Surface Chemistry Modulation of BaGd0.8La0.2Co2O6-δ As Active Air Electrode for Solid Oxide Cells.

Modulation of the surface chemistry of air electrodes makes it possible to significantly improve the electrocatalytic performance of solid oxide cells (SOCs). Here, the surface chemistry of BaGd0.8La0.2Co2O6-δ (BGLC) double perovskite is modulated by treatment in an acidic citric acid solution. The treatment leads to corrosion on the surface of BGLC particles, and the effect is dependent on the acidity of the solution. As the acidity of solution is low, Ba cations are selectively dissolved out of the BGLC surface, while as the acidity increases, the corrosion becomes more homogeneous. The Ba surface deficiency remarkably increases the concentration of surface oxygen vacancies and electrocatalytic activity of BGLC. To avoid the loss of Ba-deficient surface during the conventional high temperature sintering process, a sintering-free fabrication route is utilized to directly assemble the Ba-deficient BGLC powder into an air electrode. A single cell with the surface Ba-deficient BGLC electrode shows a peak power density of 1.04 W cm-2 at 750 °C and an electrolysis current density of 1.48 A cm-2 at 1.3 V, much greater than 0.64 W cm-2 and 1.02 A cm-2 of the cell with the pristine BGLC, respectively. This work provides a simple and effective surface chemistry modulation strategy for the development of an efficient air electrode for SOCs.

[Anti-tumor mechanism of total saponins of Paridis Rhizoma on inducing ferroptosis of breast cancer MCF-7 cells].

This study aims to investigate the mechanism of total saponins of Paridis Rhizoma in inducing the ferroptosis of MCF-7 cells and provide a theoretical basis for the clinical treatment of breast cancer with total saponins of Paridis Rhizoma. The methyl thiazolyl tetrazolium(MTT) assay was employed to examine the effects of different concentrations of total saponins of Paridis Rhizoma on the proliferation of MCF-7 cells. A phase contrast inverted microscope was used to observe the morphological changes of MCF-7 cells. The colony formation assay was employed to test the colony formation of MCF-7 cells. The lactate dehydrogenase(LDH) release test was conducted to determine the cell membrane integrity of MCF-7 cells. The cell scratch assay was employed to examine the migration of MCF-7 cells. After that, the level of reactive oxygen species(ROS) in MCF-7 cells was observed by an inverted fluorescence microscope, and the content of Fe~(2+) in MCF-7 cells was detected by the corresponding kit. Transmission electron microscopy was employed to observe the mitochondrial ultrastructure of MCF-7 cells. Western blot was employed to determine the expression of ferroptosis-related proteins, such as p53, solute carrier family 7 member 11(SLC7A11), glutathione peroxidase 4(GPX4), acyl-CoA synthetase long-chain family member 4(ACSL4), and transferrin receptor protein 1(TFR1) in MCF-7 cells. The results showed that 1.5, 3, 4.5, 6, 7.5, and 9 µg·mL~(-1) total saponins of Paridis Rhizoma significantly inhibited the proliferation of MCF-7 cells, with the IC_(50) of 4.12 µg·mL~(-1). Total saponins of Paridis Rhizoma significantly damaged the morphology of MCF-7 cells, leading to the formation of vacuoles and the gradual shrinkage and detachment of cells. Meanwhile, total saponins of Paridis Rhizoma inhibited the colony formation of MCF-7 cells, destroyed the cell membrane(leading to the release of LDH), and shortened the migration distance of MCF-7 cells. Total saponins of Paridis Rhizoma treatment significantly increased the content of ROS, induced oxidative damage, and led to the accumulation of Fe~(2+) in MCF-7 cells. Furthermore, total saponins of Paridis Rhizoma changed the mitochondrial structure, increased the mitochondrial membrane density, led to the decrease or even disappear of ridges, promoted the expression of p53 protein, down-regulated the expression of SLC7A11 and GPX4, and up-regulated the expression of ACSL4 and TFR1. In summary, total saponins of Paridis Rhizoma can significantly inhibit the proliferation and migration of MCF-7 cells and destroy the cell structure by inducing ferroptosis.

