10 results on '"Kameda, Takuya"'
Search Results
2. Walking ability after resection of soft tissue sarcoma of the thigh and the sciatic nerve.
- Author
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Isobe, Mizuki, Hakozaki, Michiyuki, Kaneuchi, Yoichi, Ogawa, Itaru, Suzuki, Takeo, Sasaki, Nobuyuki, Kameda, Takuya, and Matsumoto, Yoshihiro
- Subjects
SCIATIC nerve ,SARCOMA ,SURGICAL margin ,THIGH - Abstract
Key Clinical Message: Walking ability may be fairly well maintained after sciatic nerve resection combined with wide resection of soft tissue sarcoma, therefore, surgeons should not hesitate to perform sciatic nerve resection to achieve an adequate surgical margin. [ABSTRACT FROM AUTHOR]
- Published
- 2024
- Full Text
- View/download PDF
3. Forearm compartment syndrome due to acquired hemophilia that required massive blood transfusions after fasciotomy: A case report
- Author
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Kameda, Takuya, primary, Yokota, Takeru, additional, Ejiri, Soichi, additional, and Konno, Shin-ichi, additional
- Published
- 2021
- Full Text
- View/download PDF
4. Expression and Activity of TRPA1 and TRPV1 in the Intervertebral Disc: Association with Inflammation and Matrix Remodeling
- Author
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Kameda, Takuya, Zvick, Joel, Vuk, Miriam, Sadowska, Aleksandra, Tam, Wai Kit, Leung, Victor Y., Bölcskei, Kata, Helyes, Zsuzsanna, Applegate, Lee Ann, Hausmann, Oliver N., Klasen, Juergen, Krupkova, Olga, and Wuertz-Kozak, Karin
- Subjects
musculoskeletal diseases ,collagen ,Nucleus Pulposus ,TRPV Cation Channels ,low back pain ,TRP channels ,pro-inflammatory cytokines ,aggrecanases ,TRPA1 ,TRPV1 ,TRPV2 ,TRPV4 ,TRPC6 ,Intervertebral Disc Degeneration ,Article ,lcsh:Chemistry ,Mice ,Animals ,Humans ,Calcium Signaling ,Intervertebral Disc ,TRPA1 Cation Channel ,lcsh:QH301-705.5 ,Physical and Theoretical Chemistry ,Inorganic Chemistry ,Organic Chemistry ,Spectroscopy ,Molecular Biology ,Catalysis ,General Medicine ,Computer Science Applications ,Inflammation ,Mice, Knockout ,musculoskeletal system ,Extracellular Matrix ,Gene Expression Regulation ,lcsh:Biology (General) ,lcsh:QD1-999 ,Inflammation Mediators ,psychological phenomena and processes - Abstract
Transient receptor potential (TRP) channels have emerged as potential sensors and transducers of inflammatory pain. The aims of this study were to investigate (1) the expression of TRP channels in intervertebral disc (IVD) cells in normal and inflammatory conditions and (2) the function of Transient receptor potential ankyrin 1 (TRPA1) and Transient receptor potential vanilloid 1 (TRPV1) in IVD inflammation and matrix homeostasis. RT-qPCR was used to analyze human fetal, healthy, and degenerated IVD tissues for the gene expression of TRPA1 and TRPV1. The primary IVD cell cultures were stimulated with either interleukin-1 beta (IL-1&beta, ) or tumor necrosis factor alpha (TNF-&alpha, ) alone or in combination with TRPA1/V1 agonist allyl isothiocyanate (AITC, 3 and 10 µ, M), followed by analysis of calcium flux and the expression of inflammation mediators (RT-qPCR/ELISA) and matrix constituents (RT-qPCR). The matrix structure and composition in caudal motion segments from TRPA1 and TRPV1 wild-type (WT) and knock-out (KO) mice was visualized by FAST staining. Gene expression of other TRP channels (A1, C1, C3, C6, V1, V2, V4, V6, M2, M7, M8) was also tested in cytokine-treated cells. TRPA1 was expressed in fetal IVD cells, 20% of degenerated IVDs, but not in healthy mature IVDs. TRPA1 expression was not detectable in untreated cells and it increased upon cytokine treatment, while TRPV1 was expressed and concomitantly reduced. In inflamed IVD cells, 10 µ, M AITC activated calcium flux, induced gene expression of IL-8, and reduced disintegrin and metalloproteinase with thrombospondin motifs 5 (ADAMTS5) and collagen 1A1, possibly via upregulated TRPA1. TRPA1 KO in mice was associated with signs of degeneration in the nucleus pulposus and the vertebral growth plate, whereas TRPV1 KO did not show profound changes. Cytokine treatment also affected the gene expression of TRPV2 (increase), TRPV4 (increase), and TRPC6 (decrease). TRPA1 might be expressed in developing IVD, downregulated during its maturation, and upregulated again in degenerative disc disease, participating in matrix homeostasis. However, follow-up studies with larger sample sizes are needed to fully elucidate the role of TRPA1 and other TRP channels in degenerative disc disease.
