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The oxygen evolution reaction (OER) frequently acts as a kinetic bottleneck in various energy storage and conversion systems. Effective electrocatalysts for the OER play a crucial role in reducing the reaction barrier and expediting the reaction. Multicomponent transition metal phosphides (TMPs) have garnered an extensive amount of attention as a result of their exceptional performance in the OER. Here, we present a direct method for preparing two intrinsic morphologies of metal-organic frameworks (MOFs), barrel-like BMM-10 and pancake-like BMM-10(Ac), achieved by establishing a protonation/deprotonation equilibrium with varying NO3-/Ac- ratios. The BMM-10(Ac)-C catalyst was synthesized via heat treatment of the BMM-10(Ac) precursor, exhibiting superior OER performance. It realized an overpotential of 286 mV at a current density of 10 mA cm-2, with a Tafel slope of 111.17 mV decade-1 and a current retention of 98.03%. This improvement arises from the synergistic interaction between Ni3P/Ni nanoparticles and the partially graphitic carbon layer, augmenting the exposure of active sites. Furthermore, alterations in the morphological features of MOF-derived Ni3P/Ni carbon nanocomposites adjusted the active electrochemical surface area, thereby modulating the overall OER performance of the corresponding TMP carbon nanocomposites. This methodology can be extended to control the morphology of other MOFs and their derivatives, providing innovative avenues for the design and synthesis of new MOF-based TMP nanomaterials.
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There is significant anticipation for high-efficiency and cost-effective non-precious metal-based catalysts to advance the industrial application of the anodic oxygen evolution reaction (OER) for hydrogen production. This study introduces an efficient strategy that utilizes ligand-induced metal-organic framework (MOF) building blocks for the synthesis of hollow binary zeolitic imidazolate frameworks 67 (ZIF-67) and Prussian blue analogues (PBAs) (ZIF-67@PBA) heterostructures through a hybrid MOF-on-MOF approach. Manipulating the Co2+/Zn2+ ratio in the precursor ZIF-67 allows for the convenient synthesis of the final product, denoted as CoxFe-ZP, after pyrolysis, where the inclusion of Zn effectively modulates the distribution of Co in the catalyst. The resulting CoxFe-ZP catalysts exhibit a positive synergistic effect between hollow graphitic carbon nanomaterials and Fe-doped Co nanoparticles. The optimal Co0.3Fe-ZP catalyst demonstrates satisfactory OER performance, achieving an overpotential of 302 mV at 10 mA cm-2 and a small Tafel slope of 60.0 mV dec-1. Further analysis of the activation energy confirms that the enhanced OER activity of Co0.3Fe-ZP can be reasonably attributed to the combined influence of its morphology and composition. This study demonstrates a ligand-induced method for examining the morphology and electrochemical properties of grown binary MOF-on-MOF heterostructures for OER applications.
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The complex process of the anodic oxygen evolution reaction (OER) severely hinders overall water splitting, which further limits the large-scale production and application of hydrogen energy. In this work, one type of bimetallic coordination polymer of ZnCoBTC using the MOF-on-MOF strategy has been synthesized where both Co(II) and Zn(II) cations exhibit the same coordination environment. By applying an electric potential, the predesigned bimetallic MOF precursor can be conveniently degraded into CoOxHy as an active species for efficient OER. Owing to the dissolution of ZnOxHy species, in situ formed disordered defects on the external surface of the catalyst increase the specific surface area as well as expose abundant active materials. Therefore, the ZnCoOxHy nanosheet shows excellent OER performance and reaches an overpotential of only 334 mV at 10 mA cm-2 with a Tafel slope of 66.4 mV dec-1, indicating fast reaction kinetics. The results demonstrate that metals with the same coordination environment can undergo in situ replacement or secondary growth on the pristine MOF, and they can be electrochemically degraded into highly efficient catalysts for future energy applications.
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PURPOSE: Cervical cancer (CC), as one of the most widespread gynecological malignancies in the world, severely threatens women health. Long non-coding RNA (lncRNA) could exert vital functions in assorted cancers, including CC. Although FLVCR heme transporter 1 antisense RNA 1 (FLVCR1-AS1) has been recognized as a critical effector in different cancers, its precise role and mechanisms have never been studied in CC. METHODS: RT-qPCR analysis was done for the measurement of the expression of FLVCR1-AS1, magnesium transporter 1 (MAGT1) and miR-381-3p in CC cells. Supported by western blot analysis, functional assays were done to evaluate the CC cell phenotype, while mechanism assays were done to explore the putative correlation among genes. RESULTS: In CC cells, FLVCR1-AS1 and MAGT1 were upregulated and miR-381-3p was downregulated. FLVCR1-AS1 or MAGT1 knockdown or miR-381-3p augment restrained CC cell proliferation, migration and invasion, but facilitated cell apoptosis. FLVCR1-AS1 sponged miR-381-3p, and MAGT1 was targeted by the FLVCR1-AS1/miR-381-3p axis. It was also revealed that the inhibitory influences of FLVCR1-AS1 silence on CC cell malignant behaviors were countervailed by MAGT1 overexpression. CONCLUSION: FLVCR1-AS1 exacerbated the malignant phenotype of CC cells via the miR-381-3p/MAGT1 axis.
