The effect of temperature on the development of Nephus includens (Kirsch) and Nephus bisignatus (Boheman) (Coleoptera: Coccinellidae), predators of Planococcus citri Risso (Hemiptera: Pseudococcidae)

The effect of temperature οη the development of the predators Nephus includens (Kirsch) and Ν. bisignatus (Boheman) (Coleoptera: Coccinellidae), was studied. The development time of immature stages and the pre-oviposition period of adult females for the two predators was recorded at eight constant temperatures (10, 15, 20, 25, 30, 32.5, 35 and 37.5°C). The beetles were reared on eggs, nymphs and female adults of Planococcus citri (Risso) (Homoptera: Pseudococcidae) that had developed on squash (Cucurbita pepo) and on sour orange leaves (CΊtrus aurantium). Using the linear model for the biological cycle of Ν. includens on squash and on sour orange leaves, the developmental zeros (lower temperature thresholds) were estimated to be 10.9 and 11.0°C respectively and the thermal constants, 490.5 and 472.8 day-degrees respectively. Using the Lactin model the lower thresholds were estimated to be 11.1 and 11.2°C respectively and the upper thresholds 36.1 and 36.0°C respectively. For the biological cycle of Ν. bisignatus, using the linear model, the lower thresholds were estimated to be 9.4°C on squash and 9.3°C on sour orange leaves and the thermal constants were 614.3 and 647.9 day-degrees respectively. Using the Lactin model the lower thresholds were estimated to be 9.9 and 1O.0°C respectively and the upper thresholds, 34.7 and 35.0°C respectively. The survival rate of Ν. includens in­stars at 10, 15, 20, 25, 30, 32.5, 35 and 37.5°C on squash and on sour orange leaves was respectively 0.0, 34.9, 63.2, 70.6, 63.3, 54.5, 19.8, 0.0, and 0.0, 32.2, 61.0, 68.0, 68.3, 56.6, 17.6, 0.0%. The survival rate of Ν. bisignatus instars at 10, 15, 20, 25, 30, 32.5 and 35°C on squash and on sour orange leaves was respectively, 0.0, 39.9, 61.1, 60.7, 47.2, 26.4, 0.0 and 0.0, 35.7, 65.7, 68.0, 44.2, 29.1, 0.0%. The results show that Ν. includens has a shorter biological cycle than Ν. bisignatus, whereas the latter species has lower temperature thresholds

BCL-2 family protein expression and platinum drug resistance in ovarian carcinoma

The expression of the BCL-2 family proteins, BCL-2, BAX, BCLXLand BAK have been determined in a panel of 12 human ovarian carcinoma cell lines encompassing a wide range in sensitivity to cisplatin. Whereas BAX, BCLXLand BAK levels did not correlate with sensitivity, there was a statistically significant inverse correlation (r = –0.81;P = 0.002) between growth inhibition by cisplatin and BCL-2 levels. In sublines possessing acquired resistance to various platinum-based drugs or across a panel of human ovarian carcinoma xenografts, there was no consistent pattern of BCL-2 expression. Two relatively sensitive lines (A2780 and CH1) have been stably transfected with bcl-2 and bclXLrespectively and two relatively resistant lines (A2780cisR and SKOV-3) stably transfected with bax. Overexpression of BCL-2 in A2780 cells led to resistance to cisplatin compared to the vector control when assayed at 48 h post-drug incubation but a significant increase in sensitivity at 96 h. Relative rates of apoptosis at 48- and 96-h post-cisplatin exposure mirrored the growth inhibition. There was no significant difference in sensitivity of the pair of lines by clonogenic assay. No significant changes in chemosensitivity to a variety of DNA-damaging or tubulin-interactive agents were observed in the remaining transfected lines. Taken together, these results suggest that, in human ovarian carcinoma cells, high BCL-2 levels (either naturally occurring or through gene transfection) confers a trend towards sensitivity not resistance to platinum drugs. © 2000 Cancer Research Campaig

