Miracle-dz/UniFAR-FTUs huggingface dataset:
Validating quantum-classical programming models with tensor network simulations

The exploration of hybrid quantum-classical algorithms and programming models on noisy near-term quantum hardware has begun. As hybrid programs scale towards classical intractability, validation and benchmarking are critical to understanding the utility of the hybrid computational model. In this paper, we demonstrate a newly developed quantum circuit simulator based on tensor network theory that enables intermediate-scale verification and validation of hybrid quantum-classical computing frameworks and programming models. We present our tensor-network quantum virtual machine (TNQVM) simulator which stores a multi-qubit wavefunction in a compressed (factorized) form as a matrix product state, thus enabling single-node simulations of larger qubit registers, as compared to brute-force state-vector simulators. Our simulator is designed to be extensible in both the tensor network form and the classical hardware used to run the simulation (multicore, GPU, distributed). The extensibility of the TNQVM simulator with respect to the simulation hardware type is achieved via a pluggable interface for different numerical backends (e.g., ITensor and ExaTENSOR numerical libraries). We demonstrate the utility of our TNQVM quantum circuit simulator through the verification of randomized quantum circuits and the variational quantum eigensolver algorithm, both expressed within the eXtreme-scale ACCelerator (XACC) programming model.
Modeling and multiscale characterization of the quantitative imaging based fibrosis index reveals pathophysiological, transcriptome and proteomic correlates of lung fibrosis induced by fractionated irradiation

Pulmonary fibrosis represents a leading cause of morbidity and mortality worldwide. Therapy induced lung fibrosis constitutes a pivotal dose‐limiting side effect of radiotherapy and other anticancer agents. We aimed to develop objective criteria for assessment of fibrosis and discover pathophysiological and molecular correlates of lung fibrosis as a function of fractionated whole thoracic irradiation. Dose–response series of fractionated irradiation was utilized to develop a non‐invasive and quantitative measure for the degree of fibrosis – the fibrosis index (FI). The correlation of FI with histopathology, blood‐gas, transcriptome and proteome responses of the lung tissue was analyzed. Macrophages infiltration and polarization was assessed by immunohistochemistry. Fibrosis development followed a slow kinetic with maximum lung fibrosis levels detected at 24‐week post radiation insult. FI favorably correlated with radiation dose and surrogates of lung fibrosis i.e., enhanced pro‐inflammatory response, tissue remodeling and extracellular matrix deposition. The loss of lung architecture correlated with decreased epithelial marker, loss of microvascular integrity with decreased endothelial and elevated mesenchymal markers. Lung fibrosis was further attributed to a switch of the inflammatory state toward a macrophage/T‐helper cell type 2‐like (M2/Th2) polarized phenotype. Together, the multiscale characterization of FI in radiation‐induced lung fibrosis (RILF) model identified pathophysiological, transcriptional and proteomic correlates of fibrosis. Pathological immune response and endothelial/epithelial to mesenchymal transition were discovered as critical events governing lung tissue remodeling. FI will be instrumental for deciphering the molecular mechanisms governing lung fibrosis and discovery of novel targets for treatment of this devastating disease with an unmet medical need.
Physical Activity from Childhood to Adulthood and Cognitive Performance in Midlife

Introduction Physical activity (PA) has been suggested to protect against old-age cognitive deficits. However, the independent role of childhood/youth PA for adulthood cognitive performance is unknown. This study investigated the association between PA from childhood to adulthood and midlife cognitive performance. Methods This study is a part of the Cardiovascular Risk in Young Finns Study. Since 1980, a population-based cohort of 3596 children (age, 3–18 yr) have been followed up in 3- to 9-yr intervals. PA has been queried in all study phases. Cumulative PA was determined in childhood (age, 6–12 yr), adolescence (age, 12–18 yr), young adulthood (age, 18–24 yr), and adulthood (age, 24–37 yr). Cognitive performance was assessed using computerized neuropsychological test, CANTAB® (N = 2026; age, 34–49 yr) in 2011. Results High PA in childhood (&bgr; = 0.119; 95% confidence interval [CI], 0.055–0.182) and adolescence (&bgr; = 0.125; 95% CI, 0.063–0.188) were associated with better reaction time in midlife independent of PA in other age frames. Additionally, an independent association of high PA in young adulthood with better visual processing and sustained attention in midlife was observed among men (&bgr; = 0.101; 95% CI, 0.001–0.200). There were no associations for other cognitive domains. Conclusions Cumulative exposure to PA from childhood to adulthood was found to be associated with better midlife reaction time. Furthermore, cumulative PA exposure in young adulthood and adulthood was associated with better visual processing and sustained attention in men. All associations were independent of participants PA level in other measured age frames. Therefore, a physically active lifestyle should be adopted already in childhood, adolescence, and young adulthood and continued into midlife to ensure the plausible benefits of PA on midlife cognitive performance.
Individual and combined effects of low dissolved oxygen and low pH on survival of early stage larval blue crabs, Callinectes sapidus

