bluuebunny/crossref_metadata_2025_split huggingface dataset:
Maladaptive Family Dysfunction and Parental Death as Risk Markers of Childhood Abuse in Women
Authors: Plaza Anna , Torres Anna , Ascaso Carlos , Navarro Purificación , Gelabert Estel , Imaz Maria Luisa , Martín-Santos Rocío , Valdés Manuel , García-Esteve Lluïsa 
Published: December 2014

AbstractThis study aims to examine the prevalence and characteristics of physical, emotional and sexual childhood abuse. It also examines whether other non-abuse types of childhood adversities related to maladaptive family functioning and separations during childhood can be used as markers for the presence of childhood abuse. Participants (N = 237) were women at 2–3 days after delivery that completed the Spanish-validated version of the Early Trauma Inventory Self Report (ETI-SR; Bremner, Bolus, & Mayer, 2007; Plaza et al., 2011), designed to assess the presence of childhood adversities. Results show that 29% of the women had experienced some type of childhood abuse, and 10% more than one type. Logistic regression analyses indicate that childhood parental death is a risk marker for childhood emotional abuse (OR: 3.77; 95% CI: 1.327–10.755; p <.013), childhood parental substance abuse is a risk marker for childhood sexual (OR: 3.72; 95% CI: 1.480–9.303; p < .005) and physical abuse (OR: 2.610; 95% CI: 1.000–6.812; p < .05) and that childhood family mental illness is a risk marker for childhood emotional (OR: 2.95; 95% CI: 1.175–7.441; p < .021) and sexual abuse (OR: 2.55; 95% CI: 1.168–5.580; p < .019). The high prevalence of childhood abuse indicates a need for assessment during the perinatal period. Screening for childhood family mental illness, parental substance abuse, and parental death - all identified risk factors for reporting childhood abuse - can help to identify women that should be assessed specifically regarding abuse.
The Escherichia coli effector EspJ blocks Src kinase activity via amidation and ADP ribosylation
Authors: Young Joanna C. , Clements Abigail , Lang Alexander E. , Garnett James A. , Munera Diana , Arbeloa Ana , Pearson Jaclyn , Hartland Elizabeth L. , Matthews Stephen J. , Mousnier Aurelie , Barry David J. , Way Michael , Schlosser Andreas , Aktories Klaus , Frankel Gad 
Published: December 2014

AbstractThe hallmark of enteropathogenic Escherichia coli (EPEC) infection is the formation of actin-rich pedestal-like structures, which are generated following phosphorylation of the bacterial effector Tir by cellular Src and Abl family tyrosine kinases. This leads to recruitment of the Nck–WIP–N-WASP complex that triggers Arp2/3-dependent actin polymerization in the host cell. The same phosphorylation-mediated signalling network is also assembled downstream of the Vaccinia virus protein A36 and the phagocytic Fc-gamma receptor FcγRIIa. Here we report that the EPEC type-III secretion system effector EspJ inhibits autophosphorylation of Src and phosphorylation of the Src substrates Tir and FcγRIIa. Consistent with this, EspJ inhibits actin polymerization downstream of EPEC, Vaccinia virus and opsonized red blood cells. We identify EspJ as a unique adenosine diphosphate (ADP) ribosyltransferase that directly inhibits Src kinase by simultaneous amidation and ADP ribosylation of the conserved kinase-domain residue, Src E310, resulting in glutamine-ADP ribose.
A simplified memory network model based on pattern formations
Authors: Xu Kesheng , Zhang Xiyun , Wang Chaoqing , Liu Zonghua 
Published: December 2014

AbstractMany experiments have evidenced the transition with different time scales from short-term memory (STM) to long-term memory (LTM) in mammalian brains, while its theoretical understanding is still under debate. To understand its underlying mechanism, it has recently been shown that it is possible to have a long-period rhythmic synchronous firing in a scale-free network, provided the existence of both the high-degree hubs and the loops formed by low-degree nodes. We here present a simplified memory network model to show that the self-sustained synchronous firing can be observed even without these two necessary conditions. This simplified network consists of two loops of coupled excitable neurons with different synaptic conductance and with one node being the sensory neuron to receive an external stimulus signal. This model can be further used to show how the diversity of firing patterns can be selectively formed by varying the signal frequency, duration of the stimulus and network topology, which corresponds to the patterns of STM and LTM with different time scales. A theoretical analysis is presented to explain the underlying mechanism of firing patterns.
VarSim: a high-fidelity simulation and validation framework for high-throughput genome sequencing with cancer applications
Authors: Mu John C. , Mohiyuddin Marghoob , Li Jian , Bani Asadi Narges , Gerstein Mark B. , Abyzov Alexej , Wong Wing H. , Lam Hugo Y.K. 
Published: December 2014

