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Article ; Online: Hansen Solubility Parameter Analysis on Dispersion of Oleylamine-Capped Silver Nanoinks and their Sintered Film Morphology

Satoshi Saita / Shin-ichi Takeda / Hideya Kawasaki

Nanomaterials, Vol 12, Iss 2004, p

2022 Volume 2004

Abstract: Optimizing stabilizers and solvents is crucial for obtaining highly dispersed nanoparticle inks. Generally, nonpolar (hydrophobic) ligand-stabilized nanoparticles show superior dispersibility in nonpolar solvents, whereas polar ligand (hydrophilic)- ... ...

Abstract	Optimizing stabilizers and solvents is crucial for obtaining highly dispersed nanoparticle inks. Generally, nonpolar (hydrophobic) ligand-stabilized nanoparticles show superior dispersibility in nonpolar solvents, whereas polar ligand (hydrophilic)-stabilized nanoparticles exhibit high dispersibility in polar solvents. However, these properties are too qualitative to select optimum stabilizers and solvents for stable nanoparticle inks, and researchers often rely on their experiences. This study presents a Hansen solubility parameter (HSP)-based analysis of the dispersibility of oleylamine-capped silver nanoparticle (OAm-Ag NP) inks for optimizing ink preparation. We determined the HSP sphere of the OAm-Ag NPs, defined as the center coordinate, and the interaction radius in 3D HSP space. The solvent’s HSP inside the HSP sphere causes high dispersibility of the OAm-Ag NPs in the solvent. In contrast, the HSPs outside the sphere resulted in low dispersibility in the solvent. Thus, we can quantitatively predict the dispersibility of the OAm-Ag NPs in a given solvent using the HSP approach. Moreover, the HSP sphere method can establish a correlation between the dispersibility of the particles in inks and the sintered film morphology, facilitating electronic application of the nanoparticle inks. The HSP method is also helpful for optimizing stabilizers and solvents for stable nanoparticle inks in printed electronics.
Keywords	Hansen solubility parameter ; dispersibility ; Ag nanoparticles ; oleylamine ; nanoink ; printed electronics ; Chemistry ; QD1-999
Subject code	660 ; 500
Language	English
Publishing date	2022-06-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Dataset for surface and internal damage after impact on CFRP laminates

Saki Hasebe / Ryo Higuchi / Tomohiro Yokozeki / Shin-ichi Takeda

Data in Brief, Vol 43, Iss , Pp 108462- (2022)

2022

Abstract: Various foreign objects can collide with CFRP structures, such as CFRP aircraft. Once something impacts with CFRP laminates, both surface damage and internal damage can occur. Even if the external damage is such invisible as called barely visible impact ... ...

Abstract	Various foreign objects can collide with CFRP structures, such as CFRP aircraft. Once something impacts with CFRP laminates, both surface damage and internal damage can occur. Even if the external damage is such invisible as called barely visible impact damage, there are matrix cracks or delamination that are the main cause of compressive strength reduction, so it is difficult to find the relationship between external and internal damage on CFRP laminates. This dataset is prepared for predicting impact information only from surface damage profiles using Machine Learning (Hasebe et al., 2022). It includes three data, surface damage image (png), surface depth contour image(png), and internal damage image after ultrasound C-scanning (jpg) after low-velocity impact testing under various impact conditions. The data are helpful for researchers and engineers who deal with the impact behavior of CFRP or data science.
Keywords	BVID ; Machine learning ; Thermoset CFRP ; Non-destructive testing ; Computer applications to medicine. Medical informatics ; R858-859.7 ; Science (General) ; Q1-390
Subject code	306
Language	English
Publishing date	2022-08-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Periostin Is Required for the Maintenance of Muscle Fibers during Muscle Regeneration

Naoki Ito / Yuko Miyagoe-Suzuki / Shin’ichi Takeda / Akira Kudo

International Journal of Molecular Sciences, Vol 22, Iss 3627, p

2021 Volume 3627

Abstract: Skeletal muscle regeneration is a well-organized process that requires remodeling of the extracellular matrix (ECM). In this study, we revealed the protective role of periostin, a matricellular protein that binds to several ECM proteins during muscle ... ...

