Hybrid Transition-Metal Oxide and Nitride@N-Doped Reduced Graphene Oxide Electrodes for High-Performance, Flexible, and All-Solid-State Supercapacitors.

Nanoscale composites for high-performance electrodes employed in flexible, all-solid-state supercapacitors are being developed. A series of binder-free composites, each consisting of a transition bimetal oxide, a metal oxide, and a metal nitride grown on N-doped reduced graphene oxide (rGO)-wrapped nickel foam are obtained by using a universal strategy. Three different transition metals, Co, Mo, and Fe, are separately compounded with nickel ions, which originate from the nickel foam, to form three composites, NiCoO2 @Co3 O4 @Co2 N, NiMoO4 @MoO3 @Mo2 N, and NiFe2 O4 @Fe3 O4 @Fe2 N, respectively. These as-prepared active materials have similar regular variation patterns in their properties, including better conductivity and battery-mimicking pseudocapacitance, which result in their high whole-electrode capacitance performance [2598.3 F g-1 (39.85 F cm-2 ), 3472.6 F g-1 (41.43 F cm-2 ) and 1907.5 F g-1 (3.41 F cm-2 ) for the composites incorporating Co, Mo, and Fe, respectively]. The as-assembled flexible, all-solid-state NiCoO2 @Co3 O4 @Co2 N//KOH/PVA//NiCoO2 @Co3 O4 @Co2 N device can be easily bent and exhibits high energy density and power density of 92.8 Wh kg-1 and 1670.4 W kg-1 , respectively. The universality of this design strategy could allow it to be employed in producing hybrid materials for high-performance energy-storage devices.

Infectious Complications in Severe Acute Pancreatitis: Pathogens, Drug Resistance, and Status of Nosocomial Infection in a University-Affiliated Teaching Hospital.

BACKGROUND: Secondary infection is an important factor affecting mortality and quality of life in patients with severe acute pancreatitis. The characteristics of secondary infection, which are well known to clinicians, need to be re-examined in detail, and their understanding among clinicians needs to be updated accordingly. AIM: This study aims to investigate the characteristics and drug resistance of pathogens causing severe acute pancreatitis (SAP) secondary infection, to objectively present infection situation, and to provide reference for improved clinical management. METHODS: A retrospective analysis was performed on 55 consecutive patients with SAP who developed secondary infection with an accurate evidence of bacterial/fungal culture from 2016 to 2018. The statistics included the spectrum and distribution of pathogens, the drug resistance of main pathogens, and associations between multiple infectious parameters and mortality. RESULTS: A total of 181 strains of pathogens were isolated from (peri)pancreas; bloodstream; and respiratory, urinary, and biliary systems in 55 patients. The strains included 98 g-negative bacteria, 58 g-positive bacteria, and 25 fungi. Bloodstream infection (36.5%) was the most frequent infectious complication, followed by (peri)pancreatic infection (32.0%). Acinetobacter baumannii, Pseudomonas aeruginosa, Klebsiella pneumoniae, Escherichia coli, and Stenotrophomonas maltophilia were predominant among gram-negative bacteria. Gram-positive bacterial infections were mainly caused by Enterococcus faecium and Staphylococcus spp. Fungal infections were predominantly caused by Candida spp. The drug resistance of pathogens causing SAP secondary infection was generally higher than the surveillance level. Patients in the death group were older (55 ± 13 years vs. 46 ± 14 years; p = 0.039) and had longer intensive care unit (ICU) stay (14 vs. 8; p = 0.026) than those in the survival group. A. baumannii infection (68.4% vs. 33%; p = 0.013), number of pathogens ≥ 4 (10 vs. 6; p = 0.005), pancreatic infection (14 vs. 15, p = 0.024), and urinary infection (8 vs. 5; p = 0.019) were significantly associated with mortality. CONCLUSION: Gram-negative bacteria are the main pathogens causing SAP secondary infection, in which nosocomial infections play a major role. The drug resistance profile of gram-negative bacteria is seriously threatening, and the commonly used antibiotics in SAP are gradually losing their effectiveness. Much attention should be paid to the rational use of antibiotics, and strategies should be established for infection prevention in SAP.

Manipulation of ionized impurity scattering for achieving high thermoelectric performance in n-type Mg3Sb2-based materials.

