Mechanistic Insights into the Inhibition of a Common CTLA-4 Gene Mutation in the Cytoplasmic Domain.

Cytotoxic T-lymphocyte antigen 4 (CTLA-4) is a pivotal immune checkpoint receptor, playing a crucial role in modulating T-cell activation. In this study, we delved into the underlying mechanism by which a common mutation, G199R, in the cytoplasmic domain of CTLA-4 impacts its inhibitory function. Utilizing nuclear magnetic resonance (NMR) spectroscopy and biochemical techniques, we mapped the conformational changes induced by this mutation and investigated its role in CTLA-4 activity. Our findings reveal that this mutation leads to a distinct conformational alteration, enhancing protein-membrane interactions. Moreover, functional assays demonstrated an improved capacity of the G199R mutant to downregulate T-cell activation, underscoring its potential role in immune-related disorders. These results not only enhance our understanding of CTLA-4 regulatory mechanisms but also provide insights for targeted therapeutic strategies addressing immune dysregulation linked to CTLA-4 mutations.

Deciphering Cholesterol's Role in PD-L2 Stability: A Distinct Regulatory Mechanism From PD-L1.

Programmed cell death 1 ligand 2 (PD-L2), a member of the B7 immune checkpoint protein family, emerges as a crucial player in immune modulation. Despite its functional overlap with programmed cell death 1 ligand 1 (PD-L1) in binding to the programmed cell death protein 1 (PD-1) on T cells, PD-L2 exhibits a divergent expression pattern and a higher affinity for PD-1. However, the regulatory mechanisms of PD-L2 remain under-explored. Here, our investigations illustrate the pivotal role of cholesterol in modulating PD-L2 stability. Using advanced nuclear magnetic resonance (NMR) and biochemical analyses, we demonstrate a direct and specific binding between cholesterol and PD-L2, mediated by an F-xxx-V-xx-LR motif in its transmembrane domain, distinct from that in PD-L1. This interaction stabilizes PD-L2 and prevents its downstream degradation. Disruption of this binding motif compromises PD-L2's cellular stability, underscoring its potential significance in cancer biology. These findings not only deepen our understanding of PD-L2 regulation in the context of tumors, but also open avenues for potential therapeutic interventions.

[Mechanobiological Mechanisms Involved in the Regualation of the Blood-Brain Barrier by Fluid Shear Force]. / æµä½“å‰ªåˆ‡åŠ›è°ƒæŽ§è¡€è„‘å±éšœçš„åŠ›å­¦ç”Ÿç‰©å­¦æœºåˆ¶ç ”ç©¶.

