CoFeBP Micro Flowers (MFs) for Highly Efficient Hydrogen Evolution Reaction and Oxygen Evolution Reaction Electrocatalysts.

Hydrogen is one of the most promising green energy alternatives due to its high gravimetric energy density, zero-carbon emissions, and other advantages. In this work, a CoFeBP micro-flower (MF) electrocatalyst is fabricated as an advanced water-splitting electrocatalyst by a hydrothermal approach for hydrogen production with the highly efficient hydrogen evolution reaction (HER) and oxygen evolution reaction (OER). The fabrication process of the CoFeBP MF electrocatalyst is systematically optimized by thorough investigations on various hydrothermal synthesis and post-annealing parameters. The best optimized CoFeBP MF electrode demonstrates HER/OER overpotentials of 20 mV and 219 mV at 20 mA/cm2. The CoFeBP MFs also exhibit a low 2-electrode (2-E) cell voltage of 1.60 V at 50 mA/cm2, which is comparable to the benchmark electrodes of Pt/C and RuO2. The CoFeBP MFs demonstrate excellent 2-E stability of over 100 h operation under harsh industrial operational conditions at 60 °C in 6 M KOH at a high current density of 1000 mA/cm2. The flower-like morphology can offer a largely increased electrochemical active surface area (ECSA), and systematic post-annealing can lead to improved crystallinity in CoFeBP MFs.

Dual-Functional Ru/Ni-B-P Electrocatalyst Toward Accelerated Water Electrolysis and High-Stability.

Development of advanced electrocatalysts for the green hydrogen production by water electrolysis is an important task to reduce the climate and environmental issues as well as to meet the future energy demands. Herein, Ru/Ni-B-P sphere electrocatalyst is demonstrated by a combination of hydrothermal and soaking approaches, meeting the industrial requirement of low cell voltage with stable high-current operation. The Ru/Ni-B-P sphere catalyst demonstrates low overpotentials of 191 and 350 mV at 300 mA cm-2 with stable high current operation, ranking it as one of the best oxygen evolution reaction (OER) electrocatalysts. The bifunctional 2-E system demonstrates a low cell voltage of 2.49 V at 2000 mA cm-2 in 6 m KOH at 60 °C of harsh industrial operation condition. It also demonstrates outstanding stability with continuous 120 h (5 days) CA operation at 1000 mA cm-2. Further, the hybrid configuration of Ru/Ni-B-P || Pt/C being paired with the conventional benchmark electrode demonstrates a record low 2-E cell voltage of 2.40 V at 2000 mA cm-2 in 6 m KOH and excellent stability at high current of 1500 mA cm-2 under industrial operational condition.

MoS2 Nanoplatelets on Hybrid Core-Shell (HyCoS) AuPd NPs for Hybrid SERS Platform for Detection of R6G.

In this work, a novel hybrid SERS platform incorporating hybrid core-shell (HyCoS) AuPd nanoparticles (NPs) and MoS2 nanoplatelets has been successfully demonstrated for strong surface-enhanced Raman spectroscopy (SERS) enhancement of Rhodamine 6G (R6G). A significantly improved SERS signal of R6G is observed on the hybrid SERS platform by adapting both electromagnetic mechanism (EM) and chemical mechanism (CM) in a single platform. The EM enhancement originates from the unique plasmonic HyCoS AuPd NP template fabricated by the modified droplet epitaxy, which exhibits strong plasmon excitation of hotspots at the nanogaps of metallic NPs and abundant generation of electric fields by localized surface plasmon resonance (LSPR). Superior LSPR results from the coupling of distinctive AuPd core-shell NP and high-density background Au NPs. The CM enhancement is associated with the charge transfer from the MoS2 nanoplatelets to the R6G. The direct contact via mixing approach with optimal mixing ratio can effectively facilitate the charges transfer to the HOMO and LUMO of R6G, leading to the orders of Raman signal amplification. The enhancement factor (EF) for the proposed hybrid platform reaches ~1010 for R6G on the hybrid SERS platform.

Hybrid UV Photodetector Design Incorporating AuPt Alloy Hybrid Nanoparticles, ZnO Quantum Dots, and Graphene Quantum Dots.

