誌 査読有り

    Sherif Rashad

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

    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. 国際誌 査読有り

    Yuan Zhou, Sherif Rashad, Kuniyasu Niizuma

    The FEBS journal　2025年1月24日

    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. 国際誌 査読有り

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

    International journal of molecular sciences　26　(2)　2025年1月15日

    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. 国際誌 招待有り 査読有り

    Sherif Rashad, Aseel Marahleh

    Wiley interdisciplinary reviews. RNA　16　(2)　e70011　2025年

    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. 国際誌 査読有り

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

    Journal of cellular physiology　2024年11月8日

    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. 国際誌 査読有り

    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年10月13日

    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. 国際誌 査読有り

    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年9月4日

    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. Angiogenin regulates mitochondrial stress and function via tRNA-derived fragments generation and impacting tRNA modifications

    Shadi Al-Mesitef, Keita Tominaga, Abdulrahman Mousa, Thomas J Begley, Peter C Dedon, Sherif Rashad, Kuniyasu Niizuma

    2024年2月14日

    DOI： 10.1101/2024.02.13.580206 　

  16. Translational response to mitochondrial stresses is orchestrated by tRNA modifications. 国際誌

    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年2月14日

    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.

  17. tRNA modifications inform tissue specific mRNA translation and codon optimization

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

    2023年10月26日

    DOI： 10.1101/2023.10.24.563884 　

  18. Codon usage and mRNA stability are translational determinants of cellular response to canonical ferroptosis inducers 査読有り

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

    Neuroscience　2022年8月

    出版者・発行元： Elsevier BV

    DOI： 10.1016/j.neuroscience.2022.08.009 　

    ISSN：0306-4522

  19. RNF213 loss of function reshapes vascular transcriptome and spliceosome leading to disrupted angiogenesis and aggravated vascular inflammatory responses. 国際誌 査読有り

    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年6月25日

    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.

  20. 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年1月1日

    出版者・発行元： {AIP} Publishing

    DOI： 10.1063/5.0076271 　

  21. Mature Neurons’ sensitivity to oxidative stress is epigenetically programmed by alternative splicing and mRNA stability

    Yuan Zhou, Sherif Rashad, Teiji Tominaga, Kuniyasu Niizuma

    2021年12月25日

    DOI： 10.1101/2021.12.25.472549 　

  22. Dysregulation of Rnf 213 gene contributes to T cell response via antigen uptake, processing, and presentation. 国際誌 査読有り

    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年5月10日

    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.

  23. The cell and stress-specific canonical and noncanonical tRNA cleavage. 国際誌 査読有り

    Sherif Rashad, Teiji Tominaga, Kuniyasu Niizuma

    Journal of cellular physiology　236　(5)　3710-3724　2021年5月

    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.

  24. Physiologic blood flow is turbulent. 国際誌 査読有り

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

    Scientific reports　10　(1)　15492-15492　2020年9月23日

    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.

  25. The stress specific impact of ALKBH1 on tRNA cleavage and tiRNA generation. 国際誌 査読有り

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

    RNA biology　1-12　2020年6月21日

    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.

  26. What does computational fluid dynamics tell us about intracranial aneurysms? A meta-analysis and critical review 査読有り

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

    Journal of Cerebral Blood Flow & Metabolism　271678X19854640　2020年5月

    DOI： 10.1177/0271678X19854640 　

    ISSN：0271-678X

  27. Metabolic basis of neuronal vulnerability to ischemia; an in vivo untargeted metabolomics approach. 国際誌 査読有り

    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年4月16日

    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.

  28. Author Correction: The hemodynamic complexities underlying transient ischemic attacks in early-stage Moyamoya disease: an exploratory CFD study. 国際誌 査読有り

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

    Scientific reports　10　(1)　6217-6217　2020年4月7日

    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.

  29. Stress Induced tRNA Halves (tiRNAs) as Biomarkers for Stroke and Stroke Therapy; Pre-clinical Study. 国際誌 査読有り

    Kanako Sato, Sherif Rashad, Kuniyasu Niizuma, Teiji Tominaga

    Neuroscience　2020年3月19日

    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.

