Miracle-dz/UniFAR-FTUs huggingface dataset:
DQ Herculis in Profile: Whole Earth Telescope Observations and Smoothed Particle Hydrodynamics Simulations of an Edge-on Cataclysmic Variable System

The old nova DQ Herculis was the Whole Earth Telescope Northern Hemisphere target for the 1997 July campaign and was observed on four nights with the SARA 0.9 m telescope during 2003 June. We present updated ephemerides for the eclipse and 71 s timings. The Fourier transform displays power at the presumed white dwarf spin period of 71.0655 s, but no significant power at either 142 or 35.5 s. The mean pulsed light curve is obtained by folding on the orbital period modulus the mean ephemeris of the 71 s period, and from this we calculate an O - C phase diagram and amplitude versus orbital phase diagrams. In addition to the phase variations during eclipse ingress and egress, the WET data reveal significant phase variations outside of eclipse. These must result from the self-eclipse of a nonaxisymmetric disk. We simulated the disk in DQ Her using smoothed particle hydrodynamics. We improve our effective spatial signal-to-noise ratio by combining 250 snapshots of the N = 20,000 phase space solution over time to obtain a 5 million particle ensemble disk. From the surface shape of the ensemble disk, the radius and vertical height above the midplane of the rim of the reprocessing region can be derived as a function of azimuthal angle. From this profile we can calculate the O - C phase and amplitude diagrams as a function of inclination angle. The calculated O - C diagrams are a remarkably good match to the observed phase and amplitude variations of the 71 s signal. The best match is for inclination angle 89. °7.
Lysophosphatidylcholine Triggers TLR2- and TLR4-Mediated Signaling Pathways but Counteracts LPS-Induced NO Synthesis in Peritoneal Macrophages by Inhibiting NF-κB Translocation and MAPK/ERK Phosphorylation

Background Lysophosphatidylcholine (LPC) is the main phospholipid component of oxidized low-density lipoprotein (oxLDL) and is usually noted as a marker of several human diseases, such as atherosclerosis, cancer and diabetes. Some studies suggest that oxLDL modulates Toll-like receptor (TLR) signaling. However, effector molecules that are present in oxLDL particles and can trigger TLR signaling are not yet clear. LPC was previously described as an attenuator of sepsis and as an immune suppressor. In the present study, we have evaluated the role of LPC as a dual modulator of the TLR-mediated signaling pathway. Methodology/Principal Findings HEK 293A cells were transfected with TLR expression constructs and stimulated with LPC molecules with different fatty acid chain lengths and saturation levels. All LPC molecules activated both TLR4 and TLR2-1 signaling, as evaluated by NF-қB activation and IL-8 production. These data were confirmed by Western blot analysis of NF-қB translocation in isolated nuclei of peritoneal murine macrophages. However, LPC counteracted the TLR4 signaling induced by LPS. In this case, NF-қB translocation, nitric oxide (NO) synthesis and the expression of inducible nitric oxide synthase (iNOS) were blocked. Moreover, LPC activated the MAP Kinases p38 and JNK, but not ERK, in murine macrophages. Interestingly, LPC blocked LPS-induced ERK activation in peritoneal macrophages but not in TLR-transfected cells. Conclusions/Significance The above results indicate that LPC is a dual-activity ligand molecule. It is able to trigger a classical proinflammatory phenotype by activating TLR4- and TLR2-1-mediated signaling. However, in the presence of classical TLR ligands, LPC counteracts some of the TLR-mediated intracellular responses, ultimately inducing an anti-inflammatory phenotype; LPC may thus play a role in the regulation of cell immune responses and disease progression.
Pharmacodynamic characterization of chemopreventive triterpenoids as exceptionally potent inducers of Nrf2-regulated genes

