A Comparative Analysis of the New -3(-n) - 1 Remer Conjecture and a Proof of the 3n + 1 Collatz Conjecture

This scientific paper is a comparative analysis of two mathematical conjectures. The newly proposed -3(-n) - 1 Remer conjecture and how it is related to and a proof of the more well known 3n + 1 Collatz conjecture. An overview of both conjectures and their respective iterative processes will be presented. Showcasing their unique properties and behavior to each other. Through a detailed comparison, we highlight the similarities and differences between these two conjectures and discuss their significance in the field of mathematics. And how they prove each other to be true.

Constructing long-cycling crystalline C_(3)N_(4)-based carbonaceous anodes for sodium-ion battery via N configuration control

Carbon nitrides with two-dimensional layered structures and high theoretical capacities are attractive as anode materials for sodium-ion batteries while their low crystallinity and insufficient structural stability strongly restrict their practical applications.Coupling carbon nitrides with conductive carbon may relieve these issues.However,little is known about the influence of nitrogen(N)configurations on the interactions between carbon and C_(3)N_(4),which is fundamentally critical for guiding the precise design of advanced C_(3)N_(4)-related electrodes.Herein,highly crystalline C_(3)N_(4)(poly(triazine imide),PTI)based all-carbon composites were developed by molten salt strategy.More importantly,the vital role of pyrrolic-N for enhancing charge transfer and boosting Na+storage of C_(3)N_(4)-based composites,which was confirmed by both theoretical and experimental evidence,was spot-highlighted for the first time.By elaborately controlling the salt composition,the composite with high pyrrolic-N and minimized graphitic-N content was obtained.Profiting from the formation of highly crystalline PTI and electrochemically favorable pyrrolic-N configurations,the composite delivered an unusual reverse growth and record-level cycling stability even after 5000 cycles along with high reversible capacity and outstanding full-cell capacity retention.This work broadens the energy storage applications of C_(3)N_(4) and provides new prospects for the design of advanced all-carbon electrodes.

3-N-Butylphthalide mitigates high glucose-induced injury to Schwann cells:association with nitrosation and apoptosis

A high glucose state readily causes peripheral axon atrophy, demyelination, loss of nerve fiber function, and delayed regeneration. However, few studies have examined whether nitration is also critical for diabetic peripheral neuropathy. Therefore, this study investigated the effects of high glucose on proliferation, apoptosis, and 3-nitrotyrosine levels of Schwann cells treated with butylphthalide. In addition, we explored potential protective mechanisms of butylphthalide on peripheral nerves. Schwann cells were cultured in vitro with high glucose then stimulated with the peroxynitrite anion inhibitors uric acid and 3-n-butylphthalide for 48 hours. Cell Counting Kit-8 and flow cytometry were used to investigate the effects of uric acid and 3-n-butylphthalide on proliferation and apoptosis of Schwann cells exposed to a high glucose environment. Effects of uric acid and 3-n-butylphthalide on levels of 3-nitrotyrosine in Schwann cells were detected by enzyme-linked immunosorbent assay. The results indicated that Schwann cells cultured in high glucose showed decreased proliferation, but increased apoptosis and intracellular 3-nitrotyrosine levels. However, intervention with uric acid or 3-n-butylphthalide could increase proliferation of Schwann cells cultured in high glucose, and inhibited apoptosis and intracellular 3-nitrotyrosine levels. According to our data, 3-n-butylphthalide may inhibit cell nitrification and apoptosis, and promote cell proliferation, thereby reducing damage to Schwann cells caused by high glucose.

Relationship between high dietary fat intake and Parkinson’s disease risk: a meta-analysis

