500 research outputs found
Tree Nash Equilibria in the Network Creation Game
In the network creation game with n vertices, every vertex (a player) buys a
set of adjacent edges, each at a fixed amount {\alpha} > 0. It has been
conjectured that for {\alpha} >= n, every Nash equilibrium is a tree, and has
been confirmed for every {\alpha} >= 273n. We improve upon this bound and show
that this is true for every {\alpha} >= 65n. To show this, we provide new and
improved results on the local structure of Nash equilibria. Technically, we
show that if there is a cycle in a Nash equilibrium, then {\alpha} < 65n.
Proving this, we only consider relatively simple strategy changes of the
players involved in the cycle. We further show that this simple approach cannot
be used to show the desired upper bound {\alpha} < n (for which a cycle may
exist), but conjecture that a slightly worse bound {\alpha} < 1.3n can be
achieved with this approach. Towards this conjecture, we show that if a Nash
equilibrium has a cycle of length at most 10, then indeed {\alpha} < 1.3n. We
further provide experimental evidence suggesting that when the girth of a Nash
equilibrium is increasing, the upper bound on {\alpha} obtained by the simple
strategy changes is not increasing. To the end, we investigate the approach for
a coalitional variant of Nash equilibrium, where coalitions of two players
cannot collectively improve, and show that if {\alpha} >= 41n, then every such
Nash equilibrium is a tree
Fractal Dimension Analysis of Solar Granulation- Boxcounting dimension
The fractal dimension of high resolution Hinode solar granulation observations and numerical simulations is
studied and the results are compared. These observations are not influenced by atmospheric seeing conditions and
therefore allow a more realistic estimate of the fractal dimension than in previous works. Though arriving at
similar results for observations and simulation data, non integer fractal dimension , some differences in the
numerical values occur, and these are discussed
Characterization of Hydrogen Plasma Defined Graphene Edges
We investigate the quality of hydrogen plasma defined graphene edges by Raman
spectroscopy, atomic resolution AFM and low temperature electronic transport
measurements. The exposure of graphite samples to a remote hydrogen plasma
leads to the formation of hexagonal shaped etch pits, reflecting the anisotropy
of the etch. Atomic resolution AFM reveals that the sides of these hexagons are
oriented along the zigzag direction of the graphite crystal lattice and the
absence of the D-peak in the Raman spectrum indicates that the edges are high
quality zigzag edges. In a second step of the experiment, we investigate
hexagon edges created in single layer graphene on hexagonal boron nitride and
find a substantial D-peak intensity. Polarization dependent Raman measurements
reveal that hydrogen plasma defined edges consist of a mixture of zigzag and
armchair segments. Furthermore, electronic transport measurements were
performed on hydrogen plasma defined graphene nanoribbons which indicate a high
quality of the bulk but a relatively low edge quality, in agreement with the
Raman data. These findings are supported by tight-binding transport
simulations. Hence, further optimization of the hydrogen plasma etching
technique is required to obtain pure crystalline graphene edges.Comment: 10 pages, 7 figure
Role of âWestern Dietâ in Inflammatory Autoimmune Diseases
Developed societies, although having successfully reduced the burden of infectious disease, constitute an environment where metabolic, cardiovascular, and autoimmune diseases thrive. Living in westernized countries has not fundamentally changed the genetic basis on which these diseases emerge, but has strong impact on lifestyle and pathogen exposure. In particular, nutritional patterns collectively termed the âWestern dietâ, including high-fat and cholesterol, high-protein, high-sugar, and excess salt intake, as well as frequent consumption of processed and âfast foodsâ, promote obesity, metabolic syndrome, and cardiovascular disease. These factors have also gained high interest as possible promoters of autoimmune diseases. Underlying metabolic and immunologic mechanisms are currently being intensively explored. This review discusses the current knowledge relative to the association of âWestern dietâ with autoimmunity, and highlights the role of T cells as central players linking dietary influences to autoimmune pathology.National Institutes of Health (U.S.) (NIH grant P30-ES002109
The number of beds occupied is an independent risk factor for discharge of trauma patients
