Covid-19 triage in the emergency department 2.0: how analytics and AI transform a human-made algorithm for the prediction of clinical pathways

The Covid-19 pandemic has pushed many hospitals to their capacity limits. Therefore, a triage of patients has been discussed controversially primarily through an ethical perspective. The term triage contains many aspects such as urgency of treatment, severity of the disease and pre-existing conditions, access to critical care, or the classification of patients regarding subsequent clinical pathways starting from the emergency department. The determination of the pathways is important not only for patient care, but also for capacity planning in hospitals. We examine the performance of a human-made triage algorithm for clinical pathways which is considered a guideline for emergency departments in Germany based on a large multicenter dataset with over 4,000 European Covid-19 patients from the LEOSS registry. We find an accuracy of 28 percent and approximately 15 percent sensitivity for the ward class. The results serve as a benchmark for our extensions including an additional category of palliative care as a new label, analytics, AI, XAI, and interactive techniques. We find significant potential of analytics and AI in Covid-19 triage regarding accuracy, sensitivity, and other performance metrics whilst our interactive human-AI algorithm shows superior performance with approximately 73 percent accuracy and up to 76 percent sensitivity. The results are independent of the data preparation process regarding the imputation of missing values or grouping of comorbidities. In addition, we find that the consideration of an additional label palliative care does not improve the results

Intracellular Serotonin Modulates Insulin Secretion from Pancreatic β-Cells by Protein Serotonylation

Non-neuronal, peripheral serotonin deficiency causes diabetes mellitus and identifies an intracellular role for serotonin in the regulation of insulin secretion

Magnetische Strukturen in [Er/Tb]-Schichtsystemen : Einfluss der magnetischen Nachbarschaft und konkurrierender Anisotropien

Magnetic structures in [Er|Tb]-multilayers: Magnetic Proximity and competing anisotropies The present work concerns the influence of the artificial superstructure and competing anisotropies on the magnetic structure in [Er|Tb] superlattices. Combining neutron diffraction and resonance x-ray magnetic scattering (RXMS) the long range magnetic ordering of localized 4f states can be related to a coherent spin density wave in the conduction bands of both Er and Tb. The direct observation of spin density wave was made possible only by the improvements of the RXMS technique, i.e., an excellent source at the beamline 6id-b of the APS at the Argonne National Lab and a very efficient polarization analysis to distinguish the magnetic signal from the much stronger charge scattering. To understand the magnetic behavior of a superlattice an precise knowledge of the structural properties is needed. Therefore the growth process for epitaxial multilayers was optimized by in situ low energy electron diffraction and Auger electron spectroscopy. Following recipes given in literature for other rare earth systems, the growth parameters have been adjusted for Er and Tb. In a superlattice the quality of the interfaces is particularly important. Their properties in complete multilayers have been analysed ex situ by grazing incidence x-ray diffraction. The interfaces extend over 3-4 atomic layers, but the roughness is vertically correlated, as seen by the diffuse scattering. Therefore a squared interface profile is obtained locally even for small layer thicknesses. Wide angle diffraction of neutrons and x-ray confirms the squared structure of [Er_nEr|Tb_nTb] superlattices, the indices denoting the layer thickness in atomic layers, with up to 150 repetitions of one bilayer unit. Ferromagnetic order sets in at a temperature of 230 K, if the Tb layer thickness is more then 20 atomic layers. The ferromagnetic blocks are coupled, depending on temperature and interlayer thickness. Bulk Tb undergoes a phase transition to a helical magnetic structure at this temperature. The suppression of the bulk helical structure in Tb is due to epitaxial strains within the superlattice. In contrast the [Er_20|Tb_5] sample forms a modulated magnetic structure below 150 K. Additionally basal plane ferromagnetic order appears below 40 K, with an antiferromagnetic coupling of ordered layers. The RXMS results confirm the existence of a common superlattice band structure which is responsible for the magnetic proximity effects. A common electronic band structure is found in an Er_0.8Tb_0.2 film, too. The comparison with the superlattice clarifies the difference between statistical lattice site occupation and an artificial superstructure. This opens the opportunity of tailored magnetic properties by a man made structure