  30. The hemodynamic complexities underlying transient ischemic attacks in early-stage Moyamoya disease: an exploratory CFD study. 国際誌 査読有り

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

    Scientific reports　10　(1)　3700-3700　2020年2月28日

    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.

  31. Octacalcium phosphate collagen composite (OCP/Col) enhance bone regeneration in a rat model of skull defect with dural defect. 国際誌 査読有り

    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年2月

    DOI： 10.1016/j.heliyon.2020.e03347 　

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    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.

  32. Epigenetic response of endothelial cells to different wall shear stress magnitudes: A report of new mechano-miRNAs. 国際誌 査読有り

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

    Journal of cellular physiology　2020年1月8日

    DOI： 10.1002/jcp.29436 　

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    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.

  33. tRNA cleavage: a new insight. 国際誌 査読有り

    Rashad S, Niizuma K, Tominaga T

    Neural regeneration research　15　(1)　47-52　2020年1月

    DOI： 10.4103/1673-5374.264447 　

    ISSN：1673-5374

  34. A novel model of cerebral hyperperfusion with blood-brain barrier breakdown, white matter injury, and cognitive dysfunction. 査読有り

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

    Journal of neurosurgery　1-13　2019年10月

    DOI： 10.3171/2019.7.JNS19212 　

    ISSN：0022-3085

  35. tiRNAs as a novel biomarker for cell damage assessment in in vitro ischemia-reperfusion model in rat neuronal PC12 cells 査読有り

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

    Brain Research　1714　8-17　2019年7月

    出版者・発行元： Elsevier {BV}

    DOI： 10.1016/j.brainres.2019.02.019 　

    ISSN：0006-8993

  36. Neuroprotective effects of minocycline and progesterone on white matter injury after focal cerebral ischemia. 査読有り

    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年4月

    DOI： 10.1016/j.jocn.2019.04.012 　

    ISSN：0967-5868

  37. Early BBB breakdown and subacute inflammasome activation and pyroptosis as a result of cerebral venous thrombosis 査読有り

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

    Brain Research　1699　54-68　2018年11月

    出版者・発行元： Elsevier {BV}

    DOI： 10.1016/j.brainres.2018.06.029 　

  38. 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年10月

    出版者・発行元： (一社)日本脳循環代謝学会

    ISSN：0915-9401

    eISSN：2188-7519

  39. A refined model of chronic cerebral hypoperfusion resulting in cognitive impairment and a low mortality rate in rats. 国際誌 査読有り

    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年9月7日

    DOI： 10.3171/2018.3.JNS172274 　

    詳細を見る 詳細を閉じる

    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.

  40. Real-World Variability in the Prediction of Intracranial Aneurysm Wall Shear Stress: The 2015 International Aneurysm CFD Challenge. 査読有り

    シェリフ ラシャード

    Cardiovasc Eng Technol.　2018年9月

  41. Intracellular S1P Levels Dictate Fate of Different Regions of the Hippocampus following Transient Global Cerebral Ischemia 査読有り

    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年8月1日

    出版者・発行元： Elsevier Ltd

    DOI： 10.1016/j.neuroscience.2018.05.015 　

    ISSN：1873-7544 0306-4522

  42. Surgery for spinal intramedullary tumors: technique, outcome and factors affecting resectability 査読有り

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

    Neurosurgical Review　41　(2)　503-511　2018年4月

    DOI： 10.1007/s10143-017-0879-z 　

  43. Impact of bifurcation angle and inflow coefficient on the rupture risk of bifurcation type basilar artery tip aneurysms 査読有り

    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年3月1日

    出版者・発行元： American Association of Neurological Surgeons

    DOI： 10.3171/2016.10.JNS161695 　

    ISSN：1933-0693 0022-3085

  44. 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年11月

    出版者・発行元： (一社)日本脳循環代謝学会

    ISSN：0915-9401

    eISSN：2188-7519

  45. Transient Global Cerebral Ischemia Induces RNF213, a Moyamoya Disease Susceptibility Gene, in Vulnerable Neurons of the Rat Hippocampus CA1 Subregion and Ischemic Cortex 査読有り

