Circulating B Cell-Derived Small RNA Delivered by Extracellular Vesicles: A Dialogue Mechanism for Long-Range Targeted Renal Mitochondrial Injury in Obesity.

The intricate processes that govern the interactions between peripatetic immune cells and distal renal injury in obesity are not fully understood. Employing transcriptomic analysis of circulating extracellular vesicles (EVs), a marked amplification of small RNA (miR-3960) is discerned within CD3-CD19+ B cells. This RNA is found to be preferentially augmented in kidney tissues, contrasting with its subdued expression in other organs. By synthesizing dual-luciferase reporter assay with co-immunoprecipitation analysis, it is pinpointed that miR-3960 specifically targets the nuclear gene TRMT5, a pivotal actor in the methylation of mitochondrial tRNA. This liaison instigates aberrations in the post-transcriptional modifications of mitochondrial tRNA, engendering deficiencies within the electron respiratory chain, primarily attributable to the diminution of the mitochondrial bioenergetic compound (NDUFA7) complex I. Such perturbations lead to a compromised mitochondrial respiratory capacity in renal tubular cells, thereby exacerbating tubular injury. In contrast, EV blockade or miR-3960 depletion markedly alleviates renal tubular injury in obesity. This investigation unveils a hitherto unexplored pathway by which obesity-induced circulating immune cells remotely manipulate mitochondrial metabolism in target organs. The strategic targeting of obese EVs or infiltrative immune cells and their specifically secreted RNAs emerges as a promising therapeutic avenue to forestall obesity-related renal afflictions.

A 400 MHz Wireless Neural Signal Processing IC With 625 $\times$ On-Chip Data Reduction and Reconfigurable BFSK/QPSK Transmitter Based on Sequential Injection Locking.

An 8-channel wireless neural signal processing IC, which can perform real-time spike detection, alignment, and feature extraction, and wireless data transmission is proposed. A reconfigurable BFSK/QPSK transmitter (TX) at MICS/MedRadio band is incorporated to support different data rate requirement. By using an Exponential Component-Polynomial Component (EC-PC) spike processing unit with an incremental principal component analysis (IPCA) engine, the detection of neural spikes with poor SNR is possible while achieving 625× data reduction. For the TX, a dual-channel at 401 MHz and 403.8 MHz are supported by applying sequential injection locked techniques while attaining phase noise of -102 dBc/Hz at 100 kHz offset. From the measurement, error vector magnitude (EVM) of 4.60%/9.55% with power amplifier (PA) output power of -15 dBm is achieved for the QPSK at 8 Mbps and the BFSK at 12.5 kbps. Fabricated in 65 nm CMOS with an active area of 1 mm 2, the design consumes a total current of 5  âˆ¼ 5.6 mA with a maximum energy efficiency of 0.7 nJ/b.