bluuebunny/crossref_metadata_2025_split huggingface dataset:
Association of serum alkaline phosphatase with mortality in non-selected European patients with CKD5D: an observational, three-centre survival analysis
Authors: Beige Joachim , Wendt Ralph , Girndt Matthias , Queck Karl-Heinz , Fiedler Roman , Jehle Peter 
Published: February 2014

ObjectivesFor characterisation of mineral bone disease in chronic kidney disease (CKD), laboratory surrogates have been suggested. This observational should investigate the association of total and skeletal alkaline phosphatase (AP) with mortality of patients undergoing maintenance renal replacement therapy.SettingThree renal outpatient centers in eastern-central Germany (secondary and tertiary care).ParticipantsComplete survival and laboratory datasets were available in 407 of 493 patients. Age and gender distribution was equivalent to a general population with end-stage CKD (CKD5D). Patients were included between 2008 and 2010 if at least 2 weeks of maintenance treatment were documented.Primary outcome measuresMortality was estimated by setting theend of dialysis dateas event date. Events other than death (change to another centre, life-sustaining renal function or transplantation) were censored.ResultsThe OR to die within follow-up for patients in the higher of two total AP strata was 2.70 (95% CI 1.76 to 4.15). In univariateKaplan-Meieranalysis, total AP had a strong association with all-cause mortality (LogRank=24.1, p<0.001). Mean total AP and individual lowest skeletal AP, but not mean skeletal AP entered step-wiseCoxmodels for survival from dialysis start (χ2=22.4; p<0.001) after adjusting for age, Kt/V, diabetes and vintage. Mean values of skeletal, total AP and parathyroid hormone were 14.8±8.9 µg/L, 91.9±55.3 U/L and 188±164 ng/L, respectively. Skeletal and total AP were highly correlated (R=0.86; p<0.001).ConclusionsThis unselected CKD5D population exhibited a clinical significant association of total AP with crude mortality and a stronger death risk association of total AP and individual lowest skeletal AP with crude mortality.
Measuring Armenia's progress on the Tobacco Control Scale: an evaluation of tobacco control in an economy in transition, 2005–2009
Authors: Movsisyan Narine K , Connolly Gregory N 
Published: February 2014

ObjectivesThis study aimed to measure the 5-year progress in the implementation of WHO Framework Convention on Tobacco Control (FCTC) in Armenia by applying the Tobacco Control Scale, a rapid assessment tool developed to assess the strength of tobacco control policies in Europe.SettingArmenia, an economy in transition, has extreme smoking rates among men (62.5%) despite acceding to FCTC in 2004. However, little research has been carried out to evaluate Armenia's progress in tobacco control.MethodsThe Tobacco Control Scale total score was estimated for Armenia using the original methodology; however, a different source of data was used in estimating the subscores on tobacco price and tobacco control spending.ResultsArmenia's total score on Tobacco Control Scale has considerably improved from 2005 to 2009, mostly due to larger health warnings and advertising ban, and increased public spending on tobacco control. The scores for smoke-free public places, advertising ban, health warnings and treatment categories were below the European average in 2005 and 2007, while the price score was higher. Neither total tobacco control score nor any of its components showed a significant predictive value in a simple regression analysis using the total score and subscores as predictors for log-transformed per capita tobacco consumption.ConclusionsHigher than the European average price score for Armenia cannot be explained by the concept of affordability alone and may reflect a measurement error due to peculiarities of transition economies. The applicability of the Tobacco Control Scale could be limited to countries with mature economies, but not to transition countries such as Armenia with different social, political and economic environment. The scale modification, such as an adjustment for the policy enforcement and the effectiveness of public tobacco control spending along with alternative measures of affordability would be warranted to enhance its applicability in low-income and middle-income countries.
Benefits and barriers to participation in colorectal cancer screening: a protocol for a systematic review and synthesis of qualitative studies
Authors: Honein-AbouHaidar Gladys N , Kastner Monika , Vuong Vincent , Perrier Laure , Rabeneck Linda , Tinmouth Jill , Straus Sharon , Baxter Nancy N 
Published: February 2014

IntroductionColorectal cancer (CRC) poses a serious health problem worldwide. While screening is effective in reducing CRC mortality, participation in screening tests is generally suboptimal and social inequities in participation are frequently reported. The goal of this review is to synthesise factors that influence an individual’s decision to participate in CRC screening, and to explore how those factors vary by sex, ethnicity and socioeconomic status.Data sourcesA primary search of Cumulative Index to Nursing and Allied Health Literature (CINAHL), MEDLINE, EMBASE, PsycINFO, and a secondary search of grey literature and articles taken from references of included articles (from inception to July 2013).DesignA systematic review and Meta-study synthesis of qualitative studies that address perceived benefits and barriers to participation in CRC screening tests among adults 50 years of age or older.Review methodsThe two-staged Meta-study methodology by Paterson will be used to conduct this review. In stage 1, similarities/differences, patterns and themes will be identified across three levels of analysis while preserving the context of original studies. In stage 2, synthesis will extend beyond the analysis to generate new theory of the phenomenon through a process called Meta-synthesis.DiscussionThis review offers to generate a framework to better understand benefits and barriers that affect decision-making to participate in CRC screening among different sectors of the population. This framework will be a relevant tool for policy makers in framing educational materials, for patient-centered communication, and for researchers interested in the science of equity. This review is registered in PROSPERO (registration number: CRD42013005025).
Asymptomatic left ventricular dysfunction with long-term clozapine treatment for schizophrenia: a multicentre cross-sectional cohort study
Authors: Chow V , Yeoh T , Ng A C C , Pasqualon T , Scott E , Plater J , Whitwell B , Hanzek D , Chung T , Thomas L , Celermajer D S , Kritharides L 
Published: February 2014