Synthetic triterpenoids have been developed, which are potent inducers of cytoprotective enzymes and inhibitors of inflammation, greatly improving on the weak activity of naturally occurring triterpenoids. An imidazolide triterpenoid derivative, 1-[2-cyano-3,12-dioxooleana-1,9(11)-dien-28-oyl]imidazole (CDDO-Im or TP235), has been previously shown to potently protect against hepatic tumorigenesis, acting in part by inducing cytoprotective genes through Keap1-Nrf2-antioxidant response element (ARE) signaling. In these studies, the pharmacodynamic activity of CDDO-Im is characterized in two distinct lines of ARE reporter mice and by measuring increases in Nqo1 transcript levels as a marker of cytoprotective gene induction. Oral administration of CDDO-Im induces ARE-regulated cytoprotective genes in many tissues in the mouse, including liver, lung, kidney, intestines, brain, heart, thymus, and salivary gland. CDDO-Im induces Nqo1 RNA transcripts in some organs at doses as low as 0.3 μmol/kg body weight (orally). A structure activity evaluation of 15 additional triterpenoids (a) confirmed the importance of Michael acceptor groups on both the A and C rings, (b) showed the requirement for a nitrile group at C-2 of the A ring, and (c) indicated that substituents at C-17 dramatically affected pharmacodynamic action in vivo. In addition to CDDO-Im, other triterpenoids, particularly the methyl ester CDDO-Me (TP155) and the dinitrile TP225, are extremely potent inducers of cytoprotective genes in mouse liver, lung, small intestine mucosa, and cerebral cortex. This pharmacodynamic characterization highlights the chemopreventive promise of several synthetic triterpenoids in multiple target organs. [Mol Cancer Ther 2007;6(1):154–62]
Software-Managed Power Reduction in Infiniband Links

The backbone of a large-scale supercomputer is the interconnection network. As compute nodes become more energy-efficient, the interconnect is accounting for an increasing proportion of the total system energy consumption. The interconnect's energy consumption is, however, only starting to receive serious attention. Some hardware-based schemes have been proposed that exploit idle periods or low utilisation, either by turning off the links or by lowering the frequency and voltage. Although these schemes are effective in certain cases, they do not have enough global information about the application's communication behaviour to efficiently manage the network power consumption. This paper proposes an alternative approach: moving the intelligence into the PMPI layer of the MPI library, and using prediction to discover repetitive patterns in the application's communication behaviour. The core of the prediction algorithm is an n-gram extraction technique, which can accurately predict not only when a link will become unused but also when it will become active again, allowing lanes to be switched off during the idle periods and switched back on again in time to avoid incurring a significant performance degradation. Many HPC applications benefit from prediction, since they have repetitive computation and communication phases. By implementing the energy-saving mechanism inside the MPI library, existing MPI programs do not need to be modified. Using an event-driven simulator, driven by representative HPC workloads, we demonstrate average energy savings in Infiniband switches up to around 33%, while the average execution time increase is only up to 1%.
Auditory M50 and M100 responses to broadband noise: functional implications

The functional significance of the M50 and M100 auditory evoked fields remains unclear. Here we report auditory evoked field data from three different studies employing wide-band noise stimuli. We find that, for the same stimuli, the strength of the M100, as well as its lateralization, are task-modulated. The M50, in contrast, shows three properties: It is dramatically more pronounced for noise stimuli than for pure tones, does not seem to be task dependent, and, is significantly stronger in the left hemisphere in all task conditions. These contrasting patterns of activation shed light on the properties of the response-generating mechanisms and suggest roles in the process of auditory figure-ground segregation.
Monsoon intra-seasonal variability in a high-resolution version of Met Office Global Coupled model

Abstract Intra-seasonal oscillation (ISO) is a key ingredient of the East Asia and western North Pacific (EAWNP) summer monsoon and particularly important for seasonal forecast. This paper evaluates the seasonal means and ISOs of the EAWNP summer monsoon simulated by the latest version of the Met Office Global Coupled Model (HadGEM3-GC2) with two different atmospheric model resolutions at ~130 and ~25 km coupled to a same 0.25° × 0.25° resolution ocean model. Results show that the mean states of sea surface temperature (SST), low-level specific humidity and the western Pacific subtropical high are all improved in HadGEM3-GC2 with higher atmosphere resolution. Moreover, although ISO variance is overestimated over the western North Pacific, the model has good fidelity in characterising ISO basic features over the EAWNP including the dominant EOF structure, northward propagation and cycle evolution, as well as the zonal displacement of western Pacific Subtropical High and South Asian High associated with the northward propagating ISOs. Increasing atmosphere model resolution yields improvements in most aspects of the Monsoon ISO over the EAWNP, especially for its northward propagation. Further analysis indicates that this improvement is mainly due to the better description of ISO-related air–sea interaction in higher resolution experiment, as evidenced by the enhanced intra-seasonal SST variance and more coherent northward propagation of rainfall, SST, and the associated surface dynamic and thermodynamic variables in the higher resolution model.
Stress and Addiction: When a Robust Stress Response Indicates Resiliency.

