MgO-Template Synthesis of Extremely High Capacity Hard Carbon for Na-Ion Battery.

Extremely high capacity hard carbon for Na-ion battery, delivering 478 mAh g-1 , is successfully synthesized by heating a freeze-dried mixture of magnesium gluconate and glucose by a MgO-template technique. Influences of synthetic conditions and nano-structures on electrochemical Na storage properties in the hard carbon are systematically studied to maximize the reversible capacity. Nano-sized MgO particles are formed in a carbon matrix prepared by pre-treatment of the mixture at 600 °C. Through acid leaching of MgO and carbonization at 1500 °C, resultant hard carbon demonstrates an extraordinarily large reversible capacity of 478 mAh g-1 with a high Coulombic efficiency of 88 % at the first cycle.

Genetic-deletion of Cyclooxygenase-2 Downstream Prostacyclin Synthase Suppresses Inflammatory Reactions but Facilitates Carcinogenesis, unlike Deletion of Microsomal Prostaglandin E Synthase-1.

Prostacyclin synthase (PGIS) and microsomal prostaglandin E synthase-1 (mPGES-1) are prostaglandin (PG) terminal synthases that function downstream of inducible cyclooxygenase (COX)-2 in the PGI2 and PGE2 biosynthetic pathways, respectively. mPGES-1 has been shown to be involved in various COX-2-related diseases such as inflammatory diseases and cancers, but it is not yet known how PGIS is involved in these COX-2-related diseases. Here, to clarify the pathophysiological role of PGIS, we investigated the phenotypes of PGIS and mPGES-1 individual knockout (KO) or double KO (DKO) mice. The results indicate that a thioglycollate-induced exudation of leukocytes into the peritoneal cavity was suppressed by the genetic-deletion of PGIS. In the PGIS KO mice, lipopolysaccharide-primed pain nociception (as assessed by the acetic acid-induced writhing reaction) was also reduced. Both of these reactions were suppressed more effectively in the PGIS/mPGES-1 DKO mice than in the PGIS KO mice. On the other hand, unlike mPGES-1 deficiency (which suppressed azoxymethane-induced colon carcinogenesis), PGIS deficiency up-regulated both aberrant crypt foci formation at the early stage of carcinogenesis and polyp formation at the late stage. These results indicate that PGIS and mPGES-1 cooperatively exacerbate inflammatory reactions but have opposing effects on carcinogenesis, and that PGIS-derived PGI2 has anti-carcinogenic effects.