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The measurements that will be presented investigate the neutron-deficient polonium isotopes in the region of A = 195-199, with a special emphasis on 195Po and 197Po. These isotopes were produced at ISOLDE/CERN and delivered to the ISOLTRAP experiment where mass measurements and α-decay spectroscopy were performed. The decay-spectroscopy studies were carried out for the first time at ISOLTRAP with the support of the multi reflection time-of-flight mass spectrometer (MR-TOF MS). The masses of (195,197)g,mPo were measured precisely with Penning-trap mass spectrometry, from which the state ordering and the energy of the 13/2⁺ states in 195,197Po were determined for the first time. Furthermore, the state ordering and the energy of the 13/2⁺ state in lead, radon, and radium were obtained through α-decay chains. The new data complete the knowledge of the energy systematics in this region. The presented mass measurements provide information on the behaviour of the 13/2⁺ states in the lead region near N = 104, which remain excited states. Additionally, 195Po half-life measurements were performed in isobarically pure conditions. The resulting 195gPo half-life value is in agreement with the one in the literature, with improving in the precision of the value, whereas the 195mPo half-life value is significantly smaller than the literature value.

Amyotrophic Lateral Sclerosis (ALS) is a rapidly progressive and almost universally fatal neurodegenerative disease of the human motor nervous system1. Multiple lines of evidence from ALS patients and animal models have suggested that intrinsic motor neuron hyperexcitability plays a key role in the disease2, but it has remained unclear whether this is a direct contributor to the early motor neuron cell death observed in ALS patients. We used motor neurons derived from induced pluripotent stem cells (iPSC) from ALS patients harboring one of three ALS-causing mutations and studied their electrophysiological properties using whole-cell patch-clamp and microelectrode array (MEA) single-unit activity. We indeed found ALS motor neurons were hyperexcitable at baseline relative to healthy controls, and determined this to be due to a reduction in delayed-rectifier potassium currents. We also found that this hyperexcitability directly contributes to the earlier cell death of ALS motor neurons in vitro. We then treated ALS motor neurons with the drug retigabine (currently an FDA- approved anticonvulsant drug), which is a Kv7 potassium channel activator, and found a reversal of this hyperexcitability as well as a normalization of cell life.