OBJECTIVE Stress reactivity research has traditionally focused on the idea that exaggerated responses to stress may have adverse effects on health. Accumulating evidence suggests that attenuated responses to stress and delayed recovery may also be problematic. METHODS This review focuses on the role of the stress response of the hypothalamic-pituitary-adrenocortical axis, the endogenous opioid system, and the cardiovascular system in hypertension, pain perception, and addictive behaviors. Results from multiple methods of assessment and stress paradigms conducted in our laboratory over the past two decades are integrated with research from other investigators and with existing theories. RESULTS Research indicates that exaggerated biological and physiological responses to stress and attenuated pain perception are associated with hypertension and risk for cardiovascular diseases. This research complements work linking reduced stress responses with enhanced pain sensitivity and discomfort. Multiple studies have also demonstrated that an attenuated stress response is linked to exacerbation of withdrawal symptoms and relapse in nicotine addiction. Evidence indicates important moderators (i.e., sex, personality traits, and early life adversity) and hypothalamic-pituitary-adrenocortical- and endogenous opioid system-related mechanisms in the altered response to stress. I integrate these findings in a conceptual model emphasizing that robust stress responses in the context of addiction and relapse should be considered as a marker of resiliency. CONCLUSIONS A blunted stress response may indicate long-term physiological dysregulation that could usher harmful consequences for cardiovascular disease, pain perception, and addictive disorders. The impact of dysregulation is influenced by multiple individual and situational factors that should be considered in evaluating the clinical significance of stress response dysregulation.
Identifying core NANDA-I nursing diagnoses, NIC interventions, NOC outcomes, and NNN linkages for heart failure.

PURPOSE The purpose of the study was to identify the core nursing diagnoses, interventions, outcomes, and linkages using standardized nursing terminologies for patients with heart failure (HF). METHODS For this study a retrospective descriptive design was used. The frequently used NANDA-I, NIC, NOC, and NNN linkages were identified through 272 inpatient records of patients discharged with HF in a midwestern community. FINDINGS The findings indicate that the top 10 NANDA-I, NIC, and NOC accounted for more than 50% of nursing diagnoses, interventions, and outcomes. The most frequently used top 10 NNN linkages were identified for patients with HF. CONCLUSION AND PRACTICE IMPLICATIONS The identified core NANDA-I, NIC, NOC, and NNN linkages for HF from this study provide scope of practice of nurses working in HF clinics.
Complementary Patents and Market Structure

Many high technology goods are based on standards that require access to several patents that are owned by different IP holders. We investigate the royalties chosen by IP holders under different market structures. Vertical integration of an IP holder and a downstream producer solves the double mark-up problem between these firms. Nevertheless, it may raise royalty rates and reduce output as compared to non-integration. Horizontal integration of IP holders (or a patent pool) solves the complements problem but not the double mark-up problem. Vertical integration discourages entry and reduces innovation incentives, while horizontal integration always encourages entry and innovation.
The structure of a 3-state finite transducer representation for Prisoner's Dilemma

