OmniFold: A Method to Simultaneously Unfold All Observables

Collider data must be corrected for detector effects ("unfolded") to be compared with many theoretical calculations and measurements from other experiments. Unfolding is traditionally done for individual, binned observables without including all information relevant for characterizing the detector response. We introduce OmniFold, an unfolding method that iteratively reweights a simulated dataset, using machine learning to capitalize on all available information. Our approach is unbinned, works for arbitrarily high-dimensional data, and naturally incorporates information from the full phase space. We illustrate this technique on a realistic jet substructure example from the Large Hadron Collider and compare it to standard binned unfolding methods. This new paradigm enables the simultaneous measurement of all observables, including those not yet invented at the time of the analysis.Comment: 8 pages, 3 figures, 1 table, 1 poem; v2: updated to approximate PRL versio

Functional effects of schizophrenia-linked genetic variants on intrinsic single-neuron excitability: A modeling study

Background: Recent genome-wide association studies (GWAS) have identified a large number of genetic risk factors for schizophrenia (SCZ) featuring ion channels and calcium transporters. For some of these risk factors, independent prior investigations have examined the effects of genetic alterations on the cellular electrical excitability and calcium homeostasis. In the present proof-of-concept study, we harnessed these experimental results for modeling of computational properties on layer V cortical pyramidal cell and identify possible common alterations in behavior across SCZ-related genes. Methods: We applied a biophysically detailed multi-compartmental model to study the excitability of a layer V pyramidal cell. We reviewed the literature on functional genomics for variants of genes associated with SCZ, and used changes in neuron model parameters to represent the effects of these variants. Results: We present and apply a framework for examining the effects of subtle single nucleotide polymorphisms in ion channel and Ca2+ transporter-encoding genes on neuron excitability. Our analysis indicates that most of the considered SCZ- related genetic variants affect the spiking behavior and intracellular calcium dynamics resulting from summation of inputs across the dendritic tree. Conclusions: Our results suggest that alteration in the ability of a single neuron to integrate the inputs and scale its excitability may constitute a fundamental mechanistic contributor to mental disease, alongside with the previously proposed deficits in synaptic communication and network behavior

Portuguese validation of the Bergen Facebook Addiction Scale: an Empirical Study

Previous research on Social Networking Sites (SNSs) addiction have suggest the need to improve assessment of this behavioral addiction. The present study aimed at validating a Portuguese version of the Bergen Facebook Addiction Scale (BFAS), a widely used instrument to assess addiction to Facebook. A study was conducted in a sample of 509 Portuguese adolescent using an online survey. The psychometric properties (construct validity, criterion validity, and reliability) of the Portuguese BFAS was scrutinized. The results from the psychometric analyses suggested that the new validated instrument had excellent psychometric properties. The CFA confirmed the original one-factor solution of the BFAS and criterion validity was warranted. The reliability of the BFAS was supported by satisfactory levels of internal consistency as measured by the Cronbach’s alpha (α = .83), composite reliability (CR = .82), and factor determinacy (FD = .91). Overall, the results provided empirical support for the validity and reliability of the Portuguese BFAS. Moreover, the results were highly comparable with the findings of the original development study of the BFAS and cross-cultural support for the scale was obtained

Admission C – reactive protein after acute ischemic stroke is associated with stroke severity and mortality: The 'Bergen stroke study'

<p>Abstract</p> <p>Background</p> <p>There is growing evidence that inflammation plays an important role in atherogenesis. Previous studies show that C-reactive protein (CRP), an inflammatory marker, is associated with stroke outcomes and future vascular events. It is not clear whether this is due a direct dose-response effect or rather an epiphenomenon. We studied the effect of CRP measured within 24 hours after stroke onset on functional outcome, mortality and future vascular events.</p> <p>Methods</p> <p>We prospectively studied 498 patients with ischemic stroke who were admitted within 24 hours after the onset of symptoms. CRP and NIH stroke scale (NIHSS) were measured at the time of admission. Short-term functional outcome was measured by modified Rankin scale (mRS) and Barthel ADL index (BI) 7 days after admission. Patients were followed for up to 2.5 years for long-term mortality and future vascular events data.</p> <p>Results</p> <p>The median CRP at admission was 3 mg/L. High CRP was associated with high NIHSS (p = 0.01) and high long-term mortality (p < 0.0001). After adjusting for confounding variables, high CRP remained to be associated with high NIHSS (p = 0.02) and high long-term mortality (p = 0.002). High CRP was associated with poor short-term functional outcomes (mRS > 3; BI < 95) (p = 0.01; p = 0.03). However, the association was not significant after adjusting for confounding variables including stroke severity (p = 0.98; p = 0.88). High CRP was not associated with future vascular events (p = 0.98).</p> <p>Conclusion</p> <p>Admission CRP is associated with stroke severity and long-term mortality when measured at least 24 hours after onset. There is a crude association between high CRP and short-term functional outcome which is likely secondary to stroke severity. CRP is an independent predictor of long-term mortality after ischemic stroke.</p

When is a new scale not a new scale? The case of the Bergen Shopping Addiction Scale and the Compulsive Online Shopping Scale

Manchiraju et al. (International Journal of Mental Health and Addiction, 1–15, 2016) published the Compulsive Online Shopping Scale (COSS) in the International Journal of Mental Health and Addiction (IJMHA). To develop their measure of compulsive online shopping, Manchiraju and colleagues adapted items from the seven-item Bergen Shopping Addiction Scale (BSAS) and its' original 28-item item pool. Manchiraju et al. did not add or remove any of the original seven items, and did not substantially change the content of any of the 28 items on which the BSAS was based. They simply added the word "online" to each existing item. Given that the BSAS was specifically developed to take into account the different ways in which people now shop and to include both online and offline shopping, there does not seem to be a good rationale for developing an online version of the BSAS. It is argued that the COSS is not really an adaptation of the BSAS but an almost identical instrument based on the original 28-item pool

Computational Modeling of Genetic Contributions to Excitability and Neural Coding in Layer V Pyramidal Cells: Applications to Schizophrenia Pathology

Pyramidal cells in layer V of the neocortex are one of the most widely studied neuron types in the mammalian brain. Due to their role as integrators of feedforward and cortical feedback inputs, they are well-positioned to contribute to the symptoms and pathology in mental disorders—such as schizophrenia—that are characterized by a mismatch between the internal perception and external inputs. In this modeling study, we analyze the input/output properties of layer V pyramidal cells and their sensitivity to modeled genetic variants in schizophrenia-associated genes. We show that the excitability of layer V pyramidal cells and the way they integrate inputs in space and time are altered by many types of variants in ion-channel and Ca2+ transporter-encoding genes that have been identified as risk genes by recent genome-wide association studies. We also show that the variability in the output patterns of spiking and Ca2+ transients in layer V pyramidal cells is altered by these model variants. Importantly, we show that many of the predicted effects are robust to noise and qualitatively similar across different computational models of layer V pyramidal cells. Our modeling framework reveals several aspects of single-neuron excitability that can be linked to known schizophrenia-related phenotypes and existing hypotheses on disease mechanisms. In particular, our models predict that single-cell steady-state firing rate is positively correlated with the coding capacity of the neuron and negatively correlated with the amplitude of a prepulse-mediated adaptation and sensitivity to coincidence of stimuli in the apical dendrite and the perisomatic region of a layer V pyramidal cell. These results help to uncover the voltage-gated ion-channel and Ca2+ transporter-associated genetic underpinnings of schizophrenia phenotypes and biomarkers