Abstract	Skeletal muscle regeneration is a well-organized process that requires remodeling of the extracellular matrix (ECM). In this study, we revealed the protective role of periostin, a matricellular protein that binds to several ECM proteins during muscle regeneration. In intact muscle, periostin was localized at the neuromuscular junction, muscle spindle, and myotendinous junction, which are connection sites between muscle fibers and nerves or tendons. During muscle regeneration, periostin exhibited robustly increased expression and localization at the interstitial space. Periostin- null mice showed decreased muscle weight due to the loss of muscle fibers during repeated muscle regeneration. Cultured muscle progenitor cells from periostin- null mice showed no deficiencies in their proliferation, differentiation, and the expression of Pax7, MyoD, and myogenin, suggesting that the loss of muscle fibers in periostin- null mice was not due to the impaired function of muscle stem/progenitor cells. Periostin- null mice displayed a decreased number of CD31-positive blood vessels during muscle regeneration, suggesting that the decreased nutritional supply from blood vessels was the cause of muscle fiber loss in periostin- null mice. These results highlight the novel role of periostin in maintaining muscle mass during muscle regeneration.
Keywords	skeletal muscle regeneration ; extracellular matrix ; periostin ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Language	English
Publishing date	2021-03-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Changes in cytosolic Ca2+ dynamics in the sarcoplasmic reticulum associated with the pathology of Duchenne muscular dystrophy

Jun Tanihata / Shin’ichi Takeda

Journal of Physical Fitness and Sports Medicine, Vol 5, Iss 4, Pp 309-

2016 Volume 312

Abstract: Duchenne muscular dystrophy (DMD) is a life-limiting X-linked genetic disorder caused by a lack of the membrane-associated protein dystrophin. The absence of dystrophin increases the susceptibility of muscle fibers to damage. Repeated damage results in ... ...

Abstract	Duchenne muscular dystrophy (DMD) is a life-limiting X-linked genetic disorder caused by a lack of the membrane-associated protein dystrophin. The absence of dystrophin increases the susceptibility of muscle fibers to damage. Repeated damage results in ineffective muscle repair and the development of pseudo-hypertrophied muscles; these bulky muscles are weak despite their size. The mechanisms underlying the functional impairments in dystrophic muscle have not yet been fully determined. However, several recent studies indicate that elevated intracellular Ca2+ homeostasis is a cause or facilitator of the development of muscle weakness in DMD. This review focuses on abnormalities of Ca2+ homeostasis and the possibilities for treatment by counteracting the Ca2+ dysregulation.
Keywords	duchenne muscular dystrophy ; ca2+ homeostasis ; sarcoplasmic reticulum (sr) ; ryanodine receptor (ryr1) ; sarcoplasmic endoplasmic reticulum atpase (serca) ; Sports medicine ; RC1200-1245 ; Physiology ; QP1-981
Subject code	570
Language	English
Publishing date	2016-10-01T00:00:00Z
Publisher	Japanese Society of Physical Fitness and Sports Medicine
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: ATP-Induced Increase in Intracellular Calcium Levels and Subsequent Activation of mTOR as Regulators of Skeletal Muscle Hypertrophy

Naoki Ito / Urs T. Ruegg / Shin’ichi Takeda

International Journal of Molecular Sciences, Vol 19, Iss 9, p

2018 Volume 2804

Abstract: Intracellular signaling pathways, including the mammalian target of rapamycin (mTOR) and the mitogen-activated protein kinase (MAPK) pathway, are activated by exercise, and promote skeletal muscle hypertrophy. However, the mechanisms by which these ... ...

