Miracle-dz/UniFAR-FTUs huggingface dataset:
Extendibility limits the performance of quantum processors

Resource theories in quantum information science are helpful for the study and quantification of the performance of information-processing tasks that involve quantum systems. These resource theories also find applications in other areas of study; e.g., the resource theories of entanglement and coherence have found use and implications in the study of quantum thermodynamics and memory effects in quantum dynamics. In this paper, we introduce the resource theory of unextendibility, which is associated with the inability of extending quantum entanglement in a given quantum state to multiple parties. The free states in this resource theory are the k-extendible states, and the free channels are k-extendible channels, which preserve the class of k-extendible states. We make use of this resource theory to derive nonasymptotic, upper bounds on the rate at which quantum communication or entanglement preservation is possible by utilizing an arbitrary quantum channel a finite number of times, along with the assistance of k-extendible channels at no cost. We then show that the bounds obtained are significantly tighter than previously known bounds for quantum communication over both the depolarizing and erasure channels.
1 VIEWS OF ECONOMIC INEQUALITY IN LATIN AMERICA

We assess the factors that affect judgments about the fairness of the distribution of wealth with pooled public opinion data from Latinobarometro surveys conducted in 1997, 2001, and 2002. We test hypotheses with a multilevel logit model that allows us not only to examine the effects of the class background and perceptions of individual respondents, but also to assess the impact of societal-level differences in economic growth, GDP per capita, income concentration, and the availability of information. Examining the direct and conditional effects of these societallevel factors, we find support for relative deprivation approaches, but much more limited evidence for hypotheses derived from distributive conflict and development theories.
Probabilistic Multiple-Bias Modeling Applied to the Canadian Data From the Interphone Study of Mobile Phone Use and Risk of Glioma, Meningioma, Acoustic Neuroma, and Parotid Gland Tumors

We undertook a re-analysis of the Canadian data from the 13-country case-control Interphone Study (2001-2004), in which researchers evaluated the associations of mobile phone use with the risks of brain, acoustic neuroma, and parotid gland tumors. In the main publication of the multinational Interphone Study, investigators concluded that biases and errors prevented a causal interpretation. We applied a probabilistic multiple-bias model to address possible biases simultaneously, using validation data from billing records and nonparticipant questionnaires as information on recall error and selective participation. In our modeling, we sought to adjust for these sources of uncertainty and to facilitate interpretation. For glioma, when comparing those in the highest quartile of use (>558 lifetime hours) to those who were not regular users, the odds ratio was 2.0 (95% confidence interval: 1.2, 3.4). After adjustment for selection and recall biases, the odds ratio was 2.2 (95% limits: 1.3, 4.1). There was little evidence of an increase in the risk of meningioma, acoustic neuroma, or parotid gland tumors in relation to mobile phone use. Adjustments for selection and recall biases did not materially affect interpretation in our results from Canadian data.
Distinct prognostic roles and heterogeneity of TTF1 copy number and TTF1 protein expression in non‐small cell lung cancer

Thyroid transcription factor 1 (TTF1) located on chromosome band 14q13.3 is an oncogene and a suppressor gene in non‐small cell lung cancer (NSCLC). The prognostic relevance of TTF1 copy number alterations (CNAs) and their association with TTF1 protein expression are poorly understood. Here, we assessed TTF1 CNAs and protein expression using microarrays in a cohort of 636 NSCLC, including 423 adenocarcinoma (ADC) and 171 squamous cell carcinoma (SCC). In addition, fluorescent in situ hybridization and immunohistochemistry were performed. TTF1 CNAs were detected in 23% of NSCLC (23% of ADC and 20% of SCC). Specifically, TTF1 amplification and polysomy were observed in 5% and 18% of NSCLC, and in 7% and 16% of ADC, respectively. TTF1 expression was detected in 85% of ADC. TTF1 CNAs were significantly associated with advanced tumor stage, EGFR mutations, and TTF1 expression. A multivariate Cox hazards model analysis of overall survival and recurrence‐free survival demonstrated that both TTF1 amplification and polysomy were independent indicators of an unfavorable prognosis in patients with NSCLC. Survival was inversely correlated with TTF1 copy number. In contrast, TTF1 protein expression was an independent favorable prognostic factor. Intratumoral and intertumoral heterogeneities of TTF1 CNAs and TTF1 protein expression were assessed using primary cores from 138 pairs of primary tumors and corresponding nodal metastases. The concordance rate for TTF1 CNAs and TTF1 protein expression was high within tumors and between primary and metastatic tumors. Altogether, these results suggest that TTF1 CNAs are correlated with TTF1 protein expression, but have opposing effects on survival.
Fat accretion and the regulation of insulin-mediated glycogen synthesis after puberty in rats.

