bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effects of CFT Legumine (5% Rotenone) on Tadpole Survival and Metamorphosis of Chiricahua Leopard Frogs Lithobates chiricahuensis, Northern Leopard Frogs L. pipiens, and American Bullfrogs L. catesbeianus
Authors: Alvarez Guillermo , Caldwell Colleen A. , Kruse Carter G. 
Published: March 2017

AbstractAmphibians may experience collateral effects if exposed to CFT Legumine (5% rotenone), a piscicide that is used to remove invasive fish. A series of 48‐h static toxicity tests assessed the acute effects of CFT Legumine on multi‐aged tadpoles of the federally listed Chiricahua leopard frog Lithobates chiricahuensis, the widespread northern leopard frog L. pipiens, and the increasingly invasive American bullfrog L. catesbeianus. At the earliest Gosner stages (GS 21–25), Chiricahua leopard frogs were more sensitive to CFT Legumine (median lethal concentration [LC50] = 0.41–0.58 mg/L) than American bullfrogs (LC50 = 0.63–0.69 mg/L) and northern leopard frogs (LC50 = 0.91 and 1.17 mg/L). As tadpoles developed (i.e., increase in GS), their sensitivity to rotenone decreased. In a separate series of 48‐h static nonrenewal toxicity tests, tadpoles (GS 21–25 and GS 31–36) of all three species were exposed to piscicidal concentrations of CFT Legumine (0.5, 1.0, and 2.0 mg/L) to assess postexposure effects on metamorphosis. In survivors of all three species at both life stages, the time to tail resorption was nearly doubled in comparison with that of controls. For example, mid‐age (GS 31–36) Chiricahua leopard frog tadpoles required 210.7 h to complete tail resorption, whereas controls required 108.5 h. However, because tail resorption is a relatively short period in metamorphosis, the total duration of development (days from posthatch to complete metamorphosis) and the final weight did not differ in either age‐group surviving nominal concentrations of 0.5‐, 1.0‐, and 2.0‐mg/L CFT Legumine relative to controls. This research demonstrates that the CFT Legumine concentrations commonly used in field applications to remove unwanted fish could result in considerable mortality of the earliest stages of Lithobates species. In addition to acute lethality, piscicide treatments may result in delayed tail resorption, which places the tadpoles at risk by increasing their vulnerability to predation and pathogens.Received October 1, 2016; accepted January 17, 2017 Published online March 30, 2017
Educational equalization stalled? Trends in inequality of educational opportunity between 1930 and 1980 across 26 European nations
Authors: Barone Carlo , Ruggera Lucia 
Published: March 2017

ABSTRACT
This article assesses trends over time in the influence of social origins on educational attainment in 26 European countries. We use a cumulative dataset that merges the European Social Survey (waves 2002–2010), the International Social Survey Programme (1999, 2009) and the European Value Study (2008). Our contribution to the literature is threefold. First, we replicate as closely as possible the previous study by Breen et al. [(2009) ‘Nonpersistent in educational attainment: Evidence from eight European countries’, American Journal of Sociology 114: 1475–1521] and extend it to a larger set of countries and to more recent cohorts. Second, we reassess the argument that equalization does not involve Higher Education. Third, we consider whether our conclusions change if we use a more comprehensive measurement of social origins that jointly incorporates indicators of social class, social status and parental education. We detect a generalized reduction of educational inequalities in the post-war decades. When we focus on Higher Education, we still detect evidence of equalization, although to a lower extent. Our analyses do not support the claim that, when using a more comprehensive treatment of social origins, the patterns for different indicators evolve in opposite directions.
Carbon Monoxide Releasing Molecules Blunt Placental Ischemia-Induced Hypertension
Authors: George Eric M , Cockrell Kathy , Arany Marietta , Stec David E , Rimoldi John M , Gadepalli Rama SV , Granger Joey P 
Published: March 2017