OBJECTIVE: To assess whether dietary fat intake influences Parkinson’s disease risk. DATA SOURCES: We systematically surveyed the Embase and PubMed databases, reviewing manuscripts published prior to October 2018. The following terms were used:(“Paralysis agitans” OR “Parkinson disease” OR “Parkinson” OR “Parkinson’s” OR “Parkinson’s disease”) AND (“fat” OR “dietary fat” OR “dietary fat intake”). DATA SELECTION: Included studies were those with both dietary fat intake and Parkinson’s disease risk as exposure factors. The Newcastle-Ottawa Scale was adapted to investigate the quality of included studies. Stata V12.0 software was used for statistical analysis. OUTCOME MEASURES: The primary outcomes included the relationship between high total energy intake, high total fat intake, and Parkinson’s disease risk. The secondary outcomes included the relationship between different kinds of fatty acids and Parkinson’s disease risk. RESULTS: Nine articles met the inclusion criteria and were incorporated into this meta-analysis. Four studies scored 7 and the other five studies scored 9 on the Newcastle-Ottawa Scale, meaning that all studies were of high quality. Meta-analysis results showed that high total energy intake was associated with an increased risk of Parkinson’s disease (P = 0.000, odds ratio (OR)= 1.49, 95% confidence interval (CI): 1.26–1.75);in contrast, high total fat intake was not associated with Parkinson’s disease risk (P = 0.123, OR = 1.07, 95% CI: 0.91–1.25). Subgroup analysis revealed that polyunsaturated fatty acid intake (P = 0.010, OR = 1.03, 95% CI: 0.88–1.20) reduced the risk of Parkinson’s disease, while arachidonic acid (P = 0.026, OR = 1.15, 95% CI: 0.97–1.37) and cholesterol (P = 0.002, OR = 1.09, 95% CI: 0.92–1.29) both increased the risk of Parkinson’s disease. Subgroup analysis also demonstrated that, although the results were not significant, consumption of n-3 polyunsaturated fatty acids (P = 0.071, OR = 0.88, 95% CI: 0.73–1.05),α-linolenic acid (P = 0.06, OR = 0.86, 95% CI: 0.72–1.02), and the n-3 to n-6 ratio (P = 0.458, OR = 0.89, 95% CI: 0.75–1.06) were all linked with a trend toward reduced Parkinson’s disease risk. Monounsaturated fatty acid (P = 0.450, OR = 1.06, 95% CI: 0.91–1.23), n-6 polyunsaturated fatty acids (P = 0.100, OR = 1.15, 95% CI: 0.96–1.36) and linoleic acid (P = 0.053, OR = 1.11, 95% CI: 0.94–1.32) intakes were associated with a non-significant trend toward higher PD risk. Saturated fatty acid (P = 0.619, OR = 1.01, 95% CI: 0.87–1.18) intake was not associated with Parkinson’s disease. CONCLUSION: Dietary fat intake affects Parkinson’s disease risk, although this depends on the fatty acid subtype. Higher intake of polyunsaturated fatty acids may reduce the risk of Parkinson’s disease, while higher cholesterol and arachidonic acid intakes may elevate Parkinson’s disease risk. However, further studies and evidence are needed to validate any link between dietary fat intake and Parkinson’s disease.

Dietary Green Tea Extract and Antioxidants Improve Insulin Secretory Functions of Pancreatic β-Cells in Mild and Severe Experimental Rodent Model of Chronic Pancreatitis

Chronic pancreatitis (CP) is a progressive inflammatory disorder of the pancreas. It is predominantly idiopathic (with an unknown cause) in India and mostly due to alcohol in the West. Diabetes that occur secondary to chronic pancreatitis (T3c Diabetes) is often brittle, and is difficult to attain normoglycemia with conventional treatment requiring multiple doses of insulin. Mild and severe model of CP was induced in mice by repeated intraperitoneal injections of cerulein and L-arginine respectively with an intent to study islet dysfunction and develop therapeutic strategy in animal models of CP. Dietary intervention of epigallocatechin-3-gallate (EGCG) was tested in both the models of CP for its beneficial effects on insulin secretory functions. Pancreata collected upon euthanasia were used to study alterations in the morphology of pancreatic parenchyma and inflammation by staining with H&E and fibrotic changes by Masson’s trichrome and picrosirius staining. Insulin secretory functions of islets were evaluated to test the efficacy of the dietary intervention on β-cell functions. Intraperitoneal glucose tolerance test was performed to monitor the glucose homeostasis before and after the dietary intervention. Both the models resulted in CP with dispersed acini, inflammation and fibrosis. The loss of acini and extent of fibrosis was more in L-arginine model. 2-fold improvement in glucose-stimulated insulin secretory functions of islets was observed with 0.5% EGCG dietary intervention in cerulein model of CP and 1.6-fold in L-arginine model of CP. A further improvement in insulin secretion by 3.2-fold was observed with additional dietary supplements like N-acetyl cysteine, curcumin in combination with EGCG. Our results thus demonstrate and highlight the therapeutic potential of dietary green tea (EGCG) supplementation in reversing islet dysfunction and improving glucose homeostasis in experimental chronic pancreatitis in mice.