Amyloid-ß1-42 oligomers enhance mGlu5R-dependent synaptic weakening via NMDAR activation and complement C5aR1 signaling.

Synaptic weakening and loss are well-correlated with the pathology of Alzheimer's disease (AD). Oligomeric amyloid beta (oAß) is considered a major synaptotoxic trigger for AD. Recent studies have implicated hyperactivation of the complement cascade as the driving force for loss of synapses caused by oAß. However, the initial synaptic cues that trigger pathological complement activity remain elusive. Here, we examined a form of synaptic long-term depression (LTD) mediated by metabotropic glutamate receptors (mGluRs) that is disrupted in rodent models of AD. Exogenous application of oAß (1-42) to mouse hippocampal slices enhanced the magnitude of mGlu subtype 5 receptor (mGlu5R)-dependent LTD. We found that the enhanced synaptic weakening occurred via both N-methyl-D-aspartate receptors (NMDARs) and complement C5aR1 signaling. Our findings reveal a mechanistic interaction between mGlu5R, NMDARs, and the complement system in aberrant synaptic weakening induced by oAß, which could represent an early trigger of synaptic loss and degeneration in AD.

Electrochemically Assisted Construction of a La2NiO4+δ@Pt Core-Shell Structure for Enhancing the Performance and Durability of La2NiO4+δ Cathodes.

Ruddlesden-Popper oxide La2NiO4+δ (LNO) has a high ionic conductivity and good thermal match with the electrolyte of solid oxide fuel cells (SOFCs); however, LNO suffers from performance decay owing to the La surface segregation under the operation conditions of SOFCs. Herein, we report an in situ electrochemical decoration strategy to improve the electrocatalytic activity and durability of LNO cathodes. We show that the electrochemical polarization leads to in situ construction of the LNO@Pt core-shell structure, significantly suppressing the detrimental effect of La surface segregation on the LNO cathode. The initial peak power density of a single cell with the LNO cathode is 0.71 W cm-2 at 750 °C, increasing to 1.39 W cm-2 by the in situ construction of the LNO@Pt core-shell structure after polarization at 0.5 A cm-2 for 20 h. The LNO@Pt core-shell structure is also highly durable without noticeable performance degradation over the duration of the test for 180 h. The findings shed light on the design and fabrication of highly active and durable LNO-based cathodes for SOFCs.

Facile Construction of Nanostructured Cermet Anodes with Strong Metal-Oxide Interaction for Efficient and Durable Solid Oxide Fuel Cells.

Nanostructured anodes generate massive reaction sites to oxidize fuels in solid oxide fuel cells (SOFCs); however, the nonexistence of a practically viable approach for the construction of nanostructures and the retention of these nanostructures under the harsh operating conditions of SOFCs poses a significant challenge. Herein, a simple procedure is reported for the construction of a nanostructured Ni-Gd-doped CeO2 anode based on the direct assembly of pre-formed nanocomposite powder with strong metal-oxide interaction. The directly assembled anode forms heterointerfaces with the electrolyte owing to the electrochemical polarization current and exhibits excellent structural robustness against thermal ripening. An electrolyte-supported cell with the directly assembled anode produces a peak power density of 0.73 W cm-2 at 800 °C, while maintaining stability for 100 h, which is in contrast to the drastic degradation of the cermet anode prepared using the conventional method. These findings provide clarity on the design and construction of durable nanostructured anodes and other electrodes for SOFCs.

Lin28a maintains a subset of adult muscle stem cells in an embryonic-like state.

