Effective collision strengths for transitions in Ni XIX

Aims. In this paper we report electron impact collision strengths and excitation rates for transitions among the lowest 89 levels of Ni XIX.
Methods. The Dirac atomic R-matrix code (DARC) is adopted for the calculations of collision strengths and subsequently the effective collision strengths.
Results. Collision strengths for resonance transitions among 89 levels arising from the (1s2) 2s22p6, 2s22p53$\ell$, 2s2p63$\ell$, 2s22p54$\ell$, and 2s2p64$\ell$ configurations of Ni XIX are reported over a wide energy range below 250 Ryd. Additionally, effective collision strengths for all 3916 transitions among the 89 levels are listed over a wide temperature range below 107 K. Comparisons are made among different calculations and the accuracy of the data is assessed. Finally, comparisons between theoretical and experimental intensity ratios of some prominent lines of Ni XIX are discussed.

Effective collision strengths for inner shell transitions of Fe XVI

Collision strengths for transitions among the energetically lowest 134 levels of the (1s(2)2s(2)) 2p(6)3l, 2p(5)3s(2), 2p(5)3s3p, 2p(5)3s3d, 2p(5)3p3d and 2p(5)3d(2) configurations of Fe XVI are computed, over an electron energy range below 570 Ryd, using the Dirac atomic R-matrix code (DARC) and the flexible atomic code (FAC). All partial waves with J

Collision strengths for transitions in Ni XIX

In this paper we present calculations of electron impact excitation collision strengths for transitions among the 89 fine-structure levels of the 2S(2) 2p(,)(6) 2S(2) 2P(5) 3l, 2s(2)p(6) 3l, 2s(2) 2p(5) 4l, and 2s(2)p(6) 2l configurations of Ni XIX, for which flexible atomic code (FAC) has been adopted. Comparisons are made with the earlier available results in the literature, and the anomalies observed have been discussed.

Electron impact excitation collision strengths for neon-like Ni XIX calculated using the relativistic R-matrix method

In a recent paper [Pramana - J. Phys. 64, 129 (2005)] results have been presented for electron impact excitation collision strengths for transitions among the fine-structure levels of the 2s(2)2p(6) and 2s(2)2p(5)3s configurations of Ni XIX. In this paper we demonstrate through an independent calculation with the relativistic R-matrix code that those results are unreliable and the conclusions drawn are invalid.

'Foreign' Terror? London Bombings, Resistance and the Failing State

The British government's response to the London bombings sought to make the terror of that day foreign, even though it appeared largely domestic. This helped construct it as unusual, contingent, part of the uncontrollable ‘otherness’ of the ‘foreign’. However, it also drew the response into the arena of British foreign policy, where the ‘failing state’ has been the dominant conceptualisation of insecurity and terrorism, especially since September 11th. When the bombings are examined through the ‘failing state’ disturbing and important problems are uncovered. Primarily, the ‘failing state’ discourse deconstructs under the influence of the terrorism in London, revealing that Britain itself is a ‘failing state’ by its own description and producing a generalisation of state ‘failure’. It thereby reveals several possible sites for responding to and resisting the government's representation.

Resistance mechanisms to cancer chemotherapy

Resistance to chemotherapy ('drug resistance') is a fundamental problem that limits the effectiveness of many chemotherapies currently used to treat cancer. Drug resistance can occur due to a variety of mechanisms, such as increased drug inactivation, drug efflux from cancer cells, enhanced repair of chemotherapy-induced damage, activation of pro-survival pathways and inactivation of cell death pathways. In this article, we review some of the major mechanisms of drug resistance and discuss how new molecularly-targeted therapies are being increasingly used to overcome these resistance mechanisms.

Src and ADAM-17-Mediated Shedding of Transforming Growth Factor-alpha Is a Mechanism of Acute Resistance to TRAIL

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL/Apo-2L) has emerged as a promising anticancer agent. However, resistance to TRAIL is likely to be a major problem, and sensitization of cancer cells to TRAIL may therefore be an important anticancer strategy. In this study, we examined the effect of the epidermal growth factor receptor (EGFR)tyrosine kinase inhibitor (TKI) gefitinib and a human epidermal receptor 2 (HER2)-TKI (M578440) on the sensitivity of human colorectal cancer (CRC) cell lines to recombinant human TRAIL (rhTRAIL). A synergistic interaction between rhTRAIL and gefitinib and rhTRAIL and M578440 was observed in both rhTRAIL-sensitive and resistant CRC cells. This synergy correlated with an increase in EGFR and HER2 activation after rhTRAIL treatment. Furthermore, treatment of CRC cells with rhTRAIL resulted in activation of the Src family kinases (SFK). Importantly, we found that rhTRAIL treatment induced shedding of transforming growth factor-alpha (TGF-alpha) that was dependent on SFK activity and the protease ADAM-17. Moreover, this shedding of TGF-alpha was critical for rhTRAIL-induced activation of EGFR. In support of this, SFK inhibitors and small interfering RNAs targeting ADAM-17 and TGF-alpha also sensitized CRC cells to rhTRAIL-mediated apoptosis. Taken together, our findings indicate that both rhTRAIL-sensitive and resistant CRC cells respond to rhTRAIL treatment by activating an EGFR/HER2-mediated survival response and that these cells can be sensitized to rhTRAIL using EGFR/HER2-targeted therapies. Furthermore, this acute response to rhTRAIL is regulated by SFK-mediated and ADAM-17-mediated shedding of TGF-alpha, such that targeting SFKs or inhibiting ADAM-17, in combination with rhTRAIL, may enhance the response of CRC tumors to rhTRAIL. [Cancer Res 2008;68(20):8312-21]

Overexpression of the rhamnose catabolism regulatory protein, RhaR: a novel mechanism for metronidazole resistance in Bacteroides thetaiotaomicron

Objectives: The aim of the investigation was to use in vitro transposon mutagenesis to generate metronidazole resistance in the obligately anaerobic pathogenic bacterium Bacteroides thetaiotaomicron, and to identify the genes involved to enable investigation of potential mechanisms for the generation of metronidazole resistance.
Methods: The genes affected by the transposon insertion were identified by plasmid rescue and sequencing. Expression levels of the relevant genes were determined by semi-quantitative RNA hybridization and catabolic activity by lactate dehydrogenase/pyruvate oxidoreductase assays.
Results: A metronidazole-resistant mutant was isolated and the transposon insertion site was identified in an intergenic region between the rhaO and rhaR genes of the gene cluster involved in the uptake and catabolism of rhamnose. Metronidazole resistance was observed during growth in defined medium containing either rhamnose or glucose. The metronidazole-resistant mutant showed improved growth in the presence of rhamnose as compared with the wild-type parent. There was increased transcription of all genes of the rhamnose gene cluster in the presence of rhamnose and glucose, likely due to the transposon providing an additional promoter for the rhaR gene, encoding the positive transcriptional regulator of the rhamnose operon. The B. thetaiotaomicron metronidazole resistance phenotype was recreated by overexpressing the rhaR gene in the B. thetaiotaomicron wild-type parent. Both the metronidazole-resistant transposon mutant and RhaR overexpression strains displayed a phenotype of higher lactate dehydrogenase and lower pyruvate oxidoreductase activity in comparison with the parent strain during growth in rhamnose.
Conclusions: These data indicate that overexpression of the rhaR gene generates metronidazole resistance in B. thetaiotaomicron