The calmodulin-dependent protein kinase II inhibitor KN-93 protects rat cerebral cortical neurons from N-methyl-D-aspartic acid-induced injury

In this study, primary cultured cerebral cortical neurons of Sprague-Dawley neonatal rats were treated with 0.25, 0.5, and 1.0 μM calmodulin-dependent protein kinase II inhibitor KN-93 after 50 μM N-methyI-D-aspartic acid-induced injury. Results showed that, compared with N-methyi-D- aspartic acid-induced injury neurons, the activity of cells markedly increased, apoptosis was significantly reduced, leakage of lactate dehydrogenase decreased, and intracellular Ca2＋ concentrations in neurons reduced after KN-93 treatment. The expression of caspase-3, phosphorylated calmodulin-dependent protein kinase II and total calmodulin-dependent protein kinase II protein decreased after KN-93 treatment. And the effect was apparent at a dose of 1.0 pM KN-93. Experimental findings suggest that KN-93 can induce a dose-dependent neuroprotective effect, and that the underlying mechanism may be related to the down-regulation of caspase-3 and calmodulin- dependent protein kinase II expression.

Lateral root elongation in maize is related to auxin synthesis and transportation mediated by N metabolism under a mixed NO_(3)^(–) and NH_(4)^(+) supply

A mixed nitrate (NO_(3)^(–)) and ammonium (NH_(4)^(+)) supply can promote root growth in maize (Zea mays),however,the changes in root morphology and the related physiological mechanism under different N forms are still unclear.Here,maize seedlings were grown hydroponically with three N supplied in three different forms (NO_(3)^(–)only,75/25 NO_(3)^(–)/NH_(4)^(+)and NH_(4)^(+)only).Compared with sole NO_(3)^(–)or NH_(4)^(+),the mixed N supply increased the total root length of maize but did not affect the number of axial roots.The main reason was the increased total lateral root length,while the average lateral root (LR) length in each axle was only slightly increased.In addition,the average LR density of 2nd whorl crown root under mixed N was also increased.Compared with sole nitrate,mixed N could improve the N metabolism of roots (such as the N influx rate,nitrate reductase (NR) and glutamine synthase (GS)enzyme activities and total amino content of the roots).Experiments with exogenously added NR and GS inhibitors suggested that the increase in the average LR length under mixed N was related to the process of N assimilation,and whether the NR mediated NO synthesis participates in this process needs further exploration.Meanwhile,an investigation of the changes in root-shoot ratio and carbon (C) concentration showed that C transportation from shoots to roots may not be the key factor in mediating lateral root elongation,and the changes in the sugar concentration in roots further proved this conclusion.Furthermore,the synthesis and transportation of auxin in axial roots may play a key role in lateral root elongation,in which the expression of ZmPIN1B and ZmPIN9 may be involved in this pathway.This study preliminarily clarified the changes in root morphology and explored the possible physiological mechanism under a mixed N supply in maize,which may provide some theoretical basis for the cultivation of crop varieties with high N efficiency.

Aspects on the Mechanism of the 1-Phenyl-1<i>H</i>-pyrazolo[3,4-<i>b</i>]quinoxaline Formation

Condensation of D-glucose, o-phenylenediamine and N,N-benzylphenylhydrazine hydrochloride (NNBPHH) in a one-pot reaction, or condensation of 2-(D-arabino-tetritol-1-yl) quinoxaline and NNBPHH, gave 3-(D-erythro-glycerol-1- yl)-1-phenyl-1H-pyrazolo[3,4-b]quinoxaline. The structure of the latter was determined by 1H NMR spectroscopy and by synthesis using phenylhydrazine hydrochloride instead of NNBPHH. Condensation of D-glucose and 4,5-dichloro-o-phenylenediamine gave 6,7-dichloro-2-(D-arabino-tetritol-1-yl)quinoxaline, which upon condensation with NNBPHH gave the corresponding 6,7-dichloro-3-(D-erythro-glycerol-1-yl)-1-phenyl-1H-pyrazolo[3,4-b]quinoxaline. The structure and mechanism of formation of these compounds are discussed.