During homeostasis and after injury, adult muscle stem cells (MuSCs) activate to mediate muscle regeneration. However, much remains unclear regarding the heterogeneous capacity of MuSCs for self-renewal and regeneration. Here, we show that Lin28a is expressed in embryonic limb bud muscle progenitors, and that a rare reserve subset of Lin28a+Pax7- skeletal MuSCs can respond to injury at adult stage by replenishing the Pax7+ MuSC pool to drive muscle regeneration. Compared with adult Pax7+ MuSCs, Lin28a+ MuSCs displayed enhanced myogenic potency in vitro and in vivo upon transplantation. The epigenome of adult Lin28a+ MuSCs showed resemblance to embryonic muscle progenitors. In addition, RNA-sequencing revealed that Lin28a+ MuSCs co-expressed higher levels of certain embryonic limb bud transcription factors, telomerase components and the p53 inhibitor Mdm4, and lower levels of myogenic differentiation markers compared to adult Pax7+ MuSCs, resulting in enhanced self-renewal and stress-response signatures. Functionally, conditional ablation and induction of Lin28a+ MuSCs in adult mice revealed that these cells are necessary and sufficient for efficient muscle regeneration. Together, our findings connect the embryonic factor Lin28a to adult stem cell self-renewal and juvenile regeneration.

Facile Approach for Improving the Interfacial Adhesion of Nanofiber Air Electrodes of Reversible Solid Oxide Cells.

Nanofibers have great promise as a highly active air electrode for reversible solid oxide cells (ReSOCs); however, one thorny issue is how to adhesively stick nanofibers to electrolyte with no damage to the original morphology. Herein, PrBa0.8Ca0.2Co2O5+δ (PBCC) nanofibers are applied as an air electrode by a facile direct assembly approach that leads to the retention of most of the unique microstructure of nanofibers, and firm adhesion of the nanofiber electrode onto the electrolyte is achieved by applying electrochemical polarization. A single cell with the PBCC nanofiber air electrode exhibits excellent maximum power density (1.97 W cm-2), electrolysis performance (1.3 A cm-2 at 1.3 V), and operating stability at 750 °C for 200 h. These findings provide a facile means for the utilization of nanofiber electrodes for high-performance and durable ReSOCs.

Ultrafine, Dual-Phase, Cation-Deficient PrBa0.8Ca0.2Co2O5+δ Air Electrode for Efficient Solid Oxide Cells.

Nanostructured air electrodes play a crucial role in improving the electrocatalytic activity of oxygen reduction and evolution reactions in solid oxide cells (SOCs). Herein, we report the fabrication of a nanostructured BaCoO3-decorated cation-deficient PrBa0.8Ca0.2Co2O5+δ (PBCC) air electrode via a combined modification and direct assembly approach. The modification approach endows the dual-phase air electrode with a large surface area and abundant oxygen vacancies. An intimate air electrode-electrolyte interface is in situ constructed with the formation of a catalytically active Co3O4 bridging layer via electrochemical polarization. The corresponding single cell exhibits a peak power density of 2.08 W cm-2, an electrolysis current density of 1.36 A cm-2 at 1.3 V, and a good operating stability at 750 °C for 100 h. This study provides insights into the rational design and facile utilization of an active and stable nanostructured air electrode of SOCs.

[Diversity and functional prediction of gut microbiota in children with autism spectrum disorder]. / å­¤ç‹¬ç—‡è°±ç³»éšœç¢å„¿ç«¥è‚ é“èŒç¾¤å¤šæ ·æ€§ç ”ç©¶åŠåŠŸèƒ½é¢„æµ‹åˆ†æž.

OBJECTIVES: To study the structure and diversity of gut microbiota in children with autism spectrum disorder (ASD), and to predict the metabolic function of gut microbiota. METHODS: Fecal samples were collected from 30 ASD children (ASD group) and 20 typically developing (TD) children (TD group). Genomic DNA was extracted, the 16S rDNA V4 region was amplified by PCR, and Illumina NovaSeq6000 platform was used for high-throughput sequencing. The composition and distribution characteristics of gut microbiota were analyzed for the two groups, and the metabolic function of gut microbiota was predicted. RESULTS: There were no significant differences in alpha diversity indices (Chao1, Shannon, and Simpson) of gut microbiota between the ASD and TD groups (P>0.05). At the phylum and class levels, there was no significant difference in the structure of gut microbiota between the two groups (P>0.05). Compared with the TD group, the ASD group had significantly higher abundance of Megamonas, Barnesiella, Dialister, Megasphaera, Ruminococcus_torques_group, and Fusobacterium at the genus level (P<0.05). Functional prediction analysis showed that compared with the TD group, the ASD group had a significantly lower abundance of the gut microbiota with the metabolic functions such as tryptophan degradation, glutamate degradation, and butyrate production (P<0.05) and a significantly higher abundance of the gut microbiota with the metabolic function of GABA degradation (P<0.05). CONCLUSIONS: There is no significant difference in the alpha diversity of gut microbiota between ASD children and TD children, while there are differences in the composition of species at the genus level and the metabolic functions of gut microbiota.

