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"Takahashi, Kazuki"
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Yu-Gi-Oh! : Zexal
In a futuristic city, augmented reality Duels are all the rage. Duelists, using devices called D-Gazers, can interact with their environment and their opponents as never before. With more awesome monsters and unbelievable cards, the future of Yu-Gi-Oh! starts right here! No one loves Dueling more than Yuma Tsukumo, but unfortunately for him, no one is worse at it! This isn't going to stop Yuma from trying though. When Yuma calls on the memory of his parents during the Duel, a strange being called Astral appears, and the encounter is the start of Yuma's amazing Duel journey!\"--Page [4].
BOOK
TNF‐α enhances TGF‐β‐induced endothelial‐to‐mesenchymal transition via TGF‐β signal augmentation
The tumor microenvironment (TME) consists of various components including cancer cells, tumor vessels, cancer‐associated fibroblasts (CAFs), and inflammatory cells. These components interact with each other via various cytokines, which often induce tumor progression. Thus, a greater understanding of TME networks is crucial for the development of novel cancer therapies. Many cancer types express high levels of TGF‐β, which induces endothelial‐to‐mesenchymal transition (EndMT), leading to formation of CAFs. Although we previously reported that CAFs derived from EndMT promoted tumor formation, the molecular mechanisms underlying these interactions remain to be elucidated. Furthermore, tumor‐infiltrating inflammatory cells secrete various cytokines, including TNF‐α. However, the role of TNF‐α in TGF‐β‐induced EndMT has not been fully elucidated. Therefore, this study examined the effect of TNF‐α on TGF‐β‐induced EndMT in human endothelial cells (ECs). Various types of human ECs underwent EndMT in response to TGF‐β and TNF‐α, which was accompanied by increased and decreased expression of mesenchymal cell and EC markers, respectively. In addition, treatment of ECs with TGF‐β and TNF‐α exhibited sustained activation of Smad2/3 signals, which was presumably induced by elevated expression of TGF‐β type I receptor, TGF‐β2, activin A, and integrin αv, suggesting that TNF‐α enhanced TGF‐β‐induced EndMT by augmenting TGF‐β family signals. Furthermore, oral squamous cell carcinoma‐derived cells underwent epithelial‐to‐mesenchymal transition (EMT) in response to humoral factors produced by TGF‐β and TNF‐α‐cultured ECs. This EndMT‐driven EMT was blocked by inhibiting the action of TGF‐βs. Collectively, our findings suggest that TNF‐α enhances TGF‐β‐dependent EndMT, which contributes to tumor progression. This study showed that TGF‐β and TNF‐α cooperate to induce the endothelial‐to‐mesenchymal transition (EndMT), in which endothelial cells (ECs) acquire mesenchymal phenotypes. The ECs that have undergone EndMT, in turn, secrete TGF‐β2 and Activin by themselves. These secreted cytokines not only stabilize the mesenchymal phenotypes of ECs, but also induce the epithelial‐to‐mesenchymal transition (EMT) of epithelial cancer cells, which contributes to formation of malignant cancer cells.
Journal Article
Yu-Gi-Oh! 3-in-1
Tenth-grader Yugi always had his head in some game--until he solved the Millennium Puzzle, an Egyptian artifact containing the spirit of a master gambler from the age of the pharoahs! Possessed by the puzzle, Yugi becomes Yu-Gi-Oh, the King of Games, and challenges evildoers to the Shadow Games--weird games with high stakes and high risks!
Book
Duplication with structural modification through extrachromosomal circular and lariat DNA in the human genome
Duplication plays an important role in creating drastic changes in genome evolution. In addition to well-known tandem duplication, duplication can occur such that a duplicated DNA fragment is inserted at another location in the genome. Here, we report several genomic regions in the human genome that could be best explained by two types of insertion-based duplication mechanisms, where a duplicated DNA fragment was modified structurally and then inserted into the genome. In one process, the DNA fragment is turned into an extrachromosomal circular DNA, cut somewhere in the circle, and reintegrated into another location in the genome. And in the other, the DNA fragment forms a “lariat structure” with a “knot”, the strand is swapped at the knot, and is then reintegrated into the genome. Our results suggest that insertion-based duplication may not be a simple process; it may involve a complicated procedures such as structural modification before reintegration. However, the molecular mechanism has yet to be fully understood.