Reducing the burden of limited capacity on medical practitioners and public health systems requires a time-dependent characterization of hospitalization rates, such that inferences can be drawn about the underlying causes for hospitalization and patient discharge. The aim of this study was to analyze non-medical risk factors that lead to the discharge of trauma patients. This retrospective cohort study includes trauma patients who were treated in Switzerland between 2011 and 2018. The national Swiss database for quality assurance in surgery (AQC) was reviewed for trauma diagnoses according to the ICD-10 code. Non-medical risk factors include seasonal changes, daily changes, holidays, and number of beds occupied by trauma patients across Switzerland. Individual patient information was aggregated into counts per day of total patients, as well as counts per day of levels of each categorical variable of interest. The ARIMA-modeling was utilized to model the number of discharges per day as a function of auto aggressive function of all previously mentioned risk factors. This study includes 226,708 patients, 118,059 male (age 48.18, standard deviation (SD) 22.34 years) and 108,649 female (age 62.57, SD 22.89 years) trauma patients. The mean length of stay was 7.16 (SD 14.84) days and most patients were discharged home (n = 168,582, 74.8%). A weekly and yearly seasonality trend can be observed in admission trends. The mean number of occupied trauma beds ranges from 3700 to 4000 per day. The number of occupied beds increases on weekdays and decreases on holidays. The number of occupied beds is a positive, independent risk factor for discharge in trauma patients; as the number of occupied beds increases at any given time, so does the risk for discharge. The number of beds occupied represents an independent non-medical risk factor for discharge. Capacity determines triage of hospitalized patients and therefore might increase the risk of premature discharge
Abnormal neonatal sodium handling in skin precedes hypertension in the SAME rat
We discovered high Na(+) and water content in the skin of newborn Sprague-Dawley rats, which reduced ~ 2.5-fold by 7 days of age, indicating rapid changes in extracellular volume (ECV). Equivalent changes in ECV post birth were also observed in C57Bl/6 J mice, with a fourfold reduction over 7 days, to approximately adult levels. This established the generality of increased ECV at birth. We investigated early sodium and water handling in neonates from a second rat strain, Fischer, and an Hsd11b2-knockout rat modelling the syndrome of apparent mineralocorticoid excess (SAME). Despite Hsd11b2(-/-) animals exhibiting lower skin Na(+) and water levels than controls at birth, they retained ~ 30% higher Na(+) content in their pelts at the expense of K(+) thereafter. Hsd11b2(-/-) neonates exhibited incipient hypokalaemia from 15 days of age and became increasingly polydipsic and polyuric from weaning. As with adults, they excreted a high proportion of ingested Na(+) through the kidney, (56.15 ± 8.21% versus control 34.15 ± 8.23%; n = 4; P < 0.0001), suggesting that changes in nephron electrolyte transporters identified in adults, by RNA-seq analysis, occur by 4 weeks of age. Our data reveal that Na(+) imbalance in the Hsd11b2(-/-) neonate leads to excess Na(+) storage in skin and incipient hypokalaemia, which, together with increased, glucocorticoid-induced Na(+) uptake in the kidney, then contribute to progressive, volume contracted, salt-sensitive hypertension. Skin Na(+) plays an important role in the development of SAME but, equally, may play a key physiological role at birth, supporting post-natal growth, as an innate barrier to infection or as a rudimentary kidney
Waveform detection by deep learning reveals multi-area spindles that are selectively modulated by memory load
Sleep is generally considered to be a state of large-scale synchrony across thalamus and neocortex; however, recent work has challenged this idea by reporting isolated sleep rhythms such as slow oscillations and spindles. What is the spatial scale of sleep rhythms? To answer this question, we adapted deep learning algorithms initially developed for detecting earthquakes and gravitational waves in high-noise settings for analysis of neural recordings in sleep. We then studied sleep spindles in non-human primate electrocorticography (ECoG), human electroencephalogram (EEG), and clinical intracranial electroencephalogram (iEEG) recordings in the human. Within each recording type, we find widespread spindles occur much more frequently than previously reported. We then analyzed the spatiotemporal patterns of these large-scale, multi-area spindles and, in the EEG recordings, how spindle patterns change following a visual memory task. Our results reveal a potential role for widespread, multi-area spindles in consolidation of memories in networks widely distributed across primate cortex
α1A-Adrenergic Receptor-Directed Autoimmunity Induces Left Ventricular Damage and Diastolic Dysfunction in Rats
