The fibrinolysis inhibitor α2-antiplasmin restricts lymphatic remodelling and metastasis in a mouse model of cancer.

Remodelling of lymphatic vessels in tumours facilitates metastasis to lymph nodes. The growth factors VEGF-C and VEGF-D are well known inducers of lymphatic remodelling and metastasis in cancer. They are initially produced as full-length proteins requiring proteolytic processing in order to bind VEGF receptors with high affinity and thereby promote lymphatic remodelling. The fibrinolytic protease plasmin promotes processing of VEGF-C and VEGF-D in vitro, but its role in processing them in cancer was unknown. Here we explore plasmin's role in proteolytically activating VEGF-D in vivo, and promoting lymphatic remodelling and metastasis in cancer, by co-expressing the plasmin inhibitor α2-antiplasmin with VEGF-D in a mouse tumour model. We show that α2-antiplasmin restricts activation of VEGF-D, enlargement of intra-tumoural lymphatics and occurrence of lymph node metastasis. Our findings indicate that the fibrinolytic system influences lymphatic remodelling in tumours which is consistent with previous clinicopathological observations correlating fibrinolytic components with cancer metastasis.

VEGF-D promotes pulmonary oedema in hyperoxic acute lung injury.

Leakage of fluid from blood vessels, leading to oedema, is a key feature of many diseases including hyperoxic acute lung injury (HALI), which can occur when patients are ventilated with high concentrations of oxygen (hyperoxia). The molecular mechanisms driving vascular leak and oedema in HALI are poorly understood. VEGF-D is a protein that promotes blood vessel leak and oedema when overexpressed in tissues, but the role of endogenous VEGF-D in pathological oedema was unknown. To address these issues, we exposed Vegfd-deficient mice to hyperoxia. The resulting pulmonary oedema in Vegfd-deficient mice was substantially reduced compared to wild-type, as was the protein content of bronchoalveolar lavage fluid, consistent with reduced vascular leak. Vegf-d and its receptor Vegfr-3 were more highly expressed in lungs of hyperoxic, versus normoxic, wild-type mice, indicating that components of the Vegf-d signalling pathway are up-regulated in hyperoxia. Importantly, VEGF-D and its receptors were co-localized on blood vessels in clinical samples of human lungs exposed to hyperoxia; hence, VEGF-D may act directly on blood vessels to promote fluid leak. Our studies show that Vegf-d promotes oedema in response to hyperoxia in mice and support the hypothesis that VEGF-D signalling promotes vascular leak in human HALI. © 2016 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of Pathological Society of Great Britain and Ireland.

A non-canonical role for desmoglein-2 in endothelial cells: implications for neoangiogenesis.

Desmogleins (DSG) are a family of cadherin adhesion proteins that were first identified in desmosomes and provide cardiomyocytes and epithelial cells with the junctional stability to tolerate mechanical stress. However, one member of this family, DSG2, is emerging as a protein with additional biological functions on a broader range of cells. Here we reveal that DSG2 is expressed by non-desmosome-forming human endothelial progenitor cells as well as their mature counterparts [endothelial cells (ECs)] in human tissue from healthy individuals and cancer patients. Analysis of normal blood and bone marrow showed that DSG2 is also expressed by CD34(+)CD45(dim) hematopoietic progenitor cells. An inability to detect other desmosomal components, i.e., DSG1, DSG3 and desmocollin (DSC)2/3, on these cells supports a solitary role for DSG2 outside of desmosomes. Functionally, we show that CD34(+)CD45(dim)DSG2(+) progenitor cells are multi-potent and pro-angiogenic in vitro. Using a 'knockout-first' approach, we generated a Dsg2 loss-of-function strain of mice (Dsg2 (lo/lo)) and observed that, in response to reduced levels of Dsg2: (i) CD31(+) ECs in the pancreas are hypertrophic and exhibit altered morphology, (ii) bone marrow-derived endothelial colony formation is impaired, (iii) ex vivo vascular sprouting from aortic rings is reduced, and (iv) vessel formation in vitro and in vivo is attenuated. Finally, knockdown of DSG2 in a human bone marrow EC line reveals a reduction in an in vitro angiogenesis assay as well as relocalisation of actin and VE-cadherin away from the cell junctions, reduced cell-cell adhesion and increased invasive properties by these cells. In summary, we have identified DSG2 expression in distinct progenitor cell subpopulations and show that, independent from its classical function as a component of desmosomes, this cadherin also plays a critical role in the vasculature.

