bluuebunny/crossref_metadata_2025_split huggingface dataset:
Higher-order power corrections in a transverse-momentum cut for colour-singlet production at NLO
Authors: Cieri Leandro , Oleari Carlo , Rocco Marco 
Published: October 2019

Abstract
We consider the production of a colourless system at next-to-leading order in the strong coupling constant $$\alpha _{{\displaystyle } {\scriptstyle } {\scriptscriptstyle } {\scriptscriptstyle } \mathrm{S}}$$αS. We impose a transverse-momentum cutoff, $$q_{{\displaystyle } {\scriptstyle } {\scriptscriptstyle } {\scriptscriptstyle } \mathrm{T}}^{{\displaystyle } {\scriptstyle } {\scriptscriptstyle } {\scriptscriptstyle } \mathrm{cut}}$$qTcut, on the colourless final state and we compute the power corrections for the inclusive cross section in the cutoff, up to the fourth power. The study of the dependence of the cross section on $$q_{{\displaystyle } {\scriptstyle } {\scriptscriptstyle } {\scriptscriptstyle } \mathrm{T}}^{{\displaystyle } {\scriptstyle } {\scriptscriptstyle } {\scriptscriptstyle } \mathrm{cut}}$$qTcut allows for an understanding of its behaviour at the boundaries of the phase space, giving hints on the structure at all orders in $$\alpha _{{\displaystyle } {\scriptstyle } {\scriptscriptstyle } {\scriptscriptstyle } \mathrm{S}}$$αS and on the identification of universal patterns. The knowledge of such power corrections is also a required ingredient in order to reduce the dependence on the transverse-momentum cutoff of the QCD cross sections at higher orders, when the $$q_{\mathrm{T}}$$qT-subtraction method is applied. We present analytic results for both Drell–Yan vector boson and Higgs boson production in gluon fusion and we illustrate a process-independent procedure for the calculation of the all-order power corrections in the cutoff. In order to show the impact of the power-correction terms, we present selected numerical results and discuss how the residual dependence on $$q_{{\displaystyle } {\scriptstyle } {\scriptscriptstyle } {\scriptscriptstyle } \mathrm{T}}^{{\displaystyle } {\scriptstyle } {\scriptscriptstyle } {\scriptscriptstyle } \mathrm{cut}}$$qTcut affects the total cross section for Drell–Yan Z production and Higgs boson production via gluon fusion at the LHC.
AN AI APPROACH TO MEASURING FINANCIAL RISK
Authors: YU LINING , HÄRDLE WOLFGANG KARL , BORKE LUKAS , BENSCHOP THIJS 
Published: October 2019

AI artificial intelligence brings about new quantitative techniques to assess the state of an economy. Here, we describe a new measure for systemic risk: the Financial Risk Meter (FRM). This measure is based on the penalization parameter (λ) of a linear quantile lasso regression. The FRM is calculated by taking the average of the penalization parameters over the 100 largest US publicly-traded financial institutions. We demonstrate the suitability of this AI-based risk measure by comparing the proposed FRM to other measures for systemic risk, such as VIX, SRISK and Google Trends. We find that mutual Granger causality exists between the FRM and these measures, which indicates the validity of the FRM as a systemic risk measure. The implementation of this project is carried out using parallel computing, the codes are published on www.quantlet.de with keyword [Formula: see text] FRM. The R package RiskAnalytics is another tool with the purpose of integrating and facilitating the research, calculation and analysis methods around the FRM project. The visualization and the up-to-date FRM can be found on hu.berlin/frm.
Direct pathway neurons in mouse dorsolateral striatum in vivo receive stronger synaptic input than indirect pathway neurons
Authors: Filipović Marko , Ketzef Maya , Reig Ramon , Aertsen Ad , Silberberg Gilad , Kumar Arvind 
Published: October 2019