Objective: To explore the mechanobiological mechanism of fluid shear force (FSF) on the protection, injury, and destruction of the structure and function of the blood-brain barrier (BBB) under normal physiological conditions, ischemic hypoperfusion, and postoperative hyperperfusion conditions. BBB is mainly composed of brain microvascular endothelial cells. Rat brain microvascular endothelial cells (rBMECs) were used as model cells to conduct the investigation. Methods: rBMECs were seeded at a density of 1×105 cells/cm2 and incubated for 48 h. FSF was applied to the rBMECs at 0.5, 2, and 20 dyn/cm2, respectively, simulating the stress BBB incurs under low perfusion, normal physiological conditions, and high FSF after bypass grafting when there is cerebral vascular stenosis. In addition, a rBMECs static culture group was set up as the control (no force was applied). Light microscope, scanning electron microscope (SEM), and laser confocal microscope (LSCM) were used to observe the changes in cell morphology and cytoskeleton. Transmission electron microscope (TEM) was used to observe the tight junctions. Immunofluorescence assay was performed to determine changes in the distribution of tight junction-associated proteins claudin-5, occludin, and ZO-1 and adherens junction-associated proteins VE-cadherin and PECAM-1. Western blot was performed to determine the expression levels of tight junction-associated proteins claudin-5, ZO-1, and JAM4, adherens junction-associated protein VE-cadherin, and key proteins in Rho GTPases signaling (Rac1, Cdc42, and RhoA) under FSF at different intensities. Results: Microscopic observation showed that the cytoskeleton exhibited disorderly arrangement and irregular orientation under static culture and low shear force (0.5 dyn/cm2). Under normal physiological shear force (2 dyn/cm2), the cytoskeleton was rearranged in the orientation of the FSF and an effective tight junction structure was observed between cells. Under high shear force (20 dyn/cm2), the intercellular space was enlarged and no effective tight junction structure was observed. Immunofluorescence results showed that, under low shear force, the gap between the cells decreased, but there was also decreased distribution of tight junction-associated proteins and adherens junction-associated proteins at the intercellular junctions. Under normal physiological conditions, the cells were tightly connected and most of the tight junction-associated proteins were concentrated at the intercellular junctions. Under high shear force, the gap between the cells increased significantly and the tight junction and adherens junction structures were disrupted. According to the Western blot results, under low shear force, the expression levels of claudin-5, ZO-1, and VE-cadherin were significantly up-regulated compared with those of the control group (P<0.05). Under normal physiological shear force, claudin-5, ZO-1, JAM4, and VE-cadherin were highly expressed compared with those of the control group (P<0.05). Under high shear force, the expressions of claudin-5, ZO-1, JAM4, and VE-cadherin were significantly down-regulated compared with those of the normal physiological shear force group (P<0.05). Under normal physiological shear force, intercellular expressions of Rho GTPases proteins (Rac1, Cdc42, and RhoA) were up-regulated and were higher than those of the other experimental groups (P<0.05). The expressions of Rho GTPases under low and high shear forces were down-regulated compared with that of the normal physiological shear force group (P<0.05). Conclusion: Under normal physiological conditions, FSF helps maintain the integrity of the BBB structure, while low or high shear force can damage or destroy the BBB structure. The regulation of BBB by FSF is closely related to the expression and distribution of tight junction-associated proteins and adherens junction-associated proteins.

Fluid shear stress induced-endothelial phenotypic transition contributes to cerebral ischemia-reperfusion injury and repair.

Long-term ischemia leads to insufficient cerebral microvascular perfusion and dysfunction. Reperfusion restores physiological fluid shear stress (FSS) but leads to serious injury. The mechanism underlying FSS-induced endothelial injury in ischemia-reperfusion injury (IRI) remains poorly understood. In this study, a rat model of middle cerebral artery occlusion was constructed to explore cerebrovascular endothelial function and inflammation in vivo. Additionally, the rat brain microvascular endothelial cells (rBMECs) were exposed to a laminar FSS of 0.5 dyn/cm2 for 6 h and subsequently restored to physiological fluid shear stress level (2 dyn/cm2) for 2 and 12 h, respectively. We found that reperfusion induced endothelial-to-mesenchymal transition (EndMT) in endothelial cells, leading to serious blood-brain barrier dysfunction and endothelial inflammation, accompanied by the nuclear accumulation of Yes-associated protein (YAP). During the later stage of reperfusion, cerebral endothelium was restored to the endothelial phenotype with a distinct change in mesenchymal-to-endothelial transition (MEndT), while YAP was translocated and phosphorylated in the cytoplasm. Knockdown of YAP or inhibition of actin polymerization markedly impaired the EndMT in rBMECs. These findings suggest that ischemia-reperfusion increased intensity of FSS triggered an EndMT process and, thus, led to endothelial inflammation and tissue injury, whereas continuous FSS induced a time-dependent reversal MEndT event contributing to the endothelial repair. This study provides valuable insight for therapeutic strategies targeting IRI.

Hemodynamic force dictates endothelial angiogenesis through MIEN1-ERK/MAPK-signaling axis.

