The protective effect of exercise on diabetic nephropathy : the role of histidine-containing dipeptides

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Private quantum decoupling and secure disposal of information

Given a bipartite system, correlations between its subsystems can be understood as information that each one carries about the other. In order to give a model-independent description of secure information disposal, we propose the paradigm of private quantum decoupling, corresponding to locally reducing correlations in a given bipartite quantum state without transferring them to the environment. In this framework, the concept of private local randomness naturally arises as a resource, and total correlations get divided into eliminable and ineliminable ones. We prove upper and lower bounds on the amount of ineliminable correlations present in an arbitrary bipartite state, and show that, in tripartite pure states, ineliminable correlations satisfy a monogamy constraint, making apparent their quantum nature. A relation with entanglement theory is provided by showing that ineliminable correlations constitute an entanglement parameter. In the limit of infinitely many copies of the initial state provided, we compute the regularized ineliminable correlations to be measured by the coherent information, which is thus equipped with a new operational interpretation. In particular, our results imply that two subsystems can be privately decoupled if their joint state is separable.Comment: Child of 0807.3594 v2: minor changes v3: presentation improved, one figure added v4: extended version with a lot of discussions and examples v5: published versio

Quantum Communication With Zero-Capacity Channels

Communication over a noisy quantum channel introduces errors in the transmission that must be corrected. A fundamental bound on quantum error correction is the quantum capacity, which quantifies the amount of quantum data that can be protected. We show theoretically that two quantum channels, each with a transmission capacity of zero, can have a nonzero capacity when used together. This unveils a rich structure in the theory of quantum communications, implying that the quantum capacity does not uniquely specify a channel's ability for transmitting quantum information.Comment: Final submitted versio

Dynamics of a Quantum Reference Frame

We analyze a quantum mechanical gyroscope which is modeled as a large spin and used as a reference against which to measure the angular momenta of spin-1/2 particles. These measurements induce a back-action on the reference which is the central focus of our study. We begin by deriving explicit expressions for the quantum channel representing the back-action. Then, we analyze the dynamics incurred by the reference when it is used to sequentially measure particles drawn from a fixed ensemble. We prove that the reference thermalizes with the measured particles and find that generically, the thermal state is reached in time which scales linearly with the size of the reference. This contrasts a recent conclusion of Bartlett et al. that this takes a quadratic amount of time when the particles are completely unpolarized. We now understand their result in terms of a simple physical principle based on symmetries and conservation laws. Finally, we initiate the study of the non-equilibrium dynamics of the reference. Here we find that a reference in a coherent state will essentially remain in one when measuring polarized particles, while rotating itself to ultimately align with the polarization of the particles

Precision medicine for suicidality: from universality to subtypes and personalization

Suicide remains a clear, present and increasing public health problem, despite being a potentially preventable tragedy. Its incidence is particularly high in people with overt or un(der)diagnosed psychiatric disorders. Objective and precise identification of individuals at risk, ways of monitoring response to treatments and novel preventive therapeutics need to be discovered, employed and widely deployed. We sought to investigate whether blood gene expression biomarkers for suicide (that is, a ‘liquid biopsy’ approach) can be identified that are more universal in nature, working across psychiatric diagnoses and genders, using larger cohorts than in previous studies. Such markers may reflect and/or be a proxy for the core biology of suicide. We were successful in this endeavor, using a comprehensive stepwise approach, leading to a wealth of findings. Steps 1, 2 and 3 were discovery, prioritization and validation for tracking suicidality, resulting in a Top Dozen list of candidate biomarkers comprising the top biomarkers from each step, as well as a larger list of 148 candidate biomarkers that survived Bonferroni correction in the validation step. Step 4 was testing the Top Dozen list and Bonferroni biomarker list for predictive ability for suicidal ideation (SI) and for future hospitalizations for suicidality in independent cohorts, leading to the identification of completely novel predictive biomarkers (such as CLN5 and AK2), as well as reinforcement of ours and others previous findings in the field (such as SLC4A4 and SKA2). Additionally, we examined whether subtypes of suicidality can be identified based on mental state at the time of high SI and identified four potential subtypes: high anxiety, low mood, combined and non-affective (psychotic). Such subtypes may delineate groups of individuals that are more homogenous in terms of suicidality biology and behavior. We also studied a more personalized approach, by psychiatric diagnosis and gender, with a focus on bipolar males, the highest risk group. Such a personalized approach may be more sensitive to gender differences and to the impact of psychiatric co-morbidities and medications. We compared testing the universal biomarkers in everybody versus testing by subtypes versus personalized by gender and diagnosis, and show that the subtype and personalized approaches permit enhanced precision of predictions for different universal biomarkers. In particular, LHFP appears to be a strong predictor for suicidality in males with depression. We also directly examined whether biomarkers discovered using male bipolars only are better predictors in a male bipolar independent cohort than universal biomarkers and show evidence for a possible advantage of personalization. We identified completely novel biomarkers (such as SPTBN1 and C7orf73), and reinforced previously known biomarkers (such as PTEN and SAT1). For diagnostic ability testing purposes, we also examined as predictors phenotypic measures as apps (for suicide risk (CFI-S, Convergent Functional Information for Suicidality) and for anxiety and mood (SASS, Simplified Affective State Scale)) by themselves, as well as in combination with the top biomarkers (the combination being our a priori primary endpoint), to provide context and enhance precision of predictions. We obtained area under the curves of 90% for SI and 77% for future hospitalizations in independent cohorts. Step 5 was to look for mechanistic understanding, starting with examining evidence for the Top Dozen and Bonferroni biomarkers for involvement in other psychiatric and non-psychiatric disorders, as a mechanism for biological predisposition and vulnerability. The biomarkers we identified also provide a window towards understanding the biology of suicide, implicating biological pathways related to neurogenesis, programmed cell death and insulin signaling from the universal biomarkers, as well as mTOR signaling from the male bipolar biomarkers. In particular, HTR2A increase coupled with ARRB1 and GSK3B decreases in expression in suicidality may provide a synergistic mechanistical corrective target, as do SLC4A4 increase coupled with AHCYL1 and AHCYL2 decrease. Step 6 was to move beyond diagnostics and mechanistical risk assessment, towards providing a foundation for personalized therapeutics. Items scored positive in the CFI-S and subtypes identified by SASS in different individuals provide targets for personalized (psycho)therapy. Some individual biomarkers are targets of existing drugs used to treat mood disorders and suicidality (lithium, clozapine and omega-3 fatty acids), providing a means toward pharmacogenomics stratification of patients and monitoring of response to treatment. Such biomarkers merit evaluation in clinical trials. Bioinformatics drug repurposing analyses with the gene expression biosignatures of the Top Dozen and Bonferroni-validated universal biomarkers identified novel potential therapeutics for suicidality, such as ebselen (a lithium mimetic), piracetam (a nootropic), chlorogenic acid (a polyphenol) and metformin (an antidiabetic and possible longevity promoting drug). Finally, based on the totality of our data and of the evidence in the field to date, a convergent functional evidence score prioritizing biomarkers that have all around evidence (track suicidality, predict it, are reflective of biological predisposition and are potential drug targets) brought to the fore APOE and IL6 from among the universal biomarkers, suggesting an inflammatory/accelerated aging component that may be a targetable common denominator

