Proton exchange membrane fuel cells convert hydrogen and oxygen into electricity without emissions. The high cost and low durability of Pt-based electrocatalysts for the oxygen reduction reaction hinder their wide application, and the development of non-precious metal electrocatalysts is limited by their low performance. Here we design a hybrid electrocatalyst that consists of atomically dispersed Pt and Fe single atoms and Pt–Fe alloy nanoparticles. Its Pt mass activity is 3.7 times higher than that of commercial Pt/C in a fuel cell. More importantly, the fuel cell with a low Pt loading in the cathode (0.015 mgPt cm−2) shows an excellent durability, with a 97% activity retention after 100,000 cycles and no noticeable current drop at 0.6 V for over 200 hours. These results highlight the importance of the synergistic effects among active sites in hybrid electrocatalysts and provide an alternative way to design more active and durable low-Pt electrocatalysts for electrochemical devices.

The electrochemical nitrate reduction reaction (NITRR) is an appealing method for ammonia synthesis, owing to the ambient conditions as well as its abundant sources, low dissociation energy, and high solubility of nitrate. The hydrogen evolution reaction is a competing process of the NITRR, which should be properly suppressed to achieve a high Faradaic efficiency of the NITRR. Herein, ultrathin CoO x nanosheets with abundant surface oxygen are designed as a low-cost NITRR catalyst, which delivers an ultrahigh ammonia yield of 82.4 ± 4.8 mg h −1 mg cat −1 with a Faradaic efficiency of 93.4 ± 3.8% at −0.3 V versus the reversible hydrogen electrode. Theoretical calculation reveals that the surface oxygen on cobalt sites can stabilize the adsorbed hydrogen on cobalt oxide, which hampers the evolution of hydrogen and leads to an enhanced NITRR activity. This work demonstrates that surface modification plays a critical role in suppressing the HER and facilitating the NITRR through a NHO pathway with a lower energy barrier.

At their proliferative limit, normal cells arrest and undergo replicative senescence, displaying large cell size, flat morphology, and senescence-associated beta-galactosidase (SA-β-Gal) activity. Normal or tumor cells exposed to genotoxic stress undergo therapy-induced senescence (TIS), displaying a similar phenotype. Senescence is considered a DNA damage response, but cellular heterogeneity has frustrated identification of senescence-specific markers and targets. To explore the senescent cell proteome, we treated tumor cells with etoposide and enriched SA-β-GalHI cells by fluorescence-activated cell sorting (FACS). The enriched TIS cells were compared to proliferating or quiescent cells by label-free quantitative LC-MS/MS proteomics and systems analysis, revealing activation of multiple lipid metabolism pathways. Senescent cells accumulated lipid droplets and imported lipid tracers, while treating proliferating cells with specific lipids induced senescence. Senescent cells also displayed increased lipid aldehydes and upregulation of aldehyde detoxifying enzymes. These results place deregulation of lipid metabolism alongside genotoxic stress as factors regulating cellular senescence.

Developing efficient electrocatalysts for an oxygen evolution reaction (OER) is important for renewable energy storage. Here, we design high-density Ir single-atom catalysts supported by CoO x amorphous nanosheets (ANSs) for the OER. Experimental results show that Ir single atoms are anchored by abundant surface-absorbed O in CoO x ANSs. Ir single-atom catalysts possess ultrahigh mass activity that is 160-fold of commercial IrO 2 . The OER of IrCoO x ANSs reached a record low onset overpotential of less than 30 mV. In situ X-ray absorption spectroscopy reveals that Ir−O−Co pairs directly boosted the OER efficiency and enhanced the Ir stability.

Helicobacter pylori (H. pylori) is a common human pathogenic bacterium. Once infected, it is difficult for the host to clear this organism using the innate immune system. Increased antibiotic resistance further makes it challenging for effective eradication. However, the mechanisms of immune evasion still remain obscure, and novel strategies should be developed to efficiently eliminate H. pylori infection in stomachs. Here we uncovered desirable anti-H. pylori effect of vitamin D3 both in vitro and in vivo, even against antibiotic-resistant strains. We showed that H. pylori can invade into the gastric epithelium where they became sequestered and survived in autophagosomes with impaired lysosomal acidification. Vitamin D3 treatment caused a restored lysosomal degradation function by activating the PDIA3 receptor, thereby promoting the nuclear translocation of PDIA3-STAT3 protein complex and the subsequent upregulation of MCOLN3 channels, resulting in an enhanced Ca 2+ release from lysosomes and normalized lysosomal acidification. The recovered lysosomal degradation function drives H. pylori to be eliminated through the autolysosomal pathway. These findings provide a novel pathogenic mechanism on how H. pylori can survive in the gastric epithelium, and a unique pathway for vitamin D3 to reactivate the autolysosomal degradation function, which is critical for the antibacterial action of vitamin D3 both in cells and in animals, and perhaps further in humans.