It is well-recognized that blood flow at branches and bends of arteries generates disturbed shear stress, which plays a crucial in driving atherosclerosis. Flow-generated fluid shear stress (FSS), as one of the key hemodynamic factors, is appreciated for its critical involvement in regulating angiogenesis to facilitate wound healing and tissue repair. Endothelial cells can directly sense FSS but the mechanobiological mechanism by which they decode different patterns of FSS to trigger angiogenesis remains unclear. In the current study, laminar shear stress (LSS, 15 dyn/cm2) was employed to mimic physiological blood flow, while disturbed shear stress (DSS, ranging from 0.5 ± 4 dyn/cm2) was applied to simulate pathological conditions. The aim was to investigate how these distinct types of blood flow regulated endothelial angiogenesis. Initially, we observed that DSS impaired angiogenesis and downregulated endogenous vascular endothelial growth factor B (VEGFB) expression compared to LSS. We further found that the changes in membrane protein, migration and invasion enhancer 1 (MIEN1) play a role in regulating ERK/MAPK signaling, thereby contributing to endothelial angiogenesis in response to FSS. We also showed the involvement of MIEN1-directed cytoskeleton organization. These findings suggest the significance of shear stress in endothelial angiogenesis, thereby enhancing our understanding of the alterations in angiogenesis that occur during the transition from physiological to pathological blood flow.

Establishing Ultralow Self-Discharge Zn-I2 Battery by Optimizing ZnSO4 Electrolyte Concentration.

As one of promising candidates for large-scale energy-storage systems, Zn-I2 aqueous battery exhibits multifaceted advantages including low cost, high energy/powder density, and intrinsic operational safety, but also suffers from fast self-discharge and short cycle/shelf lifespan associating with I3 - shuttle, Zn dendrite growth, and corrosion. In this paper, the battery's self-discharge rate is successfully suppressed down to an unprecedent level of 17.1% after an ultralong shelf-time of 1 000 h (i.e., 82.9% capacity retention after 41 days open-circuit storage), by means of manipulating solvation structures of traditional ZnSO4 electrolyte via simply adjusting electrolyte concentration. Better yet, the optimized 2.7 m ZnSO4 electrolyte further prolongs the cycle lifespan of the battery up to >10 000 and 43 000 cycles at current density of 1 and 5 A g-1 , respectively, thanks to the synthetic benefits from reduced free water content, modified solvation structure and lowered I2 dissolution in the electrolyte. With both long lifespan and ultralow self-discharge, this reliable and affordable Zn-I2 battery may provide a feasible alternative to the centuries-old lead-acid battery.

The influence of microenvironment stiffness on endothelial cell fate: Implication for occurrence and progression of atherosclerosis.

Atherosclerosis, the primary cause of cardiovascular diseases (CVDs), is characterized by phenotypic changes in fibrous proliferation, chronic inflammation and lipid accumulation mediated by vascular endothelial cells (ECs) and vascular smooth muscle cells (SMCs) which are correlated with the stiffening and ectopic remodeling of local extracellular matrix (ECM). The native residents, ECs and SMCs, are not only affected by various chemical factors including inflammatory mediators and chemokines, but also by a range of physical stimuli, such as shear stress and ECM stiffness, presented in the microenvironmental niche. Especially, ECs, as a semi-selective barrier, can sense mechanical forces, respond quickly to changes in mechanical loading and provide context-specific adaptive responses to restore homeostasis. However, blood arteries undergo stiffening and lose their elasticity with age. Reports have shown that the ECM stiffening could influence EC fate by changing the cell adhesion, spreading, proliferation, cell to cell contact, migration and even communication with SMCs. The cell behaviour changes mediated by ECM stiffening are dependent on the activation of a signaling cascade of mechanoperception and mechanotransduction. Although the substantial evidence directly indicates the importance of ECM stiffening on the native ECs, the understanding about this complex interplay is still largely limited. In this review, we systematically summarize the roles of ECM stiffening on the behaviours of endothelial cells and elucidate the underlying details in biological mechanism, aiming to provide the process of how ECs integrate ECM mechanics and the highlights for bioaffinity of tissue-specific engineered scaffolds.