- Published
- 2019
- Full Text
- View/download PDF
5. Osmosensing, osmosignalling and inflammation
- Author
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Sadowska, Aleksandra, Kameda, Takuya, Krupkova, Olga, and Würtz-Kozak, Karin
- Subjects
ddc:540 ,Department Sport- und Gesundheitswissenschaften ,ddc:610 - Abstract
Intervertebral disc (IVD) cells are naturally exposed to high osmolarity and complex mechanical loading, which drive microenvironmental osmotic changes. Age- and degeneration-induced degradation of the IVD's extracellular matrix causes osmotic imbalance, which, together with an altered function of cellular receptors and signalling pathways, instigates local osmotic stress. Cellular responses to osmotic stress include osmoadaptation and activation of pro-inflammatory pathways. This review summarises the current knowledge on how IVD cells sense local osmotic changes and translate these signals into physiological or pathophysiological responses, with a focus on inflammation. Furthermore, it discusses the expression and function of putative membrane osmosensors (e.g. solute carrier transporters, transient receptor potential channels, aquaporins and acid-sensing ion channels) and osmosignalling mediators [e.g. tonicity responseelement-binding protein/nuclear factor of activated T-cells 5 (TonEBP/NFAT5), nuclear factor kappa-lightchain-enhancer of activated B cells (NF-kappa B)] in healthy and degenerated IVDs. Finally, an overview of the potential therapeutic targets for modifying osmosensing and osmosignalling in degenerated IVDs is provided.
- Published
- 2018
6. Osmosensing, osmosignalling and inflammation: how intervertebral disc cells respond to altered osmolarity
- Author
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Sadowska, Aleksandra, Kameda, Takuya, Krupkova, Olga, and Würtz-Kozak, Karin
- Subjects
lcsh:Diseases of the musculoskeletal system ,transient receptor potential channel ,lcsh:Surgery ,osmotic ,IVD ,inflammatory ,lcsh:RD1-811 ,degenerative disc disease ,Intervertebral disc degeneration ,osmolarity ,Transient receptor potential channels (TRP) ,tonicity-responsive enhancer binding protein ,aquaporin ,540 Chemie und zugeordnete Wissenschaften ,hyper-osmolarity ,lcsh:RC925-935 ,610 Medizin und Gesundheit ,hypo-osmolarity - Abstract
Intervertebral disc (IVD) cells are naturally exposed to high osmolarity and complex mechanical loading, which drive microenvironmental osmotic changes. Age- and degeneration-induced degradation of the IVD’s extracellular matrix causes osmotic imbalance, which, together with an altered function of cellular receptors and signalling pathways, instigates local osmotic stress. Cellular responses to osmotic stress include osmoadaptation and activation of pro-inflammatory pathways. This review summarises the current knowledge on how IVD cells sense local osmotic changes and translate these signals into physiological or pathophysiological responses, with a focus on inflammation. Furthermore, it discusses the expression and function of putative membrane osmosensors (e.g. solute carrier transporters, transient receptor potential channels, aquaporins and acid-sensing ion channels) and osmosignalling mediators [e.g. tonicity response-element-binding protein/nuclear factor of activated T-cells 5 (TonEBP/NFAT5), nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB)] in healthy and degenerated IVDs. Finally, an overview of the potential therapeutic targets for modifying osmosensing and osmosignalling in degenerated IVDs is provided., European Cells & Materials, 36, ISSN:1473-2262
- Published
- 2018
7. p38 MAPK Facilitates Crosstalk Between Endoplasmic Reticulum Stress and IL-6 Release in the Intervertebral Disc
- Author
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Krupkova, Olga, Sadowska, Aleksandra, Kameda, Takuya, Hitzl, Wolfgang, Hausmann, Oliver Nic, Klasen, Juergen, and Wuertz-Kozak, Karin
- Subjects
GRP78 ,IL-6 ,inflammation ,endoplasmic reticulum stress ,Department Sport- und Gesundheitswissenschaften ,intervertebral disc ,GADD153 ,ddc:610 ,p38 MAPK ,CHOP ,610 Medizin und Gesundheit ,Strukturbereich Kognitionswissenschaften - Abstract
Degenerative disc disease is associated with increased expression of pro-inflammatory cytokines in the intervertebral disc (IVD). However, it is not completely clear how inflammation arises in the IVD and which cellular compartments are involved in this process. Recently, the endoplasmic reticulum (ER) has emerged as a possible modulator of inflammation in age-related disorders. In addition, ER stress has been associated with the microenvironment of degenerated IVDs. Therefore, the aim of this study was to analyze the effects of ER stress on inflammatory responses in degenerated human IVDs and associated molecular mechanisms. Gene expression of ER stress marker GRP78 and pro-inflammatory cytokines IL-6, IL-8, IL-1β, and TNF-α was analyzed in human surgical IVD samples (n = 51, Pfirrmann grade 2–5). The