For the large-scale sustainable implementation of polymer electrolyte membrane fuel cells in vehicles, high-performance electrocatalysts with low platinum consumption are desirable for use as cathode material during the oxygen reduction reaction in fuel cells. Here we report a carbon black-supported cost-effective, efficient and durable platinum single-atom electrocatalyst with carbon monoxide/methanol tolerance for the cathodic oxygen reduction reaction. The acidic single-cell with such a catalyst as cathode delivers high performance, with power density up to 680 mW cm−2 at 80 °C with a low platinum loading of 0.09 mgPt cm−2, corresponding to a platinum utilization of 0.13 gPt kW−1 in the fuel cell. Good fuel cell durability is also observed. Theoretical calculations reveal that the main effective sites on such platinum single-atom electrocatalysts are single-pyridinic-nitrogen-atom-anchored single-platinum-atom centres, which are tolerant to carbon monoxide/methanol, but highly active for the oxygen reduction reaction.
The electrochemical reduction reaction of carbon dioxide (CO2RR) to carbon monoxide (CO) is the basis for the further synthesis of more complex carbon-based fuels or attractive feedstock. Single-atom catalysts have unique electronic and geometric structures with respect to their bulk counterparts, thus exhibiting unexpected catalytic activities. A nitrogen-anchored Zn single-atom catalyst is presented for CO formation from CO2RR with high catalytic activity (onset overpotential down to 24 mV), high selectivity (Faradaic efficiency for CO (FE ) up to 95 % at -0.43 V), remarkable durability (>75 h without decay of FE ), and large turnover frequency (TOF, up to 9969 h ). Further experimental and DFT results indicate that the four-nitrogen-anchored Zn single atom (Zn-N ) is the main active site for CO2RR with low free energy barrier for the formation of *COOH as the rate-limiting step.
The occurrence and prognosis of many complex diseases, such as cancers, is associated with the variation of various molecules, including DNA at the genetic level, RNA at the regulatory level, proteins at the functional level and small molecules at the metabolic level (defined collectively as multilevel molecules). Thus it is highly desirable to develop a single platform for detecting multilevel biomarkers for early-stage diagnosis. Here we report a protocol on DNA-nanostructure-based programmable engineering of the biomolecular recognition interface, which provides a universal electrochemical biosensing platform for the ultrasensitive detection of nucleic acids (DNA/RNA), proteins, small molecules and whole cells. The protocol starts with the synthesis of a series of differentially sized, self-assembled tetrahedral DNA nanostructures (TDNs) with site-specifically modified thiol groups that can be readily anchored on the surface of a gold electrode with high reproducibility. By exploiting the rigid structure, nanoscale addressability and versatile functionality of TDNs, one can tailor the type of biomolecular probes appended on individual TDNs for the detection of specific molecules of interest. Target binding occurring on the gold surface patterned with TDNs is quantitatively translated into electrochemical signals via a coupled enzyme-based catalytic process. This uses a sandwich assay strategy in which biotinylated reporter probes recognize TDN-bound target biomolecules, which then allow binding of horseradish-peroxidase-conjugated avidin (avidin-HRP). Hydrogen peroxide (H2O2) is then reduced by avidin-HRP in the presence of TMB (3,3',5,5'-tetramethylbenzidine) to generate a quantitative electrochemical signal. The time range for the entire protocol is ∼1 d, whereas the detection process takes ∼30 min to 3 h.
The authors report first a new type of nitrogen-triggered Zn single atom catalyst, demonstrating high catalytic activity and remarkable durability for the oxygen reduction reaction process. Both X-ray absorption fine structure spectra and theoretical calculations suggest that the atomically dispersed Zn-N 4 site is the main, as well as the most active, component with O adsorption as the rate-limiting step at a low overpotential of 1.70 V. This work opens a new field for the exploration of high-performance Pt-free electrochemical oxygen reduction catalysts for fuel cells.
Bismuth (Bi) has been known as a highly efficient electrocatalyst for CO 2 reduction reaction. Stable free-standing two-dimensional Bi monolayer (Bismuthene) structures have been predicted theoretically, but never realized experimentally. Here, we show the first simple large-scale synthesis of free-standing Bismuthene, to our knowledge, and demonstrate its high electrocatalytic efficiency for formate (HCOO −) formation from CO 2 reduction reaction. The catalytic performance is evident by the high Faradaic efficiency (99% at −580 mV vs. Reversible Hydrogen Electrode (RHE)), small onset overpotential (<90 mV) and high durability (no performance decay after 75 h and annealing at 400°C). Density functional theory calculations show the structure-sensitivity of the CO 2 reduction reaction over Bismuthene and thicker nanosheets, suggesting that selective formation of HCOO − indeed can proceed easily on Bismuthene (111) facet due to the unique compressive strain. This work paves the way for the extensive experimental investigation of Bismuthene in many different fields.
