Truncate

Abstract: The invention provides a self-adaptive modulating and coding method, which comprises the following steps: selecting a special service sub-frame for UE to transmit downlink data, wherein PRB in the special service sub-frame is truncate PRB; determining TBS and the number of truncate PRB pairs transmitted to the UE according to the loaded service; and dispatching and transmitting the downlink data for the UE according to the determined TBS, sending the number of the adopted truncate PRB pairs and an MCS sequence number to the UE, converting the number of the truncate PRB pairs into the number of complete PRB pairs through the UE, determining a modulating mode and a TBS sequence number according to the MCS sequence number, and determining the TBS of the downlink data according to the number of the complete PRB pairs and the TBS sequence number. By converting the number of the complete PRB and the number of the truncate PRB, the special conditions during transmitting the downlink data through the truncate PRB can be processed based on using the self-adaptive processing process and the resources of the prior common sub-frame, and the realization is simple and efficient.

Abstract: Gelsolin is a calcium-activated actin-binding protein with six subdomains. The N-terminal (G1) domain is essential for actin-filament-severing activity while other domains within G2–3 position the protein on the filament side allowing G1 to sever. In order to generate reagents capable of competitively inhibiting endogenous gelsolin and, potentially, other actin filament regulatory protein, we expressed several truncates of gelsolin in Escherichia coli, and analyzed how they affected the in vitro activity of two different actin-binding proteins, gelsolin and cofilin. A CA2+-sensitive truncate containing G2–6 inhibited the F-actin-depolymerizing activities of both gelsolin and cofilin, while a G2–3 truncate was less effective. Using two independent assays, our results support the idea that gelsolin truncates inhibit actin filament severing and do not markedly affect actin subunit dissociation kinetics. Cosedimentation assays in the presence of calcium demonstrate that the G2–6 truncate binds to F-actin more strongly than the G2–3 truncate consistent with a protection mechanism by conformational change of F-actin and/or competitive binding to actin filaments which depends upon the presence of actin filament binding domains.

Abstract: This invention provides an isolated polypeptide comprising an amino acid sequence of a N-terminal choline binding protein A truncate in which the amino acid sequence is set forth in any of SEQ ID NOS: 1, 3-7, or 9-11, including fragments, mutants, variants, analogs, or derivatives, thereof. Also, this invention provides a isolated polypeptide comprising an amino acid sequence of a N-terminal choline binding protein A truncate, wherein the amino acid is set forth in SEQ ID NO: 24, wherein the polypeptide retains its native tertiary structure and methods of preparation. This invention provides an isolated polypeptide comprising an amino acid sequence of a N-terminal choline binding protein A truncate, wherein the polypeptide has lectin activity and does not bind to choline. This invention provides an isolated immunogenic polypeptide comprising an amino acid sequence of a N-terminal choline binding protein A truncate. This invention provides an isolated nucleic acid encoding a polypeptide comprising an amino acid sequence of a N-terminal choline binding protein A truncate. Lastly, this invention provides pharmaceutical compositions, vaccines, and diagnostic and therapeutic methods of use.