Achieving higher carrier mobility plays a pivotal role for obtaining potentially high thermoelectric performance. In principle, the carrier mobility is governed by the band structure as well as by the carrier scattering mechanism. Here, we demonstrate that by manipulating the carrier scattering mechanism in n-type Mg3Sb2-based materials, a substantial improvement in carrier mobility, and hence the power factor, can be achieved. In this work, Fe, Co, Hf, and Ta are doped on the Mg site of Mg3.2Sb1.5Bi0.49Te0.01, where the ionized impurity scattering crosses over to mixed ionized impurity and acoustic phonon scattering. A significant improvement in Hall mobility from ∼16 to ∼81 cm2⋅V-1⋅s-1 is obtained, thus leading to a notably enhanced power factor of ∼13 µW⋅cm-1⋅K-2 from ∼5 µW⋅cm-1⋅K-2 A simultaneous reduction in thermal conductivity is also achieved. Collectively, a figure of merit (ZT) of ∼1.7 is obtained at 773 K in Mg3.1Co0.1Sb1.5Bi0.49Te0.01 The concept of manipulating the carrier scattering mechanism to improve the mobility should also be applicable to other material systems.

Adenosine A2a Receptor Stimulation Attenuates Ischemia-Reperfusion Injury and Improves Survival in A Porcine Model of DCD Liver Transplantation.

Orthotopic liver transplantation (OLT) using allografts from donation after circulatory death (DCD) is potentially associated with compromised clinical outcomes due to ischemia-reperfusion injury (IRI)-induced organ damage and graft-related complications. The aim of this study was to provide in vivo data on the effects of adenosine A2a receptor stimulation in a clinically relevant large animal model of DCD liver transplantation. Cardiac arrest was induced in German Landrace pigs (n = 10; 20-25 kg). After 30 min of warm ischemia, the donor liver was retrieved following a cold flush with 3 L of histidine-tryptophan-ketoglutarate-HTK solution. Animals of the treatment group (n = 5/group) received a standard dose of the selective adenosine receptor agonist CGS 21680 added to the cold flush. All grafts were stored for 4.5 h at 4 °C in HTK-solution before OLT. Hepatocellular injury, apoptosis, protein kinase A-PKA activity, graft microcirculation, liver function, and animal survival were assessed. Compared to untreated livers, adenosine A2a receptor stimulation resulted in improved tissue microcirculation (103% ± 5% vs. 38% ± 4% compared to baseline; p < 0.05), accelerated functional recovery of the graft (indocyanine green-plasma disappearance rate (ICG-PDR) of 75% ± 18% vs. 40% ± 30% after 3 h), increased PKA activity ratio (56% ± 3% vs. 32% ± 3%; p < 0.001 after 1 h), and consequently reduced tissue necrosis and apoptosis. The potent protective effects were clinically manifested in significantly improved survival in the treatment group after 72 h (100% vs. 40%; p = 0.04). The ex vivo administration of adenosine A2a receptor agonist during the back-table flush mitigates IRI-mediated tissue damage and improves functional graft recovery and survival in a large animal model of DCD liver transplantation.

Inactivation of ATF-2 enhances epithelial-mesenchymal transition and gemcitabine sensitivity in human pancreatic cancer cells.

OBJECTIVE: This work aimed to study the activating transcription factor 2 or AMP-dependent transcription factor-2 (ATF-2) inhibition mediated gemcitabine sensitivity in human pancreatic cancer cells. METHODS: The protein and messenger RNA expressions of ATF-2 in 42 pancreatic cancer tissues and adjacent nontumorous tissues were detected. Kaplan-Meier survival analysis was performed based on the expression level of ATF-2 protein in tumor tissues. Then the pancreatic cancer cells were transduced with ATF-2-expressing lentivirus and small interfering RNAs (siRNAs) to investigate the effect of ATF-2 on pancreatic cancer cell invasion, epithelium to mesenchyme transition, apoptosis, and gemcitabine sensitivity. RESULTS: The expression of phosphorylated (p)-ATF-2 protein was upregulated in pancreatic cancer tissues compared with adjacent nontumorous tissues. Patients with relative higher p-ATF-2 level showed significantly lower survival time. Then we found that the transfection ATF-2 siRNA into BxPC3 cells inhibited cell proliferation, invasion, and epithelium to mesenchyme transition, but enhanced cell apoptosis. These changes could be enhanced by the additional administration of gemcitabine. In addition, we confirmed that the overexpression of ATF-2 in Panc-1 cells promoted cell invasion and epithelium to mesenchyme transition. CONCLUSION: We concluded that inhibition-promoted ATF-2 expression was responsible for epithelium to mesenchyme transition and invasion of pancreatic cancer cells, while the inhibition of ATF-2 confers to gemcitabine sensitivity in human pancreatic cancer cells in vitro.