AbstractBACKGROUNDPreeclampsia is a pregnancy complication which manifests as new-onset hypertension, proteinuria, and a spectrum of other symptoms. While the underlying causes are still a subject of much debate, it is commonly believed that placental ischemia is a central cause. The ischemic placenta secretes factors which are believed to be responsible for the maternal syndrome; most notably the anti-angiogenic protein soluble fms-like tyrosine kinase 1 (sFlt-1). We have reported that induction of the carbon monoxide (CO) producing protein heme oxygenase-1 restored angiogenic imbalance and reduced blood pressure in a rat model of placental ischemia, and that CO blocks hypoxia-induced sFlt-1 production from placental tissue in vitro. We therefore hypothesized that direct administration of CO by a CO-releasing molecule (CORM) would blunt the placental ischemia-induced increase in sFlt-1 and thus the hypertension characteristic of this model.METHODSWe administered a soluble CO donor molecule (CORM-3) daily i.v. in control animals or those undergoing placental ischemia from GD14. Blood pressure and renal function were measured on GD19, and angiogenic markers measured by ELISA.RESULTSInterestingly, though we found that CORM administration significantly blunted the hypertensive response to placental ischemia, there was no concomitant normalization of sFlt-1 in either the placenta or maternal circulation. We did find, however, that CORM administration caused a significant increase in glomerular filtration rate, presumably by vasodilation of the renal arteries and increased renal plasma flow.CONCLUSIONSAll in all these data suggest that administration of CO by CORMs do lower blood pressure during placental ischemia mechanisms independent of changes in angiogenic balance.
BEESEM: estimation of binding energy models using HT-SELEX data
Authors: Ruan Shuxiang , Swamidass S Joshua , Stormo Gary D 
Published: March 2017

Abstract

Motivation
Characterizing the binding specificities of transcription factors (TFs) is crucial to the study of gene expression regulation. Recently developed high-throughput experimental methods, including protein binding microarrays (PBM) and high-throughput SELEX (HT-SELEX), have enabled rapid measurements of the specificities for hundreds of TFs. However, few studies have developed efficient algorithms for estimating binding motifs based on HT-SELEX data. Also the simple method of constructing a position weight matrix (PWM) by comparing the frequency of the preferred sequence with single-nucleotide variants has the risk of generating motifs with higher information content than the true binding specificity.

Results
We developed an algorithm called BEESEM that builds on a comprehensive biophysical model of protein–DNA interactions, which is trained using the expectation maximization method. BEESEM is capable of selecting the optimal motif length and calculating the confidence intervals of estimated parameters. By comparing BEESEM with the published motifs estimated using the same HT-SELEX data, we demonstrate that BEESEM provides significant improvements. We also evaluate several motif discovery algorithms on independent PBM and ChIP-seq data. BEESEM provides significantly better fits to in vitro data, but its performance is similar to some other methods on in vivo data under the criterion of the area under the receiver operating characteristic curve (AUROC). This highlights the limitations of the purely rank-based AUROC criterion. Using quantitative binding data to assess models, however, demonstrates that BEESEM improves on prior models.

Availability and Implementation
Freely available on the web at http://stormo.wustl.edu/resources.html.

Supplementary information
Supplementary data are available at Bioinformatics online.
Removal of batch effects using distribution-matching residual networks
Authors: Shaham Uri , Stanton Kelly P , Zhao Jun , Li Huamin , Raddassi Khadir , Montgomery Ruth , Kluger Yuval 
Published: March 2017

