Tuning Electrocatalytic Activities of Dealloyed Nanoporous Catalysts by Macroscopic Strain Engineering.

It is technically challenging to quantitatively apply strains to tune catalysis because most heterogeneous catalysts are nanoparticles, and lattice strains can only be applied indirectly via core-shell structures or crystal defects. Herein, we report quantitative relations between macroscopic strains and hydrogen evolution reaction (HER) activities of dealloyed nanoporous gold (NPG) by directly applying macroscopic strains upon bulk NPG. It was found that macroscopic compressive strains lead to a decrease, while macroscopic tensile strains improve the HER activity of NPG, which is in line with the d-band center model. The overpotential and onset potential of HER display approximately a linear relation with applied macroscopic strains, revealing an ∼2.9 meV decrease of the binding energy per 0.1% lattice strains from compressive to tensile. The methodology with the high strain sensitivity of electrocatalysis, developed in this study, paves a new way to investigate the insights of strain-dependent electrocatalysis with high precision.

Stereolithography 3D Printed Carbon Microlattices with Hierarchical Porosity for Structural and Functional Applications.

Hierarchically porous carbon microlattices (HPCMLs) fabricated by using a composite photoresin and stereolithography (SLA) 3D printing is reported. Containing magnesium oxide nanoparticles (MgO NPs) as porogens and multilayer graphene nanosheets as UV-scattering inhibitors, the composite photoresin is formed to simple cubic microlattices with digitally designed porosity of 50%. After carbonization in vacuum at 1000 °C and chemical removal of MgO NPs, it is realized that carbon microlattices possessing hierarchical porosity are composed of the lattice architecture (≈100 µm), macropores (≈5 µm), mesopores (≈50 nm), and micropores (≈1 nm). The linear shrinkage after pyrolysis is as small as 33%. Compressive strength of 7.45 to 10.45 MPa and Young's modulus of 375 to 736 MPa are achieved, proving HPCMLs a robust mechanical component among reported carbon materials with a random pore structure. Having a few millimeters in thickness, the HPCMLs can serve as thick supercapacitor electrodes that demonstrate gravimetric capacitances 105 and 13.8 F g-1 in aqueous and organic electrolyte, reaching footprint areal capacitances beyond 10 and 1 F cm-2 , respectively. The results present that the composite photoresin for SLA can yield carbon microarchitectures that integrate structural and functional properties for structural energy storages .

A 3D-Printed, Freestanding Carbon Lattice for Sodium Ion Batteries.

Increasing mass loadings of battery electrodes critically enhances the energy density of an overall battery by eliminating much of the inactive components, while compacting the battery size and lowering the costs of the ingredients. A hard carbon microlattice, digitally designed and fabricated by stereolithography 3D-printing and pyrolysis, offers enormous potential for high-mass-loading electrodes. In this work, sodium-ion batteries using hard carbon microlattices produced by an inexpensive 3D printer are demonstrated. Controlled periodic carbon microlattices are created with enhanced ion transport through microchannels. Carbon microlattices with a beam width of 32.8 µm reach a record-high areal capacity of 21.3 mAh cm-2 at a loading of 98 mg cm-2 without degrading performance, which is much higher than the conventional monolithic electrodes (≈5.2 mAh cm-2 at 92 mg cm-2 ). Furthermore, binder-free, pure-carbon elements of microlattices enable the tracking of structural changes in hard carbon that support the hypothesized intercalation of ions at plateau regions by temporal ex situ X-ray diffraction measurements. These results will advance the development of high-performance and low-cost anodes for sodium-ion batteries as well as help with understanding the mechanisms of ion intercalations in hard carbon, expanding the utilities of 3D-printed carbon architectures in both applications and fundamental studies.

Effect of Local Atomic Structure on Sodium Ion Storage in Hard Amorphous Carbon.

The fundamental understanding of sodium storage mechanisms in amorphous carbon is essential to develop high-performance anode materials for sodium-ion batteries. However, the intrinsic relation between the structure of amorphous carbon and Na+ storage remains to be debated due to the difficulty in controlling and characterizing the local atomic configurations of amorphous carbon. Here we report quantitative measurements of Na+ storage in a low-temperature dealloyed hard carbon with a tunable local structure from completely disordered micropores to gradually increased graphitic order domains. The structure-capacity-potential correlation not only verifies the disputing "adsorption-intercalation" mechanisms, i.e., Na+ intercalation into local graphitic domains for the low-voltage plateaus and adsorption in fully disordered carbon for the sloping voltage profiles, but also unveils a new mechanism of Na+ adsorption on defective sites of graphitic carbon in the medium-potential sloping region. The quantitative investigations provide essential insights into the reaction mechanisms of Na+ with amorphous carbon for designing advanced sodium-ion battery anodes.