The propeptides of VEGF-D determine heparin binding, receptor heterodimerization, and effects on tumor biology.

VEGF-D is an angiogenic and lymphangiogenic glycoprotein that can be proteolytically processed generating various forms differing in subunit composition due to the presence or absence of N- and C-terminal propeptides. These propeptides flank the central VEGF homology domain, that contains the binding sites for VEGF receptors (VEGFRs), but their biological functions were unclear. Characterization of propeptide function will be important to clarify which forms of VEGF-D are biologically active and therefore clinically relevant. Here we use VEGF-D mutants deficient in either propeptide, and in the capacity to process the remaining propeptide, to monitor the functions of these domains. We report for the first time that VEGF-D binds heparin, and that the C-terminal propeptide significantly enhances this interaction (removal of this propeptide from full-length VEGF-D completely prevents heparin binding). We also show that removal of either the N- or C-terminal propeptide is required for VEGF-D to drive formation of VEGFR-2/VEGFR-3 heterodimers which have recently been shown to positively regulate angiogenic sprouting. The mature form of VEGF-D, lacking both propeptides, can also promote formation of these receptor heterodimers. In a mouse tumor model, removal of only the C-terminal propeptide from full-length VEGF-D was sufficient to enhance angiogenesis and tumor growth. In contrast, removal of both propeptides is required for high rates of lymph node metastasis. The findings reported here show that the propeptides profoundly influence molecular interactions of VEGF-D with VEGF receptors, co-receptors, and heparin, and its effects on tumor biology.

3D printing of hierarchically micro/nanostructured electrodes for high-performance rechargeable batteries.

3D printing, also known as additive manufacturing, is capable of fabricating 3D hierarchical micro/nanostructures by depositing a layer-upon-layer of precursor materials and solvent-based inks under the assistance of computer-aided design (CAD) files. 3D printing has been employed to construct 3D hierarchically micro/nanostructured electrodes for rechargeable batteries, endowing them with high specific surface areas, short ion transport lengths, and high mass loading. This review summarizes the advantages and limitations of various 3D printing methods and presents the recent developments of 3D-printed electrodes in rechargeable batteries, such as lithium-ion batteries, sodium-ion batteries, and lithium-sulfur batteries. Furthermore, the challenges and perspectives of the 3D printing technique for electrodes and rechargeable batteries are put forward. This review will provide new insight into the 3D printing of hierarchically micro/nanostructured electrodes in rechargeable batteries and promote the development of 3D printed electrodes and batteries in the future.

UHRF1/UBE2L6/UBR4-mediated ubiquitination regulates EZH2 abundance and thereby melanocytic differentiation phenotypes in melanoma.

Cellular heterogeneity in cancer is linked to disease progression and therapy response, although mechanisms regulating distinct cellular states within tumors are not well understood. We identified melanin pigment content as a major source of cellular heterogeneity in melanoma and compared RNAseq data from high-pigmented (HPCs) and low-pigmented melanoma cells (LPCs), suggesting EZH2 as a master regulator of these states. EZH2 protein was found to be upregulated in LPCs and inversely correlated with melanin deposition in pigmented patient melanomas. Surprisingly, conventional EZH2 methyltransferase inhibitors, GSK126 and EPZ6438, had no effect on LPC survival, clonogenicity and pigmentation, despite fully inhibiting methyltransferase activity. In contrast, EZH2 silencing by siRNA or degradation by DZNep or MS1943 inhibited growth of LPCs and induced HPCs. As the proteasomal inhibitor MG132 induced EZH2 protein in HPCs, we evaluated ubiquitin pathway proteins in HPC vs LPCs. Biochemical assays and animal studies demonstrated that in LPCs, the E2-conjugating enzyme UBE2L6 depletes EZH2 protein in cooperation with UBR4, an E3 ligase, via ubiquitination at EZH2's K381 residue, and is downregulated in LPCs by UHRF1-mediated CpG methylation. Targeting UHRF1/UBE2L6/UBR4-mediated regulation of EZH2 offers potential for modulating the activity of this oncoprotein in contexts in which conventional EZH2 methyltransferase inhibitors are ineffective.