A hybrid device scheme is an attractive strategy in the construction of advanced UV photodetectors due to the flexibility in selecting the components and correspondingly improved optoelectronic properties by the cooperation of various components, which cannot be achieved by a single component device. In this work, a novel hybrid UV photodetector (PD) is demonstrated by adapting AuPt alloy hybrid nanoparticles (AHNPs), ZnO quantum dots (QDs), and graphene quantum dots (GQDs), namely, GQD/ZnO/AHNP PD. The optimized device achieves high-end figure-of-merit performance with a responsivity of 2299 mA/W, detectivity of 7.04 × 1010 jones, and external quantum efficiency of 741%. Enhanced photocurrent can be associated with the hot electron generation around the AuPt AHNPs and swift transfer to the conduction band of ZnO QDs. At the same time, the added carrier injection is achieved by a thin layer of GQDs. High density of hotspots and electromagnetic fields are generated by the strong localized surface plasmon resonance (LSPR) by the uniquely designed AuPt AHNPs with the fully alloyed AuPt NPs and adjacent small background Au NPs. The e-field distribution of various NP configurations is systematically investigated with finite-difference time-domain (FDTD) simulations.

Vanadium-Doped FeBP Microsphere Croissant for Significantly Enhanced Bi-Functional HER and OER Electrocatalyst.

Ultra-fine hydrogen produced by electrochemical water splitting without carbon emission is a high-density energy carrier, which could gradually substitute the usage of traditional fossil fuels. The development of high-performance electrocatalysts at affordable costs is one of the major research priorities in order to achieve the large-scale implementation of a green hydrogen supply chain. In this work, the development of a vanadium-doped FeBP (V-FeBP) microsphere croissant (MSC) electrocatalyst is demonstrated to exhibit efficient bi-functional water splitting for the first time. The FeBP MSC electrode is synthesized by a hydrothermal approach along with the systematic control of growth parameters such as precursor concentration, reaction duration, reaction temperature and post-annealing, etc. Then, the heteroatom doping of vanadium is performed on the best FeBP MSC by a simple soaking approach. The best optimized V-FeBP MSC demonstrates the low HER and OER overpotentials of 52 and 180 mV at 50 mA/cm2 in 1 M KOH in a three-electrode system. In addition, the two-electrode system, i.e., V-FeBP || V-FeBP, demonstrates a comparable water-splitting performance to the benchmark electrodes of Pt/C || RuO2 in 1 M KOH. Similarly, exceptional performance is also observed in natural sea water. The 3D MSC flower-like structure provides a very high surface area that favors rapid mass/electron-transport pathways, which improves the electrocatalytic activity. Further, the V-FeBP electrode is examined in different pH solutions and in terms of its stability under industrial operational conditions at 60 °C in 6 M KOH, and it shows excellent stability.

Significant role of long non-coding RNA MALAT1 in deep vein thrombosis via the regulation of vascular endothelial cell physiology through the microRNA-383-5p/BCL2L11 axis.

Deep vein thrombosis (DVT) is a vascular disease. The long non-coding RNA (lncRNA), metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), is positively expressed in DVT tissues, and regulates the biological behavior of endothelial progenitor cells. Here, we explored whether MALAT1 affected the physiology of human vascular endothelial cells (HUVECs) and analyzed its underlying mechanism. To overexpress/silence the expression of MALAT1 in HUVECs, MALAT1-plasmid/MALAT1-small interfering RNA (siRNA) was used. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide and flow cytometry analyses were performed to observe the cell viability and apoptosis. Reverse transcription-quantitative polymerase chain reaction and western blotting were used to determine the apoptosis-related protein and gene expression levels. We used Starbase software to predict the associations among MALAT1, microRNA (miR)-383-5p, and BCL2-like 11 (BCL2L11). Luciferase reporter assay was used to validate their relationship. Compared to the control vector group, MALAT1-plasmid suppressed the viability and induced apoptosis of HUVECs, while improving Bcl-2-associated X protein (Bax) expression and decreasing Bcl-2 expression. There was an interaction between MALAT1 and miR-383-5p. Compared to the control siRNA group, MALAT1-siRNA increased the cell viability, reduced cell apoptosis, upregulated Bcl-2 expression, and suppressed Bax expression. These changes were reversed by the miR-383-5p inhibitor. Additionally, we verified that BCL2L11 is a target of miR-383-5p. miR-383-5p improved the cell proliferation, while decreasing cell apoptosis in HUVECs by targeting BCL2L11. Therefore, the lncRNA-MALAT1/miR-383-5p/BCL2L11 axis may be effective for DVT treatment.