Abstract	Intracellular signaling pathways, including the mammalian target of rapamycin (mTOR) and the mitogen-activated protein kinase (MAPK) pathway, are activated by exercise, and promote skeletal muscle hypertrophy. However, the mechanisms by which these pathways are activated by physiological stimulation are not fully understood. Here we show that extracellular ATP activates these pathways by increasing intracellular Ca2+ levels ([Ca2+]i), and promotes muscle hypertrophy. [Ca2+]i in skeletal muscle was transiently increased after exercise. Treatment with ATP induced the increase in [Ca2+]i through the P2Y2 receptor/inositol 1,4,5-trisphosphate receptor pathway, and subsequent activation of mTOR in vitro. In addition, the ATP-induced increase in [Ca2+]i coordinately activated Erk1/2, p38 MAPK and mTOR that upregulated translation of JunB and interleukin-6. ATP also induced an increase in [Ca2+]i in isolated soleus muscle fibers, but not in extensor digitorum longus muscle fibers. Furthermore, administration of ATP led to muscle hypertrophy in an mTOR- and Ca2+-dependent manner in soleus, but not in plantaris muscle, suggesting that ATP specifically regulated [Ca2+]i in slow muscles. These findings suggest that ATP and [Ca2+]i are important mediators that convert mechanical stimulation into the activation of intracellular signaling pathways, and point to the P2Y receptor as a therapeutic target for treating muscle atrophy.
Keywords	skeletal muscle ; muscle hypertrophy ; muscle atrophy ; ATP ; Ca2+ ; P2Y receptor ; IP3 receptor ; mammalian target of rapamycin (mTOR) ; mitogen-activated protein kinase (MAPK) ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Language	English
Publishing date	2018-09-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Role of Ca2+ signaling in skeletal muscle hypertrophy and atrophy

Naoki Ito / Shin’ichi Takeda

Journal of Physical Fitness and Sports Medicine, Vol 4, Iss 2, Pp 171-

2015 Volume 176

Abstract: Skeletal muscle maintains an adequate volume that is commensurate with its surrounding environment. Although intracellular signaling molecules and pathways underlying the regulation of protein synthesis/degradation and subsequent muscle hypertrophy/ ... ...

Abstract	Skeletal muscle maintains an adequate volume that is commensurate with its surrounding environment. Although intracellular signaling molecules and pathways underlying the regulation of protein synthesis/degradation and subsequent muscle hypertrophy/atrophy are well studied, upstream regulators are largely unknown. In this review, we summarize the recent advances relating to the role of Ca2+ signaling as an upstream regulator of intracellular signaling pathways that regulate muscle plasticity, suggesting a new therapeutic target to control muscle mass.
Keywords	skeletal muscle ; muscle hypertrophy ; muscle atrophy ; ca2+ ; calcium signaling ; Sports medicine ; RC1200-1245 ; Physiology ; QP1-981
Language	English
Publishing date	2015-05-01T00:00:00Z
Publisher	Japanese Society of Physical Fitness and Sports Medicine
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Antioxidants restore store‐operated Ca2+ entry in patient‐iPSC‐derived myotubes with tubular aggregate myopathy‐associated Ile484ArgfsX21 STIM1 mutation via upregulation of binding immunoglobulin protein

Fusako Sakai‐Takemura / Fumiaki Saito / Ken'ichiro Nogami / Yusuke Maruyama / Ahmed Elhussieny / Kiichiro Matsumura / Shin'ichi Takeda / Yoshitsugu Aoki / Yuko Miyagoe‐Suzuki

FASEB BioAdvances, Vol 5, Iss 11, Pp 453-

2023 Volume 469

Abstract: Abstract Store‐operated Ca2+ entry (SOCE) is indispensable for intracellular Ca2+ homeostasis in skeletal muscle, and constitutive activation of SOCE causes tubular aggregate myopathy (TAM). To understand the pathogenesis of TAM, we induced pluripotent ... ...