A large number of coastal ecosystems globally are subjected to concurrent hypoxic and acidified conditions that will likely intensify and expand with continued climate change. In temperate regions, the spawning of many important organisms including the Atlantic blue crab Callinectes sapidus occurs during the summer months when the severity of coastal hypoxia and acidification is the greatest. While the blue crab earliest larval stage can be exposed to co-occurring hypoxia and acidification observed in many coastal ecosystems, the effects of these concurrent stressors on larval blue crab survival is unknown. This study investigated the individual and combined consequences of low dissolved oxygen (DO) and low pH on blue crab larvae survival through a series of short-term experiments. During 14-day experiments with moderately hypoxic conditions (117–127 μM O2 or 3.74–4.06 mg L-1) and acidified conditions (pH on total scale of 7.16–7.33), low DO and low pH individually and significantly reduced larval survival by 60% and 49%, respectively, with the combination of stressors reducing survival by 87% compared to the control treatment (210–269 μM O2 or 6.72–8.61 mg L-1, 7.91–7.94 DO and pH, respectively). During 4-day experiments with lower DO levels (68–83 μM O2 or 2.18–2.62 mg L-1) and comparable pH levels of 7.29–7.39, low DO individually reduced survival by >90% compared to the control (261–267 μM O2 or 8.35–8.54 mg L-1, 7.92–7.97 DO and pH, respectively), whereas low pH had no effect and there was no interaction between stressors. Over a 4-day period, the DO threshold at which 50% of the larval blue crab population died (LC50) was 121 μM O2 (3.86 mgL-1). In 14-day experiments, the DO and pH effects were additive, yielding survival rates lower than the individual treatments, and significantly correlated with DO and pH concentrations. Collectively, these findings indicate that blue crab sensitivity to both low DO and low pH are acute within the larval stage, depend on the intensity and duration of exposure, and leads to mortality, thereby potentially contributing to the interannual variability and possible regional declines of this fishery.
Protein‐Bound Freestanding 2D Metal Film for Stealth Information Transmission

The welding and sintering of nanomaterials is usually achieved at high temperatures and high pressures. Here, it is found that merging of metal nanoparticles occurs under ambient conditions in an aqueous solution via protein bonding. It is discovered that the silver nanoparticles from the in situ reduction of silver ammonium ions by glucose undergo confined nucleation and growth and are bound by ultrathin amyloid‐like β‐sheet stacking of lysozyme. This merging of silver nanoparticles creates a freestanding large‐area (e.g., 400 cm2) 2D silver film at the air/water interface with a purity up to 98% and controls nanoscale thickness. This reaction system is general to other proteins and metals, and shows the great ability for controlled synthesis of highly reflective and highly conductive silver films with elongation nearly 10 times higher than that of pure metal without protein bonding. The ultrathin protein‐bonding layer functions as a key mediator to dynamically tune the silver conductance in response to external pressures and strains. The sensors exhibit ultrasensitive capability for stealth transmission of Morse code and for silent speech recording via the detection of tiny vibrations of the human throat. This approach will shed light on the development of protein bonding of a given material for bespoke functions.
APLICAÇÃO DE ESTABILIZADORES MULTI-BANDA EM UMA ESTRUTURA CENTRALIZADA DE CONTROLE PARA O AMORTECIMENTO DE OSCILAÇÕES ELETROMECÂNICAS EM SEP