Striatal projection neurons, the medium spiny neurons (MSNs), play a crucial role in various motor and cognitive functions. MSNs express either D1- or D2-type dopamine receptors and initiate the direct-pathway (dMSNs) or indirect pathways (iMSNs) of the basal ganglia, respectively. dMSNs have been shown to receive more inhibition than iMSNs from intrastriatal sources. Based on these findings, computational modeling of the striatal network has predicted that under healthy conditions dMSNs should receive more total input than iMSNs. To test this prediction, we analyzed in vivo whole cell recordings from dMSNs and iMSNs in healthy and dopamine-depleted (6OHDA) anaesthetized mice. By comparing their membrane potential fluctuations, we found that dMSNs exhibited considerably larger membrane potential fluctuations over a wide frequency range. Furthermore, by comparing the spike-triggered average membrane potentials, we found that dMSNs depolarized toward the spike threshold significantly faster than iMSNs did. Together, these findings (in particular the STA analysis) corroborate the theoretical prediction that direct-pathway MSNs receive stronger total input than indirect-pathway neurons. Finally, we found that dopamine-depleted mice exhibited no difference between the membrane potential fluctuations of dMSNs and iMSNs. These data provide new insights into the question of how the lack of dopamine may lead to behavioral deficits associated with Parkinson’s disease. NEW & NOTEWORTHY The direct and indirect pathways of the basal ganglia originate from the D1- and D2-type dopamine receptor expressing medium spiny neurons (dMSNs and iMSNs). Theoretical results have predicted that dMSNs should receive stronger synaptic input than iMSNs. Using in vivo intracellular membrane potential data, we provide evidence that dMSNs indeed receive stronger input than iMSNs, as has been predicted by the computational model.
Оценка качества жизни в отдаленном периоде у больных с послеоперационными вентральными грыжами
Authors: Davlatov S. S. 
Published: October 2019

Цель работы: анализ качества жизни пациентов по усовершенствованной шкале у больных с послеоперационными вентральными грыжами.
Материалы и методы. Основу для исследования составили 217 больных с послеоперационными вентральными грыжами, которые находились под наблюдением и поступившие в хирургические отделения 1 и 2 клиники Самаркандского государственного медицинского института в сроки с 2009 по 2017 год. Больные были разделены на две группы, которые в зависимости от вида герниопластики (аутогерниопластика или аллогернипластика) были распределены ещё на две подгруппы: 1 – группа сравнения – 135 больных (2009–2014 гг.), которым применены стандартные меры по предоперационной подготовке; 2 – основная группа – 82 больных (2015–2017 гг.), при лечении которых применён усовершенствованный алгоритм выбора оптимального способа хирургического лечения.
Результаты исследований и их обсуждение. После применение предложенных разработок и инновационных подходов качество жизни больных с послеоперационными вентральными грыжами, перенесших герниопластику, в основной группе улучшилось в отличие от пациентов группы сравнения.
Abstract 171: The Effects of Adolescent Binge Alcohol Exposure to Cardiovascular Structure and Function
Authors: Ai Lizhuo , Perez Edith , Heroux Maxime , Zlobin Andrei , Asimes AnnaDorothea , Cao Quan , Chung Charles S , Pak Toni R , Kirk Jonathan A 
Published: October 2019

While the effects of alcohol consumption on the adult heart have been well studied, the impact to the adolescent heart is almost entirely unknown. Adolescents primarily consume alcohol in a binge pattern, which elevates blood alcohol content (BAC) to 0.08 g/dL within 2 hours. During adolescence the body grows rapidly, and the heart must also grow (through cellular hypertrophy) to meet this increasing demand. Our goal was to determine the impact of adolescent binge alcohol exposure on the heart, using an outbred rat model.
On postnatal day (PND) 37 (adolescence), rats were gavaged 3 g/kg EtOH for 3 days, H2O for 2 days, and EtOH for 3 more days, then sacrificed following the last dose (Binge). The control group received only H2O (Water). Both groups had normal food and water intake and weight gain. BAC was 0.08 g/dL in the Binge group and 0 in the Water group. Water rats experienced a ~40% increase in LV end-diastolic volume (LVEDV) due to normal growth along with a parallel increase in end-systolic volume such that ejection fraction (EF) was preserved. Conversely, Binge rats only had half that increase in LVEDV, and a decrease in systolic diameter resulting in increased EF. We hypothesize alcohol impaired normal cardiac growth, and systolic function increased to maintain cardiac output. Increased systolic function suggested beta-adrenergic activation, which was supported by increased troponin I phosphorylation at the PKA sites in the Binge group.
Doppler indicated the E/A ratio increased with age in the Water group, but in the Binge group the E/A ratio did not change with age. Further, the Binge group displayed increased single cell passive stiffness level (sarcomere length: 1.7-2.4 μm) compared to Water, likely due to altered titin phosphorylation. Lastly, we performed RNA-seq and identified 58 down-regulated and 10 up-regulated genes in the Binge group. Many of these genes suggest a switch in substrate utilization from fatty acid to glucose metabolism in the Binge rats.
These data reveal a previously unappreciated pathological impact of adolescent binge alcohol exposure. The young heart can compensate for these consequences at first and appear healthy. However, the long term impact of these effects may be significant and whose underlying cause was previously unknown.
Abstract 241: Pharmacological Evaluation of Novel Anti-thrombospondin-1 Decoy Strategy for Prophylaxis of Atrial Fibrillation-associated Ischemic Stroke
Authors: Elbayoumi Tamer , Sturdivant Jalicia , Ganguly Samayita , Yao Mingyi 
Published: October 2019