Abstract
Summary: VarSim is a framework for assessing alignment and variant calling accuracy in high-throughput genome sequencing through simulation or real data. In contrast to simulating a random mutation spectrum, it synthesizes diploid genomes with germline and somatic mutations based on a realistic model. This model leverages information such as previously reported mutations to make the synthetic genomes biologically relevant. VarSim simulates and validates a wide range of variants, including single nucleotide variants, small indels and large structural variants. It is an automated, comprehensive compute framework supporting parallel computation and multiple read simulators. Furthermore, we developed a novel map data structure to validate read alignments, a strategy to compare variants binned in size ranges and a lightweight, interactive, graphical report to visualize validation results with detailed statistics. Thus far, it is the most comprehensive validation tool for secondary analysis in next generation sequencing.
Availability and implementation: Code in Java and Python along with instructions to download the reads and variants is at http://bioinform.github.io/varsim.
Contact: rd@bina.com
Supplementary information: Supplementary data are available at Bioinformatics online.
Bone and kidney toxicity induced by nucleotide analogues in patients affected by HBV-related chronic hepatitis: a longitudinal study
Authors: Maggi Paolo , Montinaro Vincenzo , Leone Armando , Fasano Massimo , Volpe Anna , Bellacosa Chiara , Grattagliano Vito , Coladonato Laura , Lapadula Giovanni , Santantonio Teresa , Angarano Gioacchino 
Published: December 2014

Abstract

Objectives
Nucleotide analogues may promote renal and bone toxicity. The aim of the present study was to evaluate markers of osteorenal toxicity in patients affected by hepatitis B virus-related chronic hepatitis treated with lamivudine plus adefovir who were switched to tenofovir.

Patients and methods
We evaluated 60 consecutive patients at the time of the switch of treatment and after 1, 3, 6, 9 and 12 months. The mean baseline estimated glomerular filtration rate (eGFR) was 89.3 ± 19.0 mL/min/1.73 m2.

Results
During the study period we observed a reduction in mean eGFR up to 6 months after switching to tenofovir, and this remained stable for the last two timepoints. At the end of study, the mean eGFR was 82.6 ± 21.5 mL/min/1.73 m2, a reduction of 7.5%. The mean baseline proteinuria was 202.6 ± 237.6 mg/24 h. Microhaematuria was observed in 22.6% of patients and hypophosphataemia in 18.6%. After 1 month of tenofovir, we observed a worsening of serum phosphate and parathyroid hormone levels, haemoglobinuria and 24 h proteinuria. After 3 and 12 months of tenofovir, these data tended to recover to baseline levels. A total of 92.6% of patients at baseline had hypovitaminosis D. After supplementation with cholecalciferol, this percentage decreased significantly. We observed a reduced bone mineral density (BMD) in 52.7% of patients at baseline; this increased to 77.8% after 6 months of tenofovir, but at the last timepoint the percentage of patients with a reduced BMD had fallen to a level above the baseline.

Conclusions
In conclusion, patients exposed to lamivudine plus adefovir showed relevant osteorenal damage. The switch to tenofovir provoked a slight reduction in eGFR that stabilized after 6 months. The reduced BMD at baseline did not worsen under tenofovir treatment.
Lichen traits responding to aridity
Authors: Matos Paula , Pinho Pedro , Aragón Gregorio , Martínez Isabel , Nunes Alice , Soares Amadeu M. V. M. , Branquinho Cristina 
Published: December 2014

Summary

Climate change is expected to cause several impacts at the global scale, and drylands will be amongst the most affected areas. Thus, investigating how these changes will affect the composition, structure and functioning of dryland ecosystems has become a priority. From an ecological indicator point of view, several works have shown that functional diversity is better than species richness to understand ecosystem functioning or response to environmental factors. However, most of these works focus on plants, while those of other organisms remain largely unknown. Lichens are amongst the ecosystem components more sensitive to climatic changes due to several physiological and ecological characteristics. Their poikilohydric nature (therefore highly dependent on the atmosphere for water supply) and their ubiquity on terrestrial ecosystems underlie their potential as indicators of climate. Nonetheless, works specifically aiming to identify lichen functional traits that respond to aridity remain poorly explored, particularly in drylands.