A Low Driving-Voltage Hybrid-Electrolyte Electrochromic Window with Only Ferreous Redox Couples.

Even after decades of development, the widespread application of electrochromic windows (ECW) is still seriously restricted by their high price and inadequate performance associated with structural/fabrication complexity and electrochemical instability. Herein, a simple hybrid electrochromic system based on PFSA (perfluorosulfonic acid)-coated Prussian blue (PB, Fe4III [FeII(CN)6]3) film and Ferricyanide-Ferrocyanide ([Fe(CN)6]4-/[Fe(CN)6]3-)-containing hybrid electrolyte is reported. The PB film and the [Fe(CN)6]4-/[Fe(CN)6]3- couple show near redox potentials well inside the electrochemical window of water, resulting in a low driven voltage (0.4 V for coloring and -0.6 V for bleaching) and a relatively long lifespan (300 cycles with 76.9% transmittance contrast retained). The PFSA layer, as a cation-exchange structure, significantly improves the transmittance modulation amplitude (ΔT: 23.3% vs. 71.9% at a wavelength of 633 nm) and optical memory abilities (ΔT retention: 10.1% vs. 67.0% after 300 s open-circuit rest increases) of the device, by means of preventing the direct contact and charge transfer between the PB film and the [Fe(CN)6]4-/[Fe(CN)6]3- couple. This "hybrid electrolyte + electron barrier layer" design provides an effective way for the construction of simple structured electrochromic devices.

Coupling dual metal active sites and low-solvation architecture toward high-performance aqueous ammonium-ion batteries.

Aqueous rechargeable ammonium-ion batteries (AIBs) possess the characteristics of safety, low cost, environmental friendliness, and fast diffusion kinetics. However, their energy density is often limited due to the low specific capacity of cathode materials and narrow electrochemical stability windows of electrolytes. Herein, high-performance aqueous AIBs were designed by coupling Fe-substituted manganese-based Prussian blue analog (FeMnHCF) cathodes and highly concentrated NH4CF3SO3 electrolytes. In FeMnHCF, Mn3+/Mn2+-N redox reaction at high potential was introduced, and two metal active redox species of Mn and Fe were achieved. To match such FeMnHCF cathodes, highly concentrated NH4CF3SO3 electrolyte was further developed, where NH4+ ion displays low-solvation structure because of the increased coordination number of CF3SO3- anions. Furthermore, the water molecules are confined by NH4+ and CF3SO3- ions in their solvation sheath, leading to weak interaction between water molecules and thus effectively extending the voltage window of electrolyte. Consequently, the FeMnHCF electrodes present high reversibility during the charge/discharge process. Moreover, owing to a small amount of free water in concentrated electrolyte, the dissolution of FeMnHCF is also inhibited. As a result, the assembled aqueous AIBs exhibit enhanced energy density, excellent rate capability, and stable cycling behavior. This work provides a creative route to construct high-performance aqueous AIBs.

Identification of a novel class of cyclic penta-peptides against hepatitis C virus as p7 channel blockers.

The hepatitis C virus (HCV) p7 viroporin protein is essential for viral assembly and release, suggesting its unrealised potential as a target for HCV interventions. Several classes of small molecules that can inhibit p7 through allosteric mechanisms have shown low efficacy. Here, we used a high throughput virtual screen to design a panel of eight novel cyclic penta-peptides (CPs) that target the p7 channel with high binding affinity. Further examination of the effects of these CPs in viral production assays indicated that CP7 exhibits the highest potency against HCV among them. Moreover, the IC50 efficacy of CP7 in tests of strain Jc1-S282T suggested that this cyclopeptide could also effectively inhibit a drug-resistant HCV strain. A combination of nuclear magnetic resonance (NMR) spectroscopy and molecular dynamics (MD) simulations revealed that CP7 blocking activity relies on direct binding to the p7 channel lumen at the N-terminal bottleneck region. These findings thus present a promising anti-HCV cyclic penta-peptide targeting p7 viroporin, while also describing an alternative strategy for designing a new class of p7 channel blockers for strains resistant to direct-acting antiviral agents (DAA).

