The integration of Fe dopant and interfacial FeOOH into Ni‐MOFs Fe‐doped‐(Ni‐MOFs)/FeOOH to construct Fe−O−Ni−O−Fe bonding is demonstrated and the origin of remarkable electrocatalytic performance of ...Ni‐MOFs is elucidated. X‐ray absorption/photoelectron spectroscopy and theoretical calculation results indicate that Fe‐O−Ni−O−Fe bonding can facilitate the distorted coordinated structure of the Ni site with a short nickel–oxygen bond and low coordination number, and can promote the redistribution of Ni/Fe charge density to efficiently regulate the adsorption behavior of key intermediates with a near‐optimal d‐band center. Here the Fe‐doped‐(Ni‐MOFs)/FeOOH with interfacial Fe−O−Ni−O−Fe bonding shows superior catalytic performance for OER with a low overpotential of 210 mV at 15 mA cm−2 and excellent stability with ≈3 % attenuation after a 120 h cycle test. This study provides a novel strategy to design high‐performance Ni/Fe‐based electrocatalysts for OER in alkaline media.
Iron doping and FeOOH decorating leads to interfacial Fe−O−Ni−O−Fe bonding in Fe‐doped‐(Ni‐MOF)/FeOOH. This interfacial bonding can regulate the active Ni site to give the appropriate adsorption behavior of intermediates for the oxygen evolution reaction (OER). As a result, Fe‐doped‐(Ni‐MOF)/FeOOH shows outstanding catalytic performance with low overpotential, small Tafel slope, and high durability.
Porous CoFe2O4/C NRAs supported on nickel foam@NC (denoted as NF@NC‐CoFe2O4/C NRAs) are directly fabricated by the carbonization of bimetal–organic framework NRAs grown on NF@poly‐aniline(PANI), and ...they exhibit high electrocatalytic activity, low overpotential, and high stability for the oxygen evolution reaction in alkaline media.
The intrinsic activity of NiFe layer double hydroxides (LDHs) for the oxygen evolution reaction (OER) suffers from its predominantly exposed (003) basal plane, which is thought to have poor activity. ...Herein, we construct a hierarchal structure of NiFe LDH nanosheet-arrays-on-microplates (NiFe NSAs-MPs) to elevate the electrocatalytic activity of NiFe LDHs for the OER by exposing a high-activity plane, such as the (012) edge plane. It is surprising that the NiFe NSAs-MPs show activity of 100 mA cm
−2
at an overpotential (
η
) of 250 mV, which is five times higher than that of (003) plane-dominated NiFe LDH microsheet arrays (NiFe MSAs) at the same
η
, representing the excellent electrocatalytic activity for the OER in alkaline media. Besides, we analyzed the OER activities of the (003) basal plane and the (012) and (110) edge planes of NiFe LDHs by density functional theory with on-site Coulomb interactions (DFT+U), and the calculation results indicated that the (012) edge plane exhibits the best catalytic performance among the various crystal planes because of the oxygen coordination of the Fe site, which is responsible for the high catalytic activity of NiFe NSAs-MPs.
The (012) edge plane of NiFe layer double hydroxides (LDHs) has been proven to be a highly active plane for water oxidation.
Altered metabolism is a hallmark of cancer, and the reprogramming of energy metabolism has historically been considered a general phenomenon of tumors. It is well recognized that long noncoding RNAs ...(lncRNAs) regulate energy metabolism in cancer. However, lncRNA‐mediated posttranslational modifications and metabolic reprogramming are unclear at present. In this review, we summarized the current understanding of the interactions between the alterations in cancer‐associated energy metabolism and the lncRNA‐mediated posttranslational modifications of metabolic enzymes, transcription factors, and other proteins involved in metabolic pathways. In addition, we discuss the mechanisms through which these interactions contribute to tumor initiation and progression, and the key roles and clinical significance of functional lncRNAs. We believe that an in‐depth understanding of lncRNA‐mediated cancer metabolic reprogramming can help to identify cellular vulnerabilities that can be exploited for cancer diagnosis and therapy.
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•miR-126 exosomes efficiently transferred miR-126 to the injured spinal cord.•Exosomes containing miR-126 promoted angiogenesis in the spinal cord after SCI by suppressing SPRED1 and ...PIK3R2.•Exosomes containing miR-126 promote neurogenesis and reduce Apoptosis after SCI.
