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Flexible and stretchable electronics have attractive applications inaccessible to conventional rigid electronics. However, the mainstream transfer printing techniques have challenges for electronic films in terms of thickness and size and limitations for target substrates in terms of curvature, depth, and interfacial adhesion. Here a facile, damage-free, and contamination-free soap film transfer printing technique is reported that enables the wrinkle-free transfer of ultrathin electronic films, precise alignment in a transparent manner, and conformal and adhesion-independent printing onto various substrates, including those too topographically and adhesively challenging by existing methods. In principle, not only the pattern, resolution, and thickness of transferred films, but also the curvature, depth, and adhesion of target substrates are unlimited, while the size of transferred films can be as high as meter-scale. To demonstrate the capabilities of soap film transfer printing, pre-fabricated ultrathin electronics with multiple patterns, single micron resolution, sub-micron thickness, and centimeter size are conformably integrated onto the ultrathin web, ultra-soft cotton, DVD-R disk with the minimum radius of curvature of 131 nm, interior cavity of Klein bottle and dandelion with ultralow adhesion. The printed ultrathin sensors show superior conformabilities and robust adhesion, leading to engineering opportunities including electrocardiogram (ECG) signal acquisition and temperature measurement in aqueous environments.
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Developing stable and highly selective two-electron oxygen reduction reaction (2e- ORR) electrocatalysts for producing hydrogen peroxide (H2 O2 ) is considered a major challenge to replace the anthraquinone process and achieve a sustainable green economy. Here, we doped Sn into Ti4 O7 (D-Sn-Ti4 O7 ) by simple polymerization post-calcination method as a high-efficiency 2e- ORR electrocatalyst. In addition, we also applied plain calcination after the grinding method to load Sn on Ti4 O7 (L-Sn-Ti4 O7 ) as a comparison. However, the performance of L-Sn-Ti4 O7 is far inferior to that of the D-Sn-Ti4 O7 . D-Sn-Ti4 O7 exhibits a starting potential of 0.769â V (versus the reversible hydrogen electrode, RHE) and a high H2 O2 selectivity of 95.7 %. Excitingly, the catalyst can maintain a stable current density of 2.43â mA â cm-2 for 3600â s in our self-made H-type cell, and the cumulative H2 O2 production reaches 359.2â mg â L-1 within 50,000â s at 0.3â V. The performance of D-Sn-Ti4 O7 is better than that of the non-noble metal 2e- ORR catalysts reported so far. The doping of Sn not only improves the conductivity but also leads to the lattice distortion of Ti4 O7 , further forming more oxygen vacancies and Ti3+ , which greatly improves its 2e- ORR performance compared with the original Ti4 O7 . In contrast, since the Sn on the surface of L-Sn-Ti4 O7 displays a synergistic effect with Tin+ (3≤n≤4) of Ti4 O7 , the active center Tin+ dissociates the O=O bond, making it more inclined to 4e- ORR.
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The development of a stable and efficient non-noble metal catalyst with both oxygen reduction reaction (ORR) and oxygen evolution reaction (OER) is paramount to achieving the widespread application of Zn-air batteries (ZABs) but remains a great challenge. Herein, a novel Co3 Fe7 alloy nanoparticle dispersed on Se, N co-doped graphitic carbon (denoted as CoFe/Se@CN) was prepared through a facile hydrothermal and pyrolysis process. The synthesized CoFe/Se@CN exhibits outstanding ORR and OER properties with an ultralow potential gap of 0.625â V, which is mainly attributed to the abundant porous structure, the rich structural defects formed by doping Se atoms, and the strong synergistic effects between the CoFe alloys and graphitic carbon nanosheet. Furthermore, the ZAB fabricated by CoFe/Se@CN shows a high peak power density of 160â mW cm-2 and a large specific capacity of 802â mA h g-1 with favorable cycling stability, outperforming that of Pt/C+RuO2 . Our study offers a plausible strategy to explore bifunctional carbon-based materials with efficient electrocatalytic properties for rechargeable ZABs.