BACKGROUND: Agonistic autoantibodies to the alpha(1)-adrenergic receptor occur in nearly half of patients with refractory hypertension; however, their relevance is uncertain. METHODS/PRINCIPAL FINDINGS: We immunized Lewis rats with the second extracellular-loop peptides of the human alpha(1A)-adrenergic receptor and maintained them for one year. Alpha(1A)-adrenergic antibodies (alpha(1A)-AR-AB) were monitored with a neonatal cardiomyocyte contraction assay by ELISA, and by ERK1/2 phosphorylation in human alpha(1A)-adrenergic receptor transfected Chinese hamster ovary cells. The rats were followed with radiotelemetric blood pressure measurements and echocardiography. At 12 months, the left ventricles of immunized rats had greater wall thickness than control rats. The fractional shortening and dp/dt(max) demonstrated preserved systolic function. A decreased E/A ratio in immunized rats indicated a diastolic dysfunction. Invasive hemodynamics revealed increased left ventricular end-diastolic pressures and decreased dp/dt(min). Mean diameter of cardiomyocytes showed hypertrophy in immunized rats. Long-term blood pressure values and heart rates were not different. Genes encoding sarcomeric proteins, collagens, extracellular matrix proteins, calcium regulating proteins, and proteins of energy metabolism in immunized rat hearts were upregulated, compared to controls. Furthermore, fibrosis was present in immunized hearts, but not in control hearts. A subset of immunized and control rats was infused with angiotensin (Ang) II. The stressor raised blood pressure to a greater degree and led to more cardiac fibrosis in immunized, than in control rats. CONCLUSIONS/SIGNIFICANCE: We show that alpha(1A)-AR-AB cause diastolic dysfunction independent of hypertension, and can increase the sensitivity to Ang II. We suggest that alpha(1A)-AR-AB could contribute to cardiovascular endorgan damage
The Long Noncoding MALAT-1 RNA Indicates a Poor Prognosis in Non-small Cell Lung Cancer and Induces Migration and Tumor Growth
Introduction:The functions of large noncoding RNAs (ncRNAs) have remained elusive in many cases. Metastasis-Associated-in-Lung-Adenocarcinoma-Transcript-1 (MALAT-1) is an ncRNA that is highly expressed in several tumor types.Methods:Overexpression and RNA interference (RNAi) approaches were used for the analysis of the biological functions of MALAT-1 RNA. Tumor growth was studied in nude mice. For prognostic analysis, MALAT-1 RNA was detected on paraffin-embedded non-small cell lung cancer (NSCLC) tissue probes (n = 352) using in situ hybridization.Results:MALAT-1 was highly expressed in several human NSCLC cell lines. MALAT-1 expression was regulated by an endogenous negative feedback loop. In A549 NSCLCs, RNAi-mediated suppression of MALAT-1 RNA suppressed migration and clonogenic growth. Forced expression of MALAT-1 in NIH 3T3 cells significantly increased migration. Upon injection into nude mice, NSCLC xenografts with decreased MALAT-1 expression were impaired in tumor formation and growth. In situ hybridization on paraffin-embedded lung cancer tissue probes revealed that high MALAT-1 RNA expression in squamous cell carcinoma of the lung was associated with a poor prognosis. On genetic level, MALAT-1 displays the strongest association with genes involved in cancer like cellular growth, movement, proliferation, signaling, and immune regulation.Conclusions:These data indicate that MALAT-1 expression levels are associated with patient survival and identify tumor-promoting functions of MALAT-1
Vitamin D depletion aggravates hypertension and target-organ damage
BACKGROUND: We tested the controversial hypothesis that vitamin D depletion aggravates hypertension and target-organ damage by influencing renin. METHODS AND RESULTS: Four-week-old double-transgenic rats (dTGR) with excess angiotensin (Ang) II production due to overexpression of the human renin (hREN) and angiotensinogen (hAGT) genes received vitamin D-depleted (n=18) or standard chow (n=15) for 3 weeks. The depleted group had very low serum 25-hydroxyvitamin D levels (mean+/-SEM; 3.8+/-0.29 versus 40.6+/-1.19 nmol/L) and had higher mean systolic BP at week 5 (158+/-3.5 versus 134.6+/-3.7 mm Hg, P<0.001), week 6 (176.6+/-3.3 versus 162.3+/-3.8 mm Hg, P<0.01), and week 7 (171.6+/-5.1 versus 155.9+/-4.3 mm Hg, P<0.05). Vitamin D depletion led to increased relative heart weights and increased serum creatinine concentrations. Furthermore, the mRNAs of natriuretic peptides, neutrophil gelatinase-associated lipocalin, hREN, and rRen were increased by vitamin D depletion. Regulatory T cells in the spleen and in the circulation were not affected. Ang metabolites, including Ang II and the counter-regulatory breakdown product Ang 1 to 7, were significantly up-regulated in the vitamin D-depleted groups, while ACE-1 and ACE-2 activities were not affected. CONCLUSIONS: Short-term severe vitamin D depletion aggravated hypertension and target-organ damage in dTGR. Our data suggest that even short-term severe vitamin D deficiency may directly promote hypertension and impacts on renin-angiotensin system components that could contribute to target-organ damage. The findings add to the evidence that vitamin D deficiency could also affect human hypertension
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