Manipulating Kondo Temperature via Single Molecule Switching

Two conformations of isolated single TBrPP-Co molecules on a Cu(111) surface are switched by applying +2.2 V voltage pulses from a scanning tunneling microscope tip at 4.6 K. The TBrPP-Co has a spin-active cobalt atom caged at its center and the interaction between the spin of this cobalt atom and free electrons from the Cu(111) substrate can cause a Kondo resonance. Tunneling spectroscopy data reveal that switching from the saddle to a planar molecular conformation enhances spin-electron coupling, which increases the associated Kondo temperature from 130 K to 170 K. This result demonstrates that the Kondo temperature can be manipulated just by changing molecular conformation without altering chemical composition of the molecule.Comment: To appear in Nano Lett (2006

Europe's rare earth element resource potential: an overview of REE metallogenetic provinces and their geodynamic setting

Security of supply of a number of raw materials is of concern for the European Union; foremost among these are the rare earth elements (REE), which are used in a range of modern technologies. A number of research projects, including the EURARE and ASTER projects, have been funded in Europe to investigate various steps along the REE supply chain. This paper addresses the initial part of that supply chain, namely the potential geological resources of the REE in Europe. Although the REE are not currently mined in Europe, potential resources are known to be widespread, and many are being explored. The most important European resources are associated with alkaline igneous rocks and carbonatites, although REE deposits are also known from a range of other settings. Within Europe, a number of REE metallogenetic belts can be identified on the basis of age, tectonic setting, lithological association and known REE enrichments. This paper reviews those metallogenetic belts and sets them in their geodynamic context. The most well-known of the REE belts are of Precambrian to Palaeozoic age and occur in Greenland and the Fennoscandian Shield. Of particular importance for their REE potential are the Gardar Province of SW Greenland, the Svecofennian Belt and subsequent Mesoproterozoic rifts in Sweden, and the carbonatites of the Central Iapetus Magmatic Province. However, several zones with significant potential for REE deposits are also identified in central, southern and eastern Europe, including examples in the Bohemian Massif, the Iberian Massif, and the Carpathians

Primary and malignant cholangiocytes undergo CD40 mediated Fas dependent Apoptosis, but are insensitive to direct activation with exogenous fas ligand

Introduction Cholangiocarcinoma is a rare malignancy of the biliary tract, the incidence of which is rising, but the pathogenesis of which remains uncertain. No common genetic defects have been described but it is accepted that chronic inflammation is an important contributing factor. We have shown that primary human cholangiocyte and hepatocyte survival is tightly regulated via co-operative interactions between two tumour necrosis family (TNF) receptor family members; CD40 and Fas (CD95). Functional deficiency of CD154, the ligand for CD40, leads to a failure of clearance of biliary tract infections and a predisposition to cholangiocarcinoma implying a direct link between TNF receptor-mediated apoptosis and the development of cholangiocarcinoma. Aims To determine whether malignant cholangiocytes display defects in CD40 mediated apoptosis. By comparing CD40 and Fas-mediated apoptosis and intracellular signalling in primary human cholangiocytes and three cholangiocyte cell lines. Results Primary cholangiocytes and cholangiocyte cell lines were relatively insensitive to direct Fas-mediated killing with exogenous FasL when compared with Jurkat cells, which readily underwent Fas-mediated apoptosis, but were extremely sensitive to CD154 stimulation. The sensitivity of cells to CD40 activation was similar in magnitude in both primary and malignant cells and was STAT-3 and AP-1 dependent in both. Conclusions 1) Both primary and malignant cholangiocytes are relatively resistant to Fas–mediated killing but show exquisite sensitivity to CD154, suggesting that the CD40 pathway is intact and fully functional in both primary and malignant cholangiocytes 2) The relative insensitivity of cholangiocytes to Fas activation demonstrates the importance of CD40 augmentation of Fas dependent death in these cells. Agonistic therapies which target CD40 and associated intracellular signalling pathways may be effective in promoting apoptosis of malignant cholangiocytes

In vitro evaluation of antibiotics' combinations for empirical therapy of suspected methicillin resistant Staphylococcus aureus severe respiratory infections