Preliminary Exploration of Clinical Efficacy and Pharmacological Mechanism of Modified Danggui-Shaoyao San in the Treatment of Depression in Patients with Chronic Kidney Disease.

Background: Depression in Chronic Kidney Disease (CKD) seriously affects the prognosis of patients and Modified Danggui-Shaoyao-San (MDSS) is based on the traditional Chinese formula Danggui-Shaoyao-San (DSS) for the treatment of depression, which is further optimized. The aim of this study was to evaluate the clinical efficacy and safety of MDSS for the treatment of depression in CKD, and to explain the molecular mechanism of MDSS for the treatment of depression in CKD through pharmacology and molecular docking. Methods: 62 patients were randomly divided into treatment group (treated with MDSS) and control group (treated with placebo) and assessed by Hamilton Depression Scale, and the primary outcome was to evaluate the efficacy of MDSS in improving depressive symptoms and the effect on liver and kidney function, electrolytes. In addition, we identified the core compounds and potential targets of MDSS through the TCMSP database. The GeneCards, OMIM and Disgenet databases were then used to identify molecular targets for CKD and depression. The target protein-protein interaction network was built using STRING database. Core targets were analyzed by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG). Molecular docking was used to verify the relationship between core active compounds and proteins. Results: Clinical results showed that CKD patients in the MDSS group had significantly improved depressive status with no significant adverse effects. By network pharmacology analysis, we found that the compound-target network mainly contained 47 compounds and 69 corresponding targets. 844 terms were analyzed by GO enrichment, and 254 signaling pathways in KEGG. Molecular docking showed that the top active compounds had high affinity with four targets. Conclusion: We preliminarily investigated the efficacy of MDSS in the treatment of depression in CKD and revealed the characteristics of multiple compounds and multiple targets in MDSS.

Selective Recruitment of Presynaptic and Postsynaptic Forms of mGluR-LTD.

In area CA1 of the hippocampus, long-term depression (LTD) can be induced by activating group I metabotropic glutamate receptors (mGluRs), with the selective agonist DHPG. There is evidence that mGluR-LTD can be expressed by either a decrease in the probability of neurotransmitter release [P(r)] or by a change in postsynaptic AMPA receptor number. However, what determines the locus of expression is unknown. We investigated the expression mechanisms of mGluR-LTD using either a low (30 µM) or a high (100 µM) concentration of (RS)-DHPG. We found that 30 µM DHPG generated presynaptic LTD that required the co-activation of NMDA receptors, whereas 100 µM DHPG resulted in postsynaptic LTD that was independent of the activation of NMDA receptors. We found that both forms of LTD occur at the same synapses and that these may constitute the population with the lowest basal P(r). Our results reveal an unexpected complexity to mGluR-mediated synaptic plasticity in the hippocampus.

Quantitative assessment of liver function with hepatocyte fraction: Comparison with T1 relaxation-based indices.