Effect of Temperature on the Reaction of 2-(N-acetylamine)-3-(3,5-di-<i>tert</i>-butyl-4-hydroxyphenyl)-propionic Acid with Oxygen in an Alkaline Condition

Results of oxidation 2-(N-acetylamine)-3-(3,5-di-tert-butyl-4-hydroxyphenyl)-propionic acid oxygen depend on temperature. At 55℃?- 60℃, 2,4-di-tert-butylbicyclo(4,3,1)deca-4,6-dien-8-(N-acetylamine)-3,9-dion-1-oxa is formed. The constitution is based on dates of spectrums 1Н and 13С NMR. At 95℃?- 97℃, mixtures of 2,4-di-tert-butylbicyclo(4,3,1)deca-4,6-dien-8-(N-acetylamine)-3,9-dion-1-oxa and of 6,8-di-tert-butyl-3-(N-acetylamine)spiro(4,5)deca-1-oxa-5,8-dien-2,7-dione are produced. Structures are calculated by the method of Hartrii-Foka. Values of enthalpies and of entropies allow to assume dynamic isomerism.

Expression of p-STAT3 and vascular endothelial growth factor in MNNG-induced precancerous lesions and gastric tumors in rats

AIM: To investigate the dynamic expression of p-signal transducer and activator of transcription 3(STAT3) and vascular endothelial growth factor(VEGF) in the formation of gastric tumors induced by drinking water containing N-methyl-N'-nitro-N-nitrosoguanidine(MNNG) in Wistar rats.METHODS: One hundred and twenty Wistar rats were randomly divided into two groups(60 in each group): Control group and Model group. The rats in each group were then randomly divided into three groups(20 in each group): C/M15, C/M25 and C/M40(15, 25 and 40 represent the number of feeding weeks from termination). Rats in the control group received normal drinking water and rats in the model group received drinking water containing 100 μg/m L MNNG. Stomach tissues were collected at the end of the 15 th, 25 th and 40 th week, respectively, for microscopic measurement using hematoxylin and eosin staining. The expression of p-STAT3 and VEGF in different pathological types of gastric tissue, including normal, inflammation, atrophy, hyperplasia and gastric stromal tumor, was observed by immunohistochemistry and Western blot, and the corelation between p-STAT3 and VEGF was analyzed. RESULTS:(1) The expression of p-STAT3 in tissue with gastritis, atrophy, dysplasia and gastric stromal tumor were significantly increased in the model group compared with the control group(2.5 ± 1.0, 2.75 ±0.36, 6.2 ± 0.45, 5.67 ± 0.55 vs 0.75 ± 0.36, P = 0.026, 0.035, 0.001, 0.002, respectively); the expression of p-STAT3 in tissue with dysplasia was higher than that in samples with gastritis or atrophy(6.2 ± 0.45 vs 2.5 ± 1.0, P = 0.006; 6.2 ± 0.45 vs 2.75 ± 0.36, P = 0.005, respectively); however, the expression of p-STAT3 in gastritis and atrophy was not significantly different(P > 0.05);(2) the expression of VEGF in tissue with gastritis, atrophy, dysplasia and gastric stromal tumor was significantly increased in the model group compared with normal gastric mucosa; and the expression of VEGF in tissue with dysplasia was higher than that in tissue with inflammation and atrophy(10.8 ± 1.96 vs 7.62 ± 0.25, P = 0.029; 10.8 ± 1.96 vs 6.26 ± 0.76, P = 0.033, respectively); similarly, the expression of VEGF in tissue with gastritis and atrophy was not significantly different(P > 0.05); and(3) the expression of VEGF was positively correlated with p-STAT3. CONCLUSION: p-STAT3 plays an important role in gastric cancer formation by regulating the expression of VEGF to promote the progression of gastric tumor from gastritis.

L-3-n-butylphthalide protects against vascular dementia via activation of the Akt kinase pathway

As a neuroprotective drug for the treatment of ischemic stroke, 3-n-butylphthalide, a celery seed ex- tract, has been approved by the State Food and Drug Administration of China as a clinical therapeutic drug for ischemic stroke patients. L-3-n-butylphthalide possesses significant efficacy in the treatment of acute ischemic stroke. The activated Akt kinase pathway can prevent the death of nerve cells and exhibit neuroprotective effects in the brain after stroke. This study provides the hypothesis that I-3-n- butylphthalide has a certain therapeutic effect on vascular dementia, and its mechanism depends on the activation of the Akt kinase pathway. A vascular dementia mouse model was established by cere- bral repetitive ischemia/reperfusion, and intragastrically administered I-3-n-butylphthalide daily for 28 consecutive days after ischemia/repedusion, or 7 consecutive days before ischemia/reperfusion. The Morris water maze test showed significant impairment of spatial learning and memory at 4 weeks after operation, but intragastric administration of I-3-n-butylphthalide, especially pretreatment with I-3-n- butylphthalide, significantly reversed these changes. Thionine staining and western blot analylsis showed that preventive and therapeutic application of I-3-n-butylphthalide can reduce loss of pyrami- dal neurons in the hippocampal CA1 region and alleviate nerve damage in mice with vascular demen- tia. In addition, phosphorylated Akt expression in hippocampal tissue increased significantly after I-3-n- butylphthalide treatment. Experimental findings demonstrate that I-3-n-butylphthalide has preventive and therapeutic effects on vascular dementia, and its mechanism may be mediated by upregulation of phosphorylated Akt in the hippocampus.

