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A formal comparison between fundamental RX amplifier configurations for capacitive micromachined ultrasonic transducers (CMUTs) is proposed in this paper. The impact on both RX and the pulse-echo frequency response and on the output SNR is thoroughly analyzed and discussed. It is shown that the resistive-feedback amplifier yields a bandpass RX frequency response, while both open-loop voltage and capacitive-feedback amplifiers exhibit a low-pass frequency response. For a given power dissipation, it is formally proved that a capacitive-feedback amplifier provides a remarkable SNR improvement against the commonly adopted resistive feedback stage, achieved at the expense of a reduced pulse-echo center frequency, making its use convenient in low-frequency and midfrequency ultrasound imaging applications. The advantage mostly comes from a much lower noise contributed by the active devices, especially with low- Q , broadband transducers. The results of the analysis are applied to the design of a CMUT front end in BIPOLAR-CMOS-DMOS Silicon-on-Insulator technology operating at 10-MHz center frequency. It comprises a low-power RX amplifier, a high-voltage Transmission/Reception switch, and a 100-V TX driver. Extensive electrical characterization, pulse-echo measurements, and imaging results are shown. Compared with previously reported CMUT front ends, this transceiver demonstrates the highest dynamic range and state-of-the-art noise performance with an RX amplifier power dissipation of 1 mW.

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Six-Transmembrane Epithelial Antigen of the Prostate 1–4 (STEAP1–4) compose a family of metalloproteinases involved in iron and copper homeostasis and other cellular processes. Thus far, five homologs are known: STEAP1, STEAP1B, STEAP2, STEAP3, and STEAP4. In prostate cancer, STEAP1, STEAP2, and STEAP4 are overexpressed, while STEAP3 expression is downregulated. Although the metalloreductase activities of STEAP1–4 are well documented, their other biological functions are not. Furthermore, the properties and expression levels of STEAP heterotrimers, homotrimers, heterodimers, and homodimers are not well understood. Nevertheless, studies over the last few decades have provided sufficient impetus to investigate STEAP1–4 as potential biomarkers and therapeutic targets for prostate cancer. In particular, STEAP1 is the target of many emerging immunotherapies. Herein, we give an overview of the structure, physiology, and pathophysiology of STEAP1–4 to provide context for past and current efforts to translate STEAP1–4 into the clinic.