PURPOSE: This study aimed to assess the use of hepatocyte fraction in gadoxetic acid-enhanced magnetic resonance imaging (MRI) for quantitatively evaluating the liver function in comparison with T1 relaxation-based indices. METHODS: This retrospective study included 79 patients with chronic liver disease, who were divided into 2 groups based on the results of the indocyanine green retention test (ICG). All patients underwent a gadoxetic acid-enhanced MRI of the liver. Pre- and post-contrast Look-Locker sequences were used 20 min after gadoxetic acid administration to acquire T1 mapping. Two readers independently identified and measured the MRI parameters [five T1 relaxation-based indices (T1pre, T1post, rrT1, R1post/R1pre and ΔR1) and two hepatocyte fraction indices (HeF and KHep)]. An Independent-samples t test was used to compare each parameter for the two groups. Pearson correlation analysis was used to analyze the correction in each parameter and 15-minute ICG retention rate (ICG-R15). Receiver operating characteristic analyses were performed to differentiate the diagnostic performance of each parameter in ICG-R15 ≤ 20 % and ICG-R15 > 20 % groups. RESULTS: T1pre and T1post were significantly lower in the ICG-R15 ≤ 20 % group than in the ICG-R15 > 20 % group (P < 0.05). rrT1, R1post/R1pre, ΔR1, HeF, and KHep were significantly higher in the ICG-R15 ≤ 20 % group than in the ICG-R15 > 20 % group (P < 0.05). The correction coefficients between T1pre, T1post, rrT1, R1post/R1pre, ΔR1, HeF, KHep, and ICG-R15 were 0.343, 0.783, -0.833, -0.781, -0.803, -0.819, and -0.832, respectively. The area under the curves (AUCs) of T1pre, T1post, rrT1, R1post/R1pre, ΔR1, HeF, and KHep in assessing the ICG-R15＞20 % groups were 0.761, 0.945, 0.912, 0.912, 0.948, 0.945, and 0.950, respectively. KHep had the highest AUC, sensitivity, and specificity. CONCLUSION: Hepatocyte fraction based on gadoxetic acid-enhanced T1-mapping MRI is an efficient diagnostic tool for the quantitative evaluation of liver function.

Efficacy and safety of regorafenib or fruquintinib plus camrelizumab in patients with microsatellite stable and/or proficient mismatch repair metastatic colorectal cancer: an observational pilot study.

This study was to investigate the efficacy and safety of regorafenib or fruquintinib combined with camrelizumab in patients with microsatellite stable (MSS) and/or proficient mismatch repair (pMMR) metastatic colorectal cancer (mCRC). Medical records of MSS/pMMR mCRC patients who received regorafenib (80 mg) or fruquintinib (3 mg) once a day (21 days on/7 days off) plus camrelizumab (200 mg) every three weeks in Yuhuangding Hospital between January 2020 and June 2020 were retrospectively collected. Follow-up data up to November 1st, 2020 was gathered. The primary endpoint was the objective response rate (ORR) and disease control rate (DCR). The safety profile was the secondary endpoint. A total of 16 patients were enrolled. The ORR was 25.0% (4/16) and the DCR was 62.5% (10/16). The main adverse events (AEs) included reactive cutaneous capillary endothelial proliferation (RCCEP) (81.3%), fatigue (43.8%), hypertension (37.5%), hand-foot skin reaction (25.0%), and thyroid dysfunction (25.0%). Most AEs were grade 1 or 2, with only 1 patient of grade 3 liver dysfunction. All the AEs were ameliorated by effective symptomatic treatment. Regorafenib or fruquintinib plus camrelizumab exhibited promising efficacy in patients with MSS/pMMR mCRC. The toxicity was moderate and manageable.

Bufalin suppresses the migration and invasion of prostate cancer cells through HOTAIR, the sponge of miR-520b.

