Revisiting Deniability in Quantum Key Exchange via Covert Communication and Entanglement Distillation

We revisit the notion of deniability in quantum key exchange (QKE), a topic that remains largely unexplored. In the only work on this subject by Donald Beaver, it is argued that QKE is not necessarily deniable due to an eavesdropping attack that limits key equivocation. We provide more insight into the nature of this attack and how it extends to other constructions such as QKE obtained from uncloneable encryption. We then adopt the framework for quantum authenticated key exchange, developed by Mosca et al., and extend it to introduce the notion of coercer-deniable QKE, formalized in terms of the indistinguishability of real and fake coercer views. Next, we apply results from a recent work by Arrazola and Scarani on covert quantum communication to establish a connection between covert QKE and deniability. We propose DC-QKE, a simple deniable covert QKE protocol, and prove its deniability via a reduction to the security of covert QKE. Finally, we consider how entanglement distillation can be used to enable information-theoretically deniable protocols for QKE and tasks beyond key exchange.Comment: 16 pages, published in the proceedings of NordSec 201

Increased mitochondrial calcium levels associated with neuronal death in a mouse model of Alzheimer's disease

Mitochondria contribute to shape intraneuronal Ca2+ signals. Excessive Ca2+ taken up by mitochondria could lead to cell death. Amyloid beta (A beta) causes cytosolic Ca2+ overload, but the effects of A beta on mitochondrial Ca2+ levels in Alzheimer's disease (AD) remain unclear. Using a ratiometric Ca2+ indicator targeted to neuronal mitochondria and intravital multiphoton microscopy, we find increased mitochondrial Ca2+ levels associated with plaque deposition and neuronal death in a transgenic mouse model of cerebral beta -amyloidosis. Naturally secreted soluble A beta applied onto the healthy brain increases Ca2+ concentration in mitochondria, which is prevented by blockage of the mitochondrial calcium uniporter. RNA-sequencing from post-mortem AD human brains shows downregulation in the expression of mitochondrial influx Ca2+ transporter genes, but upregulation in the genes related to mitochondrial Ca2+ efflux pathways, suggesting a counteracting effect to avoid Ca2+ overload. We propose lowering neuronal mitochondrial Ca2+ by inhibiting the mitochondrial Ca2+ uniporter as a novel potential therapeutic target against AD. Calvo-Rodriguez et al. show elevated calcium levels in neuronal mitochondria in a mouse model of cerebral beta -amyloidosis after plaque deposition, which precede rare neuron death events in this model. The mechanism involves toxic extracellular A beta oligomers and the mitochondrial calcium uniporter

Revisiting Deniability in Quantum Key Exchange via Covert Communication and Entanglement Distillation

We revisit the notion of deniability in quantum key exchange (QKE), a topic that remains largely unexplored. In the only work on this subject by Donald Beaver, it is argued that QKE is not necessarily deniable due to an eavesdropping attack that limits key equivocation. We provide more insight into the nature of this attack and how it extends to other constructions such as QKE obtained from uncloneable encryption. We then adopt the framework for quantum authenticated key exchange, developed by Mosca et al., and extend it to introduce the notion of coercer-deniable QKE, formalized in terms of the indistinguishability of real and fake coercer views. Next, we apply results from a recent work by Arrazola and Scarani on covert quantum communication to establish a connection between covert QKE and deniability. We propose DC-QKE, a simple deniable covert QKE protocol, and prove its deniability via a reduction to the security of covert QKE. Finally, we consider how entanglement distillation can be used to enable information-theoretically deniable protocols for QKE and tasks beyond key exchange

Clinical standards for the dosing and management of TB drugs

BACKGROUND: Optimal drug dosing is important to ensure adequate response to treatment, prevent development of drug resistance and reduce drug toxicity. The aim of these clinical standards is to provide guidance on 'best practice´ for dosing and management of TB drugs.METHODS: A panel of 57 global experts in the fields of microbiology, pharmacology and TB care were identified; 51 participated in a Delphi process. A 5-point Likert scale was used to score draft standards. The final document represents the broad consensus and was approved by all participants.RESULTS: Six clinical standards were defined: Standard 1, defining the most appropriate initial dose for TB treatment; Standard 2, identifying patients who may be at risk of sub-optimal drug exposure; Standard 3, identifying patients at risk of developing drug-related toxicity and how best to manage this risk; Standard 4, identifying patients who can benefit from therapeutic drug monitoring (TDM); Standard 5, highlighting education and counselling that should be provided to people initiating TB treatment; and Standard 6, providing essential education for healthcare professionals. In addition, consensus research priorities were identified.CONCLUSION: This is the first consensus-based Clinical Standards for the dosing and management of TB drugs to guide clinicians and programme managers in planning and implementation of locally appropriate measures for optimal person-centred treatment to improve patient care