expression of GRP78 positively correlated with the degeneration grade in lumbar IVDs and IL-6, but not with IL-1β and TNF-α. Another set of human surgical IVD samples (n = 25) was used to prepare primary cell cultures. ER stress inducer thapsigargin (Tg, 100 and 500 nM) activated gene and protein expression of IL-6 and induced phosphorylation of p38 MAPK. Both inhibition of p38 MAPK by SB203580 (10 µM) and knockdown of ER stress effector CCAAT-enhancer-binding protein homologous protein (CHOP) reduced gene and protein expression of IL-6 in Tg-treated cells. Furthermore, the effects of an inflammatory microenvironment on ER stress were tested. TNF-α (5 and 10 ng/mL) did not activate ER stress, while IL-1β (5 and 10 ng/mL) activated gene and protein expression of GRP78, but did not influence [Ca2+]i flux and expression of CHOP, indicating that pro-inflammatory cytokines alone may not induce ER stress in vivo. This study showed that IL-6 release in the IVD can be initiated following ER stress and that ER stress mediates IL-6 release through p38 MAPK and CHOP. Therapeutic targeting of ER stress response may reduce the consequences of the harsh microenvironment in degenerated IVD., Frontiers in Immunology, 9, ISSN:1664-3224
- Published
- 2018
- Full Text
- View/download PDF
8. Antibacterial effects of nano-imprinted moth-eye film in practical settings
- Author
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Yamada, Miho, primary, Minoura, Kiyoshi, additional, Mizoguchi, Takashi, additional, Nakamatsu, Kenichiro, additional, Taguchi, Tokio, additional, Kameda, Takuya, additional, Sekiguchi, Miho, additional, Suzutani, Tatsuo, additional, and Konno, Shinichi, additional
- Published
- 2018
- Full Text
- View/download PDF
9. Measurement of mechanical withdrawal thresholds and gait analysis using the CatWalk method in a nucleus pulposus-applied rodent model
- Author
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Kameda, Takuya, primary, Kaneuchi, Yoichi, additional, Sekiguchi, Miho, additional, and Konno, Shin-ichi, additional
- Published
- 2017
- Full Text
- View/download PDF
10. Expression and Activity of TRPA1 and TRPV1 in the Intervertebral Disc: Association with Inflammation and Matrix Remodeling.
- Author
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Zvick, Joel, Vuk, Miriam, Sadowska, Aleksandra, Krupkova, Olga, Kameda, Takuya, Wuertz-Kozak, Karin, Tam, Wai Kit, Leung, Victor Y., Bölcskei, Kata, Helyes, Zsuzsanna, Applegate, Lee Ann, Hausmann, Oliver N., and Klasen, Juergen
- Subjects
LUMBAR pain ,TRP channels ,CYTOKINES ,COLLAGEN ,INFLAMMATION - Abstract
Transient receptor potential (TRP) channels have emerged as potential sensors and transducers of inflammatory pain. The aims of this study were to investigate (1) the expression of TRP channels in intervertebral disc (IVD) cells in normal and inflammatory conditions and (2) the function of Transient receptor potential ankyrin 1 (TRPA1) and Transient receptor potential vanilloid 1 (TRPV1) in IVD inflammation and matrix homeostasis. RT-qPCR was used to analyze human fetal, healthy, and degenerated IVD tissues for the gene expression of TRPA1 and TRPV1. The primary IVD cell cultures were stimulated with either interleukin-1 beta (IL-1β) or tumor necrosis factor alpha (TNF-α) alone or in combination with TRPA1/V1 agonist allyl isothiocyanate (AITC, 3 and 10 µM), followed by analysis of calcium flux and the expression of inflammation mediators (RT-qPCR/ELISA) and matrix constituents (RT-qPCR). The matrix structure and composition in caudal motion segments from TRPA1 and TRPV1 wild-type (WT) and knock-out (KO) mice was visualized by FAST staining. Gene expression of other TRP channels (A1, C1, C3, C6, V1, V2, V4, V6, M2, M7, M8) was also tested in cytokine-treated cells. TRPA1 was expressed in fetal IVD cells, 20% of degenerated IVDs, but not in healthy mature IVDs. TRPA1 expression was not detectable in untreated cells and it increased upon cytokine treatment, while TRPV1 was expressed and concomitantly reduced. In inflamed IVD cells, 10 µM AITC activated calcium flux, induced gene expression of IL-8, and reduced disintegrin and metalloproteinase with thrombospondin motifs 5 (ADAMTS5) and collagen 1A1, possibly via upregulated TRPA1. TRPA1 KO in mice was associated with signs of degeneration in the nucleus pulposus and the vertebral growth plate, whereas TRPV1 KO did not show profound changes. Cytokine treatment also affected the gene expression of TRPV2 (increase), TRPV4 (increase), and TRPC6 (decrease). TRPA1 might be expressed in developing IVD, downregulated during its maturation, and upregulated again in degenerative disc disease, participating in matrix homeostasis. However, follow-up studies with larger sample sizes are needed to fully elucidate the role of TRPA1 and other TRP channels in degenerative disc disease. [ABSTRACT FROM AUTHOR]
- Published
- 2019
- Full Text
- View/download PDF
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