On the Use of Wigner Distribution in Ultrasonic NDE

The application of signal processing techniques to nondestructive evaluation(NDE) has proven successful for years. The research on this issue has been directed into two types of techniques, namely, the time-domain methods and frequency methods. Techniques of frequency-domain analysis such as Fourier transform and power spectral density reveal important information concerning decomposition of frequency components which may not be available from the time-domain analysis. However, in the case of ultrasonic NDE, the observed echo from a material can be viewed as a superposition of successive time arrivals of different components each characterized by different spectral contents. Both the time domain waveform and the spectrum can be very confusing and are simultaneously relevant for a complete description of a signal [2]. Neither the spectral analysis nor the time-domain methods alone can provide needed information. Therefore, mixed tools are often necessary to be introduced to overcome the limits imposed on these two mutually complementary families of techniques. These tools are generally referred to as time-frequency distribution or time-frequency analysis and have been found useful in numerous applications such as speech processing, sonar analysis, detection of electrocardiography (EEG) signals and X-ray diffraction. Among them, the Wigner distribution has been studied intensively in the last few years due to its high resolution propert

Identification of Herpes Simplex Virus Type 1 Latency-Associated Transcript Sequences That both Inhibit Apoptosis and Enhance the Spontaneous Reactivation Phenotype

The herpes simplex virus type 1 (HSV-1) latency-associated transcript (LAT) gene is essential for the high spontaneous and induced reactivation phenotype of HSV-1 in the rabbit ocular model and for the high induced reactivation phenotype in the mouse ocular model. Recently we showed that LAT has an antiapoptosis function, and we hypothesized that LAT’s ability to inhibit apoptosis played an important role in LAT’s ability to enhance the reactivation phenotype. Expression of just the first 1.5 kb of the 8.3-kb LAT gene is sufficient for both inhibition of apoptosis in an in vitro transient-transfection assay and the high spontaneous reactivation phenotype in vivo. Here we show the results of more complex mapping studies in which inhibition of apoptosis and the enhanced spontaneous reactivation phenotype also appear to be linked. The HSV-1 mutant virus dLAT371 has a high spontaneous reactivation phenotype in rabbits, suggesting that the LAT region deleted in this mutant (LAT nucleotides 76 to 447) is not required for this phenotype. The LAT3.3A viral mutant (which expresses LAT nucleotides 1 to 1499) also has a high spontaneous reactivation phenotype, suggesting that the region of LAT not expressed by this mutant (LAT nucleotide 1500 to the end of LAT) is also not required for this phenotype. Surprisingly, LAT2.9A, which is a combination of dLAT371 and LAT3.3A (i.e., it expresses LAT nucleotides 1 to 76 and 447 to 1499), has a low spontaneous reactivation phenotype indistinguishable from that of LAT null mutants. We report here that consistent with the low spontaneous reactivation phenotype of LAT2.9A, a plasmid expressing the identical LAT RNA did not inhibit caspase 9-induced apoptosis. In contrast, plasmids containing the same deletion but able to transcribe up to or past LAT nucleotide 2850 (rather than just up to LAT nucleotide 1499) inhibited caspase 9-induced apoptosis, consistent with the high spontaneous reactivation phenotype of dLAT371. Thus, LAT2.9A may have a low spontaneous reactivation phenotype because the LAT RNA that is made cannot block apoptosis, and dLAT371 apparently has a high spontaneous reactivation phenotype because the LAT RNA made has significant antiapoptosis activity. Furthermore, LAT appeared to have at least two regions capable of interfering with caspase 9-induced apoptosis. One region partially overlaps LAT nucleotides 76 to 447. The second region is partially (or completely) downstream of LAT nucleotide 1499

The Gene That Encodes the Herpes Simplex Virus Type 1 Latency-Associated Transcript Influences the Accumulation of Transcripts (Bcl-x\u3csub\u3eL\u3c/sub\u3e and Bcl-x\u3csub\u3es\u3c/sub\u3e) That Encode Apoptotic Regulatory Proteins

The herpes simplex virus type 1 latency-associated transcript (LAT) inhibits apoptosis. We demonstrate here that LAT influences the accumulation of the Bcl-xL transcript versus the Bcl-xS transcript in Neuro-2A cells. Bcl-xL encodes an antiapoptotic protein, whereas Bcl-xS encodes a proapoptotic protein. Promoting the accumulation of Bcl-xL in neurons may inhibit apoptosis, thus enhancing the latency-reactivation cycle

The Gene That Encodes the Herpes Simplex Virus Type 1 Latency-Associated Transcript Influences the Accumulation of Transcripts (Bcl-x\u3csub\u3eL\u3c/sub\u3e and Bcl-x\u3csub\u3es\u3c/sub\u3e) That Encode Apoptotic Regulatory Proteins

