The Sedimentary records of the Hapcheon impact crater basin in Korea over the past 1.3 Ma

The Hapcheon impact crater is the only meteorite impact crater identified on the Korean peninsula. However, the morphology of the impact crater and the nature of the meteorite collision are unknown. In this study, we analyzed the sedimentary facies using grain size data; computed tomography images, 14C, 10Be, and optically stimulated luminescence dating on a >66-m-long sediment core (20HCL04) recovered from the Hapcheon Basin. Four sedimentary units and 10 types of facies were documented in the Hapcheon Basin sediment core. The sedimentary units comprise 1) a lower part (unit 1) that is dominated by moderately to well-sorted coarse gravel, which contains some impact-related sediments; 2) a middle part (units 2 and 3) dominated by well-laminated mud; and 3) an upper part (Unit 4) that is dominated by poorly sorted coarse gravel supplied from the surrounding mountain slopes by alluvial and fluvial processes. After the meteorite impact, the Hapcheon impact crater was filled with deposits from the crater wall after ca. 1.3 Ma and the Hapcheon Basin became a deep lake environment. After ca. 0.5 Ma, sediments were supplied from the surrounding mountains until the lake was filled. Finally, sediments were deposited in an alluvial fan setting. In addition, the Hapcheon Basin sedimentary cores contain a tephra layer and deformed soft sediments that can be used to investigate volcanic and seismic events on the Korean Peninsula over the past 1.3 Ma

Directly converted patient-specific induced neurons mirror the neuropathology of FUS with disrupted nuclear localization in amyotrophic lateral sclerosis

Background Mutations in the fused in sarcoma (FUS) gene have been linked to amyotrophic lateral sclerosis (ALS). ALS patients with FUS mutations exhibit neuronal cytoplasmic mislocalization of the mutant FUS protein. ALS patients fibroblasts or induced pluripotent stem cell (iPSC)-derived neurons have been developed as models for understanding ALS-associated FUS (ALS-FUS) pathology; however, pathological neuronal signatures are not sufficiently present in the fibroblasts of patients, whereas the generation of iPSC-derived neurons from ALS patients requires relatively intricate procedures. Results Here, we report the generation of disease-specific induced neurons (iNeurons) from the fibroblasts of patients who carry three different FUS mutations that were recently identified by direct sequencing and multi-gene panel analysis. The mutations are located at the C-terminal nuclear localization signal (NLS) region of the protein (p.G504Wfs*12, p.R495*, p.Q519E): two de novo mutations in sporadic ALS and one in familial ALS case. Aberrant cytoplasmic mislocalization with nuclear clearance was detected in all patient-derived iNeurons, and oxidative stress further induced the accumulation of cytoplasmic FUS in cytoplasmic granules, thereby recapitulating neuronal pathological features identified in mutant FUS (p.G504Wfs*12)-autopsied ALS patient. Importantly, such FUS pathological hallmarks of the patient with the p.Q519E mutation were only detected in patient-derived iNeurons, which contrasts to predominant FUS (p.Q519E) in the nucleus of both the transfected cells and patient-derived fibroblasts. Conclusions Thus, iNeurons may provide a more reliable model for investigating FUS mutations with disrupted NLS for understanding FUS-associated proteinopathies in ALS

Synaptic Plasticity and Metaplasticity of Biological Synapse Realized in a KNbO₃ Memristor for Application to Artificial Synapse

Amorphous KNbO₃ (KN) films were grown on a TiN/SiO₂/Si substrate to synthesize a KN memristor as a potential artificial synapse. The Pt/KN/TiN memristor exhibited typical and reliable bipolar switching behavior with multiple resistance levels. It also showed the transmission properties of a biological synapse, with a good conductance modulation linearity. Moreover, the KN memristor can emulate various biological synaptic plasticity characteristics including short-term plasticity, long-term plasticity, spike-rate dependent plasticity, paired-pulse facilitation, and post-tetanic potentiation by controlling the number and rate of the potentiation spike. Spike-timing-dependent plasticity (STDP), which is an essential property of biological synapses, is also realized in the KN memristor. The synaptic plasticity of the KN memristor can be explained by oxygen vacancy movement and oxygen vacancy filaments. The metaplasticity of biological synapses was also implemented in the KN memristor, including the metaplasticity of long-term potentiation and depression, and of STDP. Therefore, the KN memristor could be used as an artificial synapse in neuromorphic computing systems