Study on the Mechanism of Platelet-Released Clusterins Inducing Restenosis after Carotid Endarterectomy by Activating TLR3/NF-κb p65 Signaling Pathway.

This study aimed to explore the role of clusterin released by platelet aggregation in restenosis after carotid endarterectomy. 35 patients who underwent carotid endarterectomy due to carotid artery stenosis were enrolled in this study. They were admitted to the Third Affiliated Hospital of Qiqihar Medical University from January 2018 to January 2019. All the patients were divided into two groups: the restenosis group and the nonrestenosis group, according to the follow-up results within 12 months. Peripheral blood was collected on the first day, 6 months, and 12 months after operation. The expression of CLU in serum of plasma and platelet culture medium was detected by an ELISA experiment. The vascular endothelial cells were cultured in vitro with 100 ng/mL of human recombinant CLU added to the medium. Cell proliferation, migration, and invasion were detected by CCK8, scratch, and Transwell invasion tests. The expression level of TLR3 and NF-κb p65 proteins in cells was detected by western blot. TLR3 knockout plasmids in vascular endothelial cell lines were transfected. Cell proliferation and migration were detected by CCK8 and the scratch assay. The CLU content in peripheral blood plasma and supernatant of platelet culture medium was significantly higher in the restenosis group than that of the control group (p=0.003) 6 months after operation (p=0.047) and 12 months after operation (p=0.011). When CLU was added to vascular endothelial cell culture medium, the proliferation and migration were significantly enhanced. The TLR3/NF-κb p65 protein expression level in cells also significantly increased. After the transfection of TLR3 knockout plasmids into vascular endothelial cell lines, CLU cannot promote the proliferation and migration of vascular endothelial cells. Platelet-released clusterin can induce vascular endothelial cell proliferation and migration by activating the TLR3/NF-kb p65 signaling pathway, leading to carotid artery restenosis after carotid endarterectomy.

Hybrid Device Architecture Using Plasmonic Nanoparticles, Graphene Quantum Dots, and Titanium Dioxide for UV Photodetectors.

In this work, a nanoscale device architecture is demonstrated for a UV photodetector application on sapphire (0001), incorporating the plasmonic hybrid nanoparticles (HNPs), graphene quantum dots (GQDs), and titanium oxide (TiO2) for the first time. The hybrid GQDs/TiO2/HNPs photodetector exhibits the photocurrent of 1.58 × 10-5 A under the 1.64 mW/mm2 of 275 nm illumination at 10 V, which is around two order increase from the bare TiO2 device. The proposed architecture demonstrates a low dark current of ∼1 × 10-10 A at 10 V and thus the device demonstrates an excellent photo to dark current ratio along with the improved rise and fall time on the order of several hundred millisecond. The enhanced performance of device architecture is attributed to the efficient utilization of localized surface plasmon resonance (LSPR) induced hot carriers as well as scattered photons from the plasmonic HNPs that are fully encapsulated by the photoactive TiO2 layers. Furthermore, the addition of GQDs on the TiO2 can offer an additional photon absorption pathway. The proposed hybrid architecture of GQDs/TiO2/HNPs demonstrates the integration of the photon absorption and carrier transfer properties of plasmonic HNPs, GQDs, and TiO2 for an enhanced ultraviolet (UV) photoresponse. The photocurrent enhancement mechanisms of the hybrid device architecture are thoroughly investigated based on the finite-difference time domain (FDTD) simulation along with the energy band analysis. This work demonstrates a great potential of the hybrid device architecture for high-performance UV photodetectors.

Circ-HOMER1 enhances the inhibition of miR-1322 on CXCL6 to regulate the growth and aggressiveness of hepatocellular carcinoma cells.

