Variational Quantum Fidelity Estimation

Computing quantum state fidelity will be important to verify and characterize states prepared on a quantum computer. In this work, we propose novel lower and upper bounds for the fidelity F(ρ,σ) based on the “truncated fidelity'” F(ρ_m,σ) which is evaluated for a state ρ_m obtained by projecting ρ onto its mm-largest eigenvalues. Our bounds can be refined, i.e., they tighten monotonically with mm. To compute our bounds, we introduce a hybrid quantum-classical algorithm, called Variational Quantum Fidelity Estimation, that involves three steps: (1) variationally diagonalize ρ, (2) compute matrix elements of σ in the eigenbasis of ρ, and (3) combine these matrix elements to compute our bounds. Our algorithm is aimed at the case where σ is arbitrary and ρ is low rank, which we call low-rank fidelity estimation, and we prove that no classical algorithm can efficiently solve this problem under reasonable assumptions. Finally, we demonstrate that our bounds can detect quantum phase transitions and are often tighter than previously known computable bounds for realistic situations

On quantum chosen-ciphertext attacks and learning with errors

Quantum computing is a significant threat to classical public-key cryptography. In strong “quantum access” security models, numerous symmetric-key cryptosystems are also vulnerable. We consider classical encryption in a model which grants the adversary quantum oracle access to encryption and decryption, but where the latter is restricted to non-adaptive (i.e., pre-challenge) queries only. We define this model formally using appropriate notions of ciphertext indistinguishability and semantic security (which are equivalent by standard arguments) and call it QCCA1 in analogy to the classical CCA1 security model. Using a bound on quantum random-access codes, we show that the standard PRF-based encryption schemes are QCCA1-secure when instantiated with quantum-secure primitives. We then revisit standard IND-CPA-secure Learning with Errors (LWE) encryption and show that leaking just one quantum decryption query (and no other queries or leakage of any kind) allows the adversary to recover the full secret key with constant success probability. In the classical setting, by contrast, recovering the key requires a linear number of decryption queries. The algorithm at the core of our attack is a (large-modulus version of) the well-known Bernstein-Vazirani algorithm. We emphasize that our results should not be interpreted as a weakness of these cryptosystems in their stated security setting (i.e., post-quantum chosen-plaintext secrecy). Rather, our results mean that, if these cryptosystems are exposed to chosen-ciphertext attacks (e.g., as a result of deployment in an inappropriate real-world setting) then quantum attacks are even more devastating than classical ones

On non-adaptive quantum chosen-ciphertext attacks and Learning with Errors

Large-scale quantum computing is a significant threat to classical public-key cryptography. In strong “quantum access” security models, numerous symmetric-key cryptosystems are also vulnerable. We consider classical encryption in a model which grants the adversary quantum oracle access to encryption and decryption, but where the latter is restricted to non-adaptive (i.e., pre-challenge) queries only. We define this model formally using appropriate notions of

The pseudokinase MLKL mediates programmed hepatocellular necrosis independently of RIPK3 during hepatitis

Although necrosis and necroinflammation are central features of many liver diseases, the role of programmed necrosis in the context of inflammation-dependent hepatocellular death remains to be fully determined. Here, we have demonstrated that the pseudokinase mixed lineage kinase domain-like protein (MLKL), which plays a key role in the execution of receptor interacting protein (RIP) lcinase-dependent necroptosis, is upregulated and activated in human autoimmune hepatitis and in a murine model of inflammation-dependent hepatitis. Using genetic and pharmacologic approaches, we determined that hepatocellular necrosis in experimental hepatitis is driven by an MLKL-dependent pathway that occurs independently of RIPK3. Moreover, we have provided evidence that the cytotoxic activity of the proinflammatory cytokine IFN-gamma in hepatic inflammation is strongly connected to induction of MLKL expression via activation of the transcription factor STAT1. In summary, our results reveal a pathway for MLKL-dependent programmed necrosis that is executed in the absence of RIPK3 and potentially drives the pathogenesis of severe liver diseases