Proteolytic processing of vascular endothelial growth factor-D is essential for its capacity to promote the growth and spread of cancer.

VEGF-D is a mitogen for endothelial cells that promotes tumor growth and metastatic spread in animal models, and expression of which correlates with lymph node metastasis in some human cancers. It is secreted from the cell as a full-length form with propeptides flanking a central region containing binding sites for VEGFR-2 and VEGFR-3, receptors that signal for angiogenesis and lymphangiogenesis. The propeptides can be cleaved from VEGF-D, enhancing affinity for VEGFR-2 and VEGFR-3 in vitro; however, the importance of this processing in cancer is unclear. To explore the necessity of processing for the effects of VEGF-D in cancer, we use a mutant full-length form that cannot be processed, and show that, in contrast to full-length VEGF-D that is processed, this mutant does not promote tumor growth and lymph node metastasis in a mouse tumor model. Processing of VEGF-D is required for tumor angiogenesis, lymphangiogenesis, and recruitment of tumor-associated macrophages. These observations may be explained by the requirement of processing for VEGF-D to bind neuropilin receptors and activate VEGFR-2. Our results indicate that proteolytic processing is necessary for VEGF-D to promote the growth and spread of cancer, and suggest that enzymes catalyzing this processing could be targets for antimetastatic therapeutics.

Rationally designing a Ti3C2Tx/CNTs-Co9S8 heterostructure as a sulfur host with multi-functionality for high-performance lithium-sulfur batteries.

Lithium-sulfur (Li-S) batteries have been regarded as potential next-generation batteries owing to their ultrahigh theoretical capacity and abundance of sulfur. However, polysulfide shuttling, poor electronic conductivity, and severe volume expansion limit their commercial prospects. In this work, we rationally constructed a 3D porous Ti3C2Tx/CNTs-Co9S8 heterostructure derived from a zeolite imidazole framework (ZIF)/Ti3C2Tx MXene composite via carbonization and subsequent sulfidation. In this 3D porous Ti3C2Tx/CNTs-Co9S8 heterostructure, the 3D porous Ti3C2Tx MXene structure can provide facilitated ion and electron transport, good structural stability, and polar bonds to anchor sulfur and polysulfides. The formed CNTs can enhance ion diffusion and electron transport. The Co9S8 nanoparticles can accelerate the conversion reaction of polysulfides to Li2S, which can further prevent polysulfide shuttling. The 3D porous structure can buffer the electrode volume change upon cycling. This rationally designed Ti3C2Tx/CNTs-Co9S8/S cathode exhibits a high initial capacity of 1389.8 mA h g-1 at 0.1C, good cyclic stability (730.7 mA h g-1 at 0.2C after 100 cycles), and excellent rate capacities (530.7 mA h g-1 at 1C). When the S loading was 2.5 mg cm-2, the Ti3C2Tx/CNTs-Co9S8/S cathode still exhibited a reversible capacity of 472.8 mA h g-1 at 0.5C after 300 cycles.

Hierarchical MXene/transition metal oxide heterostructures for rechargeable batteries, capacitors, and capacitive deionization.

2D MXenes have attracted considerable attention due to their high electronic conductivity, tunable metal compositions, functional termination groups, low ion diffusion barriers, and abundant active sites. However, MXenes suffer from sheet stacking and partial surface oxidation, limiting their energy storage and water treatment development. To solve these problems and enhance the performance of MXenes in practical applications, various hierarchical MXene/transition metal oxide (MXene/TMO) heterostructures are rationally designed and constructed. The hierarchical MXene/TMO heterostructures can not only prevent the stacking of MXene sheets and improve the electronic conductivity and buffer the volume change of TMOs during the electrochemical reaction process. The synergistic effect of conductive MXenes and active TMOs also makes MXene/TMO heterostructures promising electrode materials for energy storage and seawater desalination. This review mainly introduces and discusses the recent research progress in MXene/TMO heterostructures, focusing on their synthetic strategies, heterointerface engineering, and applications in rechargeable batteries, capacitors, and capacitive deionization (CDI). Finally, the key challenges and prospects for the future development of the MXene/TMO heterostructures in rechargeable batteries, capacitors, and CDI are proposed.

