Redesign of a thioflavin-T-binding protein with a flat β-sheet to evaluate a thioflavin-T-derived photocatalyst with enhanced affinity.

Amyloids, proteinous aggregates with β-sheet-rich fibrils, are involved in several neurodegenerative diseases such as Alzheimer's disease; thus, their detection is critically important. The most common fluorescent dye for amyloid detection is thioflavin-T (ThT), which shows on/off fluorescence upon amyloid binding. We previously reported that an engineered globular protein with a flat β-sheet, peptide self-assembly mimic (PSAM), can be used as an amyloid binding model.

Residue-Specific Binding Mechanisms of Thioflavin T to a Surface of Flat β-Sheets within a Peptide Self-Assembly Mimic.

Thioflavin T (ThT) is a popular fluorescent dye for detecting amyloid, a protein aggregate with a β-sheet-rich structure that causes many neurodegenerative diseases. Despite the dye's popularity, a detailed understanding of its molecular binding mechanism remains elusive. We previously reported a protein model that can bind ThT on a single-layer β-sheet and revealed that a channel formed by aromatic rings with a confined length enhanced ThT binding.

Phagocytosis of splenetic neutrophils of mice enhanced by orally administered peptidoglycan from Bifidobacterium thermophilum.

A preparation of peptidoglycan (PG) of swine Bifidobacterium thermophilum was orally administered to SPF-BALB/C and ICR mice and its effect on phagocytosis splenetic neutrophils from PG administered mice was measured by chemiluminescent response (CL) and fluorometric analysis and the result was compared with that of non-treated mice. PG stimulated phagocytosis of neutrophils in a dose-dependent manner, whereas dosage exceeding the optimum concentration (500 microgram) inhibited phagocytosis. The maximum effect on phagocytosis of neutrophils was observed at 3 days after administration of PG 500 microgram.

Characterization of DBT cell clones derived from cells persistently infected with the JHM strain of mouse hepatitis virus.

Twelve clones derived from the cells persistently infected with the JHM strain (JHMV) of mouse hepatitis virus (MHV) were established from mouse astrocytoma-derived DBT cells and characterized. All the cell clones were resistant to superinfection with MHV. Only one of the persistently infected cell clone synthesized viral RNA and proteins and produced virus particles.

Inhibition of viral multiplication in cells chronically infected with mouse hepatitis virus by antisense RNA against the polymerase gene.

Recently, we showed that the antisense RNA containing a hammerhead ribozyme sequence against the polymerase gene of mouse hepatitis virus (MHV) inhibited viral multiplication in acute infection [10]. In the present study, we examined the inhibitory effects of an antisense RNA on viral multiplication in chronic MHV infection. In cell line LR-2, in which the 926-nucleotide (nt) antisense RNA containing a ribozyme sequence against the polymerase gene was expressed constitutively at a high level, chronic MHV infection was established through the maintenance of infection over 100 days postinfection (d.