Studies on the Lithium Alloys-Chlorine Secondary Battery

A new type of lithium alloys-chlorine secondary battery, by using molten salt of LiCl and KCl as an electrolyte, was constructed as an automobile and a stand-by battery. In this kind of battery, the electromotive force is somewhat less than that of a conventional lithium-chlorine battery ; but the cell structure is much simpler and the operating temperature much lower. Also, the self discharge rate is much lower. The output coulombic capacity, output power and output energy were calculated to be 55 Ahr, 260 W and 150 Whr respectively, when zinc of 1 kg was used as the substratum metal. From these data it may be concluded that this type of secondary battery is very promising for automotive and stand-by uses

The Diffusion of Lithium in Lithium-Zinc Alloy

In a new type of secondary battery with a Li-Zn alloy as one electrode, chlorine as the other and a molten salt solution of LiCl-KCl, polarizations during charge and discharge at the Li-Zn alloy electrode may occur due to the slow diffusion of Li companying K in the alloy. This was examined by the use of chronoamperometric and chronopotentiometric methods. With a cathodic charge, the apparent diffusion coefficient of Li companying K was about 3.5×lO⁻⁵ cm²/sec at 500°C, whereas that of Li alone was about 6.0×l0⁻⁵ cm²/sec. Underan anodic discharge, the apparent diffusion coefficient was extremely large (the order of 10⁻⁴ cm²/sec), and this may be caused by the existence of convection at the alloy-electrolyte interface. The optimum charging and discharging current densities of the battery were estimated to be 0.2 and 0.3 A/cm² respectively

Phosphoramidon inhibits the generation of endothelin-1 from exogenously applied big endothelin-1 in cultured vascular endothelial cells and smooth muscle cells

AbstractWhen cultured porcine aortic endothelial cells (ECs) were incubated with porcine big endothelin-1 (bit ET-I1–39), there was a time-dependent increase in immunoreactive (IR)-ET in the culture supernatant, in addition to an endogenous IR-ET release fron the cells. Reverse-phase HPLC of the culture supernatant revealed one major IR-ET component corresponding to the elution position of synthetic ET-1, thereby indicating that the additional increase in IR-ET was due to the conversion of big ET-1 to mature ET-11–21. Phosphoramidon, a metalloproteinase inhibitor, strongly suppressed this increase in IR-ET as well as the endogenous IR-ET release. Cultured vascular smooth muscle cells (VSMCs) also released IR-ET. The apparent conversion of exogenously applied big ET-1 to ET-1 and its inhibition by phosphoramidon were observed using cultured VSMCs, although the enzyme inhibitor did not influence the basal secretion of IR-ET from VSMCs. These results suggest that both cultured ECs and VSMCs can generate ET-1 from exogenously applied big ET-1 via action of the same type of phosphoramidon-sensitive metalloproteinase, which is also involved in the endogenous ET-1 generation in ECs

Acceptedfor publicationMay 19

ABSTRACT We and other investigators obtained evidence that platelets stimulate endothelin-i (ET-i) production at both message and protein levels in vascular endothelial cells (EC5),and that plate let-derived transforming growth factor-f31 (TGF-j3i) is respon sible for this stimulation. In the present study, we examined the effects of acidification or heat treatment, known to activate latent TGF-f31, on the platelet supernatant-induced Er-i pro duction in cultured porcine aortic ECs. Supematant of platelets (6.0 x 1O@ platelets/mI) aggregated by adenosine diphosphate contained large amounts of TGF-pi, but were almost in a latent form, and the proportion of active TGF-j31 in the supematant was increased markedly in the case of acidification or heat treatment. These treatments also significantly potentiated the supematant-induced stimulation of prepro Er-i mRNA expres sion and the Er-i release in ECs. Purified TGF-@i also en hanced Er-i release, dose-dependently, but the enhancement declined at the higher concentrations. Thus, powerful stimula tion of Er-i production by platelet supematant after acidifica tion or heat treatment cannot be explained only by increments in active TGF-131. The supematant-induced stimulation of Er-i synthesis was significantly inhibited by concomitant treatment of TGF-@i neutralizing antibody, but this inhibition was incom plete even at a concentration that abolished TGF-31 -induced maximal stimulation. These resutts suggest that platelet-induced stimulation and subsequent acidification and heat treatment induced potentiation on endothelial Er-i production depend closely on release and activation of TGF-@i derived from plate lets. However, when TGF-fii concentration is increased, this peptide may further stimulate Er-i production, probably through interactions with other platelet-derived substances

慢性腎臓病では血中可溶型fms様チロシンキナーゼ-1産生の減少が動脈硬化症を悪化させる

Patients with chronic kidney disease (CKD) die of cardiovascular diseases for unknown reasons. Blood vessel formation in plaques and its relationship with plaque stability could be involved with signaling through the Flt-1 receptor and its ligands, vascular endothelial growth factor, and the closely related placental growth factor (PlGF). Flt-1 also exists as a circulating regulatory splice variant short-inhibitory form (sFlt-1) that serves as a decoy receptor, thereby inactivating PlGF. Heparin releases sFlt-1 by displacing the sFlt-1 heparin-binding site from heparin sulfate proteoglycans. Heparin could provide diagnostic inference or could also induce an antiangiogenic state. In the present study, postheparin sFlt-1 levels were lower in CKD patients than in control subjects. More importantly, sFlt-1 levels were inversely related to atherosclerosis in CKD patients, and this correlation was more robust after heparin injection, as verified by subsequent cardiovascular events. Knockout of apolipoprotein E (ApoE) and/or sFlt-1 showed that the absence of sFlt-1 worsened atherogenesis in ApoE-deficient mice. Thus, the relationship between atherosclerosis and PlGF signaling, as regulated by sFlt-1, underscores the underappreciated role of heparin in sFlt-1 release. These clinical and experimental data suggest that novel avenues into CKD-dependent atherosclerosis and its detection are warranted.博士（医学）・甲614号・平成26年3月17