Spinal cord injury (SCI) is a devastating neurological event that results in incomplete or complete loss of voluntary motor and sensory function. Until recently, there has been no effective curative strategy for SCI. Our previous study showed that microRNA (miR)-126 promoted angiogenesis and attenuated inflammation after SCI; however, the effect of miR-126-based treatment is limited because of the low efficiency of miR delivery in vivo. Recently, accumulating evidence has indicated that exosomes can serve as a valuable therapeutic vehicle for miR delivery to the central nervous system (CNS). Thus, the present study aimed to investigate whether exosomes derived from mesenchymal stem cells (MSCs) can be used to deliver miR-126 to treat SCI. In this study, we found that MSCs can load miR-126 into secreted exosomes. In a rat model of SCI, exosomes transferred miR-126 to the injured site of the spinal cord, reduced the lesion volume and improved functional recovery after SCI. Additionally, miR-126-loaded exosomes promoted angiogenesis post-SCI. Moreover, the administration of miR-126 exosomes promoted neurogenesis and reduced cell apoptosis after SCI. In vitro, we observed that exosomes derived from miR-126-modified MSCs promoted the angiogenesis and migration of human umbilical venous endothelial cells (HUVECs) by inhibiting the expression of Sprouty-related EVH1 domain-containing protein 1 (SPRED1) and phosphoinositide-3-kinase regulatory subunit 2 (PIK3R2). In conclusion, our study demonstrated that exosomes derived from MSCs transfected with miR-126 may promote angiogenesis and neurogenesis, inhibit apoptosis and promote functional recovery after SCI. These findings suggest that exosomes derived from miR-126-modified MSCs may serve as a novel potential therapeutic strategy for treating SCI.
Spinal cord injury (SCI) is one of the most common devastating injuries, which causes permanent disabilities such as paralysis and loss of movement or sensation. The precise pathogenic mechanisms of ...the disease remain unclear, and, as of yet, there is no effective cure. Mesenchymal stem cells (MSCs) show promise as an effective therapy in the experimental models of SCI. MSCs secrete various factors that can modulate a hostile environment, which is called the paracrine effect. Among these paracrine molecules, exosome is considered to be the most valuable therapeutic factor. Thus, exosomes from MSCs (MSCs-exosomes) can be a potential candidate of therapeutic effects of stem cells. The present study was designed to investigate the effect of whether systemic administration of exosomes generated from MSCs can promote the function recovery on the rat model of SCI in vivo. In the present study, we observed that systemic administration of MSCs-exosomes significantly attenuated lesion size and improved functional recovery post-SCI. Additionally, MSCs-exosomes treatment attenuated cellular apoptosis and inflammation in the injured spinal cord. Expression levels of proapoptotic protein (Bcl-2-associated X protein) and proinflammatory cytokines (tumor necrosis factor alpha and interleukin IL-1β) were significantly decreased after MSCs-exosomes treatment, whereas expression levels of antiapoptotic (B-cell lymphoma 2) and anti-inflammatory (IL-10) proteins were upregulated. Further, administration of MSCs-exosomes significantly promoted angiogenesis. These results show, for the first time, that systemic administration of MSCs-exosomes attenuated cell apoptosis and inflammation, promoted angiogenesis, and promoted functional recovery post-SCI, suggesting that MSCs-exosomes hold promise as a novel therapeutic strategy for treating SCI.
Based on the control measures at different stages of COVID‐19 and its transmission characteristics, we propose a dynamical model to describe the transmission of this virus among wild animals, human ...population, and the environment, where the migration of humans, asymptomatic infected humans, and the self‐protection awareness of susceptible humans are also introduced. We discuss, firstly, the existence and stability of the disease‐free and endemic equilibrium of wild animals and environment‐only model; this happens to be the initial stage of disease transmission. Further, with the intervention of control measures, the model degenerates into a subsystem with only human population and environment; the existence and stability of the disease‐free equilibrium of this subsystem are studied. With the strengthening of control strategies, the environment and human population subsystems have further degenerated into a human population‐only model with blocking migration and environment; the ultimate extinction of this disease and the peak of the outbreak are researched. Finally, some numerical simulations are carried to explain the main results and the impacts of various control strategies on the disease outbreak. In particular, we also fit the confirmed cases in Wuhan from 24 January to 5 March to illustrate the rationality and effectiveness of our model. The results show that, in the early stage of the outbreak of COVID‐19, stopping all the migration of humans, increasing the intensity of treatment, enhancing the awareness of personal protection, and especially increasing the ability to identify asymptomatic infections are indispensable control means to control this disease.
