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We demonstrate a novel avalanche photodiode (APD) design which fundamentally relaxes the trade-off between responsivity and saturation-current performance at receiver end in coherent system. Our triple In0.52Al0.48As based multiplication (M-) layers with a stepped electric (E-) field inside has more pronounced avalanche process with significantly less effective critical-field than the dual M-layer. Reduced E-field in active M-layers ensures stronger E-field allocation to the thick absorption-layer with a smaller breakdown voltage (Vbr) resulting in less serious space-charge screening effect, less device heating at high output photocurrent. Compared to the dual M-layer reference sample, the demonstrated APD exhibits lower punch-through (− 9 vs. − 24 V)/breakdown voltages (− 43 vs. − 51 V), higher responsivity (19.6 vs. 13.5 A/W), higher maximum gain (230 vs. 130), and higher 1-dB saturation-current (> 5.6 vs. 2.5 mA) under 0.95 Vbr operation. Extremely high saturation-current (> 14.6 mA), high responsivity (7.3 A/W), and decent O-E bandwidth (1.4 GHz) can be simultaneously achieved using the demonstrated APD with a 200 µm active window diameter. In coherent FMCW LiDAR test bed, this novel APD exhibits a larger signal-to-noise ratio and high-quality 3-D images than the reference dual M-layer and high-performance commercial p-i-n PD modules, while requiring significantly less optical local-oscillator (LO) power (0.5 vs 4 mW). [ABSTRACT FROM AUTHOR]

Recessive variants of the SLC26A4 gene are an important cause of hereditary hearing impairment. Several transgenic mice with different Slc26a4 variants have been generated. However, none have recapitulated the auditory phenotypes in humans. Of the SLC26A4 variants identified thus far, the p.T721M variant is of interest, as it appears to confer a more severe pathogenicity than most of the other missense variants, but milder pathogenicity than non-sense and frameshift variants. Using a genotype-driven approach, we established a knock-in mouse model homozygous for p.T721M. To verify the pathogenicity of p.T721M, we generated mice with compound heterozygous variants by intercrossing Slc26a4+/T721M mice with Slc26a4919-2A>G/919-2A>G mice, which segregated the c.919-2A > G variant with abolished Slc26a4 function. We then performed serial audiological assessments, vestibular evaluations, and inner ear morphological studies. Surprisingly, both Slc26a4T721M/T721M and Slc26a4919-2A>G/T721M showed normal audiovestibular functions and inner ear morphology, indicating that p.T721M is non-pathogenic in mice and a single p.T721M allele is sufficient to maintain normal inner ear physiology. The evidence together with previous reports on mouse models with Slc26a4 p.C565Y and p.H723R variants, support our speculation that the absence of audiovestibular phenotypes in these mouse models could be attributed to different protein structures at the C-terminus of human and mouse pendrin. [ABSTRACT FROM AUTHOR]