To facilitate systematic and automated analysis of game playing strategies, the fingerprint, a mathematical technique that generates a functional summary independent of representation, was developed. This study attempts to push the boundaries of full state space investigation, looking at 3-state finite transducers as a representation for playing Prisoner's Dilemma. There are a staggering 23,000 unique strategies in this space, which severely limits the choice of analysis methods. These strategies are fingerprinted and pairwise distances computed, then hierarchical clustering reduces them to a manageable size for further experiments with multidimensional scaling and the mutational connectivity network. Results indicate there are no obvious cutoff scales of structure; mutational distance is not correlated with fingerprint distance; and a level of similarity with past results on smaller state spaces.
Dysregulation of iodothyronine deiodinase enzyme expression and function in human pituitary tumours

objective Thyroid hormones (THs) perform essential roles in pituitary function. They regulate anterior pituitary hormone secretion and are also key determinants of pituitary cell proliferation and differentiation. The critical role of deiodinase enzymes, which serve as prereceptor regulators of TH action, remains largely unexplored. Three deiodinase enzymes metabolize active and inactive THs and thereby determine tissue concentrations of the biologically active ligand, tri‐iodothyronine (T3). We hypothesized that aberrant expression of deiodinase enzymes and/or altered enzyme activity in pituitary tumours may change tissue concentrations of THs and influence their growth and secretory characteristics.
Effects of the Age of Donor or Host Tissue on Astrocyte Migration from Intracerebral Xenografts of Corpus Callosum

Our previous studies in which neural tissue was transplanted into neonatal rat brains have demonstrated that the patterns of astrocyte migration are stereotypic and are mainly influenced by local factors in the host brain. Here we examine how these patterns are affected by the relative maturity of donor cells and recipient brains. In one group of animals, adult mouse corpus callosum was transplanted into the cortex or midbrain of neonatal rat brains; in a second group, corpus callosum from 2- to 3-day-old mice was placed in adult rats. The location of the grafts and the distribution of donor astrocytes were defined by using a monoclonal antibody (anti-M2) specific for mouse astrocytes. In marked contrast to previous studies involving transplantation into neonatal hosts, very few neonatal astrocytes placed into adult brains invaded the gray matter and these never migrated more than 250 microns from the graft. The migration in adult brains also failed to show targeted migration to regions such as the substantia nigra. In the second group, astrocytes from adult grafts implanted in neonatal hosts migrated in both gray and white matter of brains in patterns similar to those of neonatal cells placed in neonatal brains. These observations suggest that the astrocyte migration in the white and gray matter is guided by different cues and that the maturation of host brain environment, but not the age of donor cells, influences the pattern of cell migration.
More Constructive Lower Bounds on Classical Ramsey Numbers

We present several new constructive lower bounds for classical Ramsey numbers. In particular, the inequality $R(k,s+1) \geq R(k,s)+2k-2$ is proved for $k \geq 5$. The general construction permits us to prove that, for all integers $k$, $l$, with $k \geq 5$ and $l \geq 3$, the connectivity of any Ramsey-critical $(k,l)$-graph is at least $k$, and if $k \geq l-1 \geq 1$, $k \geq 3$ and $(k,l) \neq (3,2)$, then such graphs are Hamiltonian. New concrete lower bounds for Ramsey numbers are obtained, some with the help of computer algorithms, including: $R(5,17) \geq 388$, $R(5,19) \geq 411$, $R(5,20) \geq 424$, $R(6,8) \geq 132$, $R(6,12) \geq 263$, $R(7,8) \geq 217$, $R(7,9) \geq 241$, $R(7,12) \geq 417$, $R(8,17) \geq 961$, $R(9,10) \geq 581$, $R(12,12) \geq 1639$, and also one three-color case $R(8,8,8) \geq 6079$.
Structural characterization of the C‐terminal coiled‐coil domains of wild‐type and kidney disease‐associated mutants of apolipoprotein L1