Periostin Is Required for the Maintenance of Muscle Fibers during Muscle Regeneration.

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.

Reiterative expression of pax1 directs pharyngeal pouch segmentation in medaka.

A striking characteristic of vertebrate development is the pharyngeal arches, which are a series of bulges on the lateral surface of the head of vertebrate embryos. Although each pharyngeal arch is segmented by the reiterative formation of endodermal outpocketings called pharyngeal pouches, the molecular network underlying the reiterative pattern remains unclear. Here, we show that pax1 plays crucial roles in pouch segmentation in medaka (Oryzias latipes) embryos. Importantly, pax1 expression in the endoderm prefigures the location of the next pouch before the cells bud from the epithelium. TALEN-generated pax1 mutants did not form pharyngeal pouches posterior to the second arch. Segmental expression of tbx1 and fgf3, which play essential roles in pouch development, was almost non-existent in the pharyngeal endoderm of pax1 mutants, with disturbance of the reiterative pattern of pax1 expression. These results suggest that pax1 plays a key role in generating the primary pattern for segmentation in the pharyngeal endoderm by regulating tbx1 and fgf3 expression. Our findings illustrate the crucial roles of pax1 in vertebrate pharyngeal segmentation and provide insights into the evolutionary origin of the deuterostome gill slit.

Fgf signalling controls diverse aspects of fin regeneration.

Studies have shown that fibroblast growth factor (Fgf) signalling is necessary for appendage regeneration, but its exact function and the ligands involved during regeneration have not yet been elucidated. Here, we performed comprehensive expression analyses and identified fgf20a and fgf3/10a as major Fgf ligands in the wound epidermis and blastema, respectively. To reveal the target cells and processes of Fgf signalling, we performed a transplantation experiment of mesenchymal cells that express the dominant-negative Fgf receptor 1 (dnfgfr1) under control of the heat-shock promoter. This mosaic knockdown analysis suggested that Fgf signalling is directly required for fin ray mesenchyme to form the blastema at the early pre-blastema stage and to activate the regenerative cell proliferation at a later post-blastema stage. These results raised the possibility that the early epidermal Fgf20a and the later blastemal Fgf3/10a could be responsible for these respective processes. We demonstrated by gain-of-function analyses that Fgf20a induces the expression of distal blastema marker junbl, and that Fgf3 promotes blastema cell proliferation. Our study highlights that Fgfs in the wound epidermis and blastema have distinct functions to regulate fin regeneration cooperatively.

Naming, History, Future.

The history of periostin and the mechanism of periostin in fibrillogenesis are described. Periostin is a matricellular protein and involved in incurable diseases.

The Structure of the Periostin Gene, Its Transcriptional Control and Alternative Splicing, and Protein Expression.

Although many studies have described the role of periostin in various diseases, the functions of periostin derived from alternative splicing and proteinase cleavage at its C-terminus remain unknown. Further experiments investigating the periostin structures that are relevant to diseases are essential for an in-depth understanding of their functions, which would accelerate their clinical applications by establishing new approaches for curing intractable diseases. Furthermore, this understanding would enhance our knowledge of novel functions of periostin related to stemness and response to mechanical stress .

Periostin in Bone Biology.

Periostin is specifically expressed in periosteum that functions in bone modeling and remodeling and bone repair, and is sensitive to mechanical stress. Thus periostin has been expected for controlling these crucial systems in bone. The results from periostin deficient mice demonstrate that periostin acts on bone remodeling though detailed mechanisms are unknown. Recent findings have revealed that periostin is essential for bone repair. In this chapter, I introduce expression and function of periostin in bone.

Liver, Stroke, Rhinosinusitis.

In addition to main types of fibrosis, other types of fibrosis in incredible diseases have been reported. Among them, liver fibrosis, stroke, and rhinosinusitis are described as new cases of periostin action. To understand periostin function in a new area of fibrosis linked with inflammation, periostin can be used as a new tool to elucidate the mechanisms of unknown diseases.

Clinical Applications Targeting Periostin.

Since periostin is expressed and functioned in incredible diseases , clinical applications have been initiated to directly target periostin for inhibition or activation, or periostin expression is utilized to indicate the disease state or a marker for curing diseases, which will provide novel methods in clinical applications.

Periostin deletion suppresses late-phase response in mouse experimental allergic conjunctivitis.