O presente trabalho objetiva investigar a aplicacao de Estabilizadores de Sistemas de Potencia Multi-Banda no segundo nivel de uma estrutura hierarquica de controle para o amortecimento de oscilacoes em sistemas de potencia. A estrutura de controle e composta de dois niveis: o primeiro e denominado de controle local e e baseado no uso de sinais locais. O segundo nivel e denominado de controle central e e baseado no uso de sinais remotos medidos por unidades de medicao fasorial sincronizada. O problema de ajuste e formulado como um problema de otimizacao visando a maximizacao do coeficiente de amortecimento do sistema em malha fechada considerando varias condicoes operativas para a garantia de robustez. Os resultados sao comparados com aqueles obtidos quando se usa controladores convencionais na estrutura centralizada.
Diel and infradian (7‐day) activity rhythms in Mexican spider monkeys (Ateles geoffroyi) kept with and without visitor contact

Diel activity rhythms in mammals are regulated by an endogenous (circadian) timing system which is synchronized by environmental 24‐hr periodicities called zeitgebers. Additional direct responses to stochastic environmental factors ensure the fine‐tuning to the actual situation and may mask the circadian time course. Following an observational study on behavioral effects of visitor activities in a group of spider monkeys (Ateles geoffroyi) kept free‐ranging on a small island of Lake Catemaco, Veracruz, Mexico, we analyzed the effect of weekly varying numbers of visiting tourist boats on the monkeys’ diel activity rhythm. With small accelerometer‐data logger devices we recorded the monkeys’ locomotor activity continuously for several months each. Then we compared the data with those from spider monkeys living without tourist contact. Neither the duration of the monkeys’ activity time (α) nor its phase relationship to the 24‐hr solar day did change on different weekdays in either site. However, their activity level showed a clear 7‐day rhythm. The monkeys of the tourist site showed highest activity on Saturday and Sunday, when the frequency of visiting tourist boats was highest, whereas those of the non‐tourist site were least active on Sunday and Monday, when human activities were lowest there. While the monkeys of the non‐tourist site usually displayed a distinct bimodal activity pattern peaking in the morning and late afternoon, the pattern in those of the tourist site mostly lacked a morning peak and varied more over time. Based on our results, we suggest that circadian entrainment is not involved in the differences between the diel activity rhythms of the spider monkeys from the two keeping sites and the differing 7‐day variation in their activity level. Rather, these differences seemingly reflect direct responses to the differing human activities and thus may correspond to circadian masking effects.
The Association of Fasting Glucose, Insulin, and C-Peptide, with 19-Year Incidence of Coronary Heart Disease in Older Japanese-American Men; the Honolulu Heart Program

The role of fasting glucose, insulin levels, and C-peptide in coronary heart disease (CHD) in non-diabetic individuals remains uncertain. We examined the association between fasting glucose, insulin and C-peptide with the long-term incidence of CHD in Japanese-American men. In 1980–1982, from a random sample of the Honolulu Heart Program men (n = 1378), aged 61–81 years, data on several CHD and metabolic risk factors were obtained to examine the relation of fasting glucose, insulin and C-peptide to 19-year CHD incidence. Age-adjusted incidence of CHD increased with increasing quintiles of glucose, insulin and C-peptide. Age-adjusted CHD rates in the glucose quintiles were 11.9, 11.6, 14.4, 18.1 and 24.1 per 1000 person-years (trend p < 0.001). In individual Cox models (lowest quintiles of glucose, insulin and C-peptide as reference) the relative risks (95% confidence interval) of CHD incidence for the glucose quintiles adjusting for age, smoking, hypertension, cholesterol, physical activity, and body mass index, were 0.9 (0.6–1.4), 1.2 (0.8–1.8), 1.4 (0.9–2.2), and 1.7 (1.1–2.6), respectively (trend p = 0.004). Insulin and C-peptide were not significantly associated with CHD on multivariate analysis. Fasting glucose remained the only significant predictor of increased CHD risk (p = 0.003) in a model combining all 3 metabolic variables. In this cohort, only fasting glucose independently predicts long-term incidence of CHD. Age-adjusted insulin and C-peptide levels were associated with CHD incidence, but after adjustment for other risk factors, do not independently predict CHD.
Protective mechanism of Wnt4 gene on Parkinson’s disease (PD) transgenic Drosophila