    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年9月

    DOI： 10.1016/j.jstrokecerebrovasdis.2017.06.032 　

    ISSN：1052-3057

    eISSN：1532-8511

  46. 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' 査読有り

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

    NEUROSURGICAL REVIEW　40　(3)　507-512　2017年7月

    DOI： 10.1007/s10143-017-0845-9 　

    ISSN：0344-5607

    eISSN：1437-2320

  47. Stereotactic radiosurgery as a feasible treatment for intramedullary spinal arteriovenous malformations: a single-center observation 査読有り

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

    NEUROSURGICAL REVIEW　40　(2)　259-266　2017年4月

    DOI： 10.1007/s10143-016-0758-z 　

    ISSN：0344-5607

    eISSN：1437-2320

  48. Impact of bifurcation angle and inflow coefficient on rupture risk of bifurcation type basilar artery top aneurysms 招待有り

    シェリフ ラシャード

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

    出版者・発行元： 公益社団法人 日本生体医工学会

    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>

  49. Daughter Sac Formation Related to Blood Inflow Jet in an Intracranial Aneurysm 査読有り

    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年12月

    DOI： 10.1016/j.wneu.2016.09.040 　

    ISSN：1878-8750

    eISSN：1878-8769

  50. Long-term follow-up of pediatric moyamoya disease treated by combined direct-indirect revascularization surgery: single institute experience with surgical and perioperative management 査読有り

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

    NEUROSURGICAL REVIEW　39　(4)　615-622　2016年10月

    DOI： 10.1007/s10143-016-0734-7 　

    ISSN：0344-5607

    eISSN：1437-2320

  51. Blood Flow Into Basilar Tip Aneurysms: A Predictor for Recanalization After Coil Embolization 査読有り

    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年10月

    DOI： 10.1161/STROKEAHA.116.013555 　

    ISSN：0039-2499

    eISSN：1524-4628

  52. Endovascular Modalities for the Treatment of Cavernous Sinus Arteriovenous Fistulas: A Single-Center Experience 査読有り

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

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

    DOI： 10.1016/j.jstrokecerebrovasdis.2015.08.016 　

    ISSN：1052-3057

    eISSN：1532-8511

  53. De Novo Giant Partially Thrombosed Aneurysm Complicating STA-MCA Bypass Site in 3 Years: Case Report with Review of the Literature 査読有り

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

    Neurosurgery Quarterly　25　(3)　296-301　2015年8月19日

    出版者・発行元： Lippincott Williams and Wilkins

    DOI： 10.1097/WNQ.0000000000000046 　

    ISSN：1534-4916 1050-6438

  54. Therapeutic Clip Occlusion of the Anterior Choroidal Artery Involved with Partially Thrombosed Fusiform Aneurysm: A Case Report 査読有り

    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年8月

    DOI： 10.1016/j.jstrokecerebrovasdis.2015.04.024 　

    ISSN：1052-3057

    eISSN：1532-8511

  55. Management of spinal dural arterio-venous fistulas. Report of 12 cases and review of literature 査読有り

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

    CLINICAL NEUROLOGY AND NEUROSURGERY　125　81-86　2014年10月

    DOI： 10.1016/j.clineuro.2014.07.028 　

    ISSN：0303-8467

    eISSN：1872-6968

  56. Carotid artery occlusion for the treatment of symptomatic giant carotid aneurysms: a proposal of classification and surgical protocol 査読有り