Effect of diets supplemented with linseed alone or combined with vitamin E and selenium or with plant extracts,on Longissimus thoracis transcriptome in growing-finishing Italian Large White pigs

Background: Supplementing farm animals diet with functional ingredients may improve the nutritional quality of meat products.Diet composition has been also demonstrated to influence the gene expression with effect on biological processes and pathways.However,the knowledge on the effect of nutrients at the molecular level is scant.In particular,studies on the effects of antioxidants and polyphenols dietary supplementation have been investigated mainly in rodents,and only scarcely in farm animals so far.RNA-Seq with next-generation sequencing is increasingly the method of choice for studying changes in the transcriptome and it has been recently employed also in pig nutrigenomics studies to identify diet-induced changes in gene expression.The present study aimed to investigate the effect of diets enriched with functional ingredients(linseed,vitamin E and plant extracts) on the transcriptome of pig Longissimus thoracis to elucidate the role of these compounds in influencing genes involved in muscle physiology and metabolism compared to a standard diet.Results: Eight hundred ninety-three significant differentially expressed genes(DEGs)(FDR adjusted P-value ≤ 0.05)were detected by RNA-Seq analysis in the three diet comparisons(D2-D1,D3-D1,D4-D1).The functional analysis of DEGs showed that the diet enriched with n-3 PUFA from linseed(D2) mostly downregulated genes in pathways and biological processes(BPs) related to muscle development,contraction,and glycogen metabolism compared to the standard diet.The diet supplemented with linseed and vitamin E/Selenium(D3) showed to mostly downregulate genes linked to oxidative phosphorylation.Only few genes involved in extracellular matrix(ECM)organization were upregulated by the D3.Finally,the comparison D4-D1 showed that the diet supplemented with linseed and plant extracts(D4) upregulated the majority of genes compared to D1 that were involved in a complex network of pathways and BPs all connected by hub genes.In particular,IGF2 was a hub gene connecting protein metabolism,ECM organization,immune system and lipid biosynthesis pathways.Conclusion: The supplementation of pig diet with n-3 PUFA from linseed,antioxidants and plant-derived polyphenols can influence the expression of a relevant number of genes in Longissimus thoracis muscle that are involved in a variety of biochemical pathways linked to muscle function and metabolism.

In situ generation of Li_(3)N concentration gradient in 3D carbon-based lithium anodes towards highly-stable lithium metal batteries

The uncontrolled dendrite growth of lithium metal anodes(LMAs)caused by unstable anode/electrolyte interface and uneven lithium deposition have impeded the practical applications of lithium metal batteries(LMBs).Constructing a robust artificial solid electrolyte interphase(SEI)and regulating the lithium deposition behavior is an effective strategy to address these issues.Herein,a three-dimensional(3D)lithium anode with gradient Li_(3)N has been in-situ fabricated on carbon-based framework by thermal diffusion method(denoted as CC/Li/Li_(3)N).Density functional theory(DFT)calculations reveal that Li_(3)N can effectively promote the transport of Li^(+)due to the low energy barrier of Li^(+)diffusion.As expected,the Li_(3)N-rich conformal artificial SEI film can not only effectively stabilize the interface and avoid parasitic reactions,but also facilitate fast Li^(+)transport across the SEI layer.The anode matrix with uniformly distributed Li3N can enable homogenous deposition of Li,thus preventing Li dendrite propagation.Benefiting from these merits,the CC/Li/Li_(3)N anode achieves ultralong-term cycling for>1000 h at a current density of 2 m A cm^(-2)and dendrite-free Li deposition at an ultrahigh rate of 20 m A cm^(-2).Moreover,the full cells coupled with LiFePO4cathodes show extraordinary cycling stability for>300 cycles in liquidelectrolyte-based batteries and display a high-capacity retention of 96.7%after 100 cycles in solid-state cells,demonstrating the promising prospects for the practical applications of LMBs.

