In this paper, we report the optoelectronic properties of multi-layered GeS nanosheet (∼28 nm thick)-based field-effect transistors (called GeS-FETs). The multi-layered GeS-FETs exhibit remarkably high photoresponsivity of Rλ ∼ 206 A W(-1) under 1.5 μW cm(-2) illumination at λ = 633 nm, Vg = 0 V, and Vds = 10 V. The obtained Rλ ∼ 206 A W(-1) is excellent as compared with a GeS nanoribbon-based and the other family members of group IV-VI-based photodetectors in the layered-materials realm, such as GeSe and SnS2. The gate-dependent photoresponsivity of GeS-FETs was further measured to be able to reach Rλ ∼ 655 A W(-1) operated at Vg = -80 V. Moreover, the multi-layered GeS photodetector holds high external quantum efficiency (EQE ∼ 4.0 × 10(4)%) and specific detectivity (D* ∼ 2.35 × 10(13) Jones). The measured D* is comparable to those of the advanced commercial Si- and InGaAs-based photodiodes. The GeS photodetector also shows an excellent long-term photoswitching stability over a long period of operation (>1 h). These extraordinary properties of high photocurrent generation, broad spectral range, and long-term stability make the GeS-FET photodetector a highly qualified candidate for future optoelectronic applications.
The concentration gradient of K across the cell membrane of a neuron determines its resting potential and cell excitability. During neurotransmission, the efflux of K from the cell via various channels will not only decrease the intracellular K content but also elevate the extracellular K concentration. However, it is not clear to what extent this change could be. In this study, we developed a multiple-parallel-connected silicon nanowire field-effect transistor (SiNW-FET) modified with K-specific DNA-aptamers (aptamer/SiNW-FET) for the real-time detection of the K efflux from cultured cortical neurons. The aptamer/SiNW-FET showed an association constant of (2.18 ± 0.44) × 10 M against K and an either less or negligible response to other alkali metal ions. The α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) stimulation induced an outward current and hyperpolarized the membrane potential in a whole-cell patched neuron under a Na/K-free buffer. When neurons were placed atop the aptamer/SiNW-FET in a Na/K-free buffer, AMPA (13 μM) stimulation elevated the extracellular K concentration to ∼800 nM, which is greatly reduced by 6,7-dinitroquinoxaline-2,3-dione, an AMPA receptor antagonist. The EC of AMPA in elevating the extracellular K concentration was 10.3 μM. By stimulating the neurons with AMPA under a normal physiological buffer, the K concentration in the isolated cytosolic fraction was decreased by 75%. These experiments demonstrate that the aptamer/SiNW-FET is sensitive for detecting cations and the K concentrations inside and outside the neurons could be greatly changed to modulate the neuron excitability.
Silicon nanowire field-effect transistors modified with specific aptamers can directly detect the minute dopamine and neuropeptide Y released from cells. The binding of these molecules to the aptamers results in a conductance change of the transistor biosensor and illustrates the differential releasing mechanisms of these molecules stored in various vesicle pools.
Earlier work has shown that siRNA-mediated reduction of the SUPT4H or SUPT5H proteins, which interact to form the DSIF complex and facilitate transcript elongation by RNA polymerase II (RNAPII), can decrease expression of mutant gene alleles containing nucleotide repeat expansions differentially. Using luminescence and fluorescence assays, we identified chemical compounds that interfere with the SUPT4H-SUPT5H interaction and then investigated their effects on synthesis of mRNA and protein encoded by mutant alleles containing repeat expansions in the huntingtin gene (
HTT
), which causes the inherited neurodegenerative disorder, Huntington’s Disease (HD). Here we report that such chemical interference can differentially affect expression of
HTT
mutant alleles, and that a prototypical chemical, 6-azauridine (6-AZA), that targets the SUPT4H-SUPT5H interaction can modify the biological response to mutant
HTT
gene expression. Selective and dose-dependent effects of 6-AZA on expression of
HTT
alleles containing nucleotide repeat expansions were seen in multiple types of cells cultured in vitro, and in a
Drosophila melanogaster
animal model for HD. Lowering of mutant HD protein and mitigation of the
Drosophila
“rough eye” phenotype associated with degeneration of photoreceptor neurons in vivo were observed. Our findings indicate that chemical interference with DSIF complex formation can decrease biochemical and phenotypic effects of nucleotide repeat expansions.
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