Compact Supercell Method Based on Opposite Parity for Bragg Fibers

The supercell- based orthonormal basis method is proposed to investigate the modal properties of the Bragg fibers. A square lattice is constructed by the whole Bragg fiber which is considered a supercell, and the periodical dielectric structure of the square lattice is decomposed using periodic functions (cosine). The modal electric field is expanded as the sum of the orthonormal set of Hermite-Gaussian basis functions based on the opposite parity of the transverse electric field. The propagation characteristics of Bragg fibers can be obtained after recasting the wave equation into an eigenvalue system. This method is implemented with very high efficiency and accuracy

Norcantharidin induces G2/M arrest and apoptosis via activation of ERK and JNK, but not p38 signaling in human renal cell carcinoma ACHN cells

Renal cell carcinoma (RCC) is generally acknowledged as the most resistant primary malignancy unresponsive to conventional radiotherapy and chemotherapy treatments. Norcantharidin (NCTD), a therapeutic compound derived from medicinal plants, has been shown to trigger apoptosis, as well as antimetastatic and antioxidant activities in several tumor cells. However, NCTD’s mechanism of antitumor activity in the RCC cell line remains unclear. In this study, we report that NCTD led to a time- and dose-dependent inhibition of cell proliferation. It had also markedly induced apoptosis and G2/M phase cell cycle arrest in a dose-dependent manner by decreasing the expressions of pro-caspase-3, pro-caspase-9, cyclin B1, and pCDC25C while increasing active caspase-3, cleaved-PARP, P21, and pCDC2 levels. Interestingly, NCTD treatment provoked the phosphorylation of extracellular-regulated protein kinase (ERK) and c-Jun-N-terminal kinase (JNK), but not of p38 MAPK. Moreover, SCH772984 and SP600125, ERK and JNK inhibitors, respectively, could partially abolish NCTD-induced apoptosis and G2/M phase cell cycle arrest. Collectively, these findings suggest that NCTD might activate JNK and ERK signaling pathways, consequently inducing apoptosis and G2/M arrest through the modulation of related proteins. This study provided evidence that NCTD is a promising therapeutic drug for the treatment of RCC

Cloning of neuraminidase (NA) gene and identification of its antiviral activity

Neuraminidase not only works as an antigen, inducing target-specific antibodies, but also plays a role of  enzyme activity and destroys the sialic acid receptor required by virus infection of the host cell surface which  protects the host from virus damage. In order to explore a new idea to use neuraminidase (NA) gene and  produce disease-resistant transgenic poultry, prokaryotic expression vector pGEX-NA was constructed to  make NA polyclone antibody. Eukaryotic expression vector pcDNA3.0-NA and pcDNA3.0/EGFP-NA was  constructed to reveal its subcelluar location by immunofluorescence and enhanced green fluorescent fusion  protein (EGFP). Chicken embryonic fibroblast (CEF) cells were transfected with pcDNA3.0-NA and selected by  G418 for two weeks, the transfected cells were challenged by Newcastle disease virus (NDV), the morphology of CEF cells were observed to detect the antiviral ability of NA gene. CEF cells were incubated by the cell  lysates extracted from the NIH 3T3 cells, which were transfected with pcDNA3.0-NA. The results show that  pGEX-NA could express NA protein in vitro and NA polyclone antibody worked very well; immunofluorescence and EGFP fusion protein revealed that NA protein located at the cytoplasm near the membrane; NDV-CEF  inhibition experiment showed the NA protein could resist and delayed CEF cells from NDV infection.Key words: Neuraminidase (NA), newcastle disease virus (NDV), antiviral activity, chicken embryonic fibroblast (CEF)

The transcription factor CREB is involved in sorafenib-inhibited renal cancer cell proliferation, migration and invasion

Our previous reports showed that the cyclic-AMP-response element-binding protein (CREB) served as a proto-oncogene in the process of tumorigenesis and mediated the growth and metastatic activity of renal cancer cells. Our study, therefore, explored the role of CREB in sorafenib-inhibited cell proliferation, migration and invasion. Renal cancer cells were cultured in medium containing sorafenib for 12, 24, 48 and 72 h. The MTT assay was used to study the cytotoxic effects of sorafenib. Cell invasion and migration were assayed in wound healing and transwell experiments, respectively. Protein expression levels were evaluated by western blotting. The results show that sorafenib treatment decreased cell viability in a dose- and time-dependent manner. Sorafenib inhibited cell migration and invasion and decreased the expression of MMP-2 and MMP-9. Moreover, addition of the recombinant plasmid pCI-neo/CREB (PN) reversed the sorafenib-induced inhibition of cell proliferation, migration and invasion. These results show that CREB is associated with the sorafenib-induced inhibition of proliferation, migration and invasion

Identification of Unequally Represented Founder Viruses Among Tissues in Very Early SIV Rectal Transmission

Characterizing the transmitted/founder (T/F) viruses of multi-variant SIV infection may shed new light on the understanding of mucosal transmission.We intrarectally inoculated six Chinese rhesus macaques with a single high dose of SIVmac251 (3.1 × 104 TCID50) and obtained 985 full-length env sequences from multiple tissues at 6 and 10 days post-infection by single genome amplification (SGA). All 6 monkeys were infected with a range of 2 to 8 T/F viruses and the dominant variants from the inoculum were still dominant in different tissues from each monkey. Interestingly, our data showed that a cluster of rare T/F viruses was unequally represented in different tissues. This cluster of rare T/F viruses phylogenetically related to the non-dominant SIV variants in the inoculum and was not detected in any rectum tissues, but could be identified in the descending colon, jejunum, spleen, or plasma. In 2 out of 6 macaques, identical SIVmac251 variants belonging to this cluster were detected simultaneously in descending colon/jejunum and the inoculum.We also demonstrated that the average CG dinucleotide frequency of these rare T/F viruses found in tissues, as well as non-dominant variants in the inoculum, was significantly higher than the dominant T/F viruses in tissues and the inoculum. Collectively, these findings suggest that descending colon/jejunum might be more susceptible than rectum to SIV in the very early phase of infection. And host CG suppression, which was previously shown to inhibit HIV replication in vitro, may also contribute to the bottleneck selection during in vivo transmission