ALKBH5 suppresses autophagic flux via N6-methyladenosine demethylation of ZKSCAN3 mRNA in acute pancreatitis

BACKGROUND Increasing evidence has demonstrated that N6-methyladenosine(m6A)RNA modification plays an essential role in a wide range of pathological conditions.Impaired autophagy is a critical hallmark of acute pancreatitis(AP).AIM To explore the role of the m6A modification of ZKSCAN3 in the regulation of autophagy in AP.METHODS The AP mouse cell model was established by cerulein-treated mouse pancreatic acinar cells(MPC-83),and the results were confirmed by the levels of amylase and inflammatory factors.Autophagy activity was evaluated by specific identification of the autophagy-related microstructure and the expression of autophagy-related genes.ZKSCAN3 and ALKBH5 were knocked down to study the function in AP.A m6A RNA binding protein immunoprecipitation assay was used to study how the m6A modification of ZKSCAN3 mRNA is regulated by ALKBH.RESULTS The increased expression of amylase and inflammatory factors in the supernatant and the accumulation of autophagic vacuoles verified that the AP mouse cell model was established.The downregulation of LAMP2 and upregulation of LC3-II/I and SQSTM1 demonstrated that autophagy was impaired in AP.The expression of ZKSCAN3 was upregulated in AP.Inhibition of ZKSCAN3 increased the expression of LAMP2 and decreased the expression of the inflammatory factors,LC3-II/I and SQSTM1.Furthermore,ALKBH5 was upregulated in AP.Knockdown of ALKBH5 downregulated ZKSCAN3 expression and restored decreased autophagic flux in AP.Notably,the bioinformatic analysis revealed 23 potential m6A modification sites on ZKSCAN3 mRNA.The m6A modification of ZKSCAN3 mRNA was significantly decreased in AP.Knockdown of ALKBH5 increased the modification of ZKSCAN3 mRNA,which confirmed that ALKBH5 upregulated ZKSCAN3 expression in a m6A-dependent manner.CONCLUSION ALKBH5 inhibits autophagic flux through m6A demethylation of ZKSCAN3 mRNA in AP,thereby aggravating the severity of the disease.

nForce2主板介绍与评析

NFII Ultra是DFI公司LANParty系列产品中的一员，顾名思义，该主板的用户是可以背着自己的机器去和朋友联机Party的，而NFII Ultra主板就提供了一个机箱背囊!除此以外，NFII Ultra还十分重视主板的视觉效果，棕黑色的PCB加上绿色的插槽，再配上荧光绿的Cable数据线等等。除了外观的别致之外，NFII Ultra也确实有几点特别之处，使得它适合于脱离机箱使用．比如主板上集成了开关和重启的按钮，另外它还配有4个LED灯用于显示错误信息，而且主板四角做得非常圆整。

Facile Fabrication of Fe2O3/Nitrogen Deficient g-C3N4-x Composite Catalysts with Enhanced Photocatalytic Performances

The modification of graphitic carbon nitride can significantly improve the photocatalytic performance of graphitic carbon nitride(g-C3N4).Fe2O3/nitrogen-deficient g-C3N4-x composite catalysts were prepared with dicyandiamide as the precursor and Fe3+doped in this study.The composite catalysts were characterized by XRD,SEM,FT-IR,XPS and photocurrent measurements.Close interaction occurred between Fe2O3 and nitrogen deficient g-C3N4-x,more photogenerated electrons were created and effectively separated from the holes,resulting in a decrease of photocarrier recombination,and thus enhancing the photocurrent.Photocatalytic performance experiments showed that Fe2O3/nitrogen deficient g-C3N4-x could utilize lowenergy visible light more efficiently than pure g-C3N4,and the removal rate was 92%in 60 minutes.