Journal Article
Yu-gi-oh! Arc-V
\"Yuzu Hiiragi and her father run a dueling school that's seen better days. If only they had a star teacher to bring in new students! When a rogue duelist known as Phantom appears in the city, Yuzu may have found a savior, but Phantom will have to deal with the Leo Corporation's special forces before he can get into any community service!\"-- Back cover, volume 1.
Book
CD40 is expressed in the subsets of endothelial cells undergoing partial endothelial–mesenchymal transition in tumor microenvironment
Tumor progression and metastasis are regulated by endothelial cells undergoing endothelial–mesenchymal transition (EndoMT), a cellular differentiation process in which endothelial cells lose their properties and differentiate into mesenchymal cells. The cells undergoing EndoMT differentiate through a spectrum of intermediate phases, suggesting that some cells remain in a partial EndoMT state and exhibit an endothelial/mesenchymal phenotype. However, detailed analysis of partial EndoMT has been hampered by the lack of specific markers. Transforming growth factor‐β (TGF‐β) plays a central role in the induction of EndoMT. Here, we showed that inhibition of TGF‐β signaling suppressed EndoMT in a human oral cancer cell xenograft mouse model. By using genetic labeling of endothelial cell lineage, we also established a novel EndoMT reporter cell system, the EndoMT reporter endothelial cells (EMRECs), which allow visualization of sequential changes during TGF‐β‐induced EndoMT. Using EMRECs, we characterized the gene profiles of multiple EndoMT stages and identified CD40 as a novel partial EndoMT‐specific marker. CD40 expression was upregulated in the cells undergoing partial EndoMT, but decreased in the full EndoMT cells. Furthermore, single‐cell RNA sequencing analysis of human tumors revealed that CD40 expression was enriched in the population of cells expressing both endothelial and mesenchymal cell markers. Moreover, decreased expression of CD40 in EMRECs enhanced TGF‐β‐induced EndoMT, suggesting that CD40 expressed during partial EndoMT inhibits transition to full EndoMT. The present findings provide a better understanding of the mechanisms underlying TGF‐β‐induced EndoMT and will facilitate the development of novel therapeutic strategies targeting EndoMT‐driven cancer progression and metastasis. The stepwise changes during EndoMT. During EndoMT, endothelial cells transdifferentiate to full EndoMT cells via partial EndoMT states.
Journal Article
Activation of β2‐adrenergic receptor signals suppresses mesenchymal phenotypes of oral squamous cell carcinoma cells
Metastasis is a primary reason related to the mortality of oral squamous cell carcinoma (OSCC) patients. A program called epithelial‐mesenchymal transition (EMT) has been shown to play a critical role in promoting metastasis in epithelium‐derived carcinoma. During EMT, epithelial cancer cells acquire motile mesenchymal phenotypes and detach from primary tumors. Recent lines of evidence have suggested that EMT confers cancer cells with tumor‐initiating ability. Therefore, selective targeting of EMT would lead to the development of effective therapeutic agents. In this study, using a chemical biology approach, we identified isoxsuprine, a β2‐adrenergic receptor (β2‐AR) agonist as a low‐molecular‐weight compound that interferes with the acquisition of mesenchymal phenotypes of oral cancer cells. Treatment of multiple types of oral cancer cells with isoxsuprine led to the downregulation of mesenchymal cell markers that was accompanied by reduced cell motility. Similar inhibitory effects were also observed for isoprenaline, a non‐selective β‐adrenergic receptor (β‐AR) agonist. In addition, inhibition of cell migration upon treatment with isoxsuprine was reverted by a non‐selective β‐AR antagonist, propranolol, and the CRISPR/Cas9 system‐mediated deletion of the β2‐AR gene, suggesting that the effects exerted by isoxsuprine involved signals mediated by β2‐AR. In addition, in a subcutaneous xenograft model of oral cancer cells, the administration of isoxsuprine effectively suppressed primary tumor growth, suggesting β2‐AR signals to be a promising cancer therapeutic target for treatment of OSCC. In this study we identified isoxsuprine, a β2‐adrenergic receptor agonist as an effective inhibitor of mesenchymal phenotypes and migration of oral squamous cell carcinoma cells suggesting that β2‐adrenergic receptor signal is a new promising therapeutic target for treatment of oral cancer.