Hierarchical MXene/transition metal chalcogenide heterostructures for electrochemical energy storage and conversion.

MXenes have gained rapidly increasing attention owing to their two-dimensional (2D) layered structures and unique mechanical and physicochemical properties. However, MXenes have some intrinsic limitations (e.g., the restacking tendency of the 2D structure) that hinder their practical applications. Transition metal chalcogenide (TMC) materials such as SnS, NiS, MoS2, FeS2, and NiSe2 have attracted much interest for energy storage and conversion by virture of their earth-abundance, low costs, moderate overpotentials, and unique layered structures. Nonetheless, the intrinsic poor electronic conductivity and huge volume change of TMC materials during the alkali metal-ion intercalation/deintercalation process cause fast capacity fading and poor-rate and poor-cycling performances. Constructing heterostructures based on metallic conductive MXenes and highly electrochemically active TMCs is a promising and effective strategy to solve these problems and enhance the electrochemical performances. This review highlights and discusses the recent research development of MXenes and hierarchical MXene/TMC heterostructures, with a focus on the synthesis strategies, surface/heterointerface engineering, and potential applications for lithium-ion batteries, sodium-ion batteries, lithium-sulfur batteries, supercapacitors, electrocatalysis, and photocatalysis. The critical challenges and perspectives of the future development of MXenes and hierarchical MXene/TMC heterostructures for electrochemical energy storage and conversion are forecasted.

Unraveling the Critical Role of Melt-Spinning Atmosphere in Enhancing the Thermoelectric Performance of p-Type Bi0.52Sb1.48Te3 Alloys.

Melt spinning has proven effective in maintaining chemical homogeneity and introducing multiscale microstructures that can reduce the lattice thermal conductivity and consequently enhance the thermoelectric performance of consolidated bulk materials. In this work, p-type Bi0.52Sb1.48Te3 bulk alloys are fabricated by melt spinning (MS) followed by subsequent plasma activated sintering (PAS). The influence of different MS atmospheres (air, Ar, N2, and He) on the morphologies of MS ribbons and the thermoelectric properties of MS-PAS bulk materials has been investigated systematically. Because of the relatively high thermal conductivity, a He atmosphere expedites the heat dissipation in the MS process and results in severe sublimation of tellurium and thus inferior thermoelectric performance. In contrast, an Ar atmosphere can essentially prevent heat loss of the fusant and suppress the sublimation of tellurium. Consequently, the corresponding Bi0.52Sb1.48Te3 sample (MS in Ar atmosphere) presents the highest peak ZT and average ZT values of 1.09 (at 340 K) and 0.81 (in 300-500 K), respectively. The average ZT of the sample prepared using an Ar atmosphere is almost three times the one prepared using a He atmosphere. This reflects the importance of using the appropriate atmosphere during the melt-spinning process. This result, which indicates that melt spinning in an Ar atmosphere is preferable to avoid heat loss, can also be extended to other materials.

The Hippo pathway oncoprotein YAP promotes melanoma cell invasion and spontaneous metastasis.

Melanoma is a deadly form of skin cancer that accounts for a disproportionally large proportion of cancer-related deaths in younger people. Compared with most other skin cancers, a feature of melanoma is its high metastatic capacity, although the mechanisms that confer this are not well understood. The Hippo pathway is a key regulator of organ growth and cell fate that is deregulated in many cancers. To analyse the Hippo pathway in cutaneous melanoma, we generated a transcriptional signature of melanoma cells that overexpressed YAP, the key downstream Hippo pathway oncoprotein. YAP-mediated transcriptional activity varied in melanoma cell lines but did not cluster with known genetic drivers of melanomagenesis such as BRAF and NRAS mutations. Instead, it correlated strongly with published gene expression profiles linked to melanoma cell invasiveness and varied throughout the metastatic cascade in melanoma patient tumours. Consistent with this, YAP was both necessary and sufficient for melanoma cell invasion in vitro. In vivo, YAP promoted spontaneous melanoma metastasis, whilst the growth of YAP-expressing primary tumours was impeded. Finally, we identified the YAP target genes AXL, THBS1 and CYR61 as key mediators of YAP-induced melanoma cell invasion. These data suggest that YAP is a critical regulator of melanoma metastasis.