A real optimal Fe content: For N and Fe co-doped carbon electrocatalysts for oxygen reduction reactions (ORRs) it is found that there is a real optimal trace Fe content (Peak II), which has never been observed before. The real optimal electrocatalyst shows superior high activity for ORR and possesses the best price/performance ratio ever.
Evidence accumulated over the past several years indicates that the AMP-activated protein kinase (AMPK) 2 may be a therapeutic target for treating insulin resistance and type 2 diabetes (1). AMPK is a heterotrimeric protein formed by an ␣ subunit, which contains the catalytic activity, and by the  and ␥ regulatory subunits important in maintaining stability of the heterotrimer complex (2). AMPK belongs to a family of energy-sensing enzymes functioning as a "fuel gauge" that monitors changes in the energy status of a cell (3, 4). When activated, AMPK shuts down anabolic pathways and promotes catabolism in response to an elevated AMP/ATP ratio by down-regulating the activity of several key enzymes of intermediary metabolism (4). Two primary acute consequences of AMPK activation are 1) an increase in glucose uptake by induction of glucose 4 transporter microvesicle cytoplasm to membrane translocation and fusion and 2) an increase in fatty acid oxidation by phosphorylation and inactivation of acetyl-CoA carboxylase (ACC), the rate-limiting enzyme in fatty acid synthesis (5). Therefore, the AMPK signal pathways are thought to play a central role in the regulation of cellular glucose and lipid homeostasis. The control of AMPK activity is complex, and the classic view is that AMPK is activated allosterically by an increase in the intracellular AMP/ATP ratios and/or by the phosphorylation of threonine 172 within the ␣ subunit. Several protein kinases responsible for this phosphorylation have been identified. They include Peutz-Jeghers syndrome kinase LKB1 (LKB1) (6), and the Ca 2ϩ /calmodulin-dependent protein kinase kinase (7). Protein phosphorylation signal transduction systems are balanced and regulated delicately by both phosphatase and kinase. Since AMPK is activated by (a) protein kinase(s) at the threonine 172 residue, one can easily assume that AMPK can be regulated negatively by (a) serine/threonine phosphatase(s). To date, a wide range of physiological stressors, pharmacological agents, and hormones associated with increase in the intracellular AMP/ATP ratios have been demonstrated to activate AMPK (8). AMPK is also thought to be regulated by glycogen (9), which is the major cellular storage form of carbohydrates and thus, an additional indicator of cellular energy status. Lipids are the other major energy source for cellular metabolism. Recent studies (10, 11) in heart and liver have revealed that AMPK may be sensitive to the "lipid status" of a cell, and activation may be influenced by intracellular fatty BSA, bovine serum albumin; eNOS, endothelial nitric-oxide synthase; LKB1, Peutz-Jeghers syndrome kinase LKB1; OA, okadaic acid; ONOO Ϫ , peroxynitrite; VSMC, vascular smooth muscle cell; siRNA, short interference RNA; FFA, free fatty acid; EBM, endothelial basal medium; 2-BrP, 2-bromopalmitate; HFD, high fat diet; PP2C, protein phosphatase 2C.
For the goal of practical industrial development of fuel cells, inexpensive, sustainable, and high performance electrocatalysts for oxygen reduction reactions (ORR) are highly desirable alternatives to platinum (Pt) and other rare materials. In this work, sustainable fluorine (F)-doped carbon blacks (CB-F) as metal-free, low-cost, and high-performance electrocatalysts for ORR were synthesized for the first time. The performance (electrocatalytic activity, long-term operation stability, and tolerance to poisons) of the best one (BP-18F, based on Black Pearls 2000 (BP)) is on the same level as Pt-based or other best non-Pt-based catalysts in alkaline medium. The maximum power density of alkaline direct methanol fuel cell with BP-18F as the cathode (3 mg/cm2) is ∼15.56 mW/cm2 at 60 °C, compared with a maximum of 9.44 mW/cm2 for commercial Pt/C (3 mgPt/cm2). All these results unambiguously demonstrate that these sustainable CB-F catalysts are the most promising alternatives to Pt in an alkaline fuel cell. Since sustainable carbon blacks are 10 000 times less expensive and much more abundant than Pt or other rare materials, these CB-F electrocatalysts possess the best price/performance ratio for ORR to date.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
334 Leonard St
Brooklyn, NY 11211
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.