Quantum Eavesdropping without Interception: An Attack Exploiting the Dead Time of Single Photon Detectors

The security of quantum key distribution (QKD) can easily be obscured if the eavesdropper can utilize technical imperfections of the actual implementation. Here we describe and experimentally demonstrate a very simple but highly effective attack which even does not need to intercept the quantum channel at all. Only by exploiting the dead time effect of single photon detectors the eavesdropper is able to gain (asymptotically) full information about the generated keys without being detected by state-of-the-art QKD protocols. In our experiment, the eavesdropper inferred up to 98.8% of the key correctly, without increasing the bit error rate between Alice and Bob significantly. Yet, we find an evenly simple and effective countermeasure to inhibit this and similar attacks

Controlling a superconducting nanowire single-photon detector using tailored bright illumination

We experimentally demonstrate that a superconducting nanowire single-photon detector is deterministically controllable by bright illumination. We found that bright light can temporarily make a large fraction of the nanowire length normally-conductive, can extend deadtime after a normal photon detection, and can cause a hotspot formation during the deadtime with a highly nonlinear sensitivity. In result, although based on different physics, the superconducting detector turns out to be controllable by virtually the same techniques as avalanche photodiode detectors. As demonstrated earlier, when such detectors are used in a quantum key distribution system, this allows an eavesdropper to launch a detector control attack to capture the full secret key without being revealed by to many errors in the key.Comment: Expanded discussions, updated references. 9 pages, 8 figure

Pyruvate kinase M2 activation may protect against the progression of diabetic glomerular pathology and mitochondrial dysfunction

Diabetic nephropathy (DN) is a major cause of end-stage renal disease, and therapeutic options for preventing its progression are limited. To identify novel therapeutic strategies, we studied protective factors for DN using proteomics on glomeruli from individuals with extreme duration of diabetes (≥ 50 years) without DN and those with histologic signs of DN. Enzymes in the glycolytic, sorbitol, methylglyoxal and mitochondrial pathways were elevated in individuals without DN. In particular, pyruvate kinase M2 (PKM2) expression and activity were upregulated. Mechanistically, we showed that hyperglycemia and diabetes decreased PKM2 tetramer formation and activity by sulfenylation in mouse glomeruli and cultured podocytes. Pkm-knockdown immortalized mouse podocytes had higher levels of toxic glucose metabolites, mitochondrial dysfunction and apoptosis. Podocyte-specific Pkm2-knockout (KO) mice with diabetes developed worse albuminuria and glomerular pathology. Conversely, we found that pharmacological activation of PKM2 by a small-molecule PKM2 activator, TEPP-46, reversed hyperglycemia-induced elevation in toxic glucose metabolites and mitochondrial dysfunction, partially by increasing glycolytic flux and PGC-1α mRNA in cultured podocytes. In intervention studies using DBA2/J and Nos3 (eNos) KO mouse models of diabetes, TEPP-46 treatment reversed metabolic abnormalities, mitochondrial dysfunction and kidney pathology. Thus, PKM2 activation may protect against DN by increasing glucose metabolic flux, inhibiting the production of toxic glucose metabolites and inducing mitochondrial biogenesis to restore mitochondrial function

Memory-assisted measurement-device-independent quantum key distribution

A protocol with the potential of beating the existing distance records for conventional quantum key distribution (QKD) systems is proposed. It borrows ideas from quantum repeaters by using memories in the middle of the link, and that of measurement-device-independent QKD, which only requires optical source equipment at the users end. For certain memories with short access times, our scheme allows a higher repetition rate than that of quantum repeaters with single-mode memories, thereby requiring lower coherence times. By accounting for various sources of nonideality, such as memory decoherence, dark counts, misalignment errors, and background noise, as well as timing issues with memories, we develop a mathematical framework within which we can compare QKD systems with and without memories. In particular, we show that with the state-of-the-art technology for quantum memories, it is potentially possible to devise memory-assisted QKD systems that, at certain distances of practical interest, outperform current QKD implementations

Quantum key distribution with hacking countermeasures and long term field trial

Quantum key distribution's (QKD's) central and unique claim is information theoretic security. However there is an increasing understanding that the security of a QKD system relies not only on theoretical security proofs, but also on how closely the physical system matches the theoretical models and prevents attacks due to discrepancies. These side channel or hacking attacks exploit physical devices which do not necessarily behave precisely as the theory expects. As such there is a need for QKD systems to be demonstrated to provide security both in the theoretical and physical implementation. We report here a QKD system designed with this goal in mind, providing a more resilient target against possible hacking attacks including Trojan horse, detector blinding, phase randomisation and photon number splitting attacks. The QKD system was installed into a 45 km link of a metropolitan telecom network for a 2.5 month period, during which time the system operated continuously and distributed 1.33 Tbits of secure key data with a stable secure key rate over 200 kbit/s. In addition security is demonstrated against coherent attacks that are more general than the collective class of attacks usually considered

The renal cortical fibroblast in renal tubulointerstitial fibrosis

Renal cortical fibroblasts have key roles in mediating intercellular communication with neighboring/infiltrating cells and extracellular matrix (ECM) and maintenance of renal tissue architecture. They express a variety of cytokines, chemokines, growth factors and cell adhesion molecules, playing an active role in paracrine and autocrine interactions and regulating both fibrogenesis and the interstitial inflammatory response. They additionally have an endocrine function in the production of epoetin. Tubulointerstitial fibrosis, the common pathological consequence of renal injury, is characterized by the accumulation of extracellular matrix largely due to excessive production in parallel with reduced degradation, and activated fibroblasts characterized by a myofibroblastic phenotype. Fibroblasts in the kidney may derive from resident fibroblasts, from the circulating fibroblast population or from haemopoetic progenitor or stromal cells derived from the bone marrow. Cells exhibiting a myofibroblastic phenotype may derive from these sources and from tubular cells undergoing epithelial to mesenchymal transformation in response to renal injury. The number of interstitial myofibroblasts correlates closely with tubulointerstitial fibrosis and progressive renal failure. Hence inhibiting myofibroblast formation may be an effective strategy in attenuating the development of renal failure in kidney disease of diverse etiology. (c) 2005 Elsevier Ltd. All rights reserved