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To determine an effective optimization strategy and facilitate the manufacture of optical metalenses, this paper extends the material-field series-expansion (MFSE) method for the topology design of metalenses. A new anisotropic material-field function with a spatially anisotropic correlation is introduced to describe the structural topology in a narrow design domain. The topological features can be implicitly controlled by material-field correlation lengths in different directions. Then, a generalized sigmoid projection is introduced to construct an interpolation relationship between the unbounded material-field value and the relative permittivity. Based on the series expansion technique, the number of design variables is greatly reduced in this topology optimization process without requiring additional material-field bounded constraints. The MFSE-based metalens design problem is efficiently solved by using a gradient-based algorithm incorporating design sensitivity analysis. Numerical examples demonstrate that the proposed optimization algorithm can successfully obtain an optimized and easy-to-manufacture design in optics inverse design problems.
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Photonic crystals can be adopted to control light propagation due to their superior band gap feature. It is well known the band gap feature of photonic crystals depends significantly on the topological design of the lattices, which is rather challenging due to the highly nonlinear objective function and multiple local minima feature of such design problems. To this end, this paper proposed a new band-gap topology optimization framework for photonic crystals considering different electromagnetic wave polarization modes. Based on the material-field series-expansion (MFSE) model and the dielectric permittivity interpolation scheme, the lattice topologies are represented by using a small number of design variables. Then, a sequential Kriging-based optimization algorithm, which shows strong global search capability and requires no sensitivity information, is employed to solve the band gap design problem as a series of sub-optimization problems with adaptive-adjusting design spaces. Numerical examples demonstrated the effectiveness of the proposed gradient-free method to maximize the band gap for transverse magnetic field (TM), transverse electric field (TE), and complete modes. Compared with previously reported designs, the present results exhibit less dependency on the guess of the initial design, larger band gaps and some interesting topology configurations.
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Dysregulation of calcium homeostasis endoplasmic reticulum protein (CHERP) has been implicated in several cancers, but it remains elusive how CHERP contributes to cancer cell proliferation and cancer development. Here, we observed that CHERP and its binding partner SR140 are significantly upregulated in human clinical colorectal cancer tissues (CRC). CHERP and SR140 could form a protein complex to stabilize each other. Knockdown of CHERP or SR140 triggers double-stranded DNA breaks and cell death. Furthermore, UPF3A, the RNA surveillance factor, was identified as a splicing target of CHERP and SR140, which bind specifically to the regulated exon4 and modulate UPF3A splicing. UPF3A knockdown recapitulates CHERP/SR140 depletion both in vitro and in mice. Importantly, overexpression of UPF3A significantly rescues proliferation defect of CHERP/SR140-depleted cells. These results confirmed that the effect of CHERP/SR140 in promoting tumorigenesis was partially mediated by UPF3A. Extending these results, upregulation of CHERP/SR140 observed in CRC remarkably parallels increased inclusion of UPF3A exon4. Together, our study clarifies how CHERP/SR140 exert an oncogenic role in CRC development partially through regulating expression of UPF3A variants.
