Auto-balancing bridge based wide impedance spectrum measurement with consideration of Op-Amp input impedance.

In an auto-balancing bridge for high impedance measurements, an operational amplifier (Op-Amp) is used to follow the intermediate potential. However, the input impedance of the Op-Amp introduces significant effects in high impedance measurements. This paper proposes a two-step excitation method (TSEM) and an incremental iterative method (IIM). The TSEM determines the magnitude of the Op-Amp input impedance and the initial value of the device under test. The IIM utilizes the TSEM results as initial conditions to quickly bring the bridge to equilibrium. To overcome the distortion issues associated with small amplitude excitation signals generated by the DAC under low resolution conditions, a programmable gain amplifier is designed. Additionally, a half-cycle difference algorithm is developed prior to the three-parameter sine fit to mitigate low-frequency direct-current drift caused by power frequency, thus improving measurement accuracy. Experimental results demonstrate that when the reference impedance is set to 1 MΩ, impedance measurements ranging from 1 kΩ to 100 MΩ can be achieved within the frequency range of 1 to 100 kHz. The precision evaluation reveals a relative standard deviation (RSD) of the modulus better than 0.384% and a standard deviation (SD) of the phase angle better than 3.49 mrad; especially for the impedance under test of 1 MΩ, the RSD is better than 0.006% and the SD is better than 0.1 mrad.

USP12 promotes CD4+ T cell responses through deubiquitinating and stabilizing BCL10.

Deubiquitinases (DUBs) regulate diverse biological processes and represent a novel class of drug targets. However, the biological function of only a small fraction of DUBs, especially in adaptive immune response regulation, is well-defined. In this study, we identified DUB ubiquitin-specific peptidase 12 (USP12) as a critical regulator of CD4+ T cell activation. USP12 plays an intrinsic role in promoting the CD4+ T cell phenotype, including differentiation, activation, and proliferation. Although USP12-deficient CD4+ T cells protected mice from autoimmune diseases, the immune response against bacterial infection was subdued. USP12 stabilized B cell lymphoma/leukemia 10 (BCL10) by deubiquitinating, and thereby activated the NF-κB signaling pathway. Interestingly, this USP12 regulatory mechanism was identified in CD4+ T cells, but not in CD8+ T cells. Our study results showed that USP12 activated CD4+ T cell signaling, and targeting USP12 might help develop therapeutic interventions for treating inflammatory diseases or pathogen infections.