Abstract Objective: The main pathological change of Parkinson’s disease (PD) is progressive degeneration and necrosis of dopaminergic neurons in the midbrain, forming a Lewy body in many of the remaining neurons. Studies have found that in transgenic Drosophila, mutations in the PTEN-inducible kinase 1 (PINK1) gene may cause indirect flight muscle defects in Drosophila, and mitochondrial structural dysfunction as well. Methods: In this study, Wnt4 gene overexpression and knockdown were performed in PINK1 mutant PD transgenic Drosophila, and the protective effect of Wnt4 gene on PD transgenic Drosophila and its possible mechanism were explored. The Wnt4 gene was screened in the previous experiment; And by using the PD transgenic Drosophila model of the MHC-Gal4/UAS system, the PINK1 gene could be specifically activated in the Drosophila muscle tissue. Results: In PINK1 mutation transgenic fruit flies, the Wnt4 gene to study its implication on PD transgenic fruit flies’ wing normality and flight ability. We found that overexpression of Wnt4 gene significantly reduced abnormality rate of PD transgenic Drosophila and improved its flight ability, and then, increased ATP concentration, enhanced mitochondrial membrane potential and normalized mitochondrial morphology were found. All of these findings suggested Wnt4 gene may have a protective effect on PD transgenic fruit flies. Furthermore, in Wnt4 gene overexpression PD transgenic Drosophila, down-regulation autophagy and apoptosis-related proteins Ref(2)P, Pro-Caspase3, and up-regulation of Beclin1, Atg8a, Bcl2 protein were confirmed by Western Blotting. Conclusion: The results imply that the restoring of mitochondrial function though Wnt4 gene overexpression in the PINK1 mutant transgenic Drosophila may be related to autophagy and/or apoptosis.
Cytidine deaminase enables Toll-like receptor 8 activation by cytidine or its analogs

Toll-like receptor 8 (TLR8), a sensor for pathogen-derived single-stranded RNA (ssRNA), binds to uridine (Uri) and ssRNA to induce defense responses. We here show that cytidine (Cyd) with ssRNA also activated TLR8 in peripheral blood leukocytes (PBLs) and a myeloid cell line U937, but not in an embryonic kidney cell line 293T. Cyd deaminase (CDA), an enzyme highly expressed in leukocytes, deaminates Cyd to Uri. CDA expression enabled TLR8 response to Cyd and ssRNA in 293T cells. CDA deficiency and a CDA inhibitor both reduced TLR8 responses to Cyd and ssRNA in U937. The CDA inhibitor also reduced PBL response to Cyd and ssRNA. A Cyd analogue, azacytidine, is used for the therapy of myelodysplastic syndrome and acute myeloid leukemia. Azacytidine with ssRNA induced tumor necrosis factor-α expression in U937 and PBLs in a manner dependent on CDA and TLR8. These results suggest that CDA enables TLR8 activation by Cyd or its analogues with ssRNA through deaminating activity. Nucleoside metabolism might impact TLR8 responses in a variety of situations such as the treatment with nucleoside analogues.
Nitric Oxide Remodels the Photosynthetic Apparatus upon S-Starvation in Chlamydomonas reinhardtii1

Nitric oxide is actively involved in cytochrome b6f and Rubisco degradation upon sulfur starvation. Many photosynthetic autotrophs have evolved responses that adjust their metabolism to limitations in nutrient availability. Here we report a detailed characterization of the remodeling of photosynthesis upon sulfur starvation under heterotrophy and photo-autotrophy in the green alga (Chlamydomonas reinhardtii). Photosynthetic inactivation under low light and darkness is achieved through specific degradation of Rubisco and cytochrome b6f and occurs only in the presence of reduced carbon in the medium. The process is likely regulated by nitric oxide (NO), which is produced 24 h after the onset of starvation, as detected with NO-sensitive fluorescence probes visualized by fluorescence microscopy. We provide pharmacological evidence that intracellular NO levels govern this degradation pathway: the addition of a NO scavenger decreases the rate of cytochrome b6f and Rubisco degradation, whereas NO donors accelerate the degradation. Based on our analysis of the relative contribution of the different NO synthesis pathways, we conclude that the NO2-dependent nitrate reductase-independent pathway is crucial for NO production under sulfur starvation. Our data argue for an active role for NO in the remodeling of thylakoid protein complexes upon sulfur starvation.
Increased Autophagy Levels Mediate Cisplatin Resistance in Cisplatin-Resistant Cells While Also Rendering Them Vulnerable to Autophagy Induction

