1,283 research outputs found

    Isolation and Identification of Acholeplasma sp. from the Mud Crab, Scylla serrata

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    For the first time, a mollicute-like organism (MLO) was cultured from moribund mud crabs (Scylla serrata) during an outbreak of clearwater disease in Zhejiang Province, China. The MLO displayed a fried-egg colony morphology in culture, did not possess a cell wall, and was not retained by 0.45 Όm and 0.2 Όm filters. It was able to ferment glucose, sucrose, lactose, and maltose, but it did not utilize arginine and urea. The MLO grew in the absence of bovine serum and was not susceptible to digitonin. Sequence analysis of the 16S rRNA gene revealed that this MLO had 99% identity with Acholeplasma laidlawii PG-8A, which indicates that the organism isolated from mud crabs is a member of the genus Acholeplasma

    SR140333 counteracts NK-1 mediated cell proliferation in human breast cancer cell line T47D

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    <p>Abstract</p> <p>Background</p> <p>It has been demonstrated that certain NK-1 antagonists could reduce proliferation of several cancer cell lines, however, it is unknown whether SR140333 exerts proliferation inhibition in breast cancer cell line.</p> <p>Methods</p> <p>Immunohistochemical staining was carried out to investigate the immunolocation of NK-1 in breast cancer tissues and T47D cell line, thereafter, various concentrations of [Sar9, Met(O2)11]substance P and SR140333 were applied alone or combined. MTT assay was applied to detect cytoactivation and coulter counter was to detect growth curve. The Hoechst33258 staining was performed to detect apoptosis.</p> <p>Results</p> <p>We found that breast cancer and T47D cells bear positive expression of NK-1. SR140333 inhibited cell growth in a dose dependent manner. Furthermore, SR140333 could counteract [Sar9, Met(O2)11]substance P induced proliferation. Hoechst33258 staining revealed the presence of apoptosis after SR140333 treatment.</p> <p>Conclusions</p> <p>Our study demonstrated SR140333 exert proliferation inhibition in breast cancer cell line T47D and indicates NK-1 play a central role in the substance P related cell proliferation in breast cancer.</p

    Cytoplasmic p21 induced by p65 prevents doxorubicin-induced cell death in pancreatic carcinoma cell line

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    <p>Abstract</p> <p>Background</p> <p>Studies have shown the existence of p21 induction in a p53-dependent and -independent pathway. Our previous study indicates that DOX-induced p65 is able to bind the p21 promoter to activate its transactivation in the cells.</p> <p>Methods</p> <p>Over-expression and knock-down experiments were performed in Human Pancreatic Carcinoma (PANC1) cells. Cell cycle and cell death related proteins were assessed by Western Blotting. Cytotoxicity assay was checked by CCK-8 kit. Cell growth was analyzed by flow cytometers.</p> <p>Results</p> <p>Here we showed that over-expression of p65 decreased the cytotoxic effect of DOX on PANC1 cells, correlating with increased induction of cytoplasmic p21. We observed that pro-caspase-3 physically associated with cytoplasmic p21, which may be contribution to prevent p21 translocation into the nucleus. Our data also suggested that no clear elevation of nuclear p21 by p65 provides a survival advantage by progression cell cycle after treatment of DOX. Likewise, down-regulation of p65 expression enhanced the cytotoxic effect of DOX, due to a significant decrease of mRNA levels of anti-apoptotic genes, such as the cellular inhibitor of apoptosis-1 (c-IAP1), and the long isoform of B cell leukemia/lymphoma-2 (Bcl-2), leading to efficient induction of caspase-3 cleavage in the cells. More, we present evidence that over-expression of p53 or p53/p65 in the PANC1 cells were more sensitive to DOX treatment, correlated with activation of caspase-3 and clear elevation of nuclear p21 level. Our previous data suggested that expression of p21 increases Gefitinib-induced cell death by blocking the cell cycle at the G1 and G2 phases. The present findings here reinforced this idea by showing p21's ability of potentiality of DOX-induced cell death correlated with its inhibition of cell cycle progression after over-expression of p53 or p53/p65.</p> <p>Conclusion</p> <p>Our data suggested p65 could increase p53-mediated cell death in response to DOX in PANC1 cells. Thus, it is worth noting that in p53 null or defective tumors, targeting in down-regulation of p65 may well be useful, leading to the potentiality of chemotherapeutic drugs.</p

    A surface-enhanced Raman scattering (SERS)-active optical fiber sensor based on a three-dimensional sensing layer

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    AbstractTo fabricate a new surface-enhanced Raman scattering (SERS)-active optical fiber sensor, the design and preparation of SERS-active sensing layer is one of important topics. In this study, we fabricated a highly sensitive three-dimensional (3D) SERS-active sensing layer on the optical fiber terminal via in situ polymerizing a porous polymer material on a flat optical fiber terminal through thermal-induced process, following with the photochemical silver nanoparticles growth. The polymerized polymer formed a 3D porous structure with the pore size of 0.29–0.81ÎŒm, which were afterward decorated with abundant silver nanoparticles with the size of about 100nm, allowing for higher SERS enhancement. This SERS-active optical fiber sensor was applied for the determination of 4-mercaptopyridine, crystal violet and maleic acid The enhancement factor of this SERS sensing layer can be reached as about 108. The optical fiber sensor with high sensitive SERS-active porous polymer is expected for online analysis and environment detection
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