Interfacial engineering of CoP/CoS2 heterostructure for efficiently electrocatalytic pH-universal hydrogen production.

The design and development of high-performance, low-cost catalysts with long-term durability are crucial for hydrogen generation from water electrolysis. Interfacial engineering is an appealing strategy to boost the catalytic performance of electrode materials toward hydrogen evolution reaction (HER). Herein, we report a simple phosphidation followed by sulfidation treatment to construct heterogeneous cobalt phosphide-cobalt sulfide nanowire arrays on carbon cloth (CoP/CoS2/CC). When evaluated as catalysts toward the HER, the resultant CoP/CoS2/CC exhibits efficient pH-universal hydrogen production due to the heterostructure, synergistic contribution of CoP and CoS2, and conductive substrate. To attain a current density of 10 mA cm-2, overpotentials of only 111.2, 58.1, and 182.9 mV for CoP/CoS2/CC are required under alkaline, acidic, and neutral conditions, respectively. In particular, the as-prepared CoP/CoS2/CC shows markedly improved HER electroactivity in 1.0 M KOH, even outperforming commercial Pt-C/CC at a current density of >50 mA cm-2. In addition, the self-assembled CoP/CoS2||NiFe layered double hydroxide electrolyzer demonstrates efficient catalytic performance and long-time stability, excelling the benchmark Pt-C||IrO2. These findings indicate an effective pathway for the fabrication of high-performance heterogeneous electrocatalysts for hydrogen production in the future.

Butter-Derived Ruminant Trans Fatty Acids Do Not Alleviate Atherosclerotic Lesions in High-Fat Diet-Fed ApoE-/- Mice.

Atherosclerosis (AS) is the most common cardiovascular disease (CVD). Currently, it is widely believed that R-TFA and I-TFA may cause different biological effects. In the present study, we aim to elucidate the effect of mixed R-TFA derived from butter on the development of AS in high-fat diet-fed ApoE-/- mice and find the possible mechanism. It was shown that butter-derived R-TFA promoted dyslipidemia, reduced thoracic and abdominal aorta diameters, and induced aortic lipid deposition and atherosclerotic lesions in high-fat diet-fed ApoE-/- mice. Meanwhile, butter-derived R-TFA affected the serum lipid profile of high-fat diet-fed ApoE-/- mice and the lipid metabolism of human umbilical vein endothelial cells (HUVECs). Through lipidomic techniques, we found that butter-derived R-TFA had a significant effect on the glycerophospholipid metabolic pathway. In conclusion, our results demonstrated that butter-derived R-TFA does not alleviate but promotes atherosclerotic lesions in high-fat diet-fed ApoE-/- mice and that the glycerophospholipid metabolic pathway plays a major role in this pro-atherosclerotic effect.

Comparative transcriptome analysis reveals key genes potentially related to organic acid and sugar accumulation in loquat.

Organic acids and sugars are the primary components that determine the quality and flavor of loquat fruits. In the present study, major organic acids, sugar content, enzyme activities, and the expression of related genes were analyzed during fruit development in two loquat cultivars, 'JieFangZhong' (JFZ) and 'BaiLi' (BL). Our results showed that the sugar content increased during fruit development in the two cultivars; however, the organic acid content dramatically decreased in the later stages of fruit development. The differences in organic acid and sugar content between the two cultivars primarily occured in the late stage of fruit development and the related enzymes showed dynamic changes in activies during development. Phosphoenolpyruvate carboxylase (PEPC) and mNAD malic dehydrogenase (mNAD-MDH) showed higher activities in JFZ at 95 days after flowering (DAF) than in BL. However, NADP-dependent malic enzyme (NADP-ME) activity was the lowest at 95 DAF in both JFZ and BL with BL showing higher activity compared with JFZ. At 125 DAF, the activity of fructokinase (FRK) was significantly higher in JFZ than in BL. The activity of sucrose synthase (SUSY) in the sucrose cleavage direction (SS-C) was low at early stages of fruit development and increased at 125 DAF. SS-C activity was higher in JFZ than in BL. vAI and sucrose phosphate synthase (SPS) activities were similar in the two both cultivars and increased with fruit development. RNA-sequencing was performed to determine the candidate genes for organic acid and sugar metabolism. Our results showed that the differentially expressed genes (DEGs) with the greated fold changes in the later stages of fruit development between the two cultivars were phosphoenolpyruvate carboxylase 2 (PEPC2), mNAD-malate dehydrogenase (mNAD-MDH), cytosolic NADP-ME (cyNADP-ME2), aluminum-activated malate transporter (ALMT9), subunit A of vacuolar H+-ATPase (VHA-A), vacuolar H+-PPase (VHP1), NAD-sorbitol dehydrogenase (NAD-SDH), fructokinase (FK), sucrose synthase in sucrose cleavage (SS-C), sucrose-phosphate synthase 1 (SPS1), neutral invertase (NI), and vacuolar acid invertase (vAI). The expression of 12 key DEGs was validated by quantitative reverese transcription PCR (RT-qPCR). Our findings will help understand the molecular mechanism of organic acid and sugar formation in loquat, which will aid in breeding high-quality loquat cultivars.

