C-C bond formation at the 3'-position of nucleosides by the use of their enol esters

Nucleosides having an enol ester structure in the sugar portion were synthesized and their reaction with several types of electrophiles were carried out. This furnished a new method for constructing C-C bond at the 3'-position.     

Protective Effect of External Ca2+ on Elongation and the Intracellular Concentration of K+ in Intact Mung Bean Roots under High NaCl Stress

The effects of Ca²⁺ in the external medium on intact mung beanroots under high NaCl stress were investigated. With increasingexternal concentrations of NaCl, mung bean roots showed suppressionof elongation and a decrease in the intracellular concentrationof K⁺. Addition of Ca²⁺ to the external medium alleviated theinhibition of root elongation under the high NaCl stress andmaintained a high intracellular concentration of K⁺ in the elongatingregion of the roots. This counter effect of Ca²⁺ against theNaCl stress on roots was correlated with the ratio of [Ca²⁺]/[Na⁺]²in the external medium. A value above 5.0 ? 10^–4 mM^–1resulted in almost complete recovery of root elongation undervarious high concentrations of NaCl. Root elongation for 24h under NaCl stress was correlated with the extent to whichthe intracellular concentration of K⁺ was in excess of 10 mM.Maintenance of an adequate concentration of K⁺ in root cellsis essential for root elongation under salt stress. These findingsindicate that Ca²⁺ prevents the leakage of intracellular K⁺and thereby supports the elongation of roots under salt stress. (Received November 13, 1989; Accepted June 5, 1990)     

Regenerants from Ajuga hairy roots with high productivity of 20-hydroxyecdysone

Summary Regenerants derived from hairy roots of Ajuga reptans var. atropurpurea induced by infection with Agrobacterium rhizogenes MAFF03-01724 harboring pRi revealed a dwarfing response, i.e. decrease in leaf size, reduction in internode distance, and increase in leaf number. These morphogenic alterations were accompanied by an increase in root mass and lack of floral differentiation. In the pRi-transformed regenerants, the proportion of root mass to whole plant mass was higher than that of the untransformed ones, although both kinds of regenerants were comparable on a fresh weight basis. High capacity of rooting and 20-hydroxyecdysone production associated with the original hairy root line were stably maintained in clonal regenerants.     

Hepatocytes release ceramide-enriched pro-inflammatory extracellular vesicles in an IRE1α-dependent manner

Nonalcoholic steatohepatitis (NASH) is a lipotoxic disease wherein activation of endoplasmic reticulum (ER) stress response and macrophage-mediated hepatic inflammation are key pathogenic features. However, the lipid mediators linking these two observations remain elusive. We postulated that ER stress-regulated release of pro-inflammatory extracellular vesicles (EVs) from lipotoxic hepatocytes may be this link. EVs were isolated from cell culture supernatants of hepatocytes treated with palmitate (PA) to induce lipotoxic ER stress, characterized by immunofluorescence, Western blotting, electron microscopy, and nanoparticle tracking analysis. Sphingolipids were measured by tandem mass spectrometry. EVs were employed in macrophage chemotaxis assays. PA induced significant EV release. Because PA activates ER stress, we used KO hepatocytes to demonstrate that PA-induced EV release was mediated by inositol requiring enzyme 1α (IRE1α)/X-box binding protein-1. PA-induced EVs were enriched in C16:0 ceramide in an IRE1α-dependent manner, and activated macrophage chemotaxis via formation of sphingosine-1-phosphate (S1P) from C16:0 ceramide. This chemotaxis was blocked by sphingosine kinase inhibitors and S1P receptor inhibitors. Lastly, elevated circulating EVs in experimental and human NASH demonstrated increased C16:0 ceramide. PA induces C16:0 ceramide-enriched EV release in an IRE1α-dependent manner. The ceramide metabolite, S1P, activates macrophage chemotaxis, a potential mechanism for the recruitment of macrophages to the liver under lipotoxic conditions.