Regulation of PD-L1 through direct binding of cholesterol to CRAC motifs.

Cholesterol, an essential molecule for cell structure, function, and viability, plays crucial roles in the development, progression, and survival of cancer cells. Earlier studies have shown that cholesterol-lowering drugs can inhibit the high expression of programmed-death ligand 1 (PD-L1) that contributes to immunoevasion in cancer cells. However, the regulatory mechanism of cell surface PD-L1 abundance by cholesterol is still controversial. Here, using nuclear magnetic resonance and biochemical techniques, we demonstrated that cholesterol can directly bind to the transmembrane domain of PD-L1 through two cholesterol-recognition amino acid consensus (CRAC) motifs, forming a sandwich-like architecture and stabilizing PD-L1 to prevent downstream degradation. Mutations at key binding residues prohibit PD-L1-cholesterol interactions, decreasing the cellular abundance of PD-L1. Our results reveal a unique regulatory mechanism that controls the stability of PD-L1 in cancer cells, providing an alternative method to overcome PD-L1-mediated immunoevasion in cancers.

NMR Detection and Structural Modeling of the Ethylene Receptor LeETR2 from Tomato.

The gaseous plant hormone ethylene influences many physiological processes in plant growth and development. Plant ethylene responses are mediated by a family of ethylene receptors, in which the N-terminal transmembrane domains are responsible for ethylene binding and membrane localization. Until now, little structural information was available on the molecular mechanism of ethylene responses by the transmembrane binding domain of ethylene receptors. Here, we screened different constructs, fusion tags, detergents, and purification methods of the transmembrane sensor domain of ethylene receptors. However, due to their highly hydrophobic transmembrane domain (TMD), only a KSI-fused LeETR21-131 from tomato yielded a good-quality nuclear magnetic resonance (NMR) spectrum in the organic solvent. Interestingly, a dimer model of LeETR21-131 built by the AlphaFold2 algorithm showed greatly converged structures. The interaction analysis of ethylene and LeETR21-131 using molecular docking and molecular dynamics (MD) simulations demonstrated the potential binding sites of ethylene in LeETR21-131. Our exploration provides valuable knowledge for further understanding of the ethylene-perception process in ethylene receptors.

Ni2+ Catalyzed Cleavage of TrpLE-Fused Small Transmembrane Peptides.

In addition to a membrane anchor, the transmembrane domain (TMD) of single-pass transmembrane proteins (SPTMPs) recently has shown essential roles in the cross-membrane activity or receptor assembly/clustering. However, these small TMD peptides are generally hydrophobic and dynamic, difficult to be expressed and purified. Here, we have integrated the power of TrpLE fusion protein and a sequence-specific nickel-assisted cleavage (SNAC)-tag to produce small TMD peptides in a highly efficient way under mild conditions, which uses Ni2+ as the cleavage reagent, avoiding the usage of toxic cyanogen bromide (CNBr). Furthermore, this method simplifies the downstream protein purification and reconstitution. Two representative TMDs, including the Spike-TMD from severe acute respiratory syndrome coronavirus 2 (SARS2), were successfully produced with high-quality nuclear magnetic resonance (NMR) spectra. Therefore, our study provides a more efficient and practical approach for general structural characterization of the small TM proteins.

Positive Charges in the Brace Region Facilitate the Membrane Disruption of MLKL-NTR in Necroptosis.