Silencing of Astrocyte elevated gene-1 (AEG-1) inhibits proliferation, migration, and invasiveness, and promotes apoptosis in pancreatic cancer cells.

To investigate the role of Astrocyte elevated gene-1 (AEG-1) in the development and progress of pancreatic cancer, short hairpin RNA (shRNA) was inserted into the RNA interference vector to knock-down the endogenous AEG-1 in two pancreatic cancer cell lines: AsPC-1 and PANC-1. Our results showed that silencing of AEG-1 suppressed the proliferation, colony formation ability, and cell stemness of AsPC-1 and PANC-1 cells, and inhibited their G1-to-S phase transition. Results from apoptosis assay showed that knock-down of AEG-1 led to cell apoptosis. The expression of anti-apoptotic Bcl-2 was downregulated and that of the pro-apoptotic Bax and cleaved caspase-3 was upregulated in AEG-1-silenced pancreatic cancer cells. Further, the capability of AEG-1-silenced cells to migrate and to invade through the Matrigel-coated membrane was weaker, and the expression of matrix metallopeptidase 2 (MMP-2) and MMP-9 were decreased. Moreover, the AKT-ß-catenin signaling pathway was inhibited in the cells with knock-down of AEG-1. In addition, the growth of xenograft tumors formed by AsPC-1 and PANC-1 cells was suppressed by AEG-1 shRNA. In conclusion, our study demonstrates that pancreatic cancer cells require AEG-1 to maintain their survival and metastasis, suggesting AEG-1 as a potential target for the treatment of pancreatic cancers.

Significant Role of Mg Stoichiometry in Designing High Thermoelectric Performance for Mg3(Sb,Bi)2-Based n-Type Zintls.

Complex structures with versatile chemistry provide considerable chemical tunability of the transport properties. Good thermoelectric materials are generally extrinsically doped semiconductors with optimal carrier concentrations, while charged intrinsic defects (e.g., vacancies, interstitials) can also adjust the carriers, even in the compounds with no apparent deviation from a stoichiometric nominal composition. Here we report that in Zintl compounds Mg3+xSb1.5Bi0.5, the carrier concentration can be tuned from p-type to n-type by simply altering the initial Mg concentration. The spherical-aberration-corrected (CS-corrected) high-angle annular dark field scanning transmission electron microscopy (HAADF-STEM) and energy-dispersive X-ray spectroscopy (EDX) mapping analysis show that the excess Mg would form a separate Mg-rich phase after Mg vacancies have been essentially compensated. Additionally, a slight Te doping at Bi site on Mg3.025Sb1.5Bi0.5 has enabled good n-type thermoelectric properties, which is comparable to the Te-doped Mg-rich sample. The actual final composition of Mg3.025Sb1.5Bi0.5 analyzed by EPMA is also close to the stoichiometry Mg3Sb1.5Bi0.5, answering the open question whether excess Mg is prerequisite to realize exceptionally high n-type thermoelectric performance by different sample preparation methods. The motivation for this work is first to understand the important role of vacancy and then to guide for discovering more promising n-type Zintl thermoelectric materials.

Silencing of ATF2 inhibits growth of pancreatic cancer cells and enhances sensitivity to chemotherapy.

Pancreatic cancer is one of the leading causes of cancer-related death worldwide. Activating transcription factor 2 (ATF2) is a multifunctional transcription factor, and is implicated in tumor progress, yet its role in pancreatic cancer remains unclear. In the present study, the level of ATF2 in pancreatic cancer tissues and the adjacent non-tumorous tissues was detected by quantitative real-time PCR and Western blot. The roles of ATF2 in the proliferation, cell cycle, and apoptosis of pancreatic cancer cells were investigated through ATF2 silencing, and the effect of ATF2 shRNA on the sensitivity of pancreatic cancer cells to gemcitabine, an anti-tumor drug, was explored. The results of our study showed that the ATF2 level in the pancreatic cancer tissues was higher than that in the adjacent non-tumorous tissues. Silencing of ATF2 was found to inhibit proliferation, arrest cell cycle at G1 phase and induce apoptosis in pancreatic cancer cells. Moreover, ATF2 silencing enhanced gemcitabine-induced growth-inhibition and apoptosis-induction effects in pancreatic cancer cells. In summary, silencing of ATF2 inhibited the growth of pancreatic cancer cells and enhanced the anti-tumor effects of gemcitabine, suggesting that ATF2 plays a pro-survival role in pancreatic cancer. Our results also propose that a high level of ATF2 may serve as a potential biomarker of pancreatic cancer, and that ATF2 may become a potential target for anti-tumor therapy.