We proposed to identify lichen functional traits and respective functional groups responding to aridity in a Mediterranean drylands ecosystem.

Lichen diversity was sampled in open holm oak woodlands along an aridity gradient in SW Europe (Iberian Peninsula). Lichen functional traits that could be easily identified and related to water uptake were selected to be tested: type of photobiont, growth form and reproduction strategy.

Lichen species composition was related to the aridity gradient. The three traits chosen were related with the community's response to aridity, but with contrasting responses in different functional groups. More specifically crustose and fruticose lichens, isidiate species and the ones with Trentepohlia as photobiont were related to the less arid part of the gradient. Foliose species and cyanolichens, on the contrary, were associated with the most arid areas.

Synthesis. We were able to identify lichen traits responding to aridity. Type of photobiont was particularly responsive, with Trentepohlia and cyanobacteria functional groups, responding clearly in contrasting ways to aridity in this drylands ecosystem. This work emphasizes functional diversity role on understanding and assessing the response to environmental factors, namely to climate. It also highlights the potential use of lichen functional groups as ecological indicators of climate change.
Identifying Possible False Matches in Anonymized Hospital Administrative Data without Patient Identifiers
Authors: Hagger‐Johnson Gareth , Harron Katie , Gonzalez‐Izquierdo Arturo , Cortina‐Borja Mario , Dattani Nirupa , Muller‐Pebody Berit , Parslow Roger , Gilbert Ruth , Goldstein Harvey 
Published: December 2014

ObjectiveTo identify data linkage errors in the form of possible false matches, where two patients appear to share the same unique identification number.Data SourceHospital Episode Statistics (HES) in England, United Kingdom.Study DesignData on births and re‐admissions for infants (April 1, 2011 to March 31, 2012; age 0–1 year) and adolescents (April 1, 2004 to March 31, 2011; age 10–19 years).Data Collection/Extraction MethodsHospital records pseudo‐anonymized using an algorithm designed to link multiple records belonging to the same person. Six implausible clinical scenarios were considered possible false matches: multiple births sharing HESID, re‐admission after death, two birth episodes sharing HESID, simultaneous admission at different hospitals, infant episodes coded as deliveries, and adolescent episodes coded as births.Principal FindingsAmong 507,778 infants, possible false matches were relatively rare (n = 433, 0.1 percent). The most common scenario (simultaneous admission at two hospitals, n = 324) was more likely for infants with missing data, those born preterm, and for Asian infants. Among adolescents, this scenario (n = 320) was more common for males, younger patients, the Mixed ethnic group, and those re‐admitted more frequently.ConclusionsResearchers can identify clinically implausible scenarios and patients affected, at the data cleaning stage, to mitigate the impact of possible linkage errors.
A Simple Method for Evaluating Within Sample Prognostic Balance Achieved by Published Comorbidity Summary Measures
Authors: Egleston Brian L. , Uzzo Robert G. , Beck J. Robert , Wong Yu‐Ning 
Published: December 2014

ObjectiveTo demonstrate how a researcher can investigate the appropriateness of a published comorbidity summary measure for use with a given sample.Data SourceSurveillance, Epidemiology, and End Results linked to Medicare claims data.Study DesignWe examined Kaplan–Meier estimated survival curves for four diseases within strata of a comorbidity summary measure, the Charlson Comorbidity Index.Data CollectionWe identified individuals with early‐stage kidney cancer diagnosed from 1995 to 2009. We recorded comorbidities present in the year before diagnosis.Principal FindingsThe use of many comorbidity summary measures is valid under appropriate conditions. One condition is that the relationships of the comorbidities with the outcome of interest in a researcher's own population are comparable to the relationships in a published algorithm's population. The original comorbidity weights from the Charlson Comorbidity Index seemed adequate for three of the diseases in our sample. We found evidence that the Charlson Comorbidity Index might underestimate the impact of one disease in our sample.ConclusionExamination of survival curves within strata defined by a comorbidity summary measure can be a useful tool for determining whether a published method appropriately accounts for comorbidities. A comorbidity score is only as good as those variables included.
Antiphospholipid syndrome: 30 years and our contribution
Authors: Koike Takao 
Published: December 2014