Nickel-Catalyzed Conversion of Enol Triflates into Alkenyl Halides

A Ni‐catalyzed halogenation of enol triflates was developed and it enables the synthesis of a broad range of alkenyl iodides, bromides, and chlorides under mild reaction conditions. The reaction utilizes inexpensive, bench‐stable Ni(OAc)_2⋅4 H_2O as a precatalyst and proceeds at room temperature in the presence of sub‐stoichiometric Zn and either 1,5‐cyclooctadiene or 4‐(N,N‐dimethylamino)pyridine

Preanalytical variables and performance of diagnostic RNA-based gene expression analysis in breast cancer

Prognostic multigene expression assays have become widely available to provide additional information to standard clinical parameters and to support clinicians in treatment decisions. In this study, we analyzed the impact of variations in tissue handling on the diagnostic EndoPredict test results. EndoPredict is a quantitative reverse transcription PCR assay conducted on RNA from formalin-fixed, paraffin-embedded (FFPE) tissue that predicts the likelihood of distant recurrence in patients with ER-positive/HER2-negative breast cancer. In this study, we performed a total of 138 EndoPredict assays to study the effects of preanalytical variables such as time to fixation, fixation time, tumor cell content, and section storage time on the EndoPredict test results. A time to fixation of up to 12 h and fixation of up to 5 days did not affect the results of the gene expression test. Paired samples of FFPE sections with tumor cell content ranging from 15 to 95 % and tumor-enriched samples showed a correlation coefficient of 0.97. Test results of tissue sections that have been stored for 12 months at +4 or +20 °C showed a correlation of 0.99 when compared to results of nonstored sections. In conclusion, preanalytical tissue handling is not a critical factor for diagnostic gene expression analysis with the EndoPredict assay. The test can therefore be easily integrated into the standard workflow of molecular pathology

High STEAP1 expression is associated with improved outcome of Ewing's sarcoma patients

Background Ewing's sarcoma (ES) is the second most common bone or soft-tissue sarcoma in childhood and adolescence and features a high propensity to metastasize. The six-transmembrane epithelial antigen of the prostate 1 (STEAP1) is a membrane-bound mesenchymal stem cell marker highly expressed in ES. Here, we investigated the role of STEAP1 as an immunohistological marker for outcome prediction in patients with ES. Patients and methods Membranous STEAP1 immunoreactivity was analyzed using immunohistochemistry in 114 primary pre-chemotherapy ES of patients diagnosed from 1983 to 2010 and compared with clinical parameters and patient outcome. Median follow-up was 3.85 years (range 0.43-17.51). Results A total of 62.3% of the ES samples displayed detectable STEAP1 expression with predominant localization of the protein at the plasma membrane. High membranous STEAP1 immunoreactivity was found in 53.5%, which correlated with better overall survival (P=0.021). Accordingly, no or low membranous STEAP1 expression was identified as an independent risk factor in multivariate analysis (hazard ratio 2.65, P=0.036). Conclusion High membranous STEAP1 expression predicts improved outcome and may help to define a specific subgroup of ES patients, who might benefit from adapted therapy regimen

Resection of the Medial Temporal Lobe Disconnects the Rostral Superior Temporal Gyrus from Some of its Projection Targets in the Frontal Lobe and Thalamus

Auditory memory in the monkey does not appear to extend beyond the limits of working memory. It is therefore surprising that this ability is impaired by medial temporal lobe (MTL) resections, because such lesions spare working memory in other sensory modalities. To determine whether MTL ablations might have caused the auditory deficit through inadvertent transection of superior temporal gyrus (STG) projections to its downstream targets, and, if so, which targets might have been compromised, we injected anterograde tracer (biotinylated dextran amine) in the STG of both the normal and MTL-lesioned hemispheres of split-brain monkeys. Interhemispheric comparison of label failed to show any effect of the MTL ablation on efferents from caudal STG, which projects to the inferior prefrontal convexity. However, the ablation did consistently interrupt the normally dense projections from rostral STG to both the ventral medial prefrontal cortex and medial thalamic nuclei. The findings support the possibility that the auditory working memory deficit after MTL ablation is due to transection of downstream auditory projections, and indicate that the candidate structures for mediating auditory working memory are the ventral medial prefrontal cortical areas, the medial thalamus, or both