Oncogenic miR-23a in Pancreatic Ductal Adenocarcinogenesis Via Inhibiting APAF1.

BACKGROUND: miR-23a, which participates in invasion of pancreatic ductal adenocarcinoma cells into the mesothelial barrier, is a critical regulator in many cancers. It, however, is still unknown whether miR-23a regulates pancreatic cell proliferation and apoptosis or not. AIMS: We sought to investigate the role of miR-23a in regulation of pancreatic cell proliferation and apoptosis. METHODS: miRNA, mRNA, and protein expressions were determined by qRT-PCR and Western blot, respectively. Dual-luciferase reporter assay was used in detection for binding ability of miR-23a to APAF1. Ectopic miR-23a and APAF 1 were introduced to pancreatic cells, and their roles in proliferation and apoptosis were detected by MTT, colony formation, and apoptosis assays, respectively. RESULTS: Up-regulation of miR-23a and down-regulation of APAF 1 were found in pancreatic ductal cancer, respectively. miR-23a significantly inhibited the luciferase activity by targeting APAF 1 3'UTR. Ectopic miR-23a significantly suppressed the APAF 1 gene expression in pancreatic cancer cells. Similar to siAPAF1, miR-23a significantly promoted pancreatic cancer cell proliferation and repressed apoptosis. Furthermore, miR-23a inhibitor and exogenous APAF 1 could recover the effects. CONCLUSIONS: It is suggested that miR-23a, acting as an oncogenic regulator by directly targeting APAF 1 in pancreatic cancer, is a useful potential biomarker in diagnosis and treatment of pancreatic cancer.

Interaction between pancreatic cancer cells and tumor-associated macrophages promotes the invasion of pancreatic cancer cells and the differentiation and migration of macrophages.

In this study, the impact of pancreatic cancer cell interaction with macrophages on the differentiation and function of macrophages and the behaviors of pancreatic cancer cells in vitro is evaluated. The expression of immunocompetent cell-associated markers in 22 pancreatic cancer specimens was characterized by immunohistochemistry. The impact of pancreatic cancer cells (PANC-1 and BxPC-3) on the differentiation and migration of human U937 monocytes and the effect of U937-derived macrophages on the proliferation and invasion of PANC-1 and BxPC-3 were determined by transwell assays. The potential effect on U937-derived macrophages or on the behaviors of pancreatic cancer cells following coculture in a transwell system was analyzed by quantitative real-time polymerase chain reaction. The high levels of macrophage-related CD68 and CD163 expression were detected in the pancreatic cancer specimens. Pancreatic cancer cells promoted the differentiation of U937 cells and migration of U937-derived macrophages, but decreased the mRNA transcripts of macrophage polarization-related genes of interleukin (IL)-10, IL-12p40, inducible nitric oxide synthase (iNOS), and CD163, particularly for iNOS. Furthermore, U937-derived M2 macrophages inhibited the proliferation of pancreatic cancer cells, but promoted their invasion. Coculture of pancreatic cancer cells with U937-derived macrophages upregulated the mRNA expression of genes associated with the epithelial-mesenchymal transition process, angiogenesis, and stemness of pancreatic cancer, but downregulated the expression of E-cadherin in pancreatic cancer cells. The interaction between pancreatic cancer cells and tumor-associated macrophages may play a pivotal role in the progression of pancreatic cancer.

Diagnosis and treatment of pancreatic metastases in 22 patients: a retrospective study.