Different Influences of trans Fatty Acids on the Phospholipase A2 and Arachidonic Acid Metabolic Pathway in Hepatocytes.

This study investigated the effects of 9t18:1 (representing I-TFAs), 9t16:1, and 11t18:1 (representing R-TFAs) and their mixtures on the normal human hepatocyte LO2 cell function, the possible mechanism of lipid metabolism by lipidomics, and the relationship between phospholipase A2 (PLA2) and the arachidonic acid (AA) metabolic pathway. Here, we found that the damaging effect of 9t18:1 on the LO2 cell function was significantly greater than those of 11t18:1 and 9t16:1 (p < 0.05), and the damaging effects of CHB and HSO were significantly greater than those of HHB and CM (p < 0.05). The lipidomic results showed that TFAs and TFA mixtures caused a significant change in the lipid profiles of LO2 cells, in which the TAG, PL, and OL contents increased significantly. Moreover, 9t18:1 regulated only the protein expression of cPLA2 but did not participate in the AA metabolic pathway, while 11t18:1 and 9t16:1 participated in the COX-2 and CYP450 pathways, respectively.

Evaluation of the lignite biotransformation capacity of Fusarium sp. NF01 cultured on different growth substrates.

The screening and studying the lignite solubilization/degradation capacities of indigenous microorganisms are key to exploring the in-situ biotransformation of lignite. Herein, a fungus was isolated from in-situ lignite samples and identified as Fusarium sp. NF01. This isolate was then cultured on four different carbon sources to evaluate its lignite-transformation capacity. When cultured on a solid agar medium containing sodium gluconate or sodium glutamate, Fusarium sp. NF01 completely liquefied 0.5 g of lignite within 6 days, and when cultured in a liquid medium containing sodium gluconate, the weight of lignite decreased by 28.4% within 7 days. Elemental analysis showed that the rate of lignite biodegradation was inversely proportional to the C:O ratio of the residual lignite samples. Additionally, a 5.9% biodesulfurization rate was achieved when Fusarium sp. NF01 was cultured in the presence of sodium gluconate. Finally, Fourier-transform infrared analysis of the residual lignite samples revealed relatively weak signal intensities of the signature peaks representing the following: aromatic ring side chains; ether, ester, and alcohol bonds; aromatic ring carbon-carbon double bonds; and aliphatic methyl and methylene. The results show that Fusarium sp. NF01 degrades lignite in a carbon-dependent manner and could be thus used for the bioconversion of subsurface coalbeds.

Consumption of Interesterified Medium- and Long-Chain Triacylglycerols Improves Lipid Metabolism and Reduces Inflammation in High-Fat Diet-Induced Obese Rats.

Medium- and long-chain triacylglycerols (MLCTs) were synthesized from rapeseed oil (RO), one kind of commonly used edible long-chain triacylglycerols (TGs), and then delivered to high-fat diet (HFD)-induced obese rats. Compared with RO, MLCT consumption exhibited more potent effects on reducing body and tissue weight gains, plasma TG, and total cholesterol (TC) levels and on improving hepatic TG, TC, fatty acid synthase, acetyl-CoA carboxylase, and lipoprteinlipase contents. Meanwhile, lower amounts of tumor necrosis factor-α (TNF-α), monocyte chemoattractant protein-1, and endotoxin in plasma, lower levels of interleukin-6 and TNF-α, and higher levels of interleukin-10 in both livers and white adipose tissues were detected in MLCT-fed rats. MLCT intake also remarkably suppressed the size of adipocytes and the number of macrophages. In conclusion, our study suggested that the interesterified MLCT was more efficacious in improving the lipid metabolism and inflammation in HFD-induced obese rats than RO.

