Optoelectronic synaptic devices are of great scientific and practical importance because of various potential applications such as ocular simulating and optical−electrical managers based on a new optoelectronic coupling mechanism. In this work, we design a novel channel layer with p-type CsPbBr 3 nanoparticles (NPs) buried in an InGaZnO (IGZO) film to construct the corresponding thin-film transistors (TFTs), which exhibits intense improvement in visible-light photosensitivity and synaptic plasticity as compared to the pure IGZO counterpart. Specifically, the composite device is able to exhibit versatile synaptic behavior under light stimuli with density as low as 0.12 μW/cm 2 and with the gain 5−20 times higher than that of the IGZO TFT in the visible-light region. Based on the band alignment between the IGZO and NPs, the excitation and decay processes of intrinsic and photoinduced carriers are discussed. Moreover, owing to the gate bias control in a threeterminal configuration, our TFT synapses can imitate complex biological behaviors including the famous "Pavlov's dog" experiment and the "reward and punishment mechanism" of the brain via editing the gate voltage/light pulse stimuli.
Disease-associated variants in the human genome are continually being identified using DNA sequencing technologies that are especially effective for Mendelian disorders. Here we sequenced whole genome to high coverage (>30×) of 6 members of a 7-generation family with dwarfism from a consanguineous tribe in Pakistan to determine the causal variant(s). We identified a missense variant rs111033552 (c.2011T>C [p.Ser671Pro]) located in COL10A1 (encodes the alpha chain of type X collagen) as the most likely contributor to the dwarfism. We further confirmed the variant in 22 family members using Sanger sequencing. All affected individuals are heterozygous for the missense mutation rs111033552 and no individual homozygous was observed. Moreover, the mutation was absent in 69,985 individuals representing >150 global populations. Taking advantage of whole-genome sequencing data, we also examined other variant forms, including copy number variation and insertion/deletion, but failed to identify such variants enriched in the affected individuals. Thus rs111033552 had priority for linkage with dwarfism.
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