六氟钽酸氨拓扑转变制备低深能级缺陷Ta_(3)N_(5)光阳极实现超低偏压光电化学分解水

Ta_(3)N_(5)是一种具有2.1 eV直接带隙的n型半导体,其带隙跨越水的氧化还原电位.此外,Ta_(3)N_(5)的理论太阳能制氢效率(STH)高达15.9%,超过商业化应用的效率门槛(10%),是一种理想的光电化学分解水制氢光阳极材料.采用Ta2O5作为前驱体,在氨气气氛下高温氮化制备Ta_(3)N_(5)是一个由表及里的非均相氮化过程,该过程会产生大量的低价钽和氮空位等本征深能级缺陷,导致费米能级钉扎效应的产生,从而使得光生电压显著降低和光电流起始电位较高.因此,开发能够进行体相均相氮化的前驱体,以抑制Ta_(3)N_(5)深能级缺陷的产生,具有重要意义.本文采用气相溶剂热法,在钽箔上制备了一种六氟钽酸氨((NH_(4))_(2)Ta_(2)O_(3)F_(6))化合物,并以其多面体锥阵列薄膜作为前驱体,通过可控的氮化过程将前驱体结构拓扑转变为低深能级缺陷含量的Ta_(3)N_(5)多孔阵列薄膜.在高温氮化过程中,(NH_(4))_(2)Ta_(2)O_(3)F_(6)会释放含氮、氢和氟的气体小分子并形成贯穿体相的多孔通道,有利于氨气及氮化过程中产生的其他小分子物质的渗透,促进体相均匀氮化过程,避免生成大量的本征深能级缺陷.同时,(NH_(4))_(2)Ta_(2)O_(3)F_(6)中的高电负性氟离子可以减弱Ta–O键,进一步促进氮化反应.扫描电镜和透射电镜(TEM)结果表明,制备的(NH_(4))_(2)Ta_(2)O_(3)F_(6)是具有实心结构的多面体锥阵列薄膜,而拓扑转变所得的Ta_(3)N_(5)多面体锥薄膜具有多孔结构.X射线光电子能谱(XPS)、紫外-可见漫反射光谱和稳态/瞬态光电压谱表征结果表明,通过(NH_(4))_(2)Ta_(2)O_(3)F_(6)拓扑转变制备Ta_(3)N_(5)可有效抑制Ta_(3)N_(5)薄膜中深能级缺陷的形成.采用两种产氧反应助催化剂依次修饰后,XPS和TEM结果显示出助催化剂的双壳层结构与化学组成.光电化学分解水测试结果表明,所制得的Ta_(3)N_(5)光阳极在AM1.5G模拟太阳光的照射下,可展现出0.2 V_(RHE)(vs.RHE)的极低光电流起始电位,且在1.23 V_(RHE)时的光电流密度可达3.28 mA cm^(–2),经过连续5 h的稳定性测试,仍能保持初始值的85%.此外,稳定性测试前后助催化剂的XPS和TEM结果表明,Ta_(3)N_(5)光阳极光电流下降的原因可能是产氧助催化剂中硼物种的消耗.而通过减小(NH_(4))_(2)Ta_(2)O_(3)F_(6)多面体锥前驱体的尺寸,可以进一步减少Ta_(3)N_(5)薄膜中的本征深能级缺陷的含量,修饰助催化剂后可在0 V_(RHE)下展现出光电催化水氧化活性.综上所述,通过(NH_(4))_(2)Ta_(2)O_(3)F_(6)新型前驱体拓扑转变制备了低深能级缺陷含量的Ta_(3)N_(5)光阳极,表现出极低的光电流起始电位,为构建无偏压下自发全分解水的低深能级缺陷浓度的Ta_(3)N_(5)光电极提供了一种新途径,该方法也可拓展至其他过渡金属氮化物的可控制备与缺陷调控.

预氧化处理对MP35N合金高温氧化行为的影响

目的 探索并优化合金成分、工艺以获得致密稳定的预氧化膜,提高合金抗氧化能力。方法 利用非自耗真空电弧炉熔炼合金,在真空容器中加热金属及其氧化物粉末获得平衡氧压。通过莱茵装置进行预氧化实验。通过FactSage计算Co-Ni-Cr-Mo-Al-Si体系的合金组织相图及其氧化相图,利用X射线衍射(XRD)和扫描电子显微镜对预氧化的试样进行物相分析。结果 在1000℃、10^(–17)atm氧压下预氧化,未含Si的MP35N合金表面出现Cr_(2)O_(3)氧化物;随着Si添加量的增加,表面氧化物变为(Al,Cr)_(2)O_(3),以Cr_(2)O_(3)为主,内氧化物为Al_(2)O_(3);当Si含量(质量分数)为3%时,内部形成了近乎连续的带状Al_(2)O_(3)氧化膜。在1 000℃、10^(–25) atm氧压下,合金表面形成连续的Al_(2)O_(3)膜;在1 000℃、10^(–17) atm氧压下,Co-Ni-20Cr-10Mo-4Al-1Si合金预氧化后的外氧化膜为Cr_(2)O_(3),内氧化物为Al_(2)O_(3);随着氧压的提高,在空气气氛下合金表面生成尖晶石相氧化物。在1 000℃、10^(–17)atm氧压下预氧化1、5、10h,Co-Ni-20Cr-10Mo-4Al-1Si合金表面外氧化膜为Cr_(2)O_(3),内氧化物为Al_(2)O_(3),随着时间延长至20 h,合金表面形成连续的Al_(2)O_(3)膜。结论 随着Si添加量的增加,Al元素的活度不断升高,从而提高了Al_(2)O_(3)的形成驱动力,提升了Al元素的扩散系数,有更多的Al元素扩散至合金表层,有利于Al元素的选择性氧化。预氧化氧压的降低和氧化时间的延长,有利于保护性外氧化Al_(2)O_(3)膜形成,可有效提高合金的抗高温氧化性能。