Peripheral insulin sensitivity decreases after puberty in both humans and rodents and can be explained mostly by a reduction in insulin-mediated glycogen synthesis. We tested the hypothesis that the increase in postpubertal fat mass (FM), reflecting an alternative energy store, regulates a decrease in the capacity to store muscle glycogen. We studied Sprague-Dawley rats ( n = 21) before puberty (Pre) or after puberty (at 4 mo of age) in groups that were either ad libitum fed (Post) or moderately caloric restricted (CR). FM (by3H2O isotope dilution technique) was decreased by >40% in CR compared with Post. Glucose uptake (Rd, by 18 mU ⋅ kg-1 ⋅ min-1hyperinsulinemic clamp) was 63 ± 8 mg ⋅ kg-1 ⋅ min-1in Pre and decreased to 39 ± 2 mg ⋅ kg-1 ⋅ min-1in Post ( P < 0.001). However, it increased in CR to 53 ± 2 mg ⋅ kg-1 ⋅ min-1( P < 0.001 vs. Post). This increase in Rd was mainly accounted for by an increase in glycogen synthesis (Rd glycolysis determined by the rate of conversion of 3H-labeled glucose to3H2O) from 23 ± 2 in Post to 33 ± 2 mg ⋅ kg-1 ⋅ min-1in CR ( P < 0.001; 38 ± 7 mg ⋅ kg-1 ⋅ min-1 in Pre). Correction of glycogen synthesis in CR to near-prepubertal levels was further supported by directly assayed muscle glycogen content after insulin stimulation that was 45% higher and by a 35% enhanced accumulation of [3H]glucose into glycogen. No changes in the enzyme kinetics of glycogen synthase or phosphorylase were observed. An additional group of 2-mo-old postpubertal ad libitum-fed rats was matched with CR for lean body mass but had more FM. This group demonstrated 25% lower rates of insulin-mediated glycogen synthesis compared with CR, further supporting the notion that a moderate reduction of FM prevents the decline in insulin responsiveness and glycogen synthesis occurring after puberty. These data suggest a cause-effect relationship between the increased deposition of fat and the reduced ability to store glucose in skeletal muscle after puberty.
Predictors of retention in care in HIV-infected patients in a large hospital cohort in Italy

Abstract Retention in care is a key feature of the cascade of continuum of care, playing an important role in achieving therapeutic success and being crucial for reduction of HIV transmission. The aim of this study was to evaluate the rate of retention in care in a large referral centre in the North of Italy and to identify predictors associated with failed retention. All new HIV-infected subjects were consecutive enrolled from 1 January 2008 to 31 December 2014. Demographics, immune-virological status, hepatitis co-infection and timing of initiation of combined antiretroviral therapy (cART) data were collected at baseline and at the time of last observation. Failed retention in care was defined as lack of laboratory data, clinical visits and drug dispensation for more than 6 months from the last visit. Cox regression analysis was used. Multivariate analysis of variables with P<0.05 in univariate analysis was performed. We enrolled 269 patients (mean age 46.1 years). Males were 197 (73%), Italian 219 (81%) with mean length of disease of 5.1 years. cART was prescribed for 257 patients (95%). The rate of retention in care was 78.4% and the rate of virological suppression was 75%. Predictors of being loss to follow-up were foreign origin (P = 0.048), CD4+ count <200/mmc (P = 0.001) and not being treated for HIV infection (P = 0.0004). Predictors of cART efficacy were shorter duration of HIV infection and baseline HIV-RNA <100 000 copies/ml. These findings underline the necessity to improve retention in care by identifying groups at increased risk of being loss to follow-up. Retention in care of vulnerable population is crucial to reach 90-90-90 UNAIDS endpoint.
Supramolecular Control over the Interparticle Distance in Gold Nanoparticle Arrays by Cyclodextrin Polyrotaxanes