Hemostatic abnormalities mainly decreased blood flow and increased stasis, and platelet hyper-aggregation increase thrombotic risk subsequent atrial fibrillation (AF) episodes. Excess elevation of extracellular glycoprotein thrombospondin 1 (TSP1) in circulation has emerged to predict prognosis of ischemic stroke. Moreover, TSP1 is found strongly associated with platelet hyper-aggregability and impaired nitric oxide response, through its cognate receptor CD47, thus exacerbating ischemic progression in AF patients. TSP1 arises as a prospective target of our candidate medicine.
Our work provides “proof-of-concept” of a novel pharmacological strategy, relying on soluble recombinant human CD47 peptide (rh-CD47p) to serve as a decoy receptor to specifically bind TSP1, and consequently neutralize TSP1-impaired vasorelaxation.

Our pilot studies were initially conducted with isolated mouse thoracic aorta. A pre-treatment with rh-CD47p (added 15 min prior to TSP1 incubation) showed a significant amelioration of TSP1-impaired endothelium-dependent vasodilation (
p
<0.0001, rh-CD47p+TSP1 vs. TSP1, n=6), indicating a prophylactic effect by rh-CD47p against vasoconstriction enhanced by excess TSP1. A post-treatment set-up, where TSP1 incubation was started 15 min prior to rh-CD47p addition to mimic pre-existing high level of TSP1 in ischemic stroke, exhibited a marked reversal of TSP1-inhibited vasodilation back to the same level as controls (
p
<0.0001, rh-CD47p+TSP1 vs. TSP1, n=4). Dose titration of rh-CD47p in molar ratios to TSP1 in both set-ups identified the dose range of rh-CD47p for prevention/recovery from TSP1-induced vascular dysfunction.

Binding of rh-CD47p and TSP1 was first verified as the primary mechanism via Western Blot, and further quantified with a modified ELISA assay. A linear correlation was found between % of rh-CD47p bound to TSP1 and dose of rh-CD47p added (r
2
=0.8).

Current results established the ground of rh-CD47p as a unique pharmacologic moiety for drug development to limit vasoconstriction and improve vasodilation against TSP1 in excess, thus showing great potential for proposed novel decoy CD47-coated formulation to abrogate/mitigate TSP1-associated cardiovascular complications in AF patients.
Abstract 375: Acetyl-CoA Production by Specific Metabolites Promotes Cardiac Repair After Myocardial Infarction via Mediating Histone Acetylation
Authors: Lei Ienglam , Tian Shuo , Gao Wenbin , Wang Zhong 
Published: October 2019

In this study, we set out to identify an interlinked metabolic and epigenetic network that produces acetyl-CoA for histone acetylation and gene regulation, and determine whether this network promotes heart repair and protection after I/R injury. Myocardial ischemic reperfusion (I/R) injury induces dramatic metabolic changes and is accompanied with extensive epigenetic changes. Recent studies reveal that energy metabolism and chromatin epigenetics are intimately linked in cellular functions. In particular, acetyl-CoA is a building block for energy metabolism and histone acetylation. However, the acetyl-CoA mediated regulatory machinery integrating metabolic pathways and chromatin modifications has been under-explored in heart repair and protection.
We conducted a screen of energy metabolites in promoting histone acetylation and heart repair both in vivo and in vitro. Our screen identified that acetate, pyruvate, and octanoic acid (8C) but not citrate and nonanoic acid (9C) improved heart function after MI in rats. In particular, 8C administration resulted in the most significant heart functional recovery after MI. More importantly, in a more clinically relevant setting, 8C injection at the time of reperfusion 45 minutes after left anterior descending coronary (LAD) ligation showed comparable repair effect to that of 8C administration before LAD ligation, suggesting that 8C could be a very effective metabolic natural product to treat MI. Mechanistically, 8C promoted histone acetylation in CM chromatin after IR injury and inhibited CM death by activating expression of anti-oxidant genes Nrf2, HO1, and NQO1. We further established that the 8C promoted histone acetylation and heart repair was transduced by metabolic enzyme medium-chain acyl-CoA dehydrogenase (MCAD) and histone acetylase GCN5/KAT2A.
Therefore, this study has elucidated an interlinked metabolic/epigenetic network comprising 8C, acetyl-CoA, MCAD, and KAT2A in stimulating histone acetylation and anti-oxidative stress gene expression to combat heart injury. This study provides a novel strategy for treating myocardial I/R disease at the interface of metabolism and epigenetics.
Abstract 656: Construction and Application of an Epigenetic Atlas of the Human Heart
Authors: Prasher Dimple , Zhang Hao , McCarthy Patrick M , Oudit Gavin , Fedak Paul W , Greenway Steven C 
Published: October 2019