Abstract	Abstract Store‐operated Ca2+ entry (SOCE) is indispensable for intracellular Ca2+ homeostasis in skeletal muscle, and constitutive activation of SOCE causes tubular aggregate myopathy (TAM). To understand the pathogenesis of TAM, we induced pluripotent stem cells (iPSCs) from a TAM patient with a rare mutation (c.1450_1451insGA; p. Ile484ArgfsX21) in the STIM1 gene. This frameshift mutation produces a truncated STIM1 with a disrupted C‐terminal inhibitory domain (CTID) and was reported to diminish SOCE. Myotubes induced from the patient's‐iPSCs (TAM myotubes) showed severely impaired SOCE, but antioxidants greatly restored SOCE partly via upregulation of an endoplasmic reticulum (ER) chaperone, BiP (GRP78), in the TAM myotubes. Our observation suggests that antioxidants are promising tools for treatment of TAM caused by reduced SOCE.
Keywords	antioxidants ; binding immunoglobulin protein ; calcium ; calcium release‐activated calcium channel protein 1 (ORAI1) ; induced pluripotent stem cells ; skeletal muscle ; Biology (General) ; QH301-705.5
Language	English
Publishing date	2023-11-01T00:00:00Z
Publisher	Wiley
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Establishment of a Triple Quadrupole HPLC-MS Quantitation Method for Dystrophin Protein in Mouse and Human Skeletal Muscle

Tsukasa Tominari / Masaru Takatoya / Toshiya Matsubara / Michio Matsunobe / Daichi Arai / Chiho Matsumoto / Michiko Hirata / Shosei Yoshinouchi / Chisato Miyaura / Yoshifumi Itoh / Hirofumi Komaki / Shin’ichi Takeda / Yoshitsugu Aoki / Masaki Inada

International Journal of Molecular Sciences, Vol 25, Iss 1, p

2023 Volume 303

Abstract: Duchenne muscular dystrophy (DMD) is the most common type of neuromuscular disease caused by mutations in the DMD gene encoding dystrophin protein. To quantitively assess human dystrophin protein in muscle biopsy samples, it is imperative to consistently ...

Abstract	Duchenne muscular dystrophy (DMD) is the most common type of neuromuscular disease caused by mutations in the DMD gene encoding dystrophin protein. To quantitively assess human dystrophin protein in muscle biopsy samples, it is imperative to consistently detect as low as 0.003% of the dystrophin protein relative to the total muscle protein content. The quantitation of dystrophin protein has traditionally been conducted using semiquantitative immunoblotting or immunohistochemistry; however, there is a growing need to establish a more precise quantitative method by employing liquid chromatography-mass spectrometry (LC-MS) to measure dystrophin protein. In this study, a novel quantification method was established using a mouse experiment platform applied to the clinical quantification of human dystrophin protein. The method using a spike-in approach with a triple quadrupole LC-MS quantitated the amount of dystrophin in wild-type and human DMD transgenic mice but not in DMD-null mice. In conclusion, we established a quantitating method of dystrophin using HPLC-LC-MS with a novel spike-in approach. These results indicate that our methodology could be applied to several LC-MS devices to enable the accurate measurement of dystrophin protein in patients with DMD.
Keywords	dystrophin ; Duchenne muscular dystrophy ; LC-MS ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Language	English
Publishing date	2023-12-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Enhanced cell survival and therapeutic benefits of IL-10-expressing multipotent mesenchymal stromal cells for muscular dystrophy

Yuko Nitahara-Kasahara / Mutsuki Kuraoka / Yuki Oda / Hiromi Hayashita-Kinoh / Shin’ichi Takeda / Takashi Okada

Stem Cell Research & Therapy, Vol 12, Iss 1, Pp 1-

2021 Volume 15

Abstract: Abstract Background Multipotent mesenchymal stromal cells (MSCs) are potentially therapeutic for muscle disease because they can accumulate at the sites of injury and act as immunosuppressants. MSCs are attractive candidates for cell-based strategies ... ...