Increasing nitrogen absorption and assimilation ability under mixed NO_(3)^(–)and NH_(4)^(+) supply is a driver to promote growth of maize seedlings

Compared with sole nitrate (NO_(3)^(-)) or sole ammonium (NH_(4)^(+)) supply,mixed nitrogen (N) supply may promote growth of maize seedlings.Previous study suggested that mixed N supply not only increased photosynthesis rate,but also enhanced leaf growth by increasing auxin synthesis to build a large sink for C and N utilization.However,whether this process depends on N absorption is unknown.Here,maize seedlings were grown hydroponically with three N forms (NO_(3)^(-)only,75/25 NO_(3)^(-)/NH_(4)^(+) and NH_(4)^(+) only).The study results suggested that maize growth rate and N content of shoots under mixed N supply was little different to that under sole NO_(3)^(-)supply at 0–3 d,but was higher than under sole NO_(3)^(-)supply at 6–9 d.^(15)N influx rate under mixed N supply was greater than under sole NO_(3)^(-) or NH_(4)^(+) supply at 6–9 d,although NO_(3)^(-) and NH_(4)^(+) influx under mixed N supply were reduced compared to sole NO_(3)^(-) and NH_(4)^(+) supply,respectively.qRT-PCR determination suggested that the increased N absorption under mixed N supply may be related to the higher expression of NO_(3)^(-) transporters in roots,such as ZmNRT1.1A,ZmNRT1.1B,ZmNRT1.1C,ZmNRT1.2 and ZmNRT1.3,or NH_(4)^(+) absorption transporters,such as Zm AMT1.1A,especially the latter.Furthermore,plants had higher nitrate reductase (NR)glutamine synthase (GS) activity and amino acid content under mixed N supply than when under sole NO_(3)^(-) supply.The experiments with inhibitors of NR reductase and GS synthase further confirmed that N assimilation ability under mixed N supply was necessary to promote maize growth,especially for the reduction of NO_(3)^(-) by NR reductase.This research suggested that the increased processes of NO_(3)^(-)and NH_(4)^(+) assimilation by improving N-absorption ability of roots under mixed N supply may be the main driving force to increase maize growth.

秸秆与生物炭对棉田碱性土壤NH_(3)挥发与N_(2)O排放的影响

为探究秸秆和秸秆生物炭连续添加5 a后对土壤氨(NH_(3))挥发和氧化亚氮(N_(2)O)排放的影响,并确定合理的秸秆还田措施,以降低碱性棉田氮损失。本研究基于等碳量输入,设置秸秆翻埋、秸秆催腐+覆盖还田、秸秆生物炭翻埋和不还田对照共4个处理,氮磷钾肥统一施用。结果表明:秸秆生物炭翻埋下土壤NH_(3)挥发和N_(2)O排放分别较不还田对照显著降低27.3%和56.7%,主要归因于生物炭显著抑制土壤羟胺还原酶与硝酸还原酶活性,增加棉花氮吸收量,也与生物炭自身的强吸附能力有关。而秸秆翻埋、秸秆催腐+覆盖还田分别较对照增加NH3挥发37.2%和21.2%,但减少N2O排放17.1%和38.3%,这两种秸秆还田方式均显著促进土壤有机氮矿化和羟胺还原酶活性,抑制硝酸还原酶活性。冗余分析(RDA)结果表明羟胺还原酶和棉花氮吸收是土壤NH3挥发和N_(2)O排放的主要影响因子,解释率分别为64.8%和20.1%。研究表明,秸秆生物炭翻埋对NH_(3)和N_(2)O减排的综合效果优于秸秆,是碱性棉田土壤值得推荐的氮减排措施。