<p>Abstract</p> <p>Background</p> <p>Methicillin resistant <it>Staphylococcus aureus </it>(MRSA) is an increasingly common cause of nosocomial infections, causing severe morbidity and mortality worldwide, and accounting in some hospitals for more than 50% of all <it>S. aureus </it>diseases. Treatment of infections caused by resistant bacterial pathogens mainly relies on two therapeutic modalities: development of new antimicrobials and use of combinations of available antibiotics.</p> <p>Combinations of antibiotics used in the empiric treatment of infections with suspected methicillin resistant <it>Staphylococcus aureus </it>etiology were investigated.</p> <p>Methods</p> <p>Double (vancomycin or teicoplanin with either levofloxacin or cefotaxime) and triple (vancomycin or teicoplanin + levofloxacin + one among amikacin, ceftazidime, cefepime, imipenem, piperacillin/tazobactam) combinations were evaluated by means of checkerboard assay and time kill curves. Mutational rates of single and combined drugs at antimicrobial concentrations equal to the resistance breakpoints were also calculated.</p> <p>Results</p> <p>Vancomycin or teicoplanin + levofloxacin showed synergy in 16/50 and in 9/50 strains respectively, while vancomycin or teicoplanin + cefotaxime resulted synergic for 43/50 and 23/50 strains, respectively. Triple combinations, involving teicoplanin, levofloxacin and ceftazidime or piperacillin/tazobactam gave synergy in 20/25 strains. Teicoplanin + levofloxacin gave synergy in triple combinations more frequently than vancomycin + levofloxacin.</p> <p>For single antibiotics, mutational frequencies ranged between 10^-5and <10^-9for levofloxacin, cefotaxime, amikacin and imipenem, and <10^-9for vancomycin and teicoplanin. When tested in combinations, mutational frequencies fell below 10^-9for all the combinations.</p> <p>Conclusion</p> <p><it>In vitro </it>evidence of synergy between glycopeptides, fluoroquinolones (levofloxacin) and β-lactams and of reduction of mutational frequencies by combinations are suggestive for a potential role in empirical therapy of severe pneumonia with suspected MRSA etiology.</p

Epstein-Barr Virus-Encoded LMP1 Interacts with FGD4 to Activate Cdc42 and Thereby Promote Migration of Nasopharyngeal Carcinoma Cells

Epstein-Barr virus (EBV) is closely associated with nasopharyngeal carcinoma (NPC), a human malignancy notorious for its highly metastatic nature. Among EBV-encoded genes, latent membrane protein 1 (LMP1) is expressed in most NPC tissues and exerts oncogenicity by engaging multiple signaling pathways in a ligand-independent manner. LMP1 expression also results in actin cytoskeleton reorganization, which modulates cell morphology and cell motility— cellular process regulated by RhoGTPases, such as Cdc42. Despite the prominent association of Cdc42 activation with tumorigenesis, the molecular basis of Cdc42 activation by LMP1 in NPC cells remains to be elucidated. Here using GST-CBD (active Cdc42-binding domain) as bait in GST pull-down assays to precipitate active Cdc42 from cell lysates, we demonstrated that LMP1 acts through its transmembrane domains to preferentially induce Cdc42 activation in various types of epithelial cells, including NPC cells. Using RNA interference combined with re-introduction experiments, we identified FGD4 (FYVE, RhoGEF and PH domain containing 4) as the GEF (guanine nucleotide exchange factor) responsible for the activation of Cdc42 by LMP1. Serial deletion experiments and co-immunoprecipitation assays further revealed that ectopically expressed FGD4 modulated LMP1-mediated Cdc42 activation by interacting with LMP1. Moreover, LMP1, through its transmembrane domains, directly bound FGD4 and enhanced FGD4 activity toward Cdc42, leading to actin cytoskeleton rearrangement and increased motility of NPC cells. Depletion of FGD4 or Cdc42 significantly reduced (∼50%) the LMP1-stimulated cell motility, an effect that was partially reversed by expression of a constitutively active mutant of Cdc42. Finally, quantitative RT-PCR and immunohistochemistry analyses showed that FGD4 and LMP1 were expressed in NPC tissues, supporting the potential physiologically relevance of this mechanism in NPC. Collectively, our results not only uncover a novel mechanism underlying LMP1-mediated Cdc42 activation, namely LMP1 interaction with FGD4, but also functionally link FGD4 to NPC tumorigenesis