BACKGROUND: Pancreatic metastases (PMs) are rare and lack of guidelines for diagnosis and treatments .The aim of this study is to explore the diagnosis, treatment, and prognosis of pancreatic metastases. METHODS: Twenty-two patients with pancreatic metastases who had been hospitalized at the First Affiliated Hospital of China Medical University from October 1980 to October 2012 were included in the present retrospective study. Seven patients had gastric cancer, five had colon cancer, two each had lung and liver cancer, and one each had bladder cancer, gallbladder cancer, breast cancer, nasopharyngeal cancer, renal cell carcinoma, and carcinoid. RESULTS: No specific syndrome or imageological change was found for the pancreatic metastases. The most common symptoms were abdominal pain and jaundice. Hypo-echoic lesions with well-defined margins were found on ultrasonic examinations, and low-density lesions with heterogeneous enhancement were identified in CT images. Nineteen of the 22 received treatment. Three of the 8 patients (34.1%) that had undergone operation experienced complications, but all patients recovered after conventional treatment. Follow-up studies were performed for 17 patients (77.3%), and the median survival time from the diagnosis of pancreatic metastases was 13.2 months (range, 2 to 68 months). Of the five patients who underwent radical resection, one was lost to follow-up, one died at fifteen months postoperation, and the other three are still alive and free from disease (disease-free survival ranging from five to thirty-three months from the diagnosis of the pancreatic metastases). CONCLUSION: Pancreatic metastases are rare lesions with no specific symptoms. Radical resection should be performed if possible; however, aggressive treatment should be performed for unresectable pancreatic metastases.

Global band convergence design for high-performance thermoelectric power generation in Zintls.

Electronic band convergence can have a beneficial impact on thermoelectric performance, but finding the right band-converged compositions is still time-consuming. We propose a method for designing a series of compositions with simultaneous band convergence in the high-entropy YbxCa1-xMgyZn2-ySb2 material by zeroing the weighted sum of crystal-field splitting energies of the parent compounds. We found that so-designed compositions have both larger power factors and lower thermal conductivities and that one of these compositions exhibits a large thermoelectric figure of merit value in comparison with to other p-type Zintls. Our material shows high stability both thermally and temporally. We then assembled an all-Zintl single-stage module, nontoxic and free of tellurium, that demonstrates an exceptional heat-to-electricity conversion efficiency exceeding 10% at a temperature difference of 475 kelvin.

Hierarchical Interconnected NiMoN with Large Specific Surface Area and High Mechanical Strength for Efficient and Stable Alkaline Water/Seawater Hydrogen Evolution.

NiMo-based nanostructures are among the most active hydrogen evolution reaction (HER) catalysts under an alkaline environment due to their strong water dissociation ability. However, these nanostructures are vulnerable to the destructive effects of H2 production, especially at industry-standard current densities. Therefore, developing a strategy to improve their mechanical strength while maintaining or even further increasing the activity of these nanocatalysts is of great interest to both the research and industrial communities. Here, a hierarchical interconnected NiMoN (HW-NiMoN-2h) with a nanorod-nanowire morphology was synthesized based on a rational combination of hydrothermal and water bath processes. HW-NiMoN-2h is found to exhibit excellent HER activity due to the accomodation of abundant active sites on its hierarchical morphology, in which nanowires connect free-standing nanorods, concurrently strengthening its structural stability to withstand H2 production at 1 A cm-2. Seawater is an attractive feedstock for water electrolysis since H2 generation and water desalination can be addressed simultaneously in a single process. The HER performance of HW-NiMoN-2h in alkaline seawater suggests that the presence of Na+ ions interferes with the reation kinetics, thus lowering its activity slightly. However, benefiting from its hierarchical and interconnected characteristics, HW-NiMoN-2h is found to deliver outstanding HER activity of 1 A cm-2 at 130 mV overpotential and to exhibit excellent stability at 1 A cm-2 over 70 h in 1 M KOH seawater.

Vacancy-mediated anomalous phononic and electronic transport in defective half-Heusler ZrNiBi.

Studies of vacancy-mediated anomalous transport properties have flourished in diverse fields since these properties endow solid materials with fascinating photoelectric, ferroelectric, and spin-electric behaviors. Although phononic and electronic transport underpin the physical origin of thermoelectrics, vacancy has only played a stereotyped role as a scattering center. Here we reveal the multifunctionality of vacancy in tailoring the transport properties of an emerging thermoelectric material, defective n-type ZrNiBi. The phonon kinetic process is mediated in both propagating velocity and relaxation time: vacancy-induced local soft bonds lower the phonon velocity while acoustic-optical phonon coupling, anisotropic vibrations, and point-defect scattering induced by vacancy shorten the relaxation time. Consequently, defective ZrNiBi exhibits the lowest lattice thermal conductivity among the half-Heusler family. In addition, a vacancy-induced flat band features prominently in its electronic band structure, which is not only desirable for electron-sufficient thermoelectric materials but also interesting for driving other novel physical phenomena. Finally, better thermoelectric performance is established in a ZrNiBi-based compound. Our findings not only demonstrate a promising thermoelectric material but also promote the fascinating vacancy-mediated anomalous transport properties for multidisciplinary explorations.