Reaction Packaging CoSe2 Nanoparticles in N-Doped Carbon Polyhedra with Bifunctionality for Overall Water Splitting.

Water electrolysis is a promising approach for green and large-scale hydrogen production; however, there are still challenges for developing efficient and stable bifunctional electrocatalysts toward the hydrogen and oxygen evolution reactions. Herein, zeolitic imidazolate framework-67 was used as the precursor for the construction of CoSe2 nanoparticles trapped in N-doped carbon (NC) polyhedra. Among as-obtained CoSe2-NC hybrid, highly active CoSe2 nanoparticles in sizes of 10-20 nm are encapsulated in N-doped few-layer carbon shell, avoiding their easy aggregations of CoSe2 nanoparticles as well as enhancing the long-term stability. The unique nanostructured CoSe2-NC hybrid with a hierarchical porosity and 3D conductive framework thus fully exerts outstanding bifunctional catalytic activity of CoSe2 centers. As a result, the CoSe2-NC hybrid as bifunctional catalysts for overall water splitting delivers a high current density of 50 mA cm-2 with an applied voltage of ∼1.73 V in an alkaline electrolyte, with a promising stability over 50 000 s.

Forensic characteristics and genetic analysis of both 27 Y-STRs and 143 Y-SNPs in Eastern Han Chinese population.

Y-chromosome short tandem repeat (Y-STR) and Y-chromosome single nucleotide polymorphism (Y-SNP) frequency distributions provide resources for assessment of male population stratification among world-wide populations. Currently, the Y-STR Haplotype Reference Database (YHRD) contains numerous Y-chromosome haplotype profiles from various populations and countries around the world. However, for many of the recently discovered and already phylogenetically mapped Y-SNPs, the population data are scarce. Herein, the typing of 27 Y-STRs (Yfiler Plus) and 143 Y-SNPs (self-designed Y-SNP panel) was performed on 1269 unrelated males from 11 Han Chinese populations. Haplogroup O-M175 was the most predominant haplogroup in our Han Chinese data, ranging from 67.34% (Henan Han) to 93.16% (Guangdong Han). The highest haplogroup diversity (0.967056) was observed in Heilongjiang Han, with a discrimination capacity (DC) value of 0.3723. The number of alleles at single-copy loci varied from 2 for DYS391 (Guangdong Han) to 16 for DYS518 (Henan Han). For the majority of the populations (8/11), both the haplotype diversity and DC values are 1.0000. Furthermore, genetic differentiations were observed between Northern and Southern Han Chinese. These genetic differences were mainly reflected in haplogroup distribution and frequency, and they were confirmed by statistical analysis.

Somatic Hypermutation of the YAP Oncogene in a Human Cutaneous Melanoma.

Melanoma is usually driven by mutations in BRAF or NRAS, which trigger hyperactivation of MAPK signaling. However, MAPK-targeted therapies are not sustainably effective in most patients. Accordingly, characterizing mechanisms that co-operatively drive melanoma progression is key to improving patient outcomes. One possible mechanism is the Hippo signaling pathway, which regulates cancer progression via its central oncoproteins YAP and TAZ, although is thought to be only rarely affected by direct mutation. As YAP hyperactivation occurs in uveal melanoma, we investigated this oncogene in cutaneous melanoma. YAP protein expression was elevated in most benign nevi and primary cutaneous melanomas but present at only very low levels in normal melanocytes. In patient-derived xenografts and melanoma cell lines, we observed variable reliance of cell viability on Hippo pathway signaling that was independent of TAZ activity and also of classical melanoma driver mutations such as BRAF and NRAS. Finally, in genotyping studies of melanoma, we observed the first ever hyperactivating YAP mutations in a human cancer, manifest as seven distinct missense point mutations that caused serine to alanine transpositions. Strikingly, these mutate four serine residues known to be targeted by the Hippo pathway and we show that they lead to hyperactivation of YAP. IMPLICATIONS: Our studies highlight the YAP oncoprotein as a potential therapeutic target in select subgroups of melanoma patients, although successful treatment with anti-YAP therapies will depend on identification of biomarkers additional to YAP protein expression.