CsA, FK506, corticosteroids and rapamycin inhibit TNFα production by cultured PTEC

CsA, FK506, corticosteroids and rapamycin inhibit TNFα production by PTEC. In this study we investigated the effect of immunosuppressive drugs on the interleukin-1 alpha (IL-1α) enhanced tumor necrosis factor alpha (TNFα) production by proximal tubular epithelial cells (PTEC). Under basal conditions cultured PTEC produce between 0 to 390 pg/ml/105 cells of TNFα. Upon stimulation with IL-1α an enhancement of TNFα production was seen in each cell line tested, ranging from 230 to 2424 pg/ml/105 cells. The presence of cyclosporin A (CsA) during stimulation with IL-1α inhibited the enhanced TNFα production in a dose dependent fashion, with a maximal inhibition of 90% at a concentration of 250 ng/ml. Inhibition was at the level of mRNA as could be demonstrated by Northern blot analysis. FK506, corticosteroids and rapamycin also inhibited TNFa production in a dose dependent fashion, although not as effectively as CsA. Two corticosteroids were tested for their inhibitory effect on TNFa production. It was found that dexamethasone at a concentration of 10 ng/ml inhibited TNFα production for almost 40%. A 100-fold higher concentration of hydrocortisone was necessary to yield similar inhibition. The effect of rapamycin on the IL-1α enhanced TNFα production differed from the effect of CsA. While CsA induced a maximal inhibition of 90%, rapamycin only induced a maximal inhibition of 37%, and even less inhibition at higher concentrations of the drug. The presence of the various drugs was essential for their inhibitory effect, because removal of the drug from the PTEC by washing immediately resulted in loss of inhibition. Combinations of CsA and FK506 or rapamycin were not additive. However, combinations of rapamycin and FK506 were antagonistic when low concentrations of rapamycin and FK506 were used. Low concentrations of rapamycin with high concentrations of FK506 were synergistic. Since TNFα is likely to be an important mediator in renal allograft rejection, these data suggest that the beneficial effect of immunosuppressive drugs after renal transplantation may partly be due to the effect on TNFα production by renal parenchymal cells

Quantum capacity under adversarial quantum noise: arbitrarily varying quantum channels

We investigate entanglement transmission over an unknown channel in the presence of a third party (called the adversary), which is enabled to choose the channel from a given set of memoryless but non-stationary channels without informing the legitimate sender and receiver about the particular choice that he made. This channel model is called arbitrarily varying quantum channel (AVQC). We derive a quantum version of Ahlswede's dichotomy for classical arbitrarily varying channels. This includes a regularized formula for the common randomness-assisted capacity for entanglement transmission of an AVQC. Quite surprisingly and in contrast to the classical analog of the problem involving the maximal and average error probability, we find that the capacity for entanglement transmission of an AVQC always equals its strong subspace transmission capacity. These results are accompanied by different notions of symmetrizability (zero-capacity conditions) as well as by conditions for an AVQC to have a capacity described by a single-letter formula. In he final part of the paper the capacity of the erasure-AVQC is computed and some light shed on the connection between AVQCs and zero-error capacities. Additionally, we show by entirely elementary and operational arguments motivated by the theory of AVQCs that the quantum, classical, and entanglement-assisted zero-error capacities of quantum channels are generically zero and are discontinuous at every positivity point.Comment: 49 pages, no figures, final version of our papers arXiv:1010.0418v2 and arXiv:1010.0418. Published "Online First" in Communications in Mathematical Physics, 201