Amphiphilic nonionic ligands, synthesized with a fixed hydrophobic moiety formed by a thiolated alkyl chain and an aromatic ring, and with a hydrophilic tail composed of a variable number of oxyethylene units, were used to functionalize spherical gold nanoparticles (AuNPs) in water. Steady-state and time-resolved fluorescence measurements of the AuNPs in the presence of α-cyclodextrin (α-CD) revealed the formation of supramolecular complexes between the ligand and macrocycle at the surface of the nanocrystals. The addition of α-CD induced the formation of inclusion complexes with a high apparent binding constant that decreased with the increasing oxyethylene chain length. The formation of polyrotaxanes at the surface of AuNPs, in which many α-CDs are trapped as hosts on the long and linear ligands, was demonstrated by the formation of large and homogeneous arrays of self-assembled AuNPs with hexagonal close packing, where the interparticle distance increased with the length of the oxyethylene chain. The estimated number of α-CDs per polyrotaxane suggests a high rigidization of the ligand upon complexation, allowing for nearly perfect control of the interparticle distance in the arrays. This degree of supramolecular control was extended to arrays formed by AuNPs stabilized with polyethylene glycol and even to binary arrays. Electromagnetic simulations showed that the enhancement and distribution of the electric field can be finely controlled in these plasmonic arrays.
Urinary Levels of IL-1β and GDNF in Preterm Neonates as Potential Biomarkers of Motor Development: A Prospective Study

Objectives. To evaluate the association between inflammatory biomarkers, neurotrophic factors, birth conditions, and the presence of motor development abnormalities in preterm neonates. Methods. Plasma and urinary levels of cytokines (IL-1β, IL-6, IL-10, TNF, and IL-12p70), chemokines (CXCL8/IL-8, CCL2/MCP-1, CCL5/RANTES, CXCL10/IP-10, and CXCL9/MIG), and neurotrophic factors (BDNF and GDNF) were evaluated in 40 preterm neonates born between 28 and 32 incomplete weeks of gestation, at four distinct time points: at birth (umbilical cord blood) (T0), at 48 (T1), at 72 hours (T2), and at 3 weeks after birth (T3). Biomarkers levels were compared between different time points and then associated with Test of Infant Motor Performance (TIMP) percentiles. Results. Maternal age, plasma, and urinary concentrations of inflammatory molecules and neurotrophic factors were significantly different between groups with normal versus lower than expected motor development. Higher levels of GDNF were found in the group with lower than expected motor development, while IL-1β and CXCL8/IL-8 values were higher in the group with typical motor development. Conclusion. Measurements of cytokines and neurotrophic factors in spot urine may be useful in the follow-up of motor development in preterm neonates.
Natural Compounds from Herbs that can Potentially Execute as Autophagy Inducers for Cancer Therapy

Accumulated evidence indicates that autophagy is a response of cancer cells to various anti-cancer therapies. Autophagy is designated as programmed cell death type II, and is characterized by the formation of autophagic vacuoles in the cytoplasm. Numerous herbs, including Chinese herbs, have been applied to cancer treatments as complementary and alternative medicines, supplements, or nutraceuticals to dampen the side or adverse effects of chemotherapy drugs. Moreover, the tumor suppressive actions of herbs and natural products induced autophagy that may lead to cell senescence, increase apoptosis-independent cell death or complement apoptotic processes. Hereby, the underlying mechanisms of natural autophagy inducers are cautiously reviewed in this article. Additionally, three natural compounds—curcumin, 16-hydroxycleroda-3,13-dien-15,16-olide, and prodigiosin—are presented as candidates for autophagy inducers that can trigger cell death in a supplement or alternative medicine for cancer therapy. Despite recent advancements in therapeutic drugs or agents of natural products in several cancers, it warrants further investigation in preclinical and clinical studies.
High extracellular glucose impairs cardiac E-C coupling in a glycosylation-dependent manner.