Necroptosis is a type of programmed cell death executed through the plasma membrane disruption by mixed lineage kinase domain-like protein (MLKL). Previous studies have revealed that an N-terminal four-helix bundle domain (NBD) of MLKL is the executioner domain for the membrane permeabilization, which is auto-inhibited by the first brace helix (H6). After necroptosis initiation, this inhibitory brace helix detaches and the NBD can integrate into the membrane, and hence leads to necroptotic cell death. However, how the NBD is released and induces membrane rupture is poorly understood. Here, we reconstituted MLKL2-154 into membrane mimetic bicelles and observed the structure disruption and membrane release of the first brace helix that is regulated by negatively charged phospholipids in a dose-dependent manner. Using molecular dynamics simulation we found that the brace region in an isolated, auto-inhibited MLKL2-154 becomes intrinsically disordered in solution after 7 ns dynamic motion. Further investigations demonstrated that a cluster of arginines in the C-terminus of MLKL2-154 is important for the molecular conformational switch. Functional mutagenesis showed that mutating these arginines to glutamates hindered the membrane disruption of full-length MLKL and thus inhibited the necroptotic cell death. These findings suggest that the brace helix also plays an active role in MLKL regulation, rather than an auto-inhibitory domain.

An amphipathic Bax core dimer forms part of the apoptotic pore wall in the mitochondrial␣membrane.

Bax proteins form pores in the mitochondrial outer membrane to initiate apoptosis. This might involve their embedding in the cytosolic leaflet of the lipid bilayer, thus generating tension to induce a lipid pore with radially arranged lipids forming the wall. Alternatively, Bax proteins might comprise part of the pore wall. However, there is no unambiguous structural evidence for either hypothesis. Using NMR, we determined a high-resolution structure of the Bax core region, revealing a dimer with the nonpolar surface covering the lipid bilayer edge and the polar surface exposed to water. The dimer tilts from the bilayer normal, not only maximizing nonpolar interactions with lipid tails but also creating polar interactions between charged residues and lipid heads. Structure-guided mutations demonstrate the importance of both types of protein-lipid interactions in Bax pore assembly and core dimer configuration. Therefore, the Bax core dimer forms part of the proteolipid pore wall to permeabilize mitochondria.

Inhibitor Development against p7 Channel in Hepatitis C Virus.

Hepatitis C Virus (HCV) is the key cause of chronic and severe liver diseases. The recent direct-acting antiviral agents have shown the clinical success on HCV-related diseases, but the rapid HCV mutations of the virus highlight the sustaining necessity to develop new drugs. p7, the viroporin protein from HCV, has been sought after as a potential anti-HCV drug target. Several classes of compounds, such as amantadine and rimantadine have been testified for p7 inhibition. However, the efficacies of these compounds are not high. Here, we screened some novel p7 inhibitors with amantadine scaffold for the inhibitor development. The dissociation constant (Kd) of 42 ARD-series compounds were determined by nuclear magnetic resonance (NMR) titrations. The efficacies of the two best inhibitors, ARD87 and ARD112, were further confirmed using viral production assay. The binding mode analysis and binding stability for the strongest inhibitor were deciphered by molecular dynamics (MD) simulation. These ARD-series compounds together with 49 previously published compounds were further analyzed by molecular docking. Key pharmacophores were identified among the structure-similar compounds. Our studies suggest that different functional groups are highly correlated with the efficacy for inhibiting p7 of HCV, in which hydrophobic interactions are the dominant forces for the inhibition potency. Our findings provide guiding principles for designing higher affinity inhibitors of p7 as potential anti-HCV drug candidates.

Encapsulation of Red Phosphorus in Carbon Nanocages with Ultrahigh Content for High-Capacity and Long Cycle Life Sodium-Ion Batteries.