9t18:1 and 11t18:1 activate the MAPK pathway to regulate the expression of PLA2 and cause inflammation in HUVECs.

trans fatty acids (TFAs) have been reported to promote vascular diseases mainly by promoting apoptosis and inflammation of vascular endothelial cells. However, it has been reported in recent years that elaidic acid (9t18:1) and vaccenic acid (11t18:1) may have different effects on vascular health. This study investigated the effects of 9t18:1 and 11t18:1 on human umbilical vein endothelial cell (HUVEC) function and the possible mechanism of inflammation by analyzing the changes in the phospholipid composition and the relationship between phospholipase A2 (PLA2) and MAPK pathway. Here we found that the effect of 11t18:1 on cell viability, membrane damage and cellular inflammation was significantly lower than that of 9t18:1 (p < 0.05). And 9t18:1 and 11t18:1 had different effects on phospholipid composition. Both 9t18:1 and 11t18:1 significantly increased the protein expression of PLA2. Moreover, the MAPK pathway regulated the expression of PLA2, inflammatory cytokines and cyclooxygenase-2 (COX-2) and the secretion of prostaglandin E2 (PGE2) in HUVECs induced by 9t18:1 and 11t18:1. In conclusion, 9t18:1 and 11t18:1 activated the MAPK pathway which regulated the expression of PLA2 to cause inflammation in HUVECs.

[Screening of chlorobenzene-degrading bacterium and purification of its degradation enzyme].

OBJECTIVE: We screened a bacterial strain capable of degrading chlorobenzene, and purified the corresponding degradation enzyme. METHODS: The strain was screened by gradient enrichment culture and sterile filter paper plate method, and identified by morphology and 16S rRNA gene sequence. Chlorobenzene concentration in the liquid culture was determined by gas chromatography. Degradation capability was assayed by the proportion of chlorobenzene degraded per cells. The purity quotient and molecular weight of the purified degradation enzyme were determined by gel per cell. electrophoresis. RESULTS: The isolated bacterium, LW13, used chlorobenzene in activated sludge as sole carbon and energy source. Cells were 2.3 microm long and 0.8 microm wide, with several terminal flagella. Strain LW13 was 95.5% similar to Lysinibacillus fusiformis, and its degradation enzyme was a positively-charged exoenzyme (molecular weight about 57 kDa). The optimal temperature and pH of the purified enzyme were approximately 40 degrees C and 8.0, respectively. CONCLUSION: Strain LW13 belongs to genus Lysinibacillus, and can degrade chlorobenzene (500-2000 mg/L).

Desferrioxamine in warm reperfusion media decreases liver injury aggravated by cold storage.

AIM: To evaluate whether desferrioxamine decreases ischemia and perfusion injury aggravated by cold storage (CS) in a rat liver perfusion model. METHODS: Isolated rat livers were kept in CS in University of Wisconsin Solution for 20 h at 4 °C, then exposed to 25 min of warm ischemia (WI) at 37 °C followed by 2 h of warm perfusion (WP) at 37 °C with oxygenated (95% oxygen and 5% carbon dioxide) Krebs-Henseleit buffer. Desferrioxamine (DFO), an iron chelator, was added at different stages of storage, ischemia and perfusion: in CS only, in WI only, in WP only, in WI and perfusion, or in all stages. Effluent samples were collected after CS and after WI. Perfusate samples and bile were collected every 30 min (0, 0.5, 1, 1.5 and 2 h) during liver perfusion. Cellular injury was assessed by the determination of lactate dehydrogenase (LDH) and aspartate aminotransferase (AST) in the effluent and perfusate samples. Total iron was analysed in the perfusate samples. After WP, the liver was collected for the determination of liver swelling (wet to dry ratio) and liver morphological examination (hematoxylin and eosin staining). RESULTS: Increased CS time caused increased liver dysfunction during WP. After 2 h of WP, liver injury was indicated by increased release of AST (0.5 h CS: 9.4 ± 2.2 U/g liver vs 20 h CS: 45.9 ± 10.8 U/g liver, P < 0.05) and LDH (0.5 h CS: 59 ± 14 U/g liver vs 20 h CS: 297 ± 71 U/g liver, P < 0.05). There was an associated increase in iron release into the perfusate (0.5 h CS: 0.11 ± 0.03 µmoL/g liver vs 20 h CS: 0.58 ± 0.10 µmoL/g liver, P < 0.05) and reduction in bile flow (0.5 h CS: 194 ± 12 µL/g vs 20 h CS: 71 ± 8 µL/g liver, P < 0.05). When DFO was added during WI and WP following 20 h of CS, release of iron into the perfusate was decreased (DFO absent 0.58 ± 0.10 µmoL/g liver vs DFO present 0.31 ± 0.06 µmoL/g liver, P < 0.05), and liver function substantially improved with decreased release of AST (DFO absent 45.9 ± 10.8 U/g liver vs DFO present 8.1 ± 0.9 U/g liver, P < 0.05) and LDH (DFO absent 297 ± 71 U/g liver vs DFO present 56 ± 7 U/g liver, P < 0.05), and increased bile flow (DFO absent 71 ± 8 µL/g liver vs DFO present 237 ± 36 µL/g liver, P < 0.05). DFO was also shown to improve liver morphology after WP. Cellular injury (the release of LDH and AST) was significantly reduced with the addition of DFO in CS medium but to a lesser extent compared to the addition of DFO in WP or WI and perfusion. There was no effect on liver swelling or bile flow when DFO was only added to the CS medium. CONCLUSION: DFO added during WI and perfusion decreased liver perfusion injury aggravated by extended CS.