Hyperglycemia is a major manifestation of all forms of diabetes mellitus and is associated with increased risk of cardiovascular disease. It is well established that cardiac excitation-contraction (E-C) coupling is adversely affected in diabetic animals such that ventricular myocyte action potential duration is prolonged and intracellular Ca2+clearing and mechanical relaxation are slowed. We now report that ventricular myocytes incubated in a culture medium containing high extracellular glucose (25.5 mM) also exhibit these same changes in E-C coupling. These effects are not manifested for ∼24 h after exposure. Furthermore, in the presence of normal glucose (5.5 mM), relaxation is also prolonged by fructose (20 mM), yet is unaffected by equimolar concentrations of nonmetabolizable sugars such as l-glucose and mannitol, implying that the high glucose effects require glucose entry into the cell and metabolic processing. The prolonged relaxation can also be produced by 5 mM glucosamine (an intermediate of glycosylation) and is blocked by 0.5 μg/ml tunicamycin (an inhibitor of N-linked glycoprotein synthesis). Culturing myocytes with an inhibitor of glycation (10 mM aminoguanidine) does not prevent the high extracellular glucose concentration effects. Thus our data indicate that high extracellular glucose impairs cellular mechanisms contributing to myocardial relaxation and that this impairment may involve glycosylation of nascent proteins.
Blood pressure and heart rate variability in early pregnancy in rats.

Changes in the autonomic control of the circulation may contribute to the maternal hemodynamic adaptation to early pregnancy. To evaluate this, we studied mean arterial pressure (MAP) and heart rate (HR) in chronically instrumented, conscious rats in early ( days 4, 6, 8, and 10) and late ( day 18) pregnancy ( n = 8) and in nonpregnant rats ( n = 9). MAP and HR were recorded on a beat-to-beat basis and analyzed by spectral analysis. Spectral density power was calculated in low- (0.047-0.305 Hz), mid- (0.305-0.598 Hz), and high-frequency (0.598-1.494 Hz) bands, which contain oscillations that are among others related to myogenic-, sympathetic/vagal-, and vagal/respiration-related influences, respectively. In addition, baroreceptor reflex sensitivity was determined from spontaneous variations in MAP and HR by a sequential time series method and by calculating the transfer gain between MAP and HR in the midfrequency band. Mean values of HR and MAP did not differ between the two groups on day 4. In the pregnant group, MAP fell gradually over days, whereas HR had significantly increased only on day 18. Overall variability in MAP and HR (expressed as coefficients of variation) did not change during pregnancy. Baroreceptor reflex sensitivity did not differ between the groups and did not change with advancing pregnancy. Spontaneous oscillations of MAP and HR at low, mid, and high frequencies were not different between pregnant and nonpregnant rats on days 4 to 10. On day 18, spectral density power of MAP, but not of HR, in the high-frequency band had significantly increased in pregnant rats only, most likely reflecting the increased impact of breathing on MAP fluctuations. We conclude that, with the methods employed, we could not discern any changes in baroreflex sensitivity and MAP and HR variability in pregnancy. This would imply that changes in autonomic activity do not contribute appreciably to the hemodynamic adaptations in early rat pregnancy.
Fast Detection and Removal of Glare in Gray Scale Laparoscopic Images

Images captured by laparoscopic cameras, often suffer from glare due to specular reflections from surgical tools and some tissue surfaces that can disturb the attention of surgeon. In this paper, inspired by their form, the photometric distortions caused by specular reflections are modeled as the superposition of a smooth and a pulse shaped curve. Based on this model a new fast technique for the detection and removal of glare in gray scale laparoscopic images is proposed. The proposed technique, as well as other state of the art image inpainting algorithms are used in a number of experiments based on artificial and real laparoscopic data, and the proposed algorithm seems to outperform its rivals.
Activin A inhibition attenuates sympathetic neural remodeling following myocardial infarction in rats