Red phosphorus (RP) has attracted great attention as a potential candidate for anode materials of high-energy density sodium-ion batteries (NIBs) due to its high theoretical capacity, appropriate working voltage, and natural abundance. However, the low electrical conductance and huge volumetric variation during the sodiation-desodiation process, causing poor rate performance and cyclability, have limited the practical application of RP in NIBs. Herein, we report a rational strategy to resolve these issues by encapsulating nanoscaled RP into conductive and networked carbon nanocages (denoted as RP@CNCs) using a combination of a phosphorus-amine based method and evacuation-filling process. The large interior cavities volume of CNCs and controllable solution-based method enable the ultrahigh RP loading amount (85.3 wt %) in the RP@CNC composite. Benefiting from the synergic effects of the interior cavities and conductive network, which afford high structure stability and rapid electron transport, the RP@CNC composite presents a high systematic capacity of 1363 mA h g-1 at a current density of 100 mA g-1 after 150 cycles, favorable high-rate capability, and splendid long-cycling performance with capacity retention over 80% after 1300 cycles at 5000 mA g-1. This prototypical design promises an efficient solution to maximize RP loading as well as to boost the electrochemical performance of RP-based anodes.

Electrocatalysis of S-doped carbon with weak polysulfide adsorption enhances lithium-sulfur battery performance.

Heteroatom-doped nanocarbons are beneficial for the performance improvement of lithium-sulfur batteries, and the reason is usually attributed to their strong adsorption to the soluble polysulfides. Herein, we found that, despite the weak polysulfide adsorption on hierarchical S-doped carbon nanocages (hSCNCs), the hSCNC-encapsulated sulfur cathode still exhibited better performance than the counterpart using undoped carbon nanocages, showing a high capacity of 579 mA h g-1 at 2 A g-1 after 400 cycles, and a high areal capacity of 4.7 mA h cm-2 with a high sulfur loading of 4.5 mg cm-2. The electrocatalysis-promoted mechanism of S-doped carbon was demonstrated, which facilitated polysulfide conversion and suppressed the polarization effect, thereby leading to superior performance.

The simplest construction of single-site catalysts by the synergism of micropore trapping and nitrogen anchoring.

Single-site catalysts feature high catalytic activity but their facile construction and durable utilization are highly challenging. Herein, we report a simple impregnation-adsorption method to construct platinum single-site catalysts by synergic micropore trapping and nitrogen anchoring on hierarchical nitrogen-doped carbon nanocages. The optimal catalyst exhibits a record-high electrocatalytic hydrogen evolution performance with low overpotential, high mass activity and long stability, much superior to the platinum-based catalysts to date. Theoretical simulations and experiments reveal that the micropores with edge-nitrogen-dopants favor the formation of isolated platinum atoms by the micropore trapping and nitrogen anchoring of [PtCl6]2-, followed by the spontaneous dechlorination. The platinum-nitrogen bonds are more stable than the platinum-carbon ones in the presence of adsorbed hydrogen atoms, leading to the superior hydrogen evolution stability of platinum single-atoms on nitrogen-doped carbon. This method has been successfully applied to construct the single-site catalysts of other precious metals such as palladium, gold and iridium.

Compressing Carbon Nanocages by Capillarity for Optimizing Porous Structures toward Ultrahigh-Volumetric-Performance Supercapacitors.

High volumetric energy density combined with high power density is highly desired for electrical double-layer capacitors. Usually the volumetric performance is improved by compressing carbon material to increase density but at the much expense of power density due to the deviation of the compressed porous structure from the ideal one. Herein the authors report an efficient approach to increase the density and optimize the porous structure by collapsing the carbon nanocages via capillarity. Three samples with decreasing sizes of meso- and macropores provide us an ideal model system to demonstrate the correlation of volumetric performance with porous structure. The results indicate that reducing the surplus macropores and, more importantly, the surplus mesopores is an efficient strategy to enhance the volumetric energy density while keeping the high power density. The optimized sample achieves a record-high stack volumetric energy density of 73 Wh L-1 in ionic liquid with superb power density and cycling stability.