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Molecular constructs define the elementary units in porous materials for efficient CO2 capture. The design of appropriate interpore and intermolecular space is crucial to stabilize CO2 molecules and maximize the capacity. While the molecular construct usually has a fixed dimension, whether its intermolecular space could be self-adjustable during CO2 capture and release, behaving as a balloon, has captured imagination. Here we report a flexible intermolecular space of the double chain structure of self-assembled 1,4-phenylene diisocyanide (PDI) molecules on Ag(110) surface, which dynamically broadens and recovers during the CO2 capture and release. The incipient PDI double chains organize along the [001] direction of Ag(110), in which individual PDI molecules stand up in a zigzag order with the interchain width defined by twice the Ag lattice distance along [11¯0] direction (2α[11¯0]). When CO2 molecules are introduced, they assemble to occupy the interchain spaces, expanding the interchain width to 3α[11¯0], 4α[11¯0] and 5α[11¯0]. Warming up the sample leads to the thermally-driven CO2 desorption that recovers the original interchain space. High-resolution scanning tunneling microscopy (STM) jointly with density functional theory (DFT) calculations determine the structural and electronic interactions of CO2 molecules with the dynamical PDI structures, providing a molecular-level perspective for the design of a self-adjustable metal-organic construct for reversible gas capture and release. 

Abstract BackgroundThe vast majority of findings from human genome-wide association studies (GWAS) map to non-coding sequences, complicating their mechanistic interpretations and clinical translations. Non-coding sequences that are evolutionarily conserved and biochemically active could offer clues to the mechanisms underpinning GWAS discoveries. However, genetic effects of such sequences have not been systematically examined across a wide range of human tissues and traits, hampering progress to fully understand regulatory causes of human complex traits. ResultsHere we develop a simple yet effective strategy to identify functional elements exhibiting high levels of human-mouse sequence conservation and enhancer-like biochemical activity, which scales well to 313 epigenomic datasets across 106 human tissues and cell types. Combined with 468 GWAS of European (EUR) and East Asian (EAS) ancestries, these elements show tissue-specific enrichments of heritability and causal variants for many traits, which are significantly stronger than enrichments based on enhancers without sequence conservation. These elements also help prioritize candidate genes that are functionally relevant to body mass index (BMI) and schizophrenia but were not reported in previous GWAS with large sample sizes. ConclusionsOur findings provide a comprehensive assessment of how sequence-conserved enhancer-like elements affect complex traits in diverse tissues and demonstrate a generalizable strategy of integrating evolutionary and biochemical data to elucidate human disease genetics. 

Machine learning and multiplexed screening elucidates enhancer networks regulating gene expression in health and disease states.