Boosting Oxygen Evolution Reaction of (Fe,Ni)OOH via Defect Engineering for Anion Exchange Membrane Water Electrolysis Under Industrial Conditions.

Developing non-precious catalysts with long-term catalytic durability and structural stability under industrial conditions is the key to practical alkaline anion exchange membrane (AEM) water electrolysis. Here, an energy-saving approach is proposed to synthesize defect-rich iron nickel oxyhydroxide for stability and efficiency toward the oxygen evolution reaction. Benefiting from in situ cation exchange, the nanosheet-nanoflake-structured catalyst is homogeneously embedded in, and tightly bonded to, its substrate, making it ultrastable at high current densities. Experimental and theoretical calculation results reveal that the introduction of Ni in FeOOH reduces the activation energy barrier for the catalytic reaction and that the purposely created oxygen defects not only ensure the exposure of active sites and maximize the effective catalyst surface but also modulate the local coordination environment and chemisorption properties of both Fe and Ni sites, thus lowering the energy barrier from *O to *OOH. Consequently, the optimized d-(Fe,Ni)OOH catalyst exhibits outstanding catalytic activity with long-term durability under both laboratory and industrial conditions. The large-area d-(Fe,Ni)OOH||NiMoN pair requires 1.795 V to reach a current density of 500 mA cm-2 at an absolute current of 12.5 A in an AEM electrolyzer for overall water electrolysis, showing great potential for industrial water electrolysis.

Screening strategy for developing thermoelectric interface materials.

Thermoelectric interface materials (TEiMs) are essential to the development of thermoelectric generators. Common TEiMs use pure metals or binary alloys but have performance stability issues. Conventional selection of TEiMs generally relies on trial-and-error experimentation. We developed a TEiM screening strategy that is based on phase diagram predictions by density functional theory calculations. By combining the phase diagram with electrical resistivity and melting points of potential reaction products, we discovered that the semimetal MgCuSb is a reliable TEiM for high-performance MgAgSb. The MgCuSb/MgAgSb junction exhibits low interfacial contact resistivity (ρc <1 microhm square centimeter) even after annealing at 553 kelvin for 16 days. The fabricated two-pair MgAgSb/Mg3.2Bi1.5Sb0.5 module demonstrated a high conversion efficiency of 9.25% under a 300 kelvin temperature gradient. We performed an international round-robin testing of module performance to confirm the measurement reliability. The strategy can be applied to other thermoelectric materials, filling a vital gap in the development of thermoelectric modules.

Efficient Alkaline Water/Seawater Hydrogen Evolution by a Nanorod-Nanoparticle-Structured Ni-MoN Catalyst with Fast Water-Dissociation Kinetics.

Achieving efficient and durable nonprecious hydrogen evolution reaction (HER) catalysts for scaling up alkaline water/seawater electrolysis is desirable but remains a significant challenge. Here, a heterogeneous Ni-MoN catalyst consisting of Ni and MoN nanoparticles on amorphous MoN nanorods that can sustain large-current-density HER with outstanding performance is demonstrated. The hierarchical nanorod-nanoparticle structure, along with a large surface area and multidimensional boundaries/defects endows the catalyst with abundant active sites. The hydrophilic surface helps to achieve accelerated gas-release capabilities and is effective in preventing catalyst degradation during water electrolysis. Theoretical calculations further prove that the combination of Ni and MoN effectively modulates the electron redistribution at their interface and promotes the sluggish water-dissociation kinetics at the Mo sites. Consequently, this Ni-MoN catalyst requires low overpotentials of 61 and 136 mV to drive current densities of 100 and 1000 mA cm-2 , respectively, in 1 m KOH and remains stable during operation for 200 h at a constant current density of 100 or 500 mA cm-2 . This good HER catalyst also works well in alkaline seawater electrolyte and shows outstanding performance toward overall seawater electrolysis with ultralow cell voltages.

The Role of Long Noncoding RNA AL161431.1 in the Development and Progression of Pancreatic Cancer.

