A series of binary-salt electrolytes of KPF6/KN­(SO2F)2 (KFSA) in carbonate ester solvents have been developed for high-voltage K-ion batteries by clarifying the effect of salt ratio and different solvents on the physical properties of the electrolyte solutions and electrochemical performance of K-ion batteries. The KPF6/KFSA carbonate ester solutions, such as KPF6/KFSA ethylene carbonate (EC)/diethyl carbonate (DEC), exhibit higher ionic conductivity than single-salt KPF6 one, and higher KFSA content results in higher ionic conductivity. The KPF6-rich binary-salt electrolytes with KPF6/KFSA ratios of ≥3 (mol/mol) provide enough oxidation stability and passivation against Al corrosion at 4.6 V over 100 h, ensuring reversible operation of a 4 V class positive electrode, K2Mn­[Fe­(CN)6] in half-cell. Graphite negative electrodes exhibit higher Coulombic efficiency and better rate performance in 0.75 mol kg–1 K­(PF6)0.9(FSA)0.1/EC/DEC and 1 mol kg–1 K­(PF6)0.75(FSA)0.25/EC/DEC electrolytes than those in the KPF6 one. Surface analysis by hard X-ray photoelectron spectroscopy reveals that the decomposition product of N­(SO2F)2 – anion contributes to stabilizing solid electrolyte interphase on a graphite electrode. From comparing different solvents of EC/DEC, EC/ethyl methyl carbonate, and EC/propylene carbonate (PC), the K2Mn­[Fe­(CN)6] electrode demonstrates the highest Coulombic efficiency in the EC/PC binary electrolyte, while graphite electrodes exhibit no significant difference. Based on the half-cell tests, we successfully achieve the 3.6 V class full cell of graphite|K­(PF6)0.75(FSA)0.25/EC/PC|K2Mn­[Fe­(CN)6] showing excellent cyclability over 500 cycles, which is far superior to that of the conventional KPF6/EC/DEC electrolyte cell.

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We examined the effect of glucagonlike peptides (GLPs), which are cleaved from preproglucagon in the enteroglucagon cells, on rat endocrine pancreas with the isolated perfused system. GLP-I-(7-36)-amide, a truncated form of full-sequence GLP-I-(1-37), showed a potent inhibitory effect on glucagon secretion. This inhibitory effect of GLP-I-(7-36)-amide was demonstrated at concentrations of 0.25, 2.5, and 25 nM in 11.2 and 2.8 mM glucose. In contrast, insulin release was significantly stimulated by GLP-I-(7-36)-amide at its concentration from 0.025 to 25 nM in a high glucose concentration, whereas in a low glucose concentration, the stimulation was seen only at the highest concentration (25 nM). Neither GLP-I-(1-37) nor GLP-II showed any effect on glucagon and insulin release. Although several gastrointestinal hormones have been nominated as incretins, none of them may suppress the glucagon secretion. A truncated form of GLP-I, GLP-I-(7-36)-amide thus seems to be a unique incretin that exerts glucagonostatic action.

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The sulfate esters of 1,3,2-dioxathiolane 2,2-dioxide (DTD) and trimethylene sulfate (TMS) are evaluated as electrolyte additives for K-metal cells. A symmetric K∥K cell filled with 0.8 M KPF6/EC:DEC + 1 wt % of DTD electrolyte delivers plating–stripping polarization of ∼20 mV, i.e., ∼10 mV per K electrode, which is significantly lower than those for the additive-free and TMS-added electrolyte cells. Moreover, a K∥K2Mn­[Fe­(CN)6] cell filled with the DTD-added electrolyte exhibits a larger reversible capacity and suppressed irreversible capacity than the DTD-free cells. Electrochemical tests and gas chromatography–mass spectrometry (GC–MS) reveal that DTD addition is efficient in passivating the K-metal surface and inhibiting the formation of electrolyte-soluble oligocarbonates, which are formed in the DTD-free electrolyte. The oligocarbonates are oxidized on the positive electrode and cause irreversible capacity. Thus, the DTD additive enables the high reversibility and low polarization of K-metal cells.

Hereditary protein C deficiency is associated with a predisposition to venous thrombosis. We identified 43 patients with protein C deficiency by screening approximately 26,800 patients admitted to the National Cardiovascular Center Hospital. The observed prevalence of protein C deficiency was 1 per 620. We performed genetic analyses of 57 Japanese families with protein C deficiency. Combined with the results of the other studies in 10 families, the 67 Japanese families with protein C deficiency have been examined and 39 different gene defects have been identified. Some changes were solely identified in Japanese subjects, whereas others showed no such ethnic bias. The recurrent defects of Phe139Val, Arg169Trp, Val297Met, and Met364Ile substitutions and a G8857 deletion were found in 33 Japanese families, accounting for 49% of Japanese families with protein C deficiency, Finally, we examined the relevance of protein C deficiency to the onset of arterial occlusive diseases. In the examination of whether protein C deficiency hastens arterial occlusion, we found a significant difference (p = 0.02) in the age at onset of acute myocardial infarction between the patients with protein C deficiency (n = 10: 49.4 +/- 14.8 years) and a group of patients with normal protein C levels (n = 42: 60.5 +/- 10.6 years). At the onset of atherothrombotic cerebral infarction, the patients with protein C deficiency were significantly (p = 0.022) younger (n = 11:57.4 +/- 12.8 years) than those with normal protein C levels (n = 48: 64.6 +/- 10.1 years). Thus, we conclude that congenital protein C deficiency hastens the onset of arterial occlusive diseases, especially acute myocardial infarction, in Japanese subjects.