Impacts of Perchloric Acid, Nafion, and Alkali Metal Ions on Oxygen Reduction Reaction Kinetics in Acidic and Alkaline Solutions

Fundamental understandings on the impacts induced by anions and cations on oxygen reduction reaction (ORR) are of great interest in designing more efficient catalysts and identifying reasons for discrepancies in activities measured in different protocols. In this study, the specific adsorption of ClO₄^–, Nafion ionomer, and cations on Pt/C, Pd/C, and transition metal, N codoped carbon-based (Me–N–C) catalysts, and their effects on the ORR kinetics were systematically investigated. It was found that ClO₄^– had a negligible impact on the ORR activity of Pt/C possibly due to its weak adsorption. Nafion ionomers, on the other hand, showed a significant poisoning effect on the bulk Pt electrode. Its impact on Pt/C, however, is negligible even with a very high I/C ratio (1.33) in acidic solutions. The three catalysts showed different behaviors in alkaline solutions. The noncovalent interaction between hydrated cations and surface OH groups was found on Pt/C and had an obvious impact on the ORR kinetics. This noncovalent interaction, however, was not observed on Pd/C, which showed the same ORR activity in all three electrolytes (LiOH, NaOH, and KOH). The ORR activity of Me–N–C increased following the order of KOH < NaOH < LiOH. This trend is totally opposite to that of Pt/C. The mechanisms for the material-dependent activity trend in different cation solutions were discussed

Formation of a G-quadruplex structure from human mature miR-5196-5p

<p>Some human mature microRNAs are featured of G_≥2N_<i>x</i>G_≥2N_<i>y</i>G_≥2N_<i>z</i>G_≥2 sequences. In this study, a human mature microRNA, miR-5196-5p, was selected as an example to probe the secondary structure of G-rich microRNA. Our results have confirmed that miR-5196-5p could form a stable G-quadruplex structure with three G-quartets and three double-chain-reversal loops by electrospray ionization mass spectrometry, nuclear magnetic resonance, circular dichroism spectroscopy, and molecular dynamics simulation. Our study showed the prevalence of G-rich microRNAs in <i>Homo sapiens</i>, rat, mouse, and <i>Arabidopsis thaliana</i>, and they have great potential to fold into intramolecular G-quadruplexes which may serve as new targets for the regulatory function of G-rich mature microRNAs.</p

Systemic Responses of Mice to Dextran Sulfate Sodium-Induced Acute Ulcerative Colitis Using ¹H NMR Spectroscopy

The interplay between genetic mutation and environmental factors is believed to contribute to the etiology of inflammatory bowel disease (IBD). While focused attention has been paid to the aforementioned research, time-specific and organ-specific metabolic changes associated with IBD are still lacking. Here, we induced acute ulcerative colitis in mice by providing water containing 3% dextran sulfate sodium (DSS) for 7 days and investigated the metabolic changes of plasma, urine, and a range of biological tissues by employing a ¹H nuclear magnetic resonance (NMR)-based metabonomics approach with complementary information on serum clinical chemistry and histopathology. We found that DSS-induced acute ulcerative colitis leads to significant elevations in the levels of amino acids in plasma and decreased levels in the membrane-related metabolites and a range of nucleotides, nucleobases, and nucleosides in the colon. In addition, acute-colitis-induced elevations in the levels of nucleotides in the liver were observed, accompanied by reduced levels of glucose. DSS-induced acute colitis also resulted in increased levels of oxidized glutathione and attenuated levels of taurine in the spleen. Furthermore, acute colitis resulted in depletion in the levels of gut microbial cometabolites in urine along with an increase in citric acid cycle intermediates. These findings suggest that DSS-induced acute colitis causes a disturbance of lipid and energy metabolism, damage to the colon and liver, a promoted antioxidative and anti-inflammatory response, and perturbed gut microbiotal communities. The information obtained here provided details of the time-dependent and holistic metabolic changes in the development of the DSS-induced acute ulcerative colitis, which could be useful in discovery of novel therapeutic targets for management of IBD

The Role of Transition Metal and Nitrogen in Metal–N–C Composites for Hydrogen Evolution Reaction at Universal pHs

For the first time, we demonstrated that transition metal and nitrogen codoped carbon nanocomposites synthesized by pyrolysis and heat treatment showed excellent catalytic activity toward hydrogen evolution reaction (HER) in both acidic and alkaline media. The overpotential at 10 mA cm^–2 was 235 mV in a 0.5 M H₂SO₄ solution at a catalyst loading of 0.765 mg cm^–2 for Co–N–C. In a 1 M KOH solution, the overpotential was only slightly increased by 35 mV. The high activity and excellent durability (negligible loss after 1000 cycles in both acidic and alkaline media) make this carbon-based catalyst a promising alternative to noble metals for HER. Electrochemical and density functional theory (DFT) calculation results suggested that transition metals and nitrogen played a critical role in activity enhancement. The active sites for HER might be associated with metal/N/C moieties, which have been also proposed as reaction centers for oxygen reduction reaction

O-PLS-DA comparison between urine spectra from <i>K. pneumoniae</i> infected rats and corresponding controls and metabolite concentration changes relative to corresponding controls at different time points after <i>K. pneumoniae</i> infection.