Pancreatic cancer is known for its notorious fast progression and poor prognosis. Long noncoding RNA (lncRNA) AL161431.1 has been reported to be involved in the pathogenesis of different cancers. In this study, we explored the role of lncRNA AL161431.1 in the development and progression of pancreatic cancer by bioinformatic analysis, in vitro and in vivo experiments in pancreatic cancer BxPC-3 and SW1990 cells, as well as clinical samples. We found that lncRNA AL161431.1 was highly expressed in pancreatic cancer cells and tissues. Knock down of lncRNA AL161431.1 led to increased cancer cell death and cell cycle arrest. Xenograft growth of SW1990 cells with stable knockdown of lncRNA AL161431.1 in mice was significantly slower than that of SW1990 cells with scrambled control shRNA. Finally, we showed the involvement of lncRNA AL161431.1 in pancreatic cancer was related to its promotion of epithelial mesenchymal transition process.

Circ-0005105 activates COL11A1 by targeting miR-20a-3p to promote pancreatic ductal adenocarcinoma progression.

Growing evidence indicates that circular RNAs (circRNAs) are closely involved in tumorigenesis, but the association between circRNAs and pancreatic ductal adenocarcinoma (PDAC) is far from clear. Here, we focused on the functional investigation of circ-0005105, a newly identified circRNA, in PDAC progression. In the present study, we assessed circ-0005105 expression in PDAC tissues and cell lines with quantitative reverse transcription-polymerase chain reaction (qRT-PCR). The biological functions of circ-0005105 in cellular proliferation and invasion were identified through gain- and loss-of-function experiments in vitro and in vivo. The interaction between circ-0005105 and the microRNA (miR)-20a-3p-COL11A1 (collagen type XI alpha 1) axis was examined using luciferase reporter and RNA immunoprecipitation assays. We found that circ-0005105 expression was upregulated in both PDAC tissues and cell lines. Higher circ-0005105 expression correlated positively with the malignant clinical phenotype and poor prognosis of patients with PDAC. Gain- and loss-of-function analysis showed that circ-0005105 facilitated both in vitro and in vivo cellular proliferation and invasion. Mechanistically, circ-000510 served as a competing endogenous RNA (ceRNA) of miR-20a-3p and indirectly modulated COL11A1 expression, leading to activation of epithelial-mesenchymal transition (EMT). Rescue experiments suggested that the oncogenic activity of circ-0005105 was dependent on the modulation of the miR-20a-3p-COL11A1 axis. More importantly, COL11A1 overexpression was significantly associated with poor prognosis in PDAC, and silencing COL11A1 reduced PDAC cell tumorigenicity and metastasis. Taken together, our findings confirm for the first time that circ-0005105 has critical functions by regulating the miR-20a-3p-COL11A1 axis. In the clinic, circ-0005105 can act as a potential prognostic marker and therapeutic target in PDAC.

A narrative review of a type of pancreatitis worthy of attention: acute pancreatitis associated with pancreatic tumors-current problems and future thinking.

OBJECTIVE: Our purpose is to explain the onset, diagnosis, and treatment of pancreatic tumor-associated pancreatitis (PTP), and inform clinicians about the management of PTP. It is hoped that clinicians can gain some experience and inspiration from this review, so that patients can obtain better treatment results. BACKGROUND: Acute pancreatitis (AP) is an inflammatory disease, and pancreatic tumors are one of the causes of pancreatitis. When pancreatic tumors and pancreatitis exist at the same time, and there is a "connection" between them, this type of pancreatitis is referred to as PTP. The manifestations of PTP can be as follows: (I) AP is the first symptom of pancreatic tumors; (II) pancreatitis is found in patients after pancreatic tumor diagnosis or during pancreatic tumor surgery. Because pancreatic tumors are not one of the most common causes of pancreatitis, PTP has not attracted the attention of researchers and clinicians, and there is no consistent and clear understanding of the diagnosis and treatment of PTP. METHODS: From the online database PubMed (https://pubmed.ncbi.nlm.nih.gov/) and Web of Science (https://webofknowledge.com/), we use specific retrieval strategies to retrieve relevant articles, and we review and discuss them. CONCLUSIONS: What we need to realize is that PTP is different from ordinary AP. It has its own characteristics in terms of diagnosis and treatment, which requires the attention of clinicians. More importantly, future research should design the best diagnosis and treatment algorithms for PTP.