Metal–organic framework (MOF) is an emerging important class of functional materials in the fields of information storage, wearable electronics and optoelectronic devices. The interaction of electrons or holes with MOFs is important for the systematic exploration of MOFtronics and to investigate the related structure–performance correlation. Herein, MOF flat nanosheets of copper tetrakis(4‐carboxyphenyl)porphyrin with sub‐10 nanometer scale in thickness are employed as the charge‐trapping layer in organic field‐effect floating‐gate transistor memory device fabricated by an air–liquid interfacial assembly and subsequent stamping operation. As charge trapping sites, MOF nanosheets with ultrathin nanoporous arrays significantly improve in comparison with the memory device using its counterpart ligand of tetrakis(4‐carboxyphenyl)porphyrin as the trapping elements. As compared to the reported widely applied nanofloating gate materials of gold nanoparticles, graphene, or macromolecular nanomaterials, a short pulse (≈20 ms) on the device gets a considerable memory window of ≈37.5 V at a programming voltage of ‐80 V, with a retention time longer than 104 s and good ON/OFF ratio of >103. Furthermore, the hybrid structure composed of metal and organic components endows it with electron and hole trapping capability. This work could push forward the fundamental research of organic–inorganic–hybrid electronics in future microelectronic research.

No abstract

No abstract

No abstract

Objective: We aimed to study the types and characteristics of TUBB1 mutations in a large Chinese cohort with congenital hypothyroidism (CH) and thyroid dysgenesis (TD). Methods: Mutation of the entire coding region of TUBB1 was analysed by Sanger sequencing in 289 children with CH and TD from China. Functional studies were further used to identify the effect of novel mutations on thyroid cells. Results: Among the 289 children with CH and TD, 4 (1.4%) had a c.952C>T(p.R318W) heterozygous mutation in TUBB1, resulting in a change from tryptophan to arginine at codon 318 of the TUBB1 protein. Functional studies indicated that the p.R318W mutant decreased TUBB1 expression and inhibited cell proliferation in a human thyroid cell line. Conclusions: A novel heterozygous missense mutation of TUBB1 in children with CH and TD was identified first in China, laying the foundations to expand the genotype-phenotype spectrum of TD.