Bufalin, the major active component of the traditional Chinese medicine ChanSu obtained from the skin and parotid venom glands of toads, has long been known as an anticancer agent. Recent studies show that microRNAs (miRs) are involved in the anticancer activities of bufalin, while long non-coding RNAs (lncRNAs) are known to interact with miRNAs to regulate various biological functions. In this paper, we investigated the possible network related to the antimetastatic effect of bufalin in prostate cancer (PCa) cells. We demonstrated that bufalin (0.05-10 µM) dose-dependently suppressed the proliferation of prostate cancer DU145 and PC3 cells with IC50 values of 0.89 and 1.28 µM, respectively. Furthermore, bufalin treatment significantly suppressed the cell migration and invasion. To explore the role of lncRNAs in the antimetastatic activity of bufalin, we used an lncRNA microarray and found that HOX transcript antisense RNA (HOTAIR) was the most markedly downregulated lncRNA in bufalin-treated PCa cells. Overexpression of HOTAIR counteracted the suppressing effects of bufalin on DU145 and PC3 cells. We then predicted and verified that HOTAIR upregulated FGFR1 expression by sponging miR-520b in PCa cells. In 40 patients with PCa bone metastasis, we used in situ hybridization or immunohistochemical assay to assess the HOTAIR and FGFR1 expression, which revealed that both HOTAIR and FGFR1 expression were significantly higher in bone metastasis tissues than in the primary PCa tissues. In addition, the level of serum HOTAIR was positively associated with the levels of serum bone metabolic markers (CTx, OST, B-ALP and PINP) and may serve as a reasonable biomarker for PCa bone metastasis. Taken together, this is the first study revealing that HOTAIR promotes PCa bone metastasis, and bufalin may be a promising candidate for the treatment of this disease.

LncRNA AWPPH and miRNA-21 regulates cancer cell proliferation and chemosensitivity in triple-negative breast cancer by interacting with each other.

Long-non-coding RNAs (lncRNA) AWPPH promotes the progression of liver and bladder cancer, indicating its oncogenic role. The current study aimed to explore the involvement of AWPPH in triple-negative breast cancer (TNBC). In the current study, we found that plasma levels of lncRNA AWPPH and microRNA-21 (miRNA-21) were upregulated in patients with TNBC than in healthy controls, and the upregulation of plasma lncRNA AWPPH and miRNA-21 distinguished early-stage patients with TNBC from healthy controls. Plasma levels of lncRNA AWPPH and miRNA-21 were significantly and positively correlated in both patients with TNBC and healthy controls. LncRNA AWPPH and miRNA-21 overexpression led to promoted cancer cells proliferation and improved cancer cell viability under carboplatin treatment, while lncRNA AWPPH small interfering RNA (siRNA) silencing played an opposite role. In addition, miRNA-21 overexpression attenuated the effects of lncRNA AWPPH siRNA silencing on of cancer cell behaviors. LncRNA AWPPH overexpression led to upregulated miRNA-21 in TNBC cells, while miRNA-21 overexpression also led to significantly upregulated lncRNA AWPPH expression. Therefore, lncRNA AWPPH and miRNA-21 may regulate cancer cell proliferation and chemosensitivity in TNBC by interacting with each other.

Macrophage-derived CCL18 promotes osteosarcoma proliferation and migration by upregulating the expression of UCA1.

Osteosarcoma (OS), which is the most common primary malignant bone tumor, has a high incidence of pulmonary metastasis. CCL18 (C-C motif chemokine ligand 18), which is secreted by tumor-associated macrophages (TAMs), has been found to be increased in various tumors and is associated with tumor metastasis. However, the role of CCL18 in OS remains unclear. Here, we evaluated the effect of CCL18 on the OS cell lines MG63 and 143B and explored its potential mechanisms. We found that CCL18 enhanced the proliferation and migration of OS cells and upregulated UCA1 through transcription factor EP300. Subsequently, we further revealed that the downstream Wnt/ß-catenin signaling pathway participated in this process. In addition, the high expression of CCL18 in both tissue and serum from patients was closely related to pulmonary metastasis and poor survival in OS patients. The tumor xenograft models also showed that CCL18 promoted the metastasis of OS cells. Collectively, our study indicated that macrophage-derived CCL18 promotes OS proliferation and metastasis via the EP300/UCA1/Wnt/ß-catenin pathway and that CCL18 may be used as a prognostic marker and therapeutic target of OS. KEY MESSAGES: CCL18 promotes proliferation and migration of osteosarcoma cells by EP300/ UCA1/ Wnt/ß-catenin pathway. CCL18+ TAMs are significantly correlated with pulmonary metastasis and poor survival in osteosarcoma patients. CCL18 may be used as a prognostic marker and therapeutic target for osteosarcoma.

The Probability of Neurotransmitter Release Governs AMPA Receptor Trafficking via Activity-Dependent Regulation of mGluR1 Surface Expression.