AbstractMotivationSources of variability in experimentally derived data include measurement error in addition to the physical phenomena of interest. This measurement error is a combination of systematic components, originating from the measuring instrument and random measurement errors. Several novel biological technologies, such as mass cytometry and single-cell RNA-seq (scRNA-seq), are plagued with systematic errors that may severely affect statistical analysis if the data are not properly calibrated.ResultsWe propose a novel deep learning approach for removing systematic batch effects. Our method is based on a residual neural network, trained to minimize the Maximum Mean Discrepancy between the multivariate distributions of two replicates, measured in different batches. We apply our method to mass cytometry and scRNA-seq datasets, and demonstrate that it effectively attenuates batch effects.Availability and Implementationour codes and data are publicly available at https://github.com/ushaham/BatchEffectRemoval.gitSupplementary informationSupplementary data are available at Bioinformatics online.
Cardiovascular outcome trials in patients with chronic kidney disease: challenges associated with selection of patients and endpoints
Authors: Rossignol Patrick , Agarwal Rajiv , Canaud Bernard , Charney Alan , Chatellier Gilles , Craig Jonathan C , Cushman William C , Gansevoort Ronald T , Fellström Bengt , Garza Dahlia , Guzman Nicolas , Holtkamp Frank A , London Gerard M , Massy Ziad A , Mebazaa Alexandre , Mol Peter G M , Pfeffer Marc A , Rosenberg Yves , Ruilope Luis M , Seltzer Jonathan , Shah Amil M , Shah Salim , Singh Bhupinder , Stefánsson Bergur V , Stockbridge Norman , Stough Wendy Gattis , Thygesen Kristian , Walsh Michael , Wanner Christoph , Warnock David G , Wilcox Christopher S , Wittes Janet , Pitt Bertram , Thompson Aliza , Zannad Faiez 
Published: March 2017

AbstractAlthough cardiovascular disease is a major health burden for patients with chronic kidney disease, most cardiovascular outcome trials have excluded patients with advanced chronic kidney disease. Moreover, the major cardiovascular outcome trials that have been conducted in patients with end-stage renal disease have not demonstrated a treatment benefit. Thus, clinicians have limited evidence to guide the management of cardiovascular disease in patients with chronic kidney disease, particularly those on dialysis. Several factors contribute to both the paucity of trials and the apparent lack of observed treatment effect in completed studies. Challenges associated with conducting trials in this population include patient heterogeneity, complexity of renal pathophysiology and its interaction with cardiovascular disease, and competing risks for death. The Investigator Network Initiative Cardiovascular and Renal Clinical Trialists (INI-CRCT), an international organization of academic cardiovascular and renal clinical trialists, held a meeting of regulators and experts in nephrology, cardiology, and clinical trial methodology. The group identified several research priorities, summarized in this paper, that should be pursued to advance the field towards achieving improved cardiovascular outcomes for these patients. Cardiovascular and renal clinical trialists must partner to address the uncertainties in the field through collaborative research and design clinical trials that reflect the specific needs of the chronic and end-stage kidney disease populations, with the shared goal of generating robust evidence to guide the management of cardiovascular disease in patients with kidney disease.
Structure and cell biology of the vessel wall
Authors: van Thiel Bibi S. , van der Pluijm I. , Kanaar Roland , Danser A.H. Jan , Essers Jeroen 
Published: March 2017

Abstract
The purpose of this chapter is to provide a general overview on the structure and composition of blood vessels. Moreover, the cellular constituents of the vessel wall, as well as the different types of blood vessels, are discussed. In addition the effect of ageing on the vascular wall and its role in the pathogenesis of vascular disease is discussed. More detailed insights into the pathogenesis of specific diseases, including atherosclerosis and aneurysms, are provided in other chapters of this book.
Animal models to study pathophysiology of the vasculature
Authors: Gu Wenduo , Xie Yao , Xu Qingbo 
Published: March 2017

Abstract
Animal models are designed to be preliminary tools for a better understanding of the pathogenesis, improvement in diagnosis, prevention, and therapy of vascular diseases in humans. Animal models are easily manageable, as compounding effects of dietary and environmental factors can be controlled experimentally. Blood vessel samples can be taken for detailed experimental and biomolecular examination. A thorough understanding of the animal models used is necessary and complete analysis must be validated so that the data can be extrapolated to humans. There are several species that are used for studying vascular pathophysiology, including mice, rats, rabbits, and pigs. Attracted by the well-defined genetic systems, a number of investigators have begun to use the mouse as an experimental system for arteriosclerosis research. Because vascular disorder is a complicated disease, which includes spontaneous (native) atherosclerosis, transplant arteriosclerosis, vein graft atherosclerosis, and angioplasty-induced restenosis, several models for studying all types of vascular disease have recently been established. Using these animal models, much knowledge concerning the pathogenesis of the disease and therapeutic intervention has been gained. This chapter will not attempt to cover all aspects of animal models, but will rather focus on the major progress in understanding the pathophysiology of the vasculature, the (dis)advantages of a variety of models, and how specific models can be appropriately chosen for different purposes of study.
The endothelial cell
Authors: Fleming Ingrid , Kwak Brenda R. , Meens Merlijn J. 
Published: March 2017

