Dependence of the decoherence of polarization states in phase-damping channels on the frequency spectrum envelope of photons

We consider the decoherence of photons suffering in phase-damping channels. By exploring the evolutions of single-photon polarization states and two-photon polarization-entangled states, we find that different frequency spectrum envelopes of photons induce different decoherence processes. A white frequency spectrum can lead the decoherence to an ideal Markovian process. Some color frequency spectrums can induce asymptotical decoherence, while, some other color frequency spectrums can make coherence vanish periodically with variable revival amplitudes. These behaviors result from the non-Markovian effects on the decoherence process, which may give rise to a revival of coherence after complete decoherence.Comment: 7 pages, 4 figures, new results added, replaced by accepted versio

Optimized detector tomography for photon-number resolving detectors with hundreds of pixels

Photon-number resolving detectors with hundreds of pixels are now readily available, while the characterization of these detectors using detector tomography is computationally intensive. Here, we present a modified detector tomography model that reduces the number of variables that need optimization. To evaluate the effectiveness and accuracy of our model, we reconstruct the photon number distribution of optical coherent and thermal states using the expectation-maximization-entropy algorithm. Our results indicate that the fidelity of the reconstructed states remains above 99%, and the second and third-order correlations agree well with the theoretical values for a mean number of photons up to 100. We also investigate the computational resources required for detector tomography and find out that our approach reduces the solving time by around a half compared to the standard detector tomography approach, and the required memory resources are the main obstacle for detector tomography of a large number of pixels. Our results suggest that detector tomography is viable on a supercomputer with 1~TB RAM for detectors with up to 340 pixels

[(E)-(1-Phenyl­ethyl­idene)amino]­urea methanol monosolvate

In the title compound, C9H11N3O·CH4O, the semicarbazone moiety is nearly planar [maximum deviation = 0.017 (2) Å] and is twisted by a dihedral angle of 29.40 (13)° with respect to the phenyl ring. The semicarbazone moiety and phenyl ring are located on opposite sides of the C=N bond, showing the E configuration. An inter­molecular O—H⋯O and N—H⋯O hydrogen-bonding network occurs in the crystal structure

Cloning and Expression Analysis of a PISTILLATA Homologous Gene from Pineapple (Ananas comosus L. Merr)

PISTILLATA (PI)-like genes are crucial regulators of flowering in angiosperms. A homologue of PI, designated as AcPI (Genbank accession number HQ717796), was isolated from pineapple cultivar Comte de Paris by reverse transcriptase polymerase chain reaction (RT-PCR) and rapid amplification of cDNA ends (RACE). The cDNA sequence of AcPI is 907 bp in length and contains an open reading frame of 594 bp, which encodes a protein of 197 amino acids. The molecular weight was 2.29 kDa and the isoelectric point was 9.28. The alignment showed that AcPI had a high identity with CsPIC2 (78.6%), AoPI (77.4%), OrcPI (75.7%) and HPI2 (72.4%). Quantitative real-time polymerase chain reaction (qRT-PCR) analyses in different tissues showed that the expression pattern of AcPI was different from the B-class genes in eudicots. AcPI was expressed in all the tissues investigated. The expression level was very low in fruit stems, bracts, leaves and sepals, high in petals and carpels, and moderate in apical meristems, flesh and stamens. The qRT-PCR analyses in different stages indicated that the expression of AcPI reached the highest level at 40 days after flower inducement, when the multiple fruit and floral organs were forming. It proved the important role of AcPI in floral organs and fruit development. The 35S::AcPI transgenic Arabidopsis plants flowered earlier and had more inflorescences or branches than wild type plants

MicroRNA-221 and microRNA-222 regulate gastric carcinoma cell proliferation and radioresistance by targeting PTEN

<p>Abstract</p> <p>Background</p> <p>MicroRNAs (miRNAs) can function as either oncogenes or tumor suppressor genes via regulation of cell proliferation and/or apoptosis. MiR-221 and miR-222 were discovered to induce cell growth and cell cycle progression via direct targeting of p27 and p57 in various human malignancies. However, the roles of miR-221 and miR-222 have not been reported in human gastric cancer. In this study, we examined the impact of miR-221 and miR-222 on human gastric cancer cells, and identified target genes for miR-221 and miR-222 that might mediate their biology.</p> <p>Methods</p> <p>The human gastric cancer cell line SGC7901 was transfected with AS-miR-221/222 or transduced with pMSCV-miR-221/222 to knockdown or restore expression of miR-221 and miR-222, respectively. The effects of miR-221 and miR-222 were then assessed by cell viability, cell cycle analysis, apoptosis, transwell, and clonogenic assay. Potential target genes were identified by Western blot and luciferase reporter assay.</p> <p>Results</p> <p>Upregulation of miR-221 and miR-222 induced the malignant phenotype of SGC7901 cells, whereas knockdown of miR-221 and miR-222 reversed this phenotype via induction of PTEN expression. In addition, knockdonwn of miR-221 and miR-222 inhibited cell growth and invasion and increased the radiosensitivity of SGC7901 cells. Notably, the seed sequence of miR-221 and miR-222 matched the 3'UTR of PTEN, and introducing a PTEN cDNA without the 3'UTR into SGC7901 cells abrogated the miR-221 and miR-222-induced malignant phenotype. PTEN-3'UTR luciferase reporter assay confirmed PTEN as a direct target of miR-221 and miR-222.</p> <p>Conclusion</p> <p>These results demonstrate that miR-221 and miR-222 regulate radiosensitivity, and cell growth and invasion of SGC7901 cells, possibly via direct modulation of PTEN expression. Our study suggests that inhibition of miR-221 and miR-222 might form a novel therapeutic strategy for human gastric cancer.</p

MiR-221 and miR-222 target PUMA to induce cell survival in glioblastoma

<p>Abstract</p> <p>Background</p> <p>MiR-221 and miR-222 (miR-221/222) are frequently up-regulated in various types of human malignancy including glioblastoma. Recent studies have reported that miR-221/222 regulate cell growth and cell cycle progression by targeting p27 and p57. However the underlying mechanism involved in cell survival modulation of miR-221/222 remains elusive.</p> <p>Results</p> <p>Here we showed that miR-221/222 inhibited cell apoptosis by targeting pro-apoptotic gene PUMA in human glioma cells. Enforced expression of miR-22/222 induced cell survival whereas knockdown of miR-221/222 rendered cells to apoptosis. Further, miR-221/222 reduced PUMA protein levels by targeting PUMA-3'UTR. Introducing PUMA cDNA without 3'UTR abrogated miR-221/222-induced cell survival. Notably, knockdown of miR-221/222 induces PUMA expression and cell apoptosis and considerably decreases tumor growth in xenograft model. Finally, there was an inverse relationship between PUMA and miR-221/222 expression in glioma tissues.</p> <p>Conclusion</p> <p>To our knowledge, these data indicate for the first time that miR-221/222 directly regulate apoptosis by targeting PUMA in glioblastoma and that miR-221/222 could be potential therapeutic targets for glioblastoma intervention.</p