BACKGROUND: To investigate the potential roles of periostin (POSTN), an extracellular matrix preferentially expressed in Th2-skewed conditions in the pathophysiology of allergic conjunctivitis. METHODS: The roles of POSTN in ragweed-induced experimental allergic conjunctivitis (RW-EAC) were evaluated using both POSTN-knockout (KO) and congenic BALB/c wild-type mice. Histological analysis was carried out to enumerate eosinophils/basophils in the conjunctival tissue. Th2 cytokine expression was evaluated by quantitative polymerase chain reaction (Q-PCR), and microarray analysis was performed to elucidate genes differentially expressed in POSTN-KO and wild-type mice in the RW-EAC model. RESULTS: Upregulation of POSTN expression and eosinophil infiltration was observed in subconjunctival tissue of RW-EAC in the wild-type mice. The number of infiltrating eosinophils in the conjunctivae of RW-EAC was diminished in POSTN-KO mice compared to wild-type mice. Q-PCR analysis of conjunctival tissue showed induction of Th2 cytokine (Ccl5, Il4, Il5, Il13) expression in the RW-EAC and attenuated Ccl5, Il4, Il13 mRNA expression in the conjunctivae of the RW-EAC using POSTN-KO mice. Microarray analysis and immunohistochemical analysis showed diminished basophil marker (Mcpt8) expression and reduced numbers of infiltrating basophils in the conjunctivae of RW-EAC in POSTN-KO mice. CONCLUSIONS: POSTN expression in conjunctival tissue plays an indispensable role in the late-phase reaction of the RW-EAC model by facilitating eosinophil/basophil infiltration and augmenting Th2 cytokine expression.

Low-Temperature Growth of Carbon Nanotubes Catalyzed by Sodium-Based Ingredients.

Synthesis of low-dimensional carbon nanomaterials such as carbon nanotubes (CNTs) is a key driver for achieving advances in energy storage, computing, and multifunctional composites, among other applications. Here, we report high-yield thermal chemical vapor deposition (CVD) synthesis of CNTs catalyzed by reagent-grade common sodium-containing compounds, including NaCl, NaHCO3 , Na2 CO3 , and NaOH, found in table salt, baking soda, and detergents, respectively. Coupled with an oxidative dehydrogenation reaction to crack acetylene at reduced temperatures, Na-based nanoparticles have been observed to catalyze CNT growth at temperatures below 400 °C. Ex situ and in situ transmission electron microscopy (TEM) reveal unique CNT morphologies and growth characteristics, including a vaporizing Na catalyst phenomenon that we leverage to create CNTs without residual catalyst particles for applications that require metal-free CNTs. Na is shown to synthesize CNTs on numerous substrates, and as the first alkali group metal catalyst demonstrated for CNT growth, holds great promise for expanding the understanding of nanocarbon synthesis.

The sp7 gene is required for maturation of osteoblast-lineage cells in medaka (Oryzias latipes) vertebral column development.

Sp7 is a zinc finger transcription factor that is essential for osteoblast differentiation in mammals. To verify the characteristic features of osteoblast-lineage cells in teleosts, we established medaka sp7 mutants using a transcription activator-like effector nuclease (TALEN) genome editing system. These mutants showed severe defects in the formation of skeletal structures. In particular, the neural and the hemal arches were not formed, although the chordal centra were formed. Analysis of the transgenic medaka revealed that sp7 mutant had normal distribution of type X collagen a1 a (col10a1a)-positive osteoblast-like cells around the centrum and at the proximal region of the vertebral arch. The sp7 mutant phenotype could be rescued by exogenous sp7 expression in col10a1a-positive cells, as well as in sp7-positive osteoblast cells. Furthermore, runx2-positive osteoblast progenitors were observed on the vertebral arches, but not on the centrum, during vertebral column development. In addition, these osteoblast progenitors differentiated into the col10a1a-positive cells. In sp7 mutant, the runx2-positive cells were normally distributed at the region of unformed vertebral arch but failed to differentiate into col10a1a-positive cells. These results indicate that osteoblast-lineage cells undergo two distinct differentiation processes during development of the vertebral arch and the centrum. Nevertheless, our results verified that sp7 gene expression in osteoblast-lineage cells is required for differentiation into mature osteoblasts to form the vertebral column and other skeletal structures.

Periostin Promotes Scar Formation through the Interaction between Pericytes and Infiltrating Monocytes/Macrophages after Spinal Cord Injury.

Scar formation is a prominent pathological feature of traumatic central nervous system (CNS) injury, which has long been implicated as a major impediment to the CNS regeneration. However, the factors affecting such scar formation remain to be elucidated. We herein demonstrate that the extracellular matrix protein periostin (POSTN) is a key player in scar formation after traumatic spinal cord injury (SCI). Using high-throughput RNA sequencing data sets, we found that the genes involved in the extracellular region, such as POSTN, were significantly expressed in the injured spinal cord. The expression of POSTN peaked at 7 days after SCI, predominantly in the scar-forming pericytes. Notably, we found that genetic deletion of POSTN in mice reduced scar formation at the lesion site by suppressing the proliferation of the pericytes. Conversely, we found that recombinant POSTN promoted the migration capacity of the monocytes/macrophages and increased the expression of tumor necrosis factor-α from the monocytes/macrophages in vitro, which facilitated the proliferation of pericytes. Furthermore, we revealed that the pharmacological blockade of POSTN suppressed scar formation and improved the long-term functional outcome after SCI. Our findings suggest a potential mechanism whereby POSTN regulates the scar formation after SCI and provide significant evidence that POSTN is a promising therapeutic target for CNS injury.