Hepatocellular carcinoma (HCC) is a common liver malignancy worldwide accompanying with the high rate of recurrence. Accumulating reports have documented the significance of circular RNAs (circRNAs) in carcinogenesis and development of HCC. This study aimed to establish the mechanism underlying circ-HOMER1 involvement in HCC. To this end, we identified a binding site for miR-1322 via bioinformatics, quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR), and dual-luciferase reporter assays providing evidence of a direct link between circ-HOMER1 and miR-1322. Similarly, the target gene of miR-1322 was investigated. Moreover, we determined the specific function of circ-HOMER1 in HCC with the aid of qRT-PCR based on patient clinical records, Cell Counting Kit-8, acridine orange/ethidium bromide double fluorescence staining, flow cytometry, and wound-healing and transwell assays. Notably, circ-HOMER1 was upregulated in both HCC cells and tissues. This aberrant expression pattern was closely correlated with larger tumor size, higher tumor-node-metastasis stage, and poorer prognosis for the patients with HCC. Moreover, silenced circ-HOMER1 inhibited cell proliferation, migration, and invasion concomitant with the promotion of apoptosis in HCC cells, and vice versa. Mechanistically, circ-HOMER1 enhanced the inhibition of miR-1322 on CXCL6 in HCC. Furthermore, we found that circ-HOMER1 promoted HCC cell growth and aggressiveness by miR-1322/CXCL6 axis. This study may provide a potential prognostic indicator and therapeutic target for patients with HCC.

IRGM rs13361189 polymorphism may contribute to susceptibility to Crohn's disease: A meta-analysis.

The aim of the present meta-analysis was to evaluate the correlation between a common polymorphism, rs13361189 C>T in the immunity-related GTPase M (IRGM) gene, and susceptibility to Crohn's disease (CD). The PubMed, CISCOM, CINAHL, Web of Science, Google Scholar, EBSCO, Cochrane Library and CBM databases were investigated from database inception through to October 1, 2013 without the application of any language restrictions. The meta-analysis was performed using STATA 12.0 software and the relative risk (RR) with a 95% confidence interval (CI) was calculated. Seven case-control studies were included with a total of 3,093 CD patients and 3,227 healthy control subjects. The results of the meta-analysis revealed that the IRGM rs13361189 polymorphism correlates with an increased risk of CD (T allele versus C allele: RR=1.25 with 95% CI, 1.04-1.50; P=0.016 and CT + TT versus CC: RR=1.21 with 95% CI, 1.03-1.42; P=0.018). A subgroup analysis conducted using a genotyping method indicated that the IRGM rs13361189 polymorphism was correlated with an increased risk of CD in the TaqMan® (T allele versus C allele: RR=1.32 with 95% CI, 1.01-1.73; P=0.042) and the polymerase chain reaction-restriction fragment length polymorphism subgroups (T allele versus C allele: RR=1.80 with 95% CI, 1.32-2.45; P<0.001 and CT + TT versus CC: RR=1.61 with 95% CI, 1.19-2.18; P=0.018). However, no correlation was observed in the direct sequencing subgroup (P>0.05). Further subgroup analysis by sample size demonstrated significant correlations between the IRGM rs13361189 polymorphism and an increased risk of CD in the large sample-size subgroup (T allele versus C allele: RR=1.46 with 95% CI, 1.26-1.68; P<0.001 and CT + TT versus CC: RR=1.40 with 95% CI, 1.21-1.62; P<0.001). However, no correlation was identified between the IRGM rs13361189 polymorphism and CD risk in the small sample-size subgroup (P>0.05). The present meta-analysis indicated that the IRGM rs13361189 polymorphism may contribute to susceptibility to CD. Thus, IRGM rs13361189 polymorphism may be a potential biomarker for the early diagnosis of CD.

Role of CDH1 promoter methylation in colorectal carcinogenesis: a meta-analysis.