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Neoplasias Colorrectales/genética , Proteínas de Unión al ADN/metabolismo , Regulación Neoplásica de la Expresión Génica , Proteínas de la Membrana/metabolismo , Proteínas de Unión al ARN/genética , Proteínas de Unión al ARN/metabolismo , Ribonucleoproteínas/metabolismo , Empalme Alternativo , Animales , Carcinogénesis/genética , Línea Celular Tumoral , Proliferación Celular , Neoplasias Colorrectales/patología , Roturas del ADN de Doble Cadena , Proteínas de Unión al ADN/genética , Femenino , Técnicas de Silenciamiento del Gen , Células HEK293 , Humanos , Masculino , Proteínas de la Membrana/genética , Ratones , Persona de Mediana Edad , ARN Interferente Pequeño/metabolismo , Ribonucleoproteínas/genética , Regulación hacia Arriba , Ensayos Antitumor por Modelo de XenoinjertoRESUMEN
Transition metal catalysts for replacing noble metals have been extensively studied, but the deficiencies in intrinsic activity and stability limit their application in electrocatalysis. Here, we present CoNi alloy nanoparticles loaded on Ti4O7 supports and embedded in N, S doped carbon nanofibers by electrospinning method. The prepared CoNi/Ti4O7@NS-CNFs exhibits satisfactory ORR and OER activities with a low potential gap of 0.664 V and shows a high stability over long periods of testing, which are superior to most of the transition metal catalysts reported so far. Accordingly, the Zn-air battery constructed with the prepared catalyst demonstrates a maximum power density of 165.7 mW cm-2 and a specific capacity of 788.4 mA h gZn-1 (1.61 and 1.14 times higher than that of Pt/C + IrO2, respectively). The addition of S element and corrosion-resistant Ti4O7 plays a significant part in the morphology and activity of the prepared catalyst, which optimizes the distribution and electronic structure of active centers, and improves the stability of the catalyst. This effort provides a possible approach to exploring the efficient performance of the other transition metals.
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BACKGROUND: Cancer-associated cachexia is a multifactorial syndrome defined by progressive weight loss with ongoing loss of adipose tissue and skeletal muscle. Adipose loss occurs in the early stage of cachexia and is associated with reduced quality of life and survival time. Although numerous lncRNAs are regarded as novel regulators in adipose metabolism, the role of lncRNAs that selectively modulate the development of adipose loss in cachexia remains limited. METHODS: In this study, we analyzed microarray data of lncRNAs in adipose loss and further explored the function and mechanism of MALAT1 in adipose loss. First, we explored the expression and function of MALAT1 in adipose cell by quantitative PCR and RNA knockdown. Subsequently, the mechanism of MALAT1 involvement in adipose loss was analyzed via RNA-seq, bioinformatics analysis and reporter gene assay. Finally, we explored the clinical significance of MALAT1 through correlation analysis. RESULTS: Cellular experiments revealed that knocking down MALAT1 significantly inhibited the process of adipogenesis. RNA-seq data showed that numerous adipogenic genes were downregulated upon MALAT1 knockdown. A protein-protein interaction network analysis identified PPAR-γ as the central node transcription factor, the inhibition of which explains the downregulation of numerous adipogenic genes. A reporter gene assay suggested that MALAT1 can regulate the gene expression of PPAR-γ at the transcriptional level. Moreover, MALAT1 was weakly expressed in the subcutaneous white adipose tissue of cancer-associated cachexia patients and was related to low fat mass index and poor prognosis in cancer patients. CONCLUSIONS: This study indicated that MALAT1 is associated with adipose loss in cancer-associated cachexia by regulating adipogenesis through PPAR-γ, which may potentially be a novel target for the diagnosis and treatment of cancer-associated cachexia in the clinic.
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Satellite cells are main muscle stem cells that could provide myonuclei for myofiber growth and synaptic-specific gene expression during the early postnatal development. Here, we observed that splicing factor SRSF1 is highly expressed in myoblasts and its expression is closely related with satellite cell activation and proliferation. By genetic deletion of SRSF1 in myogenic progenitors, we found that SRSF1 is critical for satellite cell proliferation in vitro and in vivo. Most notably we also observed that SRSF1 is required for the functional neuromuscular junction (NMJ) formation, as SRSF1-deficient mice fail to form mature pretzel-like NMJs, which leads to muscle weakness and premature death in mice. Finally, we demonstrated that SRSF1 contributes to muscle innervation and muscle development likely by regulating a restricted set of tissue-specific alternative splicing events. Thus, our data define a unique role for SRSF1 in postnatal skeletal muscle growth and function in mice.