<p>(A) Cross validated O-PLS-DA scores (left hand side) and coefficient plots (right hand side) generated from NMR spectral data of urine of rats at 8 hours after <i>K. pneumoniae</i> infection (red dots), compared with those of non-infected (black squares). (B) a-f plots show metabolites changes in urine. C_inf and C_con stand for the averaged concentration in the infection and control group, respectively.</p

Comparison of influencing factors on outcomes of single and multiple road traffic injuries: A regional study in Shanghai, China (2011-2014)

<div><p>Introduction</p><p>To identify key intervention factors and reduce road traffic injury (RTI)-associated mortality, this study compared outcomes and influencing factors of single and multiple road traffic injuries (RTIs) in Shanghai.</p><p>Methods</p><p>Based on the design of National Trauma Data Bank, this study collected demographic, injury, and outcome data from RTI patients treated at the four largest trauma centers in Shanghai from January 2011 to January 2015. Data were analyzed with descriptive statistics, univariate analysis, and hierarchical logistic regression analysis.</p><p>Results</p><p>Among 2397 participants, 59.4% had a single injury, and 40.6% had multiple injuries. Most patients’ outcome was cure or improvement. For single-RTI patients, length of stay, body region, central nervous system injury, acute renal failure, multiple organ dysfunction syndrome, bacterial infection, and coma were significantly related to outcome. For multiple-RTI patients, age, admission pathway, prehospital time, length of stay, number of body regions, body region, injury condition, injury severity score, and coma were significantly related to outcome.</p><p>Conclusions</p><p>Emergency rescue in road traffic accidents should focus on high-risk groups (the elderly), high-incidence body regions (head, thorax, pelvis) and number of injuries, injury condition (central nervous system injury, coma, complications, admission pathway), injury severity (critically injured patients), and time factors (particularly prehospital time).</p></div

Trajectories of plasma and urinary metabolic profiles of the control group and the infected group at different time intervals.

<p>Time-dependent trajectories of plasma (A, R²X = 0.928, Q² = 0.918) and urinary (B, R²X = 0.789, Q² = 0.614) metabolic profiles of the control group (black squares) and the infection group (red squares) from hour 0 to day 14. Bars denote the standard deviations of each group.</p

Schematic representation of the metabolites and metabolic pathways in <i>K. pneumoniae</i> bacteremia.

<p>The metabolites in red indicate the changes in plasma and those in blue indicate the changes in urine whereas those in black were not observed; the arrows pointing up and down denoted relative increase and decrease in the infected group compared with the controls.</p

¹H NMR spectra of plasma and urine from control and <i>K. pneumoniae</i> infected rats for 8 hours.

<p>Typical 500 MHz ¹H (CPMG) NMR spectra of plasma obtained from a non-infected SD rat (P_A) and a rat infected with <i>K. pneumoniae</i> for 8 hours (P_B). The region of δ 5.0–9.0 in the blood plasma spectra was vertically expanded 16 times compared with the region of δ 0.5–4.5; Representative 600 MHZ ¹H NMR spectra of urine samples obtained from a non-infected SD rat (U_A) and a rat infected with <i>K. pneumoniae</i> for 8 hours (U_B). The spectral region, δ 6.2–9.5, was vertically expanded 4 times compared with the region of δ 0.5–4.4. Key: 1,lipoprotein; 2,valine; 3,leucine; 4,isoleucine; 5,creatine; 6,<i>N</i>-acetyl glycoprotein; 7,<i>O</i>-acetyl glycoprotein; 8,alanine; 9,lactate; 10,acetoacetate; 11,α-glucose; 12,acetate; 13,pyruvate; 14,dihydrothymine; 15,threonine; 16,unsaturated fatty acid; 17,choline; 18,phosphorylcholine; 19,glycerophosphocholine; 20,lysine; 21,citrate; 22,_D-3-hydroxybutyrate; 23,glutamine; 24,glutamate; 25,histidine; 26,phenylalanine; 27,tyrosine; 28,formate; 29,trimethylamine; 30,urea; 31,triglyceride; 32,arginine; 33,ω-3 fatty acid; 34,poly unsaturated fatty acid; 35,glucose and amino acids α-CH resonances; 36,2-oxoglutarate; 37,creatinine; 38,hippurate; 39,1-methylnicotimamide; 40,acetamide; 41,fumarate; 42,phenylacetylglycine; 43,cis-aconitate; 44,pantothenic acid; 45,succinate; 46,<i>N</i>-methylnicotinate; 47,malate; 48,indoxyl sulfate; 49,dimethylamine; 50,glycine; 51,isovalerate; 52,2-(4-hydroxyphenyl)propanoic acid; 53,2,3-dihydroxybutyrate; 54,4-cresol glucuronide; 55,dimethylglycine; 56,taurine; 57,hypotaurine; 58,4-deoxyerythronate; 59,trimethylamine <i>N</i>-oxide.</p