Abstract	Abstract Background Multipotent mesenchymal stromal cells (MSCs) are potentially therapeutic for muscle disease because they can accumulate at the sites of injury and act as immunosuppressants. MSCs are attractive candidates for cell-based strategies that target diseases with chronic inflammation, such as Duchenne muscular disease (DMD). We focused on the anti-inflammatory properties of IL-10 and hypothesized that IL-10 could increase the typically low survival of MSCs by exerting a paracrine effect after transplantation. Methods We developed a continuous IL-10 expression system of MSCs using an adeno-associated virus (AAV) vector. To investigate the potential benefits of IL-10 expressing AAV vector-transduced MSCs (IL-10-MSCs), we examined the cell survival rates in the skeletal muscles after intramuscular injection into mice and dogs. Systemic treatment with IL-10-MSCs derived from dental pulp (DPSCs) was comprehensively analyzed using the canine X-linked muscular dystrophy model in Japan (CXMDJ), which has a severe phenotype similar to that of DMD patients. Results In vivo bioluminescence imaging analysis revealed higher retention of IL-10-MSCs injected into the hindlimb muscle of mice. In the muscles of dogs, myofiber-like tissue was formed after the stable engraftment of IL-10-MSCs. Repeated systemic administration of IL-10-DPSCs into the CXMDJ model resulted in long-term engraftment of cells and slightly increased the serum levels of IL-10. IL-10-hDPSCs showed significantly reduced expression of pro-inflammatory MCP-1 and upregulation of stromal-derived factor-1 (SDF-1). MRI and histopathology of the hDPSC-treated CXMDJ indicated the regulation of inflammation in the muscles, but not myogenic differentiation from treated cells. hDPSC-treated CXMDJ showed improved running capability and recovery in tetanic force with concomitant increase in physical activity. Serum creatine kinase levels, which increased immediately after exercise, were suppressed in IL-10-hDPSC-treated CXMDJ. Conclusions In case of local ...
Keywords	Mesenchymal stromal cells ; IL-10 ; DMD ; Dental pulp stromal cells ; Medicine (General) ; R5-920 ; Biochemistry ; QD415-436
Subject code	610 ; 570
Language	English
Publishing date	2021-02-01T00:00:00Z
Publisher	BMC
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Current Challenges and Future Directions in Recombinant AAV-Mediated Gene Therapy of Duchenne Muscular Dystrophy

Shin'ichi Takeda / Takashi Okada

Pharmaceuticals, Vol 6, Iss 7, Pp 813-

2013 Volume 836

Abstract: Various characteristics of adeno-associated virus (AAV)-based vectors with long-term safe expression have made it an exciting transduction tool for clinical gene therapy of Duchenne muscular dystrophy (DMD). Although host immune reactions against the ... ...

Abstract	Various characteristics of adeno-associated virus (AAV)-based vectors with long-term safe expression have made it an exciting transduction tool for clinical gene therapy of Duchenne muscular dystrophy (DMD). Although host immune reactions against the vector as well as transgene products were detected in some instances of the clinical studies, there have been promising observations. Methods of producing AAV vectors for considerable in vivo experimentation and clinical investigations have been developed and a number of studies with AAV vector-mediated muscle transduction were attempted. Notably, an intravenous limb perfusion transduction technique enables extensive transgene expression in the skeletal muscles without noticeable adverse events. Furthermore, cardiac transduction by the rAAV9-microdystrophin would be promising to prevent development of cardiac dysfunction. Recent achievements in transduction technology suggest that long-term transgene expression with therapeutic benefits in DMD treatment would be achieved by the rAAV-mediated transduction strategy with an adequate regimen to regulate host immune response.
Keywords	DMD ; AAV ; immune response ; Medicine ; R ; Pharmacy and materia medica ; RS1-441
Language	English
Publishing date	2013-06-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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