AbstractIn 1983, Graham Hughes first described the concept of antiphospholipid syndrome (APS). In 1984, we described the enzyme‐linked immunosorbent assay (ELISA) system which directly detected circulating aCL in patients with systemic lupus erythematosus (SLE) who revealed biological false positive serological test for syphilis. In 1990, three groups, including our group, independently reported the necessity of a cofactor for the binding of autoimmune anticardiolipin antibodies (aCL) to the solid phase phospholipids. β2‐glycoprotein I (β2GPI) was identified as this cofactor. In 1994,the epitope for aCL was shown to develop when β2GPI is adsorbed on polyoxygenated polystyrene plates. In 2000, we described antiprothrombin antibodies bind to prothrombin exposed to immobilized phosphatidylserine and established a phosphatidylserine dependent monoclonal antiprothrombin antibody. In 2004, a novel role of nicked β2GPI was identified in the negative feedback pathway of extrinsic fibrinolysis. Nicked β2GPI was found to bind angiostatin 4.5 and to attenuate its antiangiogenic property. In 2004, we demonstrated that the p38 MAPK pathway mediates induction of the TF gene in stimulated with human monoclonal anti‐ β2GPI antibodies. Very recently, β2GPI was identified as a complement regulator. The cross‐link between complement activation and prothrombotic status in patients with APS has been drawn much attention. Genetic factors are hypothesized to play a role in the susceptibility to APS based on several family studies in patients with antiphospholipid antibodies (aPL) and/or clinical manifestations of APS. The genetics of β2GPI has been extensively studied. 247 Val/Leu polymorphism can affect the conformational change of β2‐GPI and the exposure of the epitopes for aCL. We found that 247 Val was correlated with anti‐β2‐GPI production in patients with primary APS, and 247 Val may be important for β2‐GPI antigenicity. STAT4 SNP in Japanese patients with SLE and/or APS. T allele frequencies in SLE and APS were significantly elevated compared with that in healthy controls. When analyzed only in primary APS patients, T allele frequency was further higher. BANK1, BLK and SNP in 1q25.1 region were associated with not only SLE but also APS in Japanese population. These results suggest that APS and SLE, in part, share a common genetic background.
Recent advances in systemic lupus erythematosus genetics in an Asian population
Authors: Lee Hye‐Soon , Bae Sang Cheol 
Published: December 2014

AbstractRecent advances in systemic lupus erythematosus (SLE) genetics in Asian populations have been achieved by genome‐wide association studies (GWASs) and following replication studies, which expanded the genetic information about shared or population‐specific risk genes between ethnic groups. Meta‐analyses and multi‐ethnic replication studies may be possible approaches that could demonstrate stronger or more suggestive evidence for multiple variants for SLE. In addition to the susceptibility of SLE itself, several genotype‐phenotype analyses have shown that the specific phenotypes of SLE can also be influenced by genetic factors. Almost all SLE genetic loci are involved in the potential pathways of SLE pathogenesis, such as Toll‐like receptor/type I interferon signaling, nuclear factor κB signaling, immune complex clearing mechanism, immune cell (B, T cell, neutrophil and monocyte) function and signaling, cell‐cycle regulation, DNA methylation and autophagy. Further studies, including the next generation sequencing technology and the systematic strategy using bioinformatics, in addition to international collaboration among SLE genetic researchers, will give us better understanding of the genetic basis of SLE.
Prenatal Screening, Reproductive Choice, and Public Health
Authors: Wilkinson Stephen 
Published: December 2014