Epigenetic modifications, including DNA methylation, regulate gene expression and contribute to the differentiation of cells. Tissues are characterized by methylation patterns that reflect their specific functions and origin. Currently, there is limited knowledge of the epigenetic patterns of the heart. To address this gap, we generated methylation profiles for all anatomical regions of the human heart. We hypothesize that unique differentially methylated regions (DMRs) of DNA exist for each cardiac region and that these patterns are disrupted in heart failure.
Using non-diseased cardiac tissue and reduced representation bisulfite sequencing on a Illumina platform, we generated genome-wide methylomes for the human right atrium (n=4), left atrium (n=4), right ventricle (n=4), left ventricle (n=4), aorta (n=3), pulmonary artery (n=2), mitral valve (n=3), tricuspid valve (n=3), aortic valve (n=3) and pulmonary valve (n=3). DMRs, defined as regions with significantly different mean methylation differences, were identified using Metilene.

For each tissue we identified between 10-20 million reads covering 8-10 million CpG methylation sites and 4-228 tissue-specific DMRs. There were relatively few (4) different DMRs between the left and right ventricles but 228 unique DMRs were found in the vessels (aorta and pulmonary artery) compared to the ventricles including regions upstream of
BMP3
and
FOXC1
, genes implicated in cardiogenesis. We then applied this approach and normal data to the analysis of disease. We generated additional left ventricular methylomes from adult (n=3) and pediatric (n=3) patients with heart failure. We identified 19 unique DMRs in the adult group and 107 in the pediatric group. Genes associated with pediatric HF DMRs included
ROCK1
and
FBLN2
that have been previously implicated in contraction and remodelling.

We have created an atlas of the human heart based upon differences in DNA methylation between the anatomical regions of the human heart. This data will help increase our understanding of cardiac development, identify new disease biomarkers and have application to a wide range of cardiac diseases
Abstract 750: Gene Signatures to Distinguish Amyloid Cardiomyopathy Risk in Multiple Myeloma Patients
Authors: Jha Alokkumar , Morgado Isabel , Lee Dian J , Alexander Kevin , Tsai Cheng-Yu , Schimmel Katharina , Ward Jennifer , Witteles R , Liedtke Michaela , Liao Ronglih , Dangwal Seema 
Published: October 2019

Amyloid light chain (AL) amyloidosis results from tissue deposition of clonal light chains, most commonly produced by clonal plasma cells. AL amyloidosis is closely associated with multiple myeloma (MM), another disease which arises from clonal plasma cell proliferation. Here we aim to identify gene signatures to distinguish AL cardiomyopathy (AL-CM) risk in MM patients.
We utilized publicly available data sets and applied Graph Cluster Perturbation approach to cluster the co-expression networks based on pathways in MM and AL-CM utilizing 225 samples from four datasets: GSE42955 study (12 dilated CM, 12 ischemic CM and 5 control LV human heart tissues), GSE95077 study (16 amiloride drug treated/untreated myeloma cell line samples), GSE24128 study (16 newly diagnosed AL with monoclonal plasma cell samples over- or under-expressing cyclin D1), and GSE6477 study (76 primary bone marrow samples from hyper-diploid myeloma patients and 80 non-hyperdiploid MM patients). From these data sets, the networks for extracellular matrix organization, immune system, innate immune system, metabolism, and neutrophil degranulation pathways for MM and amyloid CM were extracted.

