Invisible Trojan-horse attack

We demonstrate the experimental feasibility of a Trojan-horse attack that remains nearly invisible to the single-photon detectors employed in practical quantum key distribution (QKD) systems, such as Clavis2 from ID Quantique. We perform a detailed numerical comparison of the attack performance against Scarani-Acin-Ribordy-Gisin (SARG04) QKD protocol at 1924nm versus that at 1536nm. The attack strategy was proposed earlier but found to be unsuccessful at the latter wavelength, as reported in N.~Jain et al., New J. Phys. 16, 123030 (2014). However at 1924nm, we show experimentally that the noise response of the detectors to bright pulses is greatly reduced, and show by modeling that the same attack will succeed. The invisible nature of the attack poses a threat to the security of practical QKD if proper countermeasures are not adopted.Comment: 8 pages, 3 figures, due to problem in the compilation of bibliography, we are uploading a corrected versio

Creation of backdoors in quantum communications via laser damage

Practical quantum communication (QC) protocols are assumed to be secure provided implemented devices are properly characterized and all known side channels are closed. We show that this is not always true. We demonstrate a laser-damage attack capable of modifying device behaviour on-demand. We test it on two practical QC systems for key distribution and coin-tossing, and show that newly created deviations lead to side channels. This reveals that laser damage is a potential security risk to existing QC systems, and necessitates their testing to guarantee security.Comment: Changed the title to match the journal version. 9 pages, 5 figure

Publisher Correction: Invisible Trojan-horse attack

A correction to this article has been published and is linked from the HTML version of this paper. The error has been fixed in the paper

A three-in-one-bullet for oesophageal cancer: Replication fork collapse, spindle attachment failure and enhanced radiosensitivity generated by a ruthenium(II) metallo-intercalator

Substitutionally inert ruthenium(II) polypyridyl complexes have been developed as DNA intercalating agents yet cellular DNA damage responses to this binding modality are largely unexplored. Here, we show the nuclear-targeting complex [Ru(phen)2(tpphz)]2+ (phen = 1,10-phenanthroline, tpphz = tetrapyridophenazine) generates rapid and pronounced stalling of replication fork progression in p53-deficient human oesophageal cancer cells. In response, replication stress and double-strand break (DSB) DNA damage response (DDR) pathways are activated and cell proliferation is inhibited by growth arrest. Moreover, mitotic progression is compromised by [Ru(phen)2(tpphz)]2+, where the generation of metaphase chromosome spindle attachment failure results in spindle assembly checkpoint (SAC) activation. This dual mechanism of action results in preferential growth inhibition of rapidly-proliferating oesophageal cancer cells with elevated mitotic indices. In addition to these single-agent effects, [Ru(phen)2(tpphz)]2+ functions as a radiosensitizer with efficiency comparable to cisplatin, which occurs through a synergistic enhancement of DNA damage. These results establish that DNA replication is the target for [Ru(phen)2(tpphz)]2+ and provide the first experimental evidence that ruthenium-based intercalation targets multiple genome integrity pathways in cancer cells, thereby achieving enhanced selectivity compared to existing DNA-damaging agents such as cisplatin

Recombining Low Homology, Functionally Rich Regions of Bacterial Subtilisins by Combinatorial Fragment Exchange

Combinatorial fragment exchange was utilised to recombine key structural and functional low homology regions of bacilli subtilisins to generate new active hybrid proteases with altered substrate profiles. Up to six different regions comprising mostly of loop residues from the commercially important subtilisin Savinase were exchanged with the structurally equivalent regions of six other subtilisins. The six additional subtilisins derive from diverse origins and included thermophilic and intracellular subtilisins as well as other academically and commercially relevant subtilisins. Savinase was largely tolerant to fragment exchange; rational replacement of all six regions with 5 of 6 donating subtilisin sequences preserved activity, albeit reduced compared to Savinase. A combinatorial approach was used to generate hybrid Savinase variants in which the sequences derived from all seven subtilisins at each region were recombined to generate new region combinations. Variants with different substrate profiles and with greater apparent activity compared to Savinase and the rational fragment exchange variants were generated with the substrate profile exhibited by variants dependent on the sequence combination at each region