Cross-seeding by prion protein inactivates TDP-43

Abstract A common pathological denominator of various neurodegenerative diseases is the accumulation of protein aggregates. Neurotoxic effects are caused by a loss of the physiological activity of the aggregating protein and/or a gain of toxic function of the misfolded protein conformers. In transmissible spongiform encephalopathies or prion diseases, neurodegeneration is caused by aberrantly folded isoforms of the prion protein (PrP). However, it is poorly understood how pathogenic PrP conformers interfere with neuronal viability. Employing in vitro approaches, cell culture, animal models, and patients’ brain samples, we show that misfolded PrP can induce aggregation and inactivation of TDP-43. Purified PrP aggregates interact with TDP-43 in vitro and in cells and induce the conversion of soluble TDP-43 into non-dynamic protein assemblies. Similarly, mislocalized PrP conformers in the cytosol bind to and sequester TDP-43 in cytosolic aggregates. As a consequence, TDP-43-dependent splicing activity in the nucleus is significantly decreased, leading to altered protein expression in cells with cytosolic PrP aggregates. Finally, we present evidence for cytosolic TDP-43 aggregates in neurons of transgenic flies expressing mammalian PrP and Creutzfeldt–Jakob disease patients. Our study identified a novel mechanism of how aberrant PrP conformers impair physiological pathways by cross-seeding

The Jülich high brilliance neutron source project - Improving access to neutrons

1.5Full digital generat a partir de la base topogràfica 1:5 000. Els fulls d'aquesta sèrie corresponen a la divisió 4 x 4 de la malla de distribució del Mapa topográfico nacional de España 1:50 000. Cada full inclou 2 finestres (Mapa índex de la sèrie; Mapa guia). - Projecció Universal Transversa Mercator (UTM), fus 31, sobre el·lipsoide internacional i datum europeu. Equidistància de les corbes de nivell: 5 m.Imatge digital de 90 x 67 cm1:5 000300 PP

All-cause mortality and disease progression in SARS-CoV-2-infected patients with or without antibiotic therapy: an analysis of the LEOSS cohort

Purpose!#!Reported antibiotic use in coronavirus disease 2019 (COVID-19) is far higher than the actual rate of reported bacterial co- and superinfection. A better understanding of antibiotic therapy in COVID-19 is necessary.!##!Methods!#!6457 SARS-CoV-2-infected cases, documented from March 18, 2020, until February 16, 2021, in the LEOSS cohort were analyzed. As primary endpoint, the correlation between any antibiotic treatment and all-cause mortality/progression to the next more advanced phase of disease was calculated for adult patients in the complicated phase of disease and procalcitonin (PCT) ≤ 0.5 ng/ml. The analysis took the confounders gender, age, and comorbidities into account.!##!Results!#!Three thousand, six hundred twenty-seven cases matched all inclusion criteria for analyses. For the primary endpoint, antibiotic treatment was not correlated with lower all-cause mortality or progression to the next more advanced (critical) phase (n = 996) (both p > 0.05). For the secondary endpoints, patients in the uncomplicated phase (n = 1195), regardless of PCT level, had no lower all-cause mortality and did not progress less to the next more advanced (complicated) phase when treated with antibiotics (p > 0.05). Patients in the complicated phase with PCT > 0.5 ng/ml and antibiotic treatment (n = 286) had a significantly increased all-cause mortality (p = 0.029) but no significantly different probability of progression to the critical phase (p > 0.05).!##!Conclusion!#!In this cohort, antibiotics in SARS-CoV-2-infected patients were not associated with positive effects on all-cause mortality or disease progression. Additional studies are needed. Advice of local antibiotic stewardship- (ABS-) teams and local educational campaigns should be sought to improve rational antibiotic use in COVID-19 patients