Assuntos
Proteínas de Transporte de Cátions , MicroRNAs , RNA Longo não Codificante , Neoplasias do Colo do Útero , Humanos , Feminino , RNA Longo não Codificante/genética , RNA Longo não Codificante/metabolismo , Neoplasias do Colo do Útero/patologia , MicroRNAs/genética , MicroRNAs/metabolismo , Regulação Neoplásica da Expressão Gênica , Proliferação de Células/genética , Transformação Celular Neoplásica , Linhagem Celular Tumoral , Movimento Celular/genética , Receptores Virais/genética , Receptores Virais/metabolismo , Proteínas de Membrana Transportadoras/genética , Proteínas de Membrana Transportadoras/metabolismo , Proteínas de Transporte de Cátions/genética , Proteínas de Transporte de Cátions/metabolismoRESUMO
In this work, we presented a long-wavelength emission fluorescent probe DCM-Cou-SePh that can discriminatively detect glutathione (GSH) and hydrogen polysulfides (H2Sn, nâ¯>â¯1) from green and red emission channels, respectively. With the addition of GSH, probe DCM-Cou-SePh displayed green fluorescence emission (λex/emâ¯=â¯430/530â¯nm). In the presence of H2Sn, the probe exhibited a significant fluorescence enhancement in red channel (λex/emâ¯=â¯560/680â¯nm). We also demonstrated that this probe was suitable to quantitatively detect GSH and H2Sn with low detection limits (0.12⯵M for GSH, 0.19⯵M for H2Sn). Furthermore, DCM-Cou-SePh can be used for sensing endogenous GSH and H2Sn in living cells by dual-color fluorescence imaging.
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AIMS: Low density lipoprotein receptor-related protein 6 (LRP6) has been demonstrated to control trophoblast cell invasion, but its regulatory gene remains undefined. In this study, microRNA (miR) regulating LRP6 were explored to elucidate the potential mechanism of preeclampsia (PE). METHODS: Firstly, the expression of LRP6 in PE tissues was detected by immunohistochemical staining and quantitative real-time polymerase chain reaction (qRT-PCR) assay. Prediction software predicted that LRP6 might be the target gene of miR-95-5p, and verified by double-luciferase reporter analysis. qRT-PCR assay measured the expression of miR-95-5p in PE tissues and trophoblast cell lines. Then, we transfected miR-95-5p mimic, inhibitor, LRP6, or mimic plus LRP6 into trophoblast cell lines, and analyzed their influences on cell migration and invasion by wound healing and Transwell experiments. The expressions of matrix metalloproteinase (MMP)-2, MMP-9 and tissue inhibitors of metalloproteinase (TIMP)-1 in transfected cells were examined by western blot (WB) analysis. RESULTS: LRP6 was low-expressed in PE tissues, while miR-95-5p expression was high-expressed. MiR-95-5p negatively regulated the LRP6 expression in trophoblast cells. Both up-regulated LRP6 and down-regulated miR-95-5p can not only promote the migration and invasion of trophoblast cells, but also raised the expressions of MMP-2 and MMP-9 and inhibited the expression of TIMP-1. The over-expression of miR-95-5p suppressed the metastasis of trophoblast cells and rescued LRP6-induced increase of MMP-2 and MMP-9 and reduction of TIMP-1. CONCLUSION: MiR-95-5p involved in the migration and invasion of trophoblast cells by targeting LRP6, which might be a potential therapeutic target for PE.