CCL27/CCL28-CCR10 Chemokine Signaling Mediates Migration of Lymphatic Endothelial Cells.

Metastasis via the lymphatic vasculature is an important step in cancer progression. The formation of new lymphatic vessels (lymphangiogenesis), or remodeling of existing lymphatics, is thought to facilitate the entry and transport of tumor cells into lymphatic vessels and on to distant organs. The migration of lymphatic endothelial cells (LEC) toward guidance cues is critical for lymphangiogenesis. While chemokines are known to provide directional navigation for migrating immune cells, their role in mediating LEC migration during tumor-associated lymphangiogenesis is not well defined. Here, we undertook gene profiling studies to identify chemokine-chemokine receptor pairs that are involved in tumor lymphangiogenesis associated with lymph node metastasis. CCL27 and CCL28 were expressed in tumor cells with metastatic potential, while their cognate receptor, CCR10, was expressed by LECs and upregulated by the lymphangiogenic growth factor VEGFD and the proinflammatory cytokine TNFα. Migration assays demonstrated that LECs are attracted to both CCL27 and CCL28 in a CCR10-dependent manner, while abnormal lymphatic vessel patterning in CCR10-deficient mice confirmed the significant role of CCR10 in lymphatic patterning. In vivo analyses showed that LECs are recruited to a CCL27 or CCL28 source, while VEGFD was required in combination with these chemokines to enable formation of coherent lymphatic vessels. Moreover, tumor xenograft experiments demonstrated that even though CCL27 expression by tumors enhanced LEC recruitment, the ability to metastasize was dependent on the expression of VEGFD. These studies demonstrate that CCL27 and CCL28 signaling through CCR10 may cooperate with inflammatory mediators and VEGFD during tumor lymphangiogenesis. SIGNIFICANCE: The study shows that the remodeling of lymphatic vessels in cancer is influenced by CCL27 and CCL28 chemokines, which may provide a future target to modulate metastatic spread.

Ultralight and Highly Elastic Graphene/Lignin-Derived Carbon Nanocomposite Aerogels with Ultrahigh Electromagnetic Interference Shielding Performance.

Ultralight and highly elastic reduced graphene oxide (RGO)/lignin-derived carbon (LDC) composite aerogels with aligned micron-sized pores and cell walls are prepared using a facile freeze-drying method. The presence of a small fraction of LDC in the cell walls enhances the interfacial polarization effect while almost maintaining the amount of charge carriers and conductivity of the cell walls, greatly boosting the wave absorption capability of the cell walls. RGO/LDC aerogels also show a greater number of large cell walls with better integrity than RGO aerogels, further improving the multiple reflection ability of the aligned cell walls. Synergistic effects of the multiphase cell walls and the preferred microstructures of the RGO/LDC aerogels lead to their high electromagnetic interference (EMI) shielding effectiveness of 21.3-49.2 dB at an ultralow density of 2.0-8.0 mg/cm3. This corresponds to the surface-specific SE (SE divided by density and thickness) up to 53 250 dB·cm2/g, which is higher than the values reported for other carbon- and metal-based shields. Furthermore, the critical roles that microstructures play in determining the EMI shielding performance are directly revealed by comparing the shielding performance in directions parallel and normal to cell walls, as well as in an in situ compression process.

Self-Assembly-Assisted Facile Synthesis of MoS2-Based Hybrid Tubular Nanostructures for Efficient Bifunctional Electrocatalysis.

