One, two, three, four: A copper(I)–phosphine complex catalyzes the diborylation of alkynes and arynes, and the tri‐ or tetraborylation of propargyl ethers (see scheme; pin=pinacolato). In the latter cases, the CO bond(s) as well as the CC bond are borylated in one pot. Furthermore, a diborylation product serves as an intermediate in the efficient synthesis of ortho‐terphenyls with pharmacological activity.
Arynes are found to be facilely inserted into bis(pinacolato)diboron by using a platinum-isocyanide catalyst, affording diverse 1,2-diborylarenes, which can be converted into o-terphenyls via Suzuki-Miyaura coupling reaction.
Eins, zwei, drei, vier: Ein Kupfer(I)‐Phosphinkomplex katalysiert die Diborylierung von Alkinen und Arinen sowie die Tri‐ oder Tetraborylierung von Propargylethern (siehe Schema; pin=Pinakolato). In den letzteren Fällen werden die C‐O‐Einfach‐ und die C‐C‐Dreifachbindung in einem Schritt boryliert. Ein Diborylierungsprodukt diente außerdem als Intermediat in der effizienten Synthese von pharmakologisch aktiven ortho‐Terphenylen.
Temperature remarkably influences the water behavior in the PEMFC. However, the temperature inside the PEMFC has not been well understood. A lot of heat comparable to the electric power is emitted out of the cell. The PEM temperature is determined by the effective thermal conductivity through the layers and the temperature gradient created in the through-plane direction for emitting the heat. By measuring the PEM temperature with thin thermocouples and thick membrane, the effective thermal conductivity was estimated. It strongly depended on the cell binding pressure. Binding the cell improves the contact between carbon paper and carbon current collector as well as compresses carbon paper, leading to rise in the apparent effective thermal conductivity in the through-plane direction. The interfacial resistance to heat transfer was found 39 % of the overall resistance.
Drug repositioning is a strategy for repurposing the approved or investigational drugs that are outside the scope of the original medical indication. Memantine is used as a non-competitive N-methyl-D-aspartate receptor antagonist to prevent glutamate-mediated excitotoxicity in Alzheimer's disease, and is one of the promising agents which is utilized for the purpose of cancer therapy. However, the association between memantine and Golgi glycoprotein 1 (GLG1), an intracellular fibroblast growth factor receptor, in cancers has not yet been clarified. The present study analyzed the expression and location of GLG1 in tumor cells treated with memantine. Memantine was found to suppress the growth of malignant glioma and breast cancer cells in a concentration-dependent manner. The mRNA expression of GLG1 was upregulated in a concentration-dependent manner, and the splicing variant profiles were altered in all cell lines examined. The results of western blot analysis revealed an increase in the full-length and truncated forms of GLG1. Moreover, GLG1 spread in the cytosol of memantine-treated cells, whereas it localized in the Golgi apparatus in control cells. Since GLG1 functions as a decoy FGF receptor, the modulation of GLG1 may prove to be one of the mechanisms underlying the cancer-suppressive effects of memantine.
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