We have employed a new route to synthesize single phase F-doped LaOFeAs compound and confirmed the superconductivity above 20 K in this Fe-based system. We show that the new superconductor has a rather high upper critical field of over 50 T. A clear signature of superconducting gap opening below T(c) was observed in the far-infrared reflectance spectra, with 2Delta/kT(c) approximately 3.5-4.2. Furthermore, we show that the new superconductor has electron-type conducting carriers with a rather low-carrier density.

We report a systematic study by 75 As nuclear-quadrupole resonance in LaFeAsO1−xFx. The antiferromagnetic spin fluctuation (AFSF) found above the magnetic ordering temperature TN = 58 K for x = 0.03 persists in the regime 0.04 ≤ x ≤ 0.08 where superconductivity sets in. A domeshaped x-dependence of the superconducting transition temperature Tc is found, with the highest Tc = 27 K at x = 0.06 which is realized under significant AFSF. With increasing x further, the AFSF decreases, and so does Tc. These features resemble closely the cuprates La2−xSrxCuO4. In x = 0.06, the spin-lattice relaxation rate (1/T1) below Tc decreases exponentially down to 0.13 Tc, which unambiguously indicates that the energy gaps are fully-opened. The temperature variation of 1/T1 below Tc is rendered nonexponential for other x by impurity scattering.

Mutations in SCN1A, the gene encoding the α subunit of Nav1.1 channel, can cause epilepsies with wide ranges of clinical phenotypes, which are associated with the contrasting effects of channel loss-of-function or gain-of-function. In this project, CRISPR/Cas9- and TALEN-mediated genome-editing techniques were applied to induced pluripotent stem cell (iPSC)-based-disease model to explore the mechanism of epilepsy caused by SCN1A loss-of-function mutation. By fluorescently labeling GABAergic subtype in iPSC-derived neurons using CRISPR/Cas9, we for the first time performed electrophysiological studies on SCN1A-expressing neural subtype and monitored the postsynaptic activity of both inhibitory and excitatory types. We found that the mutation c.A5768G, which led to no current of Nav1.1 in exogenously transfected system, influenced the properties of not only Nav current amount, but also Nav activation in Nav1.1-expressing GABAergic neurons. The two alterations in Nav further reduced the amplitudes and enhanced the thresholds of action potential in patient-derived GABAergic neurons, and led to weakened spontaneous inhibitory postsynaptic currents (sIPSCs) in the patient-derived neuronal network. Although the spontaneous excitatory postsynaptic currents (sEPSCs) did not change significantly, when the frequencies of both sIPSCs and sEPSCs were further analyzed, we found the whole postsynaptic activity transferred from the inhibition-dominated state to excitation in patient-derived neuronal networks, suggesting that changes in sIPSCs alone were sufficient to significantly reverse the excitatory level of spontaneous postsynaptic activity. In summary, our findings fill the gap of our knowledge regarding the relationship between SCN1A mutation effect recorded on exogenously transfected cells and on Nav1.1-expressing neurons, and reveal the physiological basis underlying epileptogenesis caused by SCN1A loss-of-function mutation.