The herpes simplex virus type 1 latency-associated transcript (LAT) inhibits apoptosis. We demonstrate here that LAT influences the accumulation of the Bcl-xL transcript versus the Bcl-xS transcript in Neuro-2A cells. Bcl-xL encodes an antiapoptotic protein, whereas Bcl-xS encodes a proapoptotic protein. Promoting the accumulation of Bcl-xL in neurons may inhibit apoptosis, thus enhancing the latency-reactivation cycle

Herpes simplex virus type 1 ICP0 localizes in the stromal layer of infected rabbit corneas and resides predominantly in the cytoplasm and/or perinuclear region of rabbit keratocytes

Herpes stromal keratitis (HSK) results from the reactivation of herpes simplex virus type-1 (HSV-1) in the cornea. The subsequent corneal inflammation and neovascularization may lead to scarring and visual loss. The cellular and molecular mechanisms underlying HSK remain unknown. The presence of stromal HSV-1 viral proteins or antigens in the HSK cornea remains a subject of debate. It was recently reported that HSV-1 ICP0 rapidly diffuses out of infected rabbit corneas. To investigate further the presence of HSV-1 ICP0 in the infected cornea, particularly in the corneal stroma, ex vivo confocal microscopy was used to scan rabbit corneas infected with the virus ICP0–EYFP, an HSV-1 derivative (strain 17+) that expresses ICP0 fused to the enhanced yellow fluorescent protein (EYFP). These results demonstrate that ICP0 is expressed in the corneal epithelium and stromal cells (keratocytes) of infected rabbit corneas throughout acute infection. Furthermore, expression of ICP0–EYFP appears localized to punctate, granular deposits within stromal keratocytes, showing both a cytoplasmic and perinuclear localization. These findings provide new data demonstrating that anterior corneal keratocytes become infected and express ICP0 during acute HSV-1 infection

Chiral Lagrangians for Radiative Decays of Heavy Hadrons

The radiative decays of heavy mesons and heavy baryons are studied in a formalism which incorporates both the heavy quark symmetry and the chiral symmetry. The chiral Lagrangians for the electromagnetic interactions of heavy hadrons consist of two pieces: one from gauging electromagnetically the strong-interaction chiral Lagrangian, and the other from the anomalous magnetic moment interactions of the heavy baryons and mesons. Due to the heavy quark spin symmetry, the latter contains only one independent coupling constant in the meson sector and two in the baryon sector. These coupling constants only depend on the light quarks and can be calculated in the nonrelativistic quark model. However, the charm quark is not heavy enough and the contribution from its magnetic moment must be included. Applications to the radiative decays $D^\ast \rightarrow D \gamma~,~B^\ast \rightarrow B \gamma~,~ \Xi^\prime_c \rightarrow \Xi_c \gamma~, \Sigma_c \rightarrow \Lambda_c \gamma$ and $\Sigma_c \rightarrow \Lambda_c \pi \gamma$ are given. Together with our previous results on the strong decay rates of $D^\ast \rightarrow D \pi$ and $\Sigma_c \rightarrow \Lambda_c \pi$, predictions are obtained for the total widths and branching ratios of $D^\ast$ and $\Sigma_c$. The decays $\Sigma^+_c \rightarrow \Lambda^+_c \pi^0 \gamma$ and $\Sigma^0_c \rightarrow \Lambda^+_c \pi^- \gamma$ are discussed to illustrate the important roles played by both the heavy quark symmetry and the chiral symmetry.Comment: 30 pages (one figure, available on request), CLNS 92/1158 and IP-ASTP-13-9

Phenomenology of Higgs bosons in the Zee-Model

To generate small neutrino masses radiatively, the Zee-model introduces two Higgs doublets and one weak-singlet charged Higgs boson to its Higgs sector. From analyzing the renormalization group equations, we determine the possibile range of the lightest CP-even Higgs boson ($h$) mass and the Higgs boson self-couplings as a function of the cut-off scale beyond which either some of the coupling constants are strong enough to invalidate the perturbative analysis or the stability of the electroweak vacuum is no longer guaranteed. Using the results obtained from the above analysis, we find that the singlet charged Higgs boson can significantly modify the partial decay width of $h \to \gamma \gamma$ via radiative corrections, and its collider phenomenology can also be drastically different from that of the charged Higgs bosons in the usual two-Higgs-doublet models.Comment: Added a paragraph and a figure in Section V, corrected typos, added references. (RevTeX, 45 pages, 16 figures included.) To appear in Physical Review