This meta-analysis was performed to evaluate the role of CDH1 promoter methylation in colorectal carcinogenesis. The PubMed, CISCOM, CINAHL, Web of Science, Google Scholar, EBSCO, Cochrane Library, and CBM databases were searched for relevant articles published before November 1st, 2013 without any language restrictions. Meta-analysis was conducted using the STATA 12.0 software. Crude odds ratios (ORs) with 95% confidence intervals (95% CIs) were calculated. Nine clinical cohort studies met all our inclusion criteria and were included in this meta-analysis. A total of 883 colorectal cancer (CRC) patients were assessed. Our meta-analysis results revealed that the frequencies of CDH1 promoter methylation in CRC tissues were higher than those in control tissues (OR=2.61, 95% CI=1.24-5.50, p=0.012). A subgroup analysis by ethnicity showed that CDH1 promoter methylation was closely linked to the pathogenesis of CRC among Asians and Africans (Asians: OR=2.90, 95% CI=1.26-6.67, p=0.012; Africans: OR=3.81, 95% CI=1.56-9.34, p=0.003; respectively), but not among Caucasians (OR=1.68, 95% CI=0.24-11.72, p=0.598). A further subgroup analysis by type of control tissues suggested that CRC tissues also exhibited higher frequencies of CDH1 promoter methylation than those of normal and adjacent tissues (normal: OR=1.57, 95% CI=1.12-2.21, p=0.009; adjacent: OR=5.07, 95% CI=2.91-8.82, p<0.001; respectively). However, we found no evidence for any significant difference in the frequencies of CDH1 promoter methylation between CRC tissues and adenomas tissues (OR=1.18, 95% CI=0.74-1.90, p=0.485). Our findings provide empirical evidence that CDH1 promoter methylation may play an important role in colorectal carcinogenesis. Thus, CDH1 promoter methylation may be a useful biomarker for the early diagnosis of CRC.

Matrix metalloproteinase 9 expression and prognosis in colorectal cancer: a meta-analysis.

Matrix metalloproteinase-9 (MMP-9) is an important member of the matrix metalloproteinase family and is considered to be involved in the invasion and metastasis of cancer cells. Many studies were published to assess the prognostic role of MMP-9 overexpression in patients with colorectal cancer, but the findings from those studies were inconsistent. We searched eligible studies in Pubmed, Embase, and Web of Science databases. Thirteen studies with a total of 2, 390 CRC patients were finally included into the meta-analysis. The pooled hazard ratios (HRs) with the corresponding 95 % confidence interval (95 % CIs) for overall and progression-free survival were calculated by using meta-analysis. There were nine studies with a total of 1,674 colorectal cancer patients relating the progression-free survival, and eight studies with a total of 1,379 colorectal cancer patients relating the overall survival. Overall, MMP-9 overexpression was associated with poorer progression-free survival in patients with colorectal cancer (fixed-effects HR 1.81, 95 % CI 1.48-2.20, P < 0.001; random-effects HR 1.92, 95 % CI 1.46-2.53, P < 0.001). In addition, MMP-9 overexpression was also associated with poorer overall survival in patients with colorectal cancer (fixed-effects HR 1.74, 95 % CI 1.39-2.19, P < 0.001; random-effects HR 1.78, 95 % CI 1.31-2.41, P < 0.001). MMP-9 expression is associated with the prognosis of patients with colorectal cancer, and patients with higher MMP-9 expression have poorer survival.

[The impact of human serum immunoglobulin treatment of refractory immune thrombocytopenic purpura. Analysis].

AIM: To observe the impact of human serum immunoglobulin treatment of refractory immune thrombocytopenic purpura in clinical efficacy. METHODS: 220 patients met the diagnostic criteria of refractory immune thrombocytopenic purpura, patients were randomly divided into treatment group and control group, 110 patients in each group. Groups were given prednisolone tablets 1 mg/ (kg x d), 2 times/d, oral, taking for 2 weeks, and than gradually reducing, the maintenance to be suspended; all-trans retinoic acid, each 10 mg, 3 times a day, oral. On this basis, the treatment group increases the employing blood immunoglobulin 400 mg/ (kg x d) infusion qd for 7 days. The two groups are 4 weeks for the course of treatment, a therapeutic effect after treatment. RESULTS: The total effective treatment group and control group were 94.56%, 80.91%, statistically significant differences between two groups (P < 0.05). Treatment serum IL-2, IFN-gamma, IL-4, IL-10, TGF-beta1, significant differences compared to other indicators (p < 0.05). Platelet counts after treatment, the rates of increase, effective hemostasis time of the treatment group compared with the control group, significant difference (p < 0.05). CONCLUSION: The impact of human serum immunoglobulin treatment of refractory immune thrombocytopenic purpura significantly shorten the bleeding time, platelet and platelet rise-time return to normal time.