AbstractOne widely held view of prenatal screening (PNS) is that its foremost aim is, or should be, to enable reproductive choice; this is the Pure Choice view. The article critiques this position by comparing it with an alternative: Public Health Pluralism. It is argued that there are good reasons to prefer the latter, including the following. (1) Public Health Pluralism does not, as is often supposed, render PNS more vulnerable to eugenics‐objections. (2) The Pure Choice view, if followed through to its logical conclusions, may have unpalatable implications, such as extending choice well beyond health screening. (3) Any sensible version of Public Health Pluralism will be capable of taking on board the moral seriousness of abortion and will advocate, where practicable, alternative means of reducing the prevalence of disease and disability. (4) Public Health Pluralism is at least as well‐equipped as the Pure Choice model to deal with autonomy and consent issues.
A New Ethical Landscape of Prenatal Testing: Individualizing Choice to Serve Autonomy and Promote Public Health: A Radical Proposal
Authors: Munthe Christian 
Published: December 2014

AbstractA new landscape of prenatal testing (PNT) is presently developing, including new techniques for risk‐reducing, non‐invasive sampling of foetal DNA and drastically enhanced possibilities of what may be rapidly and precisely analysed, surrounded by a growing commercial genetic testing industry and a general trend of individualization in healthcare policies. This article applies a set of established ethical notions from past debates on PNT for analysing PNT screening‐programmes in this new situation. While some basic challenges of PNT stay untouched, the new development supports a radical individualization of how PNT screening is organized. This reformation is, at the same time, difficult to reconcile with responsible spending of resources in a publicly funded healthcare context. Thus, while the ethical imperative of individualization holds and applies to PNT, the new landscape of PNT provides reasons to start rolling back the type of mass‐screening programmes currently established in many countries. Instead, more limited offers are suggested, based on considerations of severity of conditions and optimized to simultaneously serve reproductive autonomy and public health within an acceptable frame of priorities. The new landscape of PNT furthermore underscores the ethical importance of supporting and including people with disabilities. For the very same reason, no ban on what may be analysed using PNT in the new landscape should be applied, although private offers must, of course, conform to strict requirements of respecting reproductive autonomy and what that means in terms of counselling.
WMJ‐S‐001, a novel aliphatic hydroxamate derivative, exhibits anti‐inflammatory properties via MKP‐1 in LPS‐stimulated RAW264.7 macrophages
Authors: Chen Wei‐Chuan , Yen Chia‐Sheng , Huang Wei‐Jan , Hsu Ya‐Fen , Ou George , Hsu Ming‐Jen 
Published: December 2014

Background and PurposeHydroxamate derivatives have attracted considerable attention because of their broad pharmacological properties. Recent studies reported their potential use in the treatment of cardiovascular diseases, arthritis and infectious diseases. However, the mechanisms of the anti‐inflammatory effects of hydroxamate derivatives remain to be elucidated. In an effort to develop a novel pharmacological agent that could suppress abnormally activated macrophages, we investigated a novel aliphatic hydroxamate derivative, WMJ‐S‐001, and explored its anti‐inflammatory mechanisms.Experimental ApproachRAW264.7 macrophages were exposed to LPS in the absence or presence of WMJ‐S‐001. COX‐2 expression and signalling molecules activated by LPS were assessed.Key ResultsLPS‐induced COX‐2 expression was suppressed by WMJ‐S‐001. WMJ‐S‐001 inhibited p38MAPK, NF‐κB subunit p65 and CCAAT/enhancer‐binding protein (C/EBP)β phosphorylation in cells exposed to LPS. Treatment of cells with a p38MAPK inhibitor (p38MAPK inhibitor III) markedly inhibited LPS‐induced p65 and C/EBPβ phosphorylation and COX‐2 expression. LPS‐increased p65 and C/EBPβ binding to the COX‐2 promoter region was suppressed in the presence of WMJ‐S‐001. In addition, WMJ‐S‐001 suppression of p38MAPK, p65 and C/EBPβ phosphorylation, and subsequent COX‐2 expression were restored in cells transfected with a dominant‐negative (DN) mutant of MAPK phosphatase‐1 (MKP‐1). WMJ‐S‐001 also caused an increase in MKP‐1 activity in RAW264.7 macrophages.Conclusions and ImplicationsWMJ‐S‐001 may activate MKP‐1, which then dephosphorylates p38MAPK, resulting in a decrease in p65 and C/EBPβ binding to the COX‐2 promoter region and COX‐2 down‐regulation in LPS‐stimulated RAW264.7 macrophages. The present study suggests that WMJ‐S‐001 may be a potential drug candidate for alleviating LPS‐associated inflammatory diseases.