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MicroRNAs , Pré-Eclâmpsia , Movimento Celular , Feminino , Humanos , Proteína-6 Relacionada a Receptor de Lipoproteína de Baixa Densidade , MicroRNAs/genética , Pré-Eclâmpsia/genética , Gravidez , TrofoblastosRESUMO
BACKGROUND: Gestational diabetes mellitus (GDM) severely threatens maternal and fetal health. Long non-coding RNA (lncRNA) participates in the regulation of various cellular processes. OBJECTIVES: Previous studies have identified the role of lncRNA MALAT1 in diabetic retinopathy-related inflammation. However, the role of lncRNA MALAT1 in GDM has not been reported yet. MATERIAL AND METHODS: Real-time polymerase chain reaction (RT-PCR) was used to measure the lncRNA MALAT1 expression level in placental tissues from GDM patients and from a normal pregnant group. Placental trophoblastic-derived cell line HTR8 cells were divided into a control group, an siRNA negative control group and a MALAT1 siRNA group. The cells underwent RT-PCR analysis of lncRNA MALAT1 expression, an MTT assay of cell proliferation, and a transwell assay of cell invasion and migration. In addition, enzyme-linked immunosorbent assay (ELISA) was used to analyze the level of tumor necrosis factor α (TNF-α) and interleukin 6 (IL-6). Western blotting was used to measure the changes of the tumor growth factor ß (TGF-ß)/nuclear factor-kappa B (NF-κB) signaling pathway. RESULTS: Gestational diabetes mellitus placental tissues showed higher lncRNA MALAT1 expression compared to a normal control group (p < 0.05). After siRNA intervention, lncRNA MALAT1 showed decreased expression in the trophoblastic layer; inhibited trophoblastic cell proliferation, migration, or invasion; decreased the secretion of inflammatory factors TNF-α and IL-6; and suppressed the expression of TGF-ß and NF-κB compared to that of the control and siRNA-NC groups (p < 0.05). CONCLUSIONS: Gestational diabetes mellitus appears to upregulate lncRNA MALAT1. Downregulation of lncRNA MALAT1 inhibits inflammation and suppresses the proliferation, invasion and migration of GDM placental trophoblastic cells, possibly by modulating the TGF-ß/NF-κB signaling pathway.
Assuntos
Diabetes Gestacional , Proliferação de Células , Diabetes Gestacional/genética , Feminino , Humanos , NF-kappa B/metabolismo , Gravidez , RNA Longo não Codificante/genética , Transdução de SinaisRESUMO
Kruppel-like factors (KLFs) are a group of transcriptional regulators, being tumor-suppressive in various types of cancers, but not clear in human endometrial carcinoma (EC). We investigated the KLF-4 expression in both mRNA and protein levels in 29 EC specimens with RT-qPCR and Western blotting methods, and then to determine its promotion to Epithelial-to-mesenchymal transition (EMT) and proliferation of EC Ishikawa cells, via analyzing EMT-associated markers and via CCK-8 and colony forming assay. We found the downregulation of KLF-4 in the 29 EC specimens, correlating with the EC malignance. Moreover, we confirmed reduced levels of EMT and cell proliferation of Ishikawa cells post-KLF-4 overexpression. In conclusion, the significantly reduced KLF-4 correlated with the EC malignance. And the overexpressed KLF-4 promoted the EMT and proliferation of EC cells in vitro. The present study recognized the tumor suppressive role of KLF-4 in EC.
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Biomarcadores Tumorais/metabolismo , Neoplasias do Endométrio/metabolismo , Transição Epitelial-Mesenquimal , Fatores de Transcrição Kruppel-Like/metabolismo , Adulto , Linhagem Celular Tumoral , Proliferação de Células , Regulação para Baixo , Feminino , Humanos , Fator 4 Semelhante a KruppelRESUMO
Understanding the association between congenital human cytomegalovirus (HCMV) infection and active maternal HCMV infection during pregnancy is important for maternal and neonatal healthcare. In the present study, a loop-mediated isothermal amplification (LAMP) method was established for the detection of CMV DNA from whole blood or amniotic fluid samples, using reverse transcription-quantitative polymerase chain reaction. The results of the present study demonstrated that the CMV LAMP assay detection was specific for CMV DNA, whereas it did not detect viral DNA from herpes simplex type 1 (HSV-1), HSV-2, varicella zoster virus, HSV-6 or HSV-7. Sensitivity determination using serially-diluted CMV glycoprotein B-containing plasmids, demonstrated that >10 copies per tube were detectable using the CMV LAMP method. Furthermore, the detection results, using the LAMP method for 336 whole blood samples, demonstrated that at a threshold of 10(1)-10(4) copies per tube, the sensitivity of this method was 86.96-100%, the specificity was 97.24-100%, the positive predictive value was 76.92-100% and the negative predictive value was 99.05-100%. The results for 11 amniotic fluid samples from pregnant women with whole blood CMV-positive and 15 control amniotic fluid samples, indicated that the CMV LAMP assay was sensitive and specific for CMV detection. In conclusion, in the present study, a CMV LAMP method was developed, which was shown to be sensitive, specific and efficient in the detection of HCMV infection. Furthermore, CMV LAMP is capable of detecting active CMV infection in pregnant women. Therefore, the current study provides novel insights into diagnostic approaches for active CMV infection in pregnant women.