Summary:
Ranking of the perturbed genes based on pathways similarity index in MM and AL resulted in a panel of genes: CD44, NRAS, GRAP2, CTLA4, GSN, CCND1, NFKB1, and IRF1 (p= <0.01). As shown in

Figure

, the high hazard ratio of this gene cluster in MM with AL-CM (3.76; p=0.021) compared to MM without CM (0.96; p=0.032) suggests the potential of this gene panel to distinguish high or low risk groups in MM based on survival.
Abstract 848: The Iron Chelator Deferiprone Clears Hemorrhagic Byproducts Following Acute Myocardial Infarction in a Swine Model of Ischemia-Reperfusion
Authors: Weyers Jill J , Thomas Reuben , Qi Xiuilng , Barry Jennifer , Rabadia Vraj , Manca Dino , Connelly John , Spino Michael , Strauss Bradley H , Wright Graham A , Ghugre Nilesh R 
Published: October 2019

Current treatments for myocardial infarction (MI) aim to remove the vascular occlusion and reperfuse the infarcted tissue. While reperfusion can salvage myocardium, it can also increase damage to the unsalvageable tissue, one mechanism of which is hemorrhage; the resulting blood and iron deposits increase edema and inflammation. We hypothesize that removing these iron deposits with the iron chelating drug deferiprone (DFP) will reduce inflammation and lead to faster healing post-MI.
Using a swine model of ischemia-reperfusion, pigs were administered either DFP or saline for four weeks post-MI. Cardiac MRI tracked heart function, infarct progression (via late gadolinium enhancement), hemorrhage (via T2* imaging), and edema (via T2 imaging) at baseline and 1 day, 1 week, and 4 weeks post-MI. Animals were then sacrificed and hearts were processed for histology.
Treatment with DFP decreased the presence of iron in the infarct compared to saline by one week post-MI, as shown by increased T2* values. DFP treatment also decreased end diastolic wall swelling, suggesting less inflammation post-MI. To support this, T2 values and histology both revealed trends toward less edema with DFP. Histology also showed trended increases in fibroblast proliferation and collagen deposition at four weeks post-MI in the treatment group, consistent with a faster resolution to scar. Ventricular remodeling (by ventricular volumes), infarct size (by MRI, histology and blood Troponin I levels), and infarct transmurality were all unaffected, but contractile function improved with DFP treatment: ejection fraction and wall thickening both improved faster.
In conclusion, DFP treatment successfully reduced hemorrhagic iron within the infarct as compared to saline, indicating a clearing of the iron byproducts. Treatment also decreased wall swelling, suggesting reduced inflammation, and improved contractile function. In the infarct, reduced swelling could indicate faster remodeling and a faster resolution to scar, and histology confirms a more progressed scar structure with DFP treatment. Overall, iron chelation appears to be a promising therapy that could reduce the negative effects of hemorrhage and speed the functional recovery of patients post-MI.
Declining Gender Differences in Low-Wage Employment in Germany, Austria and Switzerland
Authors: Fritsch Nina-Sophie , Verwiebe Roland , Liedl Bernd 
Published: October 2019

Abstract
Although the low-wage employment sector has enlarged over the past 20 years in the context of pronounced flexibility in restructured labor markets, gender differences in low-wage employment have declined in Germany, Austria and Switzerland. In this article, the authors examine reasons for declining gender inequalities, and most notably concentrate on explanations for the closing gender gap in low-wage employment risks. In addition, they identify differences and similarities among the German-speaking countries. Based on regression techniques and decomposition analyses (1996-2016), the authors find significantly decreasing labor market risks for the female workforce. Detailed analysis reveals that (1) the concrete positioning in the labor market shows greater importance in explaining declining gender differences compared to personal characteristics. (2) The changed composition of the labor markets has prevented the low-wage sector from increasing even more in general and works in favor of the female workforce and their low-wage employment risks in particular.
Generalization in Comparative History
Authors: Clark Samuel 
Published: October 2019

Abstract
This article examines a sample of comparative-historical literature to assess when convincing generalizations are made and when they are not. Although a variety of factors can affect the potential for generalization, the focus here is on the difference between diachronic and synchronic generalizations. Separate sections are devoted to synchronic-idiographic, synchronic-nomothetic, diachronic-idiographic, and diachronic-nomothetic analysis and research. Evidence is presented to demonstrate that synchronic generalizations are common in comparative history. The most attention in the article is, however, given to the challenges faced when generalizing diachronically and especially when generalizing sequentially. The article ends with a discussion of the effects of inter-societal forces on comparative-historical generalization and with a conclusion outlining when comparative-historical generalizations seem to be more or less successful.