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Diferenciación Celular , Unión Neuromuscular/citología , Células Satélite del Músculo Esquelético/citología , Células Satélite del Músculo Esquelético/metabolismo , Factores de Empalme Serina-Arginina/metabolismo , Empalme Alternativo/genética , Animales , Animales Recién Nacidos , Biomarcadores/metabolismo , Proliferación Celular , Eliminación de Gen , Ratones Endogámicos C57BL , Ratones Noqueados , Atrofia Muscular/patología , Factores de Empalme Serina-Arginina/deficienciaRESUMEN
Splicing factor SRSF2 is frequently mutated or up-regulated in human cancers. Here, we observe that hepatocyte-specific deletion of Srsf2 trigger development of hepatocellular carcinoma (HCC) in mice, which also involves inflammation and fibrosis. Importantly, we find that, when compensatory hepatocyte proliferation is impaired, activation of hepatic progenitor cells (HPCs) play an important role in liver regeneration and tumor formation. Moreover, the cells of HCC- bearing livers display both HPC and hepatocyte markers, with gene expression profiling suggesting HPC origin and embryonic origin. Mechanically, we demonstrate that levels of oncofetal genes insulin-like growth factor 2 (Igf2) and H19 are significantly increased in the tumors, likely due to decreased DNA methylation of the Igf2/H19 locus. Consequently, signaling via the Igf2 pathway is highly activated in the tumors. Thus, our data demonstrate that loss of Srsf2 triggers HPC-mediated regeneration and activation of oncofetal genes, which altogether promote HCC development and progression in mice.
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Carcinoma Hepatocelular/genética , Eliminación de Gen , Hepatocitos , Neoplasias Hepáticas/genética , Factores de Empalme Serina-Arginina/deficiencia , Células Madre/metabolismo , Regulación Neoplásica de la Expresión GénicaRESUMEN
A new method for the simulation of the mass distribution of cancellous bone is presented on the basis of finite element analysis (FEA). In this method,the process of bone remodelling is considered as a process of the topology optimization of a corresponding continuum structure. Fabric tensor is used to express the microstructure and the constitutive properties of cancellous bone. The effective volume fraction or the relative density of a point in the design domain is expressed by the invariables of the fabric tensor. A reference strain interval, which is corresponding to the strain dead zone of a bone in biomechanics, is applied to detect the the final topology of the structure. By the present approach, several numerical results are given, i. e., the simulation on the shape of the coronal plane of vertebrae, the predictions of the mass distributions of the two-dimensional and the three-dimensional proximal femurs. The validity and feasibility of this new method are verified by the comparison between the results of the present work and those in the published literatures.
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Densidad Ósea/fisiología , Remodelación Ósea/fisiología , Huesos/fisiología , Análisis de Elementos Finitos , Modelos Biológicos , Adaptación Fisiológica , Algoritmos , Fenómenos Biomecánicos , Simulación por Computador , Cabeza Femoral/fisiología , Humanos , Estrés MecánicoRESUMEN
Calorie restriction (CR) extends lifespan and elicits numerous effects beneficial to health and metabolism in various model organisms, but the underlying mechanisms are not completely understood. Gut microbiota has been reported to be associated with the beneficial effects of CR; however, it is unknown whether these effects of CR are causally mediated by gut microbiota. In this study, we employed an antibiotic-induced microbiota-depleted mouse model to investigate the functional role of gut microbiota in CR. Depletion of gut microbiota rendered mice resistant to CR-induced loss of body weight, accompanied by the increase in fat mass, the reduction in lean mass and the decline in metabolic rate. Depletion of gut microbiota led to increases in fasting blood glucose and cholesterol levels independent of CR. A few metabolism-modulating hormones including leptin and insulin were altered by CR and/or gut microbiota depletion. In addition, CR altered the composition of gut microbiota with significant increases in major probiotic genera such as Lactobacillus and Bifidobacterium, together with the decrease of Helicobacter. In addition, we performed fecal microbiota transplantation in mice fed with high-fat diet. Mice with transferred microbiota from calorie-restricted mice resisted high fat diet-induced obesity and exhibited metabolic improvement such as alleviated hepatic lipid accumulation. Collectively, these data indicate that CR-induced metabolic improvement especially in body weight reduction is mediated by intestinal microbiota to a certain extent.