[Experimental research of the inhibition of vascular endothelial growth factor C expression in gastric cancer by targeting RNA interference].

OBJECTIVE: To construct the plasmid expression vector pSIH1-H1-copGFP for RNA interference against vascular endothelial growth factor C (VEGF-C) and to evaluate its effect on the expression of VEGF-C mRNA in gastric cancer cells after transfection. METHODS: Three siRNAs of genome sequence of VEGF-C gene were retrieved from GenBank and one negative chain was used as control. Four siRNAs were cloned into plasmid pSIH1-H1-copGFP,which were then transfected into gastric cancer cells (SGC7901). The expression of VEGF-C mRNA was analyzed by RT-PCR. RESULTS: The recombinant plasmid of pSIH1-H1-copGFP specific for VEGF-C was confirmed by gene sequencing analysis. The target sequence obtained was completely consistent with the design. Transfection efficiency of the three siRNAs ranged from 60% to 70%. After transfection, the expression of VEGF-C mRNA in SGC7901 cells was significantly inhibited. Inhibition rates of VEGF-C mRNA expression were 35.4%, 33.8% and 81.5% in the three siRNA plasmid vectors, respectively. CONCLUSION: The siRNA expression plasmid vector against VEGF-C mRNA is successfully constructed, and RNAi may be a useful technique to inhibit the lymphangiogenesis of gastric cancer.

catena-Poly[[diaqua-(2,2'-bipyridine-κN,N')nickel(II)]-µ-biphenyl-2,2'-dicarboxyl-ato-κO:O'].

In the title compound, [Ni(C(14)H(8)O(4))(C(10)H(8)N(2))(H(2)O)(2)](n), the Ni(II) atom is coordinated in a slightly distorted octa-hedral geometry by two water mol-ecules, two N atoms from a 2,2'-bipyridine ligand and two O atoms from the carboxyl-ate groups of two 2,2'-biphenyl-dicarboxyl-ate (2,2'-dpa) ligands. The 2,2'-dpa ligand acts as a bridge between neighbouring Ni(II) atoms, forming one-dimensional coordination polymers along [100]. The coordinated water mol-ecules form hydrogen bonds to the carboxyl-ate O atoms of 2,2'-dpa within the same coordination polymer, and one O-H⋯π inter-action is also formed to 2,2'-dpa.

Bis(µ-biphenyl-2,2'-dicarboxyl-ato)bis-[(2,2'-bipyridine)cobalt(II)].

In the title compound, [Co(2)(C(14)H(8)O(4))(2)(C(10)H(8)N(2))(2)], the Co(II) atom is coordinated by two N atoms from one 2,2'-bipyridine ligand and two O atoms from two biphenyl-2,2'-dicarboxyl-ate (2,2'-dpa) ligands in a distorted planar geometry. Longer Co-O contacts [2.437 (3) and 2.552 (3) Å] are formed to the second O atom of each coordinated carboxyl-ate group so that these groups approximate a bidentate coordination mode and the coordination geometry around Co(II) approaches distorted octa-hedral. The 2,2'-dpa ligands bridge two Co(II) atoms, forming a cyclic dinuclear complex around a centre of inversion.