A major mechanism contributing to synaptic plasticity involves alterations in the number of AMPA receptors (AMPARs) expressed at synapses. Hippocampal CA1 synapses, where this process has been most extensively studied, are highly heterogeneous with respect to their probability of neurotransmitter release, P(r). It is unknown whether there is any relationship between the extent of plasticity-related AMPAR trafficking and the initial P(r) of a synapse. To address this question, we induced metabotropic glutamate receptor (mGluR) dependent long-term depression (mGluR-LTD) and assessed AMPAR trafficking and P(r) at individual synapses, using SEP-GluA2 and FM4-64, respectively. We found that either pharmacological or synaptic activation of mGluR1 reduced synaptic SEP-GluA2 in a manner that depends upon P(r); this process involved an activity-dependent reduction in surface mGluR1 that selectively protects high-P(r) synapses from synaptic weakening. Consequently, the extent of postsynaptic plasticity can be pre-tuned by presynaptic activity.

Knockdown of LINC01614 inhibits lung adenocarcinoma cell progression by up-regulating miR-217 and down-regulating FOXP1.

We tried to identify the function of LINC01614 in lung adenocarcinoma (LUAD) and reveal its underlying mechanisms. qRT-PCR was applied to assess the expression of LINC016014 in LUAD tissues, noncancerous tissues and cells. Through colony formation assay, MTT assay and apoptosis analysis, we examined the variation of cell proliferation and apoptosis ability after silencing LINC01614. Moreover, the targeting interactions among LINC01614, miR-217 and FOXP1 were validated via luciferase reporter assay, and then, we regulated the expression of miR-217 and FOXP1 to ascertain their importance in cell proliferation and apoptosis. LINC01614 and FOXP1 were found to be up-regulated in LUAD tumours and cells, whereas miR-217 was down-regulated. The experiment showed that target-specific selectivity exists between LINC01614-miR-217 and miR-217-FOXP1 3'UTR. Furthermore, we disclosed that inhibition of LINC01614 could activate miR-217, which subsequently restrained FOXP1. It was proved that LINC01614 promoted FOXP1 by inhibiting miR-217, which ultimately stimulated the development of LUAD.

[Research on classification of brain functional network features during mental fatigue].

This study is aimed to investigate objective indicators of mental fatigue evaluation to improve the accuracy of mental fatigue evaluation. Mental fatigue was induced by a sustained cognitive task. The brain functional networks in two states (normal state and mental fatigue state) were constructed based on electroencephalogram (EEG) data. This study used complex network theory to calculate and analyze nodal characteristics parameters (degree, betweenness centrality, clustering coefficient and average path length of node), and served them as the classification features of support vector machine (SVM). Parameters of the SVM model were optimized by gird search based on 6-fold cross validation. Then, the subjects were classified. The results show that characteristic parameters of node of brain function networks can be divided into normal state and mental fatigue state, which can be used in the objective evaluation of mental fatigue state.

Ultrahigh adsorption and singlet-oxygen mediated degradation for efficient synergetic removal of bisphenol A by a stable zirconium-porphyrin metal-organic framework.

Bisphenol A (BPA), one of 23 most important endocrine disrupting chemicals, was efficiently removed and sequentially photodegraded by a zirconium-porphyrin metal-organic framework (MOF) catalyst under visible light for water treatment. Well control of photodegradation allows the kinetic separation of adsorption step and photodegradation step. Ultrahigh adsorption uptake of 487.69 ± 8.37 mg g-1 is observed, while efficient photodegradation could be observed within 20 min at the rate of 0.004 mg min-1. The synergetic effect boosts the photocatalytic efficiency and confirms that the catalysis happens inside the MOF pores other than in the solution phase. Furthermore, the mechanism was elucidated by diverse control experiments, such as in the conditions of 1O2 scavenger, in darkness and with the changes of light sensitizing ligands. It confirmed that BPA was oxidized by the 1O2 which was generated from porphyrin ligand within MOFs under visible-light. The excellent reusability and wide range of suitable pH range make the Zr-porphyrin MOFs practical for the photocatalytic water treatment processes.