Abstract
The endothelium, a monolayer of cells that lines blood vessels, acts as a physical barrier between circulating blood and vascular smooth muscle cells. The purpose of this chapter is to provide a general overview on the structural heterogeneity of the endothelium. Moreover, the most important physiological functions of the vascular endothelium in blood vessels are discussed. More detailed insights into the pathogenesis of specific diseases, including atherosclerosis and hypertension, are provided in other chapters of this book.
The lymphatic system
Authors: Karaman Sinem , Aspelund Aleksanteri , Detmar Michael , Alitalo Kari 
Published: March 2017

Abstract
The lymphatic vascular system is an integral component of the circulatory system; it forms a one-way conduit that transports tissue interstitial components back to the venous circulation through lymph nodes. Lymphatic vessels extend to most tissues and contribute to the regulation of interstitial fluid homeostasis, trafficking of immune cells, and absorption of dietary fats from the gut. Developmentally, lymphatic vessels originate from embryonic veins and specialized angioblasts. A number of molecules have been identified in the commitment of endothelial cells to the lymphatic lineage, and the sprouting, expansion and maturation of the lymphatic vascular tree. Importantly, the vascular endothelial growth factor (VEGF) family members VEGFC and VEGFD, together with their receptors VEGFR2 and VEGFR3 have been implicated as critical regulators of lymphangiogenesis. Lymphatic vessels are involved in several human diseases, including cancer, where they contribute to tumour metastasis, the leading cause of cancer-related deaths. Lymphatic vessels regulate immune responses against foreign pathogens by transporting leucocytes to lymph nodes, but are also in involved in the regulation of self-tolerance. Defects in the lymphatic vascular system are causal for the development of lymphoedema.
Valvular heart disease
Authors: Kovanen Petri T. , Bäck Magnus 
Published: March 2017

Abstract
The heart valves, which maintain a unidirectional cardiac blood flow, are covered by endothelial cells and structurally composed by valvular interstitial cells and extracellular matrix. Valvular heart disease can be either stenotic, causing obstruction of the valvular flow, or regurgitant, referring to a back-flow through the valve. The pathophysiological changes in valvular heart disease include, for example, lipid and inflammatory cell infiltration, calcification, neoangiogenesis, and extracellular matrix remodelling. The present chapter addresses the biology of the aortic and mitral valves, and the pathophysiology of aortic stenosis and mitral valve prolapse.
Pathophysiology of thrombosis
Authors: Badimon Lina , Tanner Felix C. , Camici Giovanni G. , Vilahur Gemma 
Published: March 2017

Abstract
Ischaemic heart disease and stroke are major causes of death and morbidity worldwide. Coronary and cerebrovascular events are mainly a consequence of a sudden thrombotic occlusion of the vessel lumen. Arterial thrombosis usually develops on top of a disrupted atherosclerotic plaque because of the exposure of thrombogenic material, such as collagen fibrils and tissue factor (TF), to the flowing blood. TF, either expressed by subendothelial cells, macrophage- and/or vascular smooth muscle-derived foam-cells in atherosclerotic plaques, is a key element in the initiation of thrombosis due to its ability to induce thrombin formation (a potent platelet agonist) and subsequent fibrin deposition at sites of vascular injury. Adhered platelets at the site of injury also play a crucial role in the pathophysiology of atherothrombosis. Platelet surface receptors (mainly glycoproteins) interact with vascular structures and/or Von Willebrand factor triggering platelet activation signalling events, including an increase in intracellular free Ca2+, exposure of a pro-coagulant surface, and secretion of platelet granule content. On top of this, interaction between soluble agonists and platelet G-coupled protein receptors further amplifies the platelet activation response favouring integrin alpha(IIb)beta(3) activation, an essential step for platelet aggregation. Blood-borne TF and microparticles have also been shown to contribute to thrombus formation and propagation. As thrombus evolves different circulating cells (red-blood cells and leukocytes, along with occasional undifferentiated cells) get recruited in a timely dependent manner to the growing thrombus and further entrapped by the formation of a fibrin mesh.
Vascular pathophysiology of hypertension
Authors: Guzik Tomasz J. , Touyz Rhian M. 
Published: March 2017