Autophagy plays an important role in tumor development because of its capacity to maintain energy homeostasis by recycling damaged intracellular proteins and organelles, and increased autophagy levels are reported to mediate drug resistance in many cancers. However, whether high autophagy levels negatively impact tumor cell growth is unknown. Herein, we found that cisplatin (ddp)-resistant cells were more sensitive to glutamine (Gln) deprivation than ddp-sensitive cells, and they showed significant G1 arrest and increased apoptosis rates under Gln-deficient conditions. Furthermore, ddp-resistant cells had a higher level of autophagy, which mediated ddp resistance. Further analysis indicated that Gln deficiency could trigger apoptosis by enhancing activation of the autophagy signaling pathway AMPK/ULK1 in ddp-resistant cells due to their high basal autophagy level. Interestingly, ddp-resistant cells were more sensitive to rapamycin, and rapamycin could efficiently suppress the growth of ddp-resistant cells in vivo. Taken together, our study demonstrated that ddp-resistant cells became vulnerable to Gln deprivation because of their increased level of autophagy, and for the first time, we showed that suppressing the growth of ddp-resistant cells via enhancing autophagy induction was possible with rapamycin treatment.
Editorial

Early Life Stress (ELS) profoundly impairs child’s brain development and behaviour giving rise to either temporary or permanent effects on cognitive, behavioural and psychological functions. Furthermore, possible long-term cumulative effects of various types of early adversity may show up in adulthood [1]. ELS-related pathological consequences greatly vary among individuals and depend on genetic and environmental factors. With regard to the onset of neurodevelopmental and psychiatric disorders associated to ELS exposure, great emphasis must be laid on the influence of various pre-, periand post-traumatic components in the environmental social context in which childhood abuse occurs. Namely, other influence factors related to the nature of the early trauma, such as its duration, chronicity, and severity, strongly predispose towards either pathological outcomes or resilient reactions. Together, genetic and environmental factors influence the individual stress responses although the most remarkable effects of such an interplay are those concerning a critical period of vulnerability spanning from fetal to postnatal development and adolescence. During this developmental window, the genome within neurons appears to be more plastic and sensitive to both positive and negative environmental stimuli. These gene-environment interactions contribute to optimal brain development, establishing a proper neural and behavioural developmental trajectory [2]. As previously anticipated, it is now clear that there is a causal link between ELS and the onset of neuropsychiatric and behavioural consequences, both with shortand long-term effects [3].
Automated Sleep Apnea Detection in Raw Respiratory Signals Using Long Short-Term Memory Neural Networks

Sleep apnea is one of the most common sleep disorders and the consequences of undiagnosed sleep apnea can be very severe, ranging from increased blood pressure to heart failure. However, many people are often unaware of their condition. The gold standard for diagnosing sleep apnea is an overnight polysomnography in a dedicated sleep laboratory. Yet, these tests are expensive and beds are limited as trained staff needs to analyze the entire recording. An automated detection method would allow a faster diagnosis and more patients to be analyzed. Most algorithms for automated sleep apnea detection use a set of human-engineered features, potentially missing important sleep apnea markers. In this paper, we present an algorithm based on state-of-the-art deep learning models for automatically extracting features and detecting sleep apnea events in respiratory signals. The algorithm is evaluated on the Sleep-Heart-Health-Study-1 dataset and provides per-epoch sensitivity and specificity scores comparable to the state of the art. Furthermore, when these predictions are mapped to the apnea–hypopnea index, a considerable improvement in per-patient scoring is achieved over conventional methods. This paper presents a powerful aid for trained staff to quickly diagnose sleep apnea.
Breaking the Borders: An Investigation of Cross-Ecosystem Software Packages

Software ecosystems are collections of projects that are developed and evolve together in the same environment. Existing literature investigates software ecosystems as isolated entities whose boundaries do not overlap and assumes they are self-contained. However, a number of software projects are distributed in more than one ecosystem. As different aspects, e.g., success, security vulnerabilities, bugs, etc., of such cross-ecosystem packages can affect multiple ecosystems, we investigate the presence and characteristics of these cross-ecosystem packages in 12 large software distributions. We found a small number of packages distributed in multiple packaging ecosystems and that such packages are usually distributed in two ecosystems. These packages tend to better support with new releases certain ecosystems, while their evolution can impact a multitude of packages in other ecosystems. Finally, such packages appear to be popular with large developer communities.