No abstract

We synthesized freestanding bulk three-dimensional nanoporous Si using dealloying in a metallic melt, a top-down process. Using this nanoporous Si, we fabricated negative electrodes with high lithium capacity, nearing their theoretical limits, and greatly extended cycle lifetimes, considerably improving the battery performance compared with those using electrodes made from silicon nanoparticles. By operating the electrodes below the accommodation volume limit of their pores, we prolonged their cycle lifetime.

Genistein, an inhibitor of protein-tyrosine kinase, inhibited the replication of herpes simplex virus type 1 (HSV-1) at genistein concentrations of more than 25 microM, whereas the related compounds, which do not inhibit protein-tyrosine kinases, did not affect the replication of HSV-1. In the presence of genistein, the phosphorylation of tyrosine residues in specific viral polypeptides was markedly reduced. These results indicate that the phosphorylation of tyrosine residues in viral polypeptides may be essential for the replication of HSV-1.

No abstract

Previously, we found the first congenital deficiency of histidine-rich glycoprotein (HRG) in a Japanese woman with thrombosis. To elucidate the genetic basis of this deficiency, we first performed Southern blot analysis and found no gross deletion or insertion in the proband's HRG gene. We then examined the nucleotide sequences of all seven exons of the proband's HRG gene. A single nucleotide substitution, G to A at nucleotide position 429, which mutates Gly85 to Glu in the first cystatin-like domain, was found in exon 3 in 13 of 22 amplified clones. This mutation generates a unique Taq I site. Exon 3 was amplified from the proband, her family members, and 50 unrelated normal Japanese individuals, and Taq I fragmentation was examined. Fragmentation of exon 3 was observed in one allele of the genes from the proband and the family members who also have decreased plasma levels of HRG. Fifty unrelated normal Japanese individuals had a normal HRG gene, indicating that the G to A mutation is not a common polymorphism. To elucidate the identified mutation as a cause for the secretion defect of HRG in the proband's plasma, we constructed and transiently expressed the recombinant Tokushima-type HRG mutant (Gly85 to Glu) in baby hamster kidney (BHK) cells, and examined an intracellular event of the mutant protein. The results showed that only about 20% of the Tokushima-type HRG was secreted into the culture medium, and intracellular degradation of the mutant was observed. Thus, the present study strongly suggests that the HRG deficiency is caused by intracellular degradation of the Gly85 to Glu mutant of HRG in the proband.