Rationale
Short‐chain fatty acids (SCFAs) are associated with intestinal microbiota and diseases in humans. SCFAs have a low response in mass spectrometry, and in order to increase sensitivity, ...reduce sample consumption, shorten analysis time, and simplify sample preparation steps, a derivatization method was developed.
Methods
We converted seven SCFAs into amide derivatives with 4‐aminomethylquinoline. The reaction occurred for 20 min at room temperature. The analytes were separated on a reversed‐phase C18 column and quantitated in the positive ion electrospray ionization mode using multiple reaction monitoring. Acetic acid‐d4 was used as the stable‐isotope‐labeled surrogate analyte for acetic acid in the working solutions, while the other stable‐isotope‐labeled standards were used as internal standards (ISs).
Results
Method validation showed that the intra‐day and inter‐day precision of quantitation for the seven SCFAs over the whole concentration range was ≤3.8% (n = 6). The quantitation accuracy ranged from 85.5% to 104.3% (n = 6). Most important, the collected feces were vortexed immediately with ethanol.
Conclusions
This study provides a new derivatization method for a precise, accurate, and rapid quantitation of SCFAs in human feces using ultra‐performance liquid chromatography/tandem mass spectrometry. This method successfully determined the concentration of SCFAs in human feces and could assist in the exploration of intestinal microbiota and diseases.
Mitochondrial dynamics plays an important role in tumour progression. However, how these dynamics integrate tumour metabolism in hepatocellular carcinoma (HCC) metastasis is still unclear.
The ...mitochondrial fusion protein mitofusin-1 (MFN1) expression and its prognostic value are detected in HCC. The effects and underlying mechanisms of MFN1 on HCC metastasis and metabolic reprogramming are analysed both in vitro and in vivo.
Mitochondrial dynamics, represented by constant fission and fusion, are found to be associated with HCC metastasis. High metastatic HCC displays excessive mitochondrial fission. Among genes involved in mitochondrial dynamics, MFN1 is identified as a leading downregulated candidate that is closely associated with HCC metastasis and poor prognosis. While promoting mitochondrial fusion, MFN1 inhibits cell proliferation, invasion and migration capacity both in vitro and in vivo. Mechanistically, disruption of mitochondrial dynamics by depletion of MFN1 triggers the epithelial-to-mesenchymal transition (EMT) of HCC. Moreover, MFN1 modulates HCC metastasis by metabolic shift from aerobic glycolysis to oxidative phosphorylation. Treatment with glycolytic inhibitor 2-Deoxy-D-glucose (2-DG) significantly suppresses the effects induced by depletion of MFN1.
Our results reveal a critical involvement of mitochondrial dynamics in HCC metastasis via modulating glucose metabolic reprogramming. MFN1 may serve as a novel potential therapeutic target for HCC.
The diagnosis of biliary atresia (BA) remains a clinical challenge because affected infants have signs, symptoms, and serum liver biochemistry that are also seen in those with other causes of ...neonatal cholestasis (non‐BA). However, an early diagnosis and prompt surgical treatment are required to improve clinical outcome. Recently, the relative abundance of serum matrix metalloproteinase‐7 (MMP‐7) was suggested to have discriminatory features for infants with BA. To test the hypothesis that elevated serum concentration of MMP‐7 is highly diagnostic for BA, we determined the normal serum concentration of MMP‐7 in healthy control infants, and then in 135 consecutive infants being evaluated for cholestasis. The median concentration for MMP‐7 was 2.86 ng/mL (interquartile range, IQR: 1.32‐5.32) in normal controls, 11.47 ng/mL (IQR: 8.54‐24.55) for non‐BA, and 121.1 ng/mL (IQR: 85.42‐224.4) for BA (P < 0.0001). The area under the curve of MMP‐7 for the diagnosis of BA was 0.9900 with a cutoff value of 52.85 ng/mL; the diagnostic sensitivity and specificity were 98.67% and 95.00%, respectively, with a negative predictive value of 98.28%. Conclusion: Serum MMP‐7 assay has high sensitivity and specificity to differentiate BA from other neonatal cholestasis, and may be a reliable biomarker for BA.
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