    Sherif Rashad, Tamer Hassan, Waseem Aziz, Ahmed Marei

    NEUROSURGICAL REVIEW　37　(3)　501-511　2014年7月

    DOI： 10.1007/s10143-014-0533-y 　

    ISSN：0344-5607

    eISSN：1437-2320

  57. Near-fatal epistaxis from traumatic giant carotid artery pseudoaneurysm: A case report 査読有り

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

    Neurosurgery Quarterly　24　(1)　56-62　2014年2月

    DOI： 10.1097/WNQ.0b013e31828cbed9 　

  58. Vein of Galen Aneurysmal Malformation Presented by Dementia and Impotence in an Adult: Case Report 査読有り

    Sherif Rashad, Tamer Hassan

    NEUROSURGERY QUARTERLY　23　(2)　140-143　2013年5月

    DOI： 10.1097/WNQ.0b013e31828c6f01 　

    ISSN：1050-6438

︎全件表示 ︎最初の5件までを表示

MISC 3

  1. 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年

  2. 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年

    ISSN： 2188-7519

  3. 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年

    ISSN： 2186-5663

講演・口頭発表等 14

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

    シェリフ ラシャード

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

  2. Impact of bifurcation angle and inflow coefficient on rupture risk of bifurcation type basilar artery aneurysms 招待有り

    シェリフ ラシャード

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

  3. Impact of bifurcation angle and inflow coefficient on rupture risk of bifurcation type basilar artery top aneurysms 招待有り

    シェリフ ラシャード

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

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

    シェリフ ラシャード

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

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

    シェリフ ラシャード

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

  6. 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

    シェリフ ラシャード

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

  7. Bifurcation configuration as a criterion affecting risk of aneurysm rupture in Basilar artery aneurysms 国際会議

    シェリフ ラシャード

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

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

    シェリフ ラシャード

    31th annual meeting of the Japanese Society for NeuroEndovascular Therapy (JSNET), Okayama, Japan 2015　2015年

  9. Radiotherapy for intramedullary AVMs

    シェリフ ラシャード

    30th annual meeting of the Japanese society of spinal Surgery 2015 (jsss2015), Sapporo, Japan　2015年

  10. Proposed Protocol for "where" to Occlude Giant Carotid Aneurysm with Mass Effect 国際会議

    シェリフ ラシャード

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

  11. De-novo Giant Partially Thrombosed Aneurysm Complicating Sta-mca Bypass Site in 3 Years; Case Report with Review of the Literature 国際会議

    シェリフ ラシャード

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

  12. Vein of Galen Aneurysmal Malformation Presented by Dementia and Impotence in an Adult; Case Report 国際会議

    シェリフ ラシャード

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

  13. Near Fatal Epistaxis from Traumatic Giant Carotid Artery Pseudoaneurysm; Case Report 国際会議

    シェリフ ラシャード

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

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

    シェリフ ラシャード

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

︎全件表示 ︎最初の5件までを表示

共同研究・競争的資金等の研究課題 2

  1. 感音難聴と嗅覚障害の病態形成における転移RNA修飾の関与

    鈴木 淳, Rashad Sherif, 新妻 邦泰

    提供機関：Japan Society for the Promotion of Science

    制度名：Grants-in-Aid for Scientific Research

    研究種目：Grant-in-Aid for Scientific Research (C)

    研究機関：Tohoku University

    2025年4月1日 ～ 2028年3月31日

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

    Rashad Sherif, 遠藤 俊毅, 七谷 圭, 新妻 邦泰, 金森 政之

    提供機関：Japan Society for the Promotion of Science

    制度名：Grants-in-Aid for Scientific Research

    研究種目：Grant-in-Aid for Scientific Research (B)

    研究機関：Tohoku University

    2023年4月1日 ～ 2026年3月31日

    詳細を見る 詳細を閉じる

    During the past year, I was able to finish 2 manuscripts related to tRNA modifications and their potential role. The manuscripts were published as preprints and currently are under review (Al-Mesitef et al, 2024; Rashad et al, 2024). I also presented the preliminary results of my work in the RNA society meeting 2023 in Singapore and The American Society for Cell Biology 2023 in Boston. I was also able to improve the mass spectrometry method and analyze patient derived glioma samples that led to major discovery in terms of tRNA modifications and glioma that is currently being explored.