Inflammation serves a critical role in driving sympathetic neural remodeling following myocardial infarction (MI), and activin A has been implicated as an important mediator of the inflammatory response post-MI. However, whether activin A impacts sympathetic neural remodeling post-MI remains unclear. In the present study, the authors assessed the effects of activin A on sympathetic neural remodeling in a rat model of MI. Rats were randomly divided into sham, MI, and MI + follistatin-300 (FS, activin A inhibitor) groups. Cardiac tissues from the peri-infarct zone were assessed for expression of sympathetic neural remodeling and inflammatory factors in rats 4 weeks post-MI by western blotting and immunohistochemical methods. Heart function was assessed by echocardiography. It is demonstrated that FS administration significantly reduced post-MI upregulation of activin A, nerve growth factor protein lever, and the density of nerve fibers with positive and protein expression of sympathetic neural remodeling markers in nerve fibers, which included growth associated protein 43 and tyrosine hydroxylase. In addition, inhibition of activin A reduced cardiac inflammation post-MI based on the reduction of i) interleukin-1 and tumor necrosis factor-α protein expression, ii) numbers and/or proportional area of infiltrating macrophages and myofibroblasts and iii) phosphorylated levels of p65 and IκBα. Furthermore, activin A inhibition lessened heart dysfunction post-MI. These results suggested that activin A inhibition reduced sympathetic neural remodeling post-MI in part through inhibition of the inflammatory response. The current study implicates activin A as a potential therapeutic target to circumvent sympathetic neural remodeling post-MI.
The Childhood Obesity Declines Project: Implications for Research and Evaluation Approaches.

BACKGROUND Childhood obesity remains prevalent and is increasing in some disadvantaged populations. Numerous research, policy and community initiatives are undertaken to impact this pandemic. Understudied are natural experiments. The need to learn from these efforts is paramount. Resulting evidence may not be readily available to inform future research, community initiatives, and policy development/implementation. METHODS We discuss the implications of using an adaptation of the Systematic Screening and Assessment (SSA) method to evaluate the Childhood Obesity Declines (COBD) project. The project examined successful initiatives, programs and policies in four diverse communities which were concurrent with significant declines in child obesity. In the context of other research designs and evaluation schemas, rationale for use of SSA is presented. Evidence generated by this method is highlighted and guidance suggested for evaluation of future studies of community-based childhood obesity prevention initiatives. Support for the role of stakeholder collaboratives, in particular the National Collaborative on Childhood Obesity Research, as a synergistic vehicle to accelerate research on childhood obesity is discussed. RESULTS/DISCUSSION SSA mapped active processes and provided contextual understanding of multi-level/component simultaneous efforts to reduce rates of childhood obesity in community settings. Initiatives, programs and policies were not necessarily coordinated. And although direct attribution of intervention/initiative/policy components could not be made, the what, by who, how, to whom was temporally associated with statistically significant reductions in childhood obesity. CONCLUSIONS SSA provides evidence for context and processes which are not often evaluated in other data analytic methods. SSA provides an additional tool to layer with other evaluation approaches.
Neurostimulation as a promising epilepsy therapy

The revolution in theory, swift technological developments, and invention of new devices have driven tremendous progress in neurostimulation as a third‐line treatment for epilepsy. Over the past decades, neurostimulation took its place in the field of epilepsy as an advanced treatment technique and opened up a new world. Numerous animal studies have proven the physical efficacy of stimulation of the brain and peripheral nerves. Based on this optimistic fundamental research, new advanced techniques are being explored in clinical practice. Over the past century, drawing on the benefits brought about by vagus nerve stimulation for the treatment of epilepsy, various new neurostimulation modalities have been developed to control seizures. Clinical studies including case reports, case series, and clinical trials have been booming in the past several years. This article gives a comprehensive review of most of these clinical studies. In addition to highlighting the advantages of neurostimulation for the treatment of epilepsy, concerns with this modality and future development directions are also discussed. The biggest advantage of neurostimulation over pharmacological treatments for epilepsy is the modulation of the epilepsy network by delivering stimuli at a specific target or the “hub. ” Conversely, however, a lack of knowledge of epilepsy networks and the mechanisms of neurostimulation may hinder further development. Therefore, theoretical research on the mechanism of epileptogenesis and epilepsy networks is needed in the future. Within the multiple modalities of neuromodulation, the final choice should be made after full discussion with a multidisciplinary team at a presurgical conference. Furthermore, the establishment of a neurostimulation system with standardized parameters and rigorous guidelines is another important issue. To achieve this goal, a worldwide collaboration of epilepsy centers is also suggested in the future.