Abstract
Hypertension is a multifactorial disease, in which vascular dysfunction plays a prominent role. It occurs in over 30% of adults worldwide and an additional 30% are at high risk of developing the disease. Vascular pathology is both a cause of the disease and a key manifestation of hypertension-associated target-organ damage. It leads to clinical symptoms and is a key risk factor for cardiovascular disease. All layers of the vascular wall and the endothelium are involved in the pathogenesis of hypertension. Pathogenetic mechanisms, whereby vascular damage contributes to hypertension, are linked to increased peripheral vascular resistance. At the vascular level, processes leading to change sin peripheral resistance include hyper-contractility of vascular smooth muscle cells, endothelial dysfunction, and structural remodelling, due to aberrant vascular signalling, oxidative and inflammatory responses. Increased vascular stiffness due to vascular remodelling, adventitial fibrosis, and inflammation are key processes involved in sustained and established hypertension. These mechanisms are linked to vascular smooth muscle and fibroblast proliferation, migration, extracellular matrix remodelling, calcification, and inflammation. Apart from the key role in the pathogenesis of hypertension, hypertensive vasculopathy also predisposes to atherosclerosis, another risk factor for cardiovascular disease. This is linked to increased transmural pressure, blood flow, and shear stress alterations in hypertension, as well as endothelial dysfunction and vascular stiffness. Therefore, understanding the mechanisms and identifying potential novel treatments targeting hypertensive vasculopathy are of primary importance in vascular medicine.
Adventitia and perivascular adipose tissue—the integral unit in vascular disease
Authors: Yang Zhihong , Ming Xiu-Fen 
Published: March 2017

Abstract
Obesity and obesity-associated metabolic disorders are highly associated with cardiovascular disease. Abnormal ectopic deposition and accumulation of adipose tissue in organs, including perivascular space (perivascular adipose tissue, PVAT) in obesity are emerging to contribute to vascular disease development through pathological paracrine and/or endocrine secretion of cytokines, namely adipokines, which are vasoactive factors including vascular relaxing and contracting factors, smooth muscle growth promoting and inhibiting factors, and pro- and anti-inflammatory factors. In obesity, production of these factors from PVAT is altered and in imbalance which favours vascular contraction, pathological remodelling, and inflammation. In cross-talk with the endothelium, the functional changes of adventitia and PVAT are detrimental and importantly contribute to the acceleration of vascular atherosclerosis and complications associated with obesity and metabolic disorders
MASSIVE SUBRETINAL GAS AFTER VITRECTOMY SURGERY: MECHANISM AND MANAGEMENT
Authors: Seamone Mark E. , Lewis Darrell R. , Almeida David , Choudhry Netan , Gupta R. Rishi 
Published: March 2017

Purpose:
To describe the complication of subretinal gas after pars plana vitrectomy for rhegmatogenous retinal detachment, as well as its management.

Methods:
The presence of subretinal gas was noted on postoperative Day 1 after pars plana vitrectomy for a chronic rhegmatogenous retinal detachment. Resolution of subretinal gas was facilitated by an infusion line and external sclerotomy to expand the vitreous cavity. Residual subretinal gas was removed through a posterior retinotomy after fluid–air exchange.

Results:
This technique resulted in the successful evacuation of subretinal gas, allowing for chorioretinal adhesion and reattachment of the retina.

Conclusion:
Subretinal gas can rarely occur after pars plana vitrectomy for rhegmatogenous retinal detachment. This complication can be successfully managed by way of external drainage, followed by evacuation of residual gas through fluid–air exchange and posterior retinotomy.