Objective Infection with Helicobacter pylori ( H pylori ), especially cytotoxin‐associated gene A‐positive (CagA+) strains, has been associated with various gastrointestinal and extragastric diseases. The aim of this study was to characterize H pylori ‐induced alterations in the gastric and tongue coating microbiota and evaluate their potential impacts on human health. Design The gastric mucosa and tongue coating specimens were collected from 80 patients with chronic gastritis, and microbiota profiles were generated by 16S rRNA gene sequencing. Samples were grouped as H pylori negative (n = 32), CagA‐negative H pylori infection (n = 13), and CagA‐positive H pylori infection (n=35). The comparison of bacterial relative abundance was made using a generalized linear model. Functional profiling of microbial communities was predicted with PICRUSt and BugBase. Microbial correlation networks were produced by utilizing SparCC method. Results Significant alterations of the gastric microbiota were found in the H pylori +/CagA+ samples, represented by a decrease in bacterial diversity, a reduced abundance of Roseburia , and increased abundances of Helicobacter and Haemophilus genera. At the community level, functions involved in biofilm forming, mobile element content, and facultative anaerobiosis were significantly decreased in gastric microbiome of the H pylori + subjects. The presence of CagA gene was linked to an increased proportion of Gram‐negative bacteria in the stomach, thereby contributing to an upregulation of lipopolysaccharide (LPS) biosynthesis. The number of bacterial interactions was greatly reduced in networks of both tongue coating and gastric microbiota of the H pylori +/CagA+ subject, and the cooperative bacterial interactions dominated the tongue coating microbiome. Conclusions Infection with H pylori strains possessing CagA may increase the risk of various diseases, by upregulating LPS biosynthesis in the stomach and weakening the defense of oral microbiota against microorganisms with pathogenic potential.

Atomically dispersed metal‐nitrogen sites show great prospect for the oxygen reduction reaction (ORR), whereas the unsatisfactory adsorption‐desorption behaviors of oxygenated intermediates on the metal centers impede improvement of the ORR performance. We propose a new conceptual strategy of introducing sacrificial bonds to remold the local coordination of Fe−Nx sites, via controlling the dynamic transformation of the Fe−S bonds in the Fe−N−C single‐atom catalyst. Spectroscopic and theoretical results reveal that the selective cleavage of the sacrificial Fe−S bonds induces the incorporation of the electron‐withdrawing oxidized sulfur on the Fe centers. The newly functionalized moieties endow the catalyst with superior ORR activity and remarkable stability, owing to the reduced electron localization around the Fe centers facilitating the desorption of ORR intermediates. These findings provide a unique perspective for precisely controlling the coordination structure of single‐atom materials to optimize their activity.

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Growth and differentiation factors (GDFs) are secreted signaling molecules within the BMP family that have critical roles in joint morphogenesis during skeletal development in mice and humans. Using genetic data obtained from a six-generation Chinese family, we identified a missense variant in GDF6 (NP_001001557.1; p.Y444N) that fully segregates with a novel autosomal dominant synostoses (SYNS) phenotype, which we designate as SYNS4. Affected individuals display bilateral wrist and ankle deformities at birth and progressive conductive deafness after age 40 years. We find that the Y444N variant affects a highly conserved residue of GDF6 in a region critical for binding of GDF6 to its receptor(s) and to the BMP antagonist NOG, and show that this mutant GDF6 is a more potent stimulator of the canonical BMP signaling pathway compared with wild-type GDF6. Further, we determine that the enhanced BMP activity exhibited by mutant GDF6 is attributable to resistance to NOG-mediated antagonism. Collectively, our findings indicate that increased BMP signaling owing to a GDF6 gain-of-function mutation is responsible for loss of joint formation and profound functional impairment in patients with SYNS4. More broadly, our study highlights the delicate balance of BMP signaling required for proper joint morphogenesis and reinforces the critical role of BMP signaling in skeletal development.

Stimulating the development of soil suppressiveness against certain pathogens represents a sustainable solution toward reducing pesticide use in agriculture. However, understanding the dynamics of suppressiveness and the mechanisms leading to pathogen control remain largely elusive.Here, we investigated the mechanisms used by the rhizosphere microbiome induces bacterial wilt disease suppression in a long-term field experiment where continuous application of bio-organic fertilizers (BFs) triggered disease suppressiveness when compared to chemical fertilizer application. We further demonstrated in a glasshouse experiment that the suppressiveness of the rhizosphere bacterial communities was triggered mainly by changes in community composition rather than only by the abundance of the introduced biocontrol strain.Metagenomics approaches revealed that members of the families Sphingomonadaceae and Xanthomonadaceae with the ability to produce secondary metabolites were enriched in the BF plant rhizosphere but only upon pathogen invasion. We experimentally validated this observation by inoculating bacterial isolates belonging to the families Sphingomonadaceae and Xanthomonadaceae into conducive soil, which led to a significant reduction in pathogen abundance and increase in nonribosomal peptide synthetase gene abundance.We conclude that priming of the soil microbiome with BF amendment fostered reactive bacterial communities in the rhizosphere of tomato plants in response to biotic disturbance.