Journal Article
Light-Driven Flying Balloons Based on Hybrids of Carbon Nanotubes and Cellulose Nanofibers
We have fabricated nanocarbon-based palm-sized cubic paper balloons that can be levitated by light irradiation. These paper balloons are composed of carbon nanotube (CNT) freestanding films and cellulose nanofiber (CNF) freestanding films. The number of CNT freestanding films (NCNT) and the number of CNF freestanding films (6-NCNT) among the six walls of the cube were varied. We investigated the effect of NCNT on the levitation behaviors under light irradiation. We found that the balloons were levitated when NCNT was greater than or equal to two. The levitation height was found to be increased by increasing NCNT.
Journal Article
Subclonal accumulation of immune escape mechanisms in microsatellite instability-high colorectal cancers
BackgroundIntratumor heterogeneity (ITH) in microsatellite instability-high (MSI-H) colorectal cancer (CRC) has been poorly studied. We aimed to clarify how the ITH of MSI-H CRCs is generated in cancer evolution and how immune selective pressure affects ITH.MethodsWe reanalyzed public whole-exome sequencing data on 246 MSI-H CRCs. In addition, we performed a multi-region analysis from 6 MSI-H CRCs. To verify the process of subclonal immune escape accumulation, a novel computational model of cancer evolution under immune pressure was developed.ResultsOur analysis presented the enrichment of functional genomic alterations in antigen-presentation machinery (APM). Associative analysis of neoantigens indicated the generation of immune escape mechanisms via HLA alterations. Multiregion analysis revealed the clonal acquisition of driver mutations and subclonal accumulation of APM defects in MSI-H CRCs. Examination of variant allele frequencies demonstrated that subclonal mutations tend to be subjected to selective sweep. Computational simulations of tumour progression with the interaction of immune cells successfully verified the subclonal accumulation of immune escape mutations and suggested the efficacy of early initiation of an immune checkpoint inhibitor (ICI) -based treatment.ConclusionsOur results demonstrate the heterogeneous acquisition of immune escape mechanisms in MSI-H CRCs by Darwinian selection, providing novel insights into ICI-based treatment strategies.
Journal Article
Ktedonoketone and 2’-oxosattabacin, benzenoid metabolites from a thermophilic bacterium Thermosporothrix hazakensis in the phylum Chloroflexi
A thermophilic bacterium Thermosporothrix hazakensis NBRC 105916 which belongs to the class Ktedonobacteria was investigated to explore its biosynthetic potential of secondary metabolites. UV-guided fractionation led to the identification of a new benzenoid metabolite designated ktedonoketone (6) and an α-diketone metabolite 2’-oxosattabacin (7) along with five known compounds. Compound 7 was previously described as a synthetic compound, but this is the first finding as a natural product. Compound 7 induced adipocyte differentiation at 10–20 μM and autophagy at 1–10 μM. Compound 6 showed weak inducing activity of adipocyte differentiation. The biosynthetic origin of hazakacin (3), an acyloin-type compound, was elucidated by 13C-labeled precursor-feeding experiments.
Journal Article