Burst packet loss concealment using multiple codebooks and comfort noise for CELP-type speech coders in wireless sensor networks.

In this paper, a packet loss concealment (PLC) algorithm for CELP-type speech coders is proposed in order to improve the quality of decoded speech under burst packet loss conditions in a wireless sensor network. Conventional receiver-based PLC algorithms in the G.729 speech codec are usually based on speech correlation to reconstruct the decoded speech of lost frames by using parameter information obtained from the previous correctly received frames. However, this approach has difficulty in reconstructing voice onset signals since the parameters such as pitch, linear predictive coding coefficient, and adaptive/fixed codebooks of the previous frames are mostly related to silence frames. Thus, in order to reconstruct speech signals in the voice onset intervals, we propose a multiple codebook-based approach that includes a traditional adaptive codebook and a new random codebook composed of comfort noise. The proposed PLC algorithm is designed as a PLC algorithm for G.729 and its performance is then compared with that of the PLC algorithm currently employed in G.729 via a perceptual evaluation of speech quality, a waveform comparison, and a preference test under different random and burst packet loss conditions. It is shown from the experiments that the proposed PLC algorithm provides significantly better speech quality than the PLC algorithm employed in G.729 under all the test conditions.

OSNR monitoring technique based on cascaded long-period fiber grating with optically tunable phase shifter.

An optical signal-to-noise ratio (OSNR) monitoring technique using a cascaded long-period fiber grating with a tunable phase shifter is proposed for non return-to-zero on-off-keying (NRZ-OOK) and differential phase shift keying (DPSK) signals. This method is based on two key points: first, the cascaded long period fiber grating (CLPG) acts as an optical delay interferometer (ODI) by Mach-Zehnder configuration consisting of the core and cladding modes inside the CLPG. Secondly, an optically tunable phase shifter using an Yb(3+) doped optical fiber (YDF) is inserted between the CLPG. The phase of the modulated signal propagating along the core mode of YDF is controlled by adjusting pumping power of 976-nm laser diode (LD). By combining the CLPG with the optically tunable phase shifter, the OSNR monitoring could be successfully executed.

Regulation of urokinase plasminogen activator by epigallocatechin-3-gallate in human fibrosarcoma cells.

(-)-Epigallocatechin-3-gallate (EGCG), a main flavanol of green tea, potently suppressed the urokinase-type plasminogen activator (uPA) expression in human fibrosarcoma HT 1080 cells. EGCG induced not only the suppression of the uPA promoter activity but also the destabilization of uPA mRNA. EGCG inhibited the phosphorylation of extracellular signal-regulated kinases 1 and 2 (Erk-1/2) and P38 mitogen-activated protein kinase (MAPK), but not the phosphorylation of c-jun N-terminal kinase (JNK) and Akt. Specific inhibitors of Erk-1/2 (2'-amino-3'-methoxyflavone, PD98059) and P38 MAPK (pyridinylimidazole, SB203580) were found to suppress the uPA expression and the uPA promoter activity. However, the specific inhibitors did not affect the uPA mRNA stability. These results suggest that EGCG could regulate the uPA expression by at least two different mechanisms: EGCG may inhibit the Erk-1/2 and P38 MAPK, leading to suppression of the uPA promoter activity, and EGCG may destabilize the uPA mRNA in an Erk-1/2- and p38 MAPK-independent way.

SB203580, a P38 MAPK Inhibitor, Blocks in vitro Invasion by Human Gastric SNU-638 Cells.

PURPOSE: The role of P38 mitogen-activated protein kinase (MAPK) in gastric cancer invasion has not yet been determined. In this study, we examined the effects of SB203580, a specific P38 MAPK inhibitor, on the in vitro invasion of gastric cancer and upon the molecules involved in this process. MATERIALS AND METHODS: Human gastric cancer SNU-638 cells were maintained in RPMI 1640 supplemented with 10% FBS. BIOCOAT matrigel invasion chambers were used to examine in vitro invasiveness, zymography for gelatinase activity, CAT assay for uPA promoter activity and Western and Northern blotting to determine protein and mRNA levels, respectively. RESULTS: Treatment of SNU-638 cells with SB203580, a specific P38 MAPK inhibitor, reduced in vitro invasiveness, dose-dependently. SB203580 treatment was found to decrease both mRNA expression and uPA promoter activity in gastric SNU-638 cells. In vitro invasion of SNU-638 cells was partially abrogated by uPA-neutralizing antibodies. The activities of MMPs were not significantly altered by SB203580. CONCLUSION: Our results suggest that P38 MAPK is a potential therapeutic target for inhibiting uPA-dependent gastric tumor invasiveness and metastasis.