Trypanosomes that cause sleeping sickness endocytose apolipoprotein L1 (APOL1)‐containing trypanolytic factors from human serum, leading to trypanolytic death through generation of APOL1‐associated lytic pores in trypanosomal membranes. The trypanosome Trypanosoma brucei rhodesiense counteracts trypanolysis by expressing the surface protein serum response‐associated (SRA), which can bind APOL1 common variant G0 to block its trypanolytic activity. However, two missense variants in the C terminal predicted coiled‐coil (CC) domains of human APOL1 G1 (S342G/I384M) and G2 (ΔN388Y389) decrease or abrogate APOL1 binding to T. brucei rhodesiense SRA, thus preserving APOL1 trypanolytic activity. These evolutionarily selected APOL1 missense variants, found at a high frequency in some populations of African descent, also confer elevated risk of kidney disease. Understanding the SRA–APOL1 interaction and the role of APOL1 G1 and G2 variants in kidney disease demands structural characterization of the APOL1 CC domain. Using CD, heteronuclear NMR, and molecular dynamics (MD) simulation on structural homology models, we report here unique and dynamic solution conformations of nephropathy variants G1 and G2 as compared with the common variant G0. Conformational plasticity in G1 and G2 CC domains led to interhelical α1–α2 approximation coupled with secondary structural changes and delimited motional properties absent in the G0 CC domain. The G1 substitutions conferred local structural changes principally along helix α1, whereas the G2 deletion altered the structure of both helix α2 and helix α1. These dynamic features of APOL1 CC variants likely reflect their intrinsic structural properties, and should help interpret future APOL1 structural studies and define the contribution of APOL1 risk variants to kidney disease.
Neuroscience and Biobehavioral Reviews Alcohol Dependence as a Chronic Pain Disorder

Dysregulation of pain neurocircuitry and neurochemistry has been increasingly recognized as playing a critical role in a diverse spectrum of diseases including migraine, fibromyalgia, depression, and PTSD. Evidence presented here supports the hypothesis that alcohol dependence is among the pathologies arising from aberrant neurobiological substrates of pain. In this review, we explore the possible influence of alcohol analgesia and hyperalgesia in promoting alcohol misuse and dependence. We examine evidence that neuroanatomical sites involved in the negative emotional states of alcohol dependence also play an important role in pain transmission and may be functionally altered under chronic pain conditions. We also consider possible genetic links between pain transmission and alcohol dependence. We propose an allostatic load model in which episodes of alcohol intoxication and withdrawal, traumatic stressors, and injury are each capable of dysregulating an overlapping set of neural substrates to engender sensory and affective pain states that are integral to alcohol dependence and comorbid conditions such as anxiety, depression, and chronic pain.
Characterizing the Impact of Intermittent Hardware Faults on Programs

Extreme complimentary metal-oxide-semiconductor (CMOS) technology scaling is causing significant concerns in the reliability of computer systems. Intermittent hardware errors are non-deterministic bursts of errors that occur in the same physical location. Recent studies have found that 40% of the processor failures in real-world machines are due to intermittent hardware errors. A study of the effects of intermittent faults on programs is a critical step in building fault-tolerance techniques of reasonable accuracy and cost. In this work, we characterize the impact of intermittent hardware faults in programs using fault-injection campaigns in a microarchitectural processor simulator. We find that 80% of the non-benign intermittent hardware errors activate a hardware trap in the processor, and the remaining 20% cause silent data corruptions. We have also investigated the possibility of using the program state at failure time in software-based diagnosis techniques, and found that much of the erroneous data are intact and can be used to identify the source of the error.
Oleic Acid Inhibits Gap Junction Permeability and Increases Glucose Uptake in Cultured Rat Astrocytes

Abstract: The role of oleic acid in the modulation of gap junction permeability was studied in cultured rat astrocytes by the scrape‐loading/Lucifer yellow transfer technique. Incubation with oleic acid caused a dose‐dependent inhibition of gap junction permeability by 79.5% at 50 µM, and no further inhibition was observed by increasing the oleic acid concentration to 100 µM. The oleic acid‐mediated inhibition of gap junction permeability was reversible and was prevented by bovine serum albumin. The potency of oleic acid‐related compounds in inhibiting gap junction permeability was arachidonic acid > oleic acid > oleyl alcohol > palmitoleic acid > stearic acid > octanol > caprylic acid > palmitic acid > methyloleyl ester. Oleic acid and arachidonic acid, but not methyloleyl ester, increased glucose uptake by astrocytes. Neither oleic acid nor arachidonic acid increased glucose uptake in the poorly coupled glioma C6 cells. These results support that the inhibition of gap junction permeability is associated with the increase in glucose uptake. We suggest that oleic acid may be a physiological mediator of the transduction pathway leading to the inhibition of intercellular communication.