Introductory review: periostin-gene and protein structure.

Although many studies have described the role of periostin in various diseases, the function of the periostin protein structures derived from alternative splicing and proteinase cleavage at the C-terminal remain unknown. Further experiments revealing the protein structures that are highly related to diseases are essential to understand the function of periostin in depth, which would accelerate its clinical application by establishing new approaches for curing intractable diseases. Furthermore, this understanding would enhance our knowledge of novel functions of periostin related to stemness and response to mechanical stress.

Osteoblast and osteoclast behaviors in the turnover of attachment bones during medaka tooth replacement.

Tooth replacement in polyphyodont is a well-organized system for maintenance of homeostasis of teeth, containing the dynamic structural change in skeletal tissues such as the attachment bone, which is the supporting element of teeth. Histological analyses have revealed the character of tooth replacement, however, the cellular mechanism of how skeletal tissues are modified during tooth replacement is largely unknown. Here, we showed the important role of osteoblasts for controlling osteoclasts to modify the attachment bone during tooth replacement in medaka pharyngeal teeth, coupled with an osterix-DsRed/TRAP-GFP transgenic line to visualize osteoblasts and osteoclasts. In the turnover of the row of attachment bones, these bones were resorbed at the posterior side where most developed functional teeth were located, and generated at the anterior side where teeth were newly erupted, which caused continuous tooth replacement. In the cellular analysis, osteoclasts and osteoblasts were located at attachment bones separately, since mature osteoclasts were localized at the resorbing side and osteoblasts gathered at the generating side. To demonstrate the role of osteoclasts in tooth replacement, we established medaka made deficient in c-fms-a by TALEN. c-fms-a deficient medaka showed hyperplasia of attachment bones along with reduced bone resorption accompanied by a low number of TRAP-positive osteoclasts, indicating an important role of osteoclasts in the turnover of attachment bones. Furthermore, nitroreductase-mediated osteoblast-specific ablation induced disappearance of osteoclasts, indicating that osteoblasts were essential for maintenance of osteoclasts for the proper turnover. Taken together, our results suggested that the medaka attachment bone provides the model to understand the cellular mechanism for tooth replacement, and that osteoblasts act in the coordination of bone morphology by supporting osteoclasts.

A diffusible signal derived from hematopoietic cells supports the survival and proliferation of regenerative cells during zebrafish fin fold regeneration.

Multicellular organisms maintain body integrity by constantly regenerating tissues throughout their lives; however, the overall mechanism for regulating regeneration remains an open question. Studies of limb and fin regeneration in teleost fish and urodeles have shown the involvement of a number of locally activated signals at the wounded site during regeneration. Here, we demonstrate that a diffusible signal from a distance also play an essential role for regeneration. Among a number of zebrafish mutants, we found that the zebrafish cloche (clo) and tal1 mutants, which lack most hematopoietic tissues, displayed a unique regeneration defect accompanying apoptosis in primed regenerative tissue. Our analyses of the mutants showed that the cells in the primed regenerative tissue are susceptible to apoptosis, but their survival is normally supported by the presence of hematopoietic tissues, mainly the myeloid cells. We further showed that a diffusible factor in the wild-type body fluid mediates this signal. Thus, our study revealed a novel mechanism that the hematopoietic tissues regulate tissue regeneration through a diffusible signal.

Periostin promotes secretion of fibronectin from the endoplasmic reticulum.

Extracellular matrix (ECM) proteins are synthesized in the endoplasmic reticulum (ER), transported to the extracellular milieu through the secretory pathway, and assembled into an extracellular architecture. A previous study of ours showed that periostin, a secretory protein, interacts with fibronectin and is involved in ECM remodeling. Here we show that periostin played a role in fibronectin secretion from the ER. Co-immunoprecipitation and in situ proximity ligation assays revealed an interaction between periostin and fibronectin in the ER. Although accumulation of fibronectin was detected in the ER of fibroblastic C3H10T1/2 cells, forced expression of periostin in those cells decreased the accumulation of fibronectin in the ER, suggesting that periostin promoted the secretion of fibronectin. A substitution mutant of tryptophan at the position 65 to alanine in the EMI domain of periostin, which caused periostin to lose its ability to interact with fibronectin, did not decrease the accumulation. Furthermore, targeted disruption of periostin in mice caused the non-fibrillar and ectopic deposition of fibronectin in the periodontal ligament. Thus, these results demonstrate a subcellular role of periostin in promotion of fibronectin secretion from the ER.