In this work, MoS2-based hybrid tubular nanostructures are facilely synthesized via a self-assembly-assisted process and evaluated as a bifunctional electrocatalyst for hydrogen evolution reactions (HERs) and oxygen reduction reactions (ORRs). By simply mixing the reactants under ambient conditions, (NH4)2MoS4/polydopamine (PDA) hybrid nanospheres are formed. The protonated dopamine is linked to tetrahedral [MoS4]2- via weak N-H···S and O-H···S interactions, causing the PDA nanospheres merging together and forming nanorods under stirring-induced shear force. Moreover, the oxidative polymerization of dopamine proceeds on the surface of the nanorods, whereas it is prohibited inside the nanorods owing to lack of oxygen, leading to outward diffusion of dopamine and hence cavitation. After annealing, the tubular morphology is perfectly retained, while ultrafine MoS2 monolayers are formed due to the confinement of the framework. Benefiting from these unique structural features, the MoS2/C hybrid nanotubes possess abundant active sites and high surface area, as well as boost electronic and ionic transport, remarkably enhancing their electrocatalytic activities. The onset and half-wave potentials are 0.91 and 0.82 V, respectively, for ORR, close to those of Pt/C. Moreover, low onset potential and small Tafel slope are also observed for HER, demonstrating the potential of the hybrid nanotubes as a promising non-noble metal bifunctional electrocatalyst.

[Age-dependent mitochondrial DNA 4977bp depletion in human skeletal muscle].

OBJECTIVE: To explore depletion of human mitochondrial DNA 4977-bp and its relation with aging. METHODS: Total DNA (nuclear and mtDNA) was extracted from 100mg muscle tissue. UV light illumination of ethidium bromide-stained PCR products was used to study the depletion of mtDNA (wild-type or mutant). RESULTS: The proportions of mtDNA depletion in human skeletal muscle could be determined. The frequency of mtDNA 4977-bp depletion in different age groups (0-9, 10-19, 20-29, 30-39, 40-49, 50-59, 60-69, 70-79, 80-89, 90-99) was: 0%, 0%, 0.003%, 0.011%, 0.015%, 0.033%, 0.038%, 0.062%, 0.069%, and 0.091%, respectively. CONCLUSION: Our findings suggest that the frequency of the mtDNA4977 depletion in human skeletal muscle increases with age. It might be useful for human age estimation.

Bacterial cellulose-based sheet-like carbon aerogels for the in situ growth of nickel sulfide as high performance electrode materials for asymmetric supercapacitors.

Electroactive materials, such as nickel sulfide (NiS), with high theoretical capacities have attracted broad interest to fabricate highly efficient supercapacitors. Preventing aggregation and increasing the conductivity of NiS particles are key challenging tasks to fully achieve excellent electrochemical properties of NiS. One effective approach to solve these problems is to combine NiS with highly porous and conductive carbon materials such as carbon aerogels. In this study, a green and facile method for the in situ growth of NiS particles on bacterial cellulose (BC)-derived sheet-like carbon aerogels (CAs) has been reported. CA prepared by the dissolution-gelation-carbonization process was used as a framework to construct NiS/CA composite aerogels with NiS uniformly decorated on the pore walls of CA. It was found that the NiS/CA composite aerogel electrodes exhibit excellent capacitive performance with high specific capacitance (1606 F g-1), good rate capacitance retention (69% at 10 A g-1), and enhanced cycling stability (91.2% retention after 10 000 continuous cyclic voltammetry cycles at 100 mV s-1). Furthermore, asymmetric supercapacitors (ASCs) were constructed utilizing NiS/CA composite and CA as the positive and negative electrode materials, respectively. Through the synergistic effect of three-dimensional porous structures and conductive networks derived from CA and the high capacitive performance offered by NiS, the ASC device exhibited an energy density of ∼21.5 Wh kg-1 and a power density of 700 W kg-1 at the working voltage of 1.4 V in 2 M KOH aqueous solution. The ASC device also showed excellent long-term cycle stability with ∼87.1% specific capacitance retention after 10 000 cycles of cyclic voltammetry scans. Therefore, the NiS/CA composite shows great potential as a promising alternative to high-performance electrode materials for supercapacitors.