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We have investigated the biological properties of the osmium analogue of a potent ruthenium-based mitochondrial calcium uniporter inhibitor and have found it to possess distinct properties. 

This paper presents the design, implementation, and experimental evaluation of a wireless biomedical implant platform exploiting the magnetoelectric effect for wireless power and bi-directional communication. As an emerging wireless power transfer method, magnetoelectric is promising for mm-scaled bio-implants because of its superior misalignment sensitivity, high efficiency, and low tissue absorption compared to other modalities [46, 59, 60]. Utilizing the same physical mechanism for power and communication is critical for implant miniaturization, but low-power magnetoelectric uplink communication has not been achieved yet. For the first time, we design and demonstrate near-zero power magnetoelectric backscatter from the mm-sized implants by exploiting the converse magnetostriction effects. The system for demonstration consists of an 8.2-mm3 wireless implantable device and a custom portable transceiver. The implant's ASIC interfacing with the magnetoelectric transducer encodes uplink data by changing the transducer's load, resulting in resonance frequency changes for frequency-shift-keying modulation. The magnetoelectrically backscattered signal is sensed and demodulated through frequency-to-digital conversion by the external transceiver. With design optimizations in data modulation and recovery, the proposed system archives > 1-kbps data rate at the 335-kHz carrier frequency, with a communication distance greater than 2 cm and a bit error rate less than 1E-3. Further, we validate the proposed system for wireless stimulation and sensing, and conducted ex-vivo tests through a 1.5-cm porcine tissue. The proposed magnetoelectric backscatter approach provides a path towards miniaturized wireless bio-implants for advanced biomedical applications like closed-loop neuromodulation. 

We report our investigation into the MCU-inhibitory activity of Co 3+ complexes in comparison to Ru265. These compounds reversibly inhibit the MCU with nanomolar potency. Mutagenesis studies and molecular docking simulations suggest that the complexes operate through interactions with the DIME motif of the MCU pore.