ObjectivesPatients with schizophrenia treated with clozapine are at risk of acute myocarditis and dilated cardiomyopathy. However, there are no data on the prevalence of subclinical cardiomyopathy or its associations.Methods100 consecutive patients with schizophrenia treated with clozapine for >1 year and without a history of cardiac pathology (group 1), 21 controls with a history of schizophrenia treated with non-clozapine antipsychotics for >1 year (group 2) and 20 controls without schizophrenia (group 3) were studied. Comprehensive evaluation by clinical examination, ECG, transthoracic echocardiography including left ventricular ejection fraction (LVEF) and global longitudinal strain (GLS) and biochemical profiles were performed.ResultsPatients with schizophrenia were of similar age, but had higher body mass index (BMI), rates of smoking and hyperlipidaemia than controls. Patients with schizophrenia had received clozapine or non-clozapine antipsychotics for a mean duration of 6.8±5.3 and 9.7±6.1 years, respectively. Patients taking clozapine demonstrated globally impaired LVEF (58.3%: group 1 vs 62.2%: group 2 vs 64.8%: group 3, p<0.001) and GLS (−16.7%: group 1 vs −18.6%: group 2 vs −20.2%: group 3, p<0.001). Moreover, LVEF was <50% in 9/100 (9%) patients receiving clozapine and in non-clozapine schizophrenia patients or healthy controls, but this was not statistically significantly different (analysis of covariance, p=0.19). Univariate analysis in patients taking clozapine found that impaired LV was not predicted by high-sensitivity troponin T, but was associated with features of the metabolic syndrome (including increased triglycerides, low high-density lipoprotein cholesterol (HDL-C), high-sensitivity C reactive protein and BMI), elevated neutrophil count, elevated heart rate, smoking and N-terminal probrain natriuretic peptide. In patients taking clozapine, multivariable analysis identified elevated neutrophil count and low HDL-C as the only independent predictors of impaired GLS.ConclusionsAsymptomatic mild LV impairment is common in patients with schizophrenia receiving long-term clozapine treatment and is associated with neutrophilia and low HDL-C.
Medical student views on the use of Facebook profile screening by residency admissions committees
Authors: George Daniel R , Green Michael J , Navarro Anita M , Stazyk Kelly K , Clark Melissa A 
Published: February 2014

Abstract

Purpose
Previous research has shown that &gt;50% of residency programmes indicate that inappropriate Facebook postings could be grounds for rejecting a student applicant. This study sought to understand medical students’ views regarding the impact of their Facebook postings on the residency admissions process.

Study design
In 2011–2012, we conducted a national survey of 7144 randomly selected medical students representing 10% of current enrollees in US medical schools. Students were presented with a hypothetical scenario of a residency admissions committee searching Facebook and finding inappropriate pictures of a student, and were asked how the committee ought to regard these pictures.

Results
The response rate was 30% (2109/7144). Respondents did not differ from medical students nationally with regard to type of medical school and regional representation. Of the three options provided, the majority of respondents (63.5%) indicated ‘the pictures should be considered along with other factors, but should not be grounds for automatic rejection of the application’. A third (33.7%) believed ‘the pictures should have no bearing on my application; the pictures are irrelevant’. A small minority of respondents (2.8%) felt ‘the pictures should be grounds for automatic rejection of the application’.

Conclusions
That the views of students regarding the consequences of their online activity differ so greatly from the views of residency admissions committees speaks to the need for better communication between these parties. It also presents opportunities for medical schools to help students in their residency application process by increasing awareness of social media screening strategies used by some residency programmes, and fostering self-awareness around the use of social media during medical school and especially during the residency application process.
Decreased serum protein associated with Mycobacterium avium subspecies paratuberculosis shedding in German Holstein cows
Authors: Donat K. , Erhardt G. , Soschinka A. , Brandt H. R. 
Published: February 2014

Using well established metabolic parameters, this study aimed to substantiate differences in protein and energy metabolism between Mycobacterium avium subspecies paratuberculosis (MAP) positive and negative dairy cows tested by faecal culture. A total of 227 MAP‐positive and 239 MAP‐negative German Holstein cows kept in 13 MAP‐positive dairy herds were selected for metabolic testing. The serum concentrations of total protein (TP), bilirubin, cholesterol and betahydroxybutyrate were measured as well as the activities of Glutamate‐Dehydrogenase (GLDH) and Aspartate‐Aminotransferase. MAP‐positive cows were characterised by a decreased mean TP (66.5 g/l) compared to the MAP‐negative controls (73.2 g/l). Mean log10 GLDH activities tended to be higher in MAP‐positive than MAP‐negative cows. Concerning TP, there was a significant interaction between MAP status and farm. Within four farms, the difference between MAP‐positive and MAP‐negative animals differed significantly, while in the other farms this difference was not significant. It is concluded that a decreased TP and an increased GLDH indicate alterations in protein metabolism. These findings suggest an enhanced liver cell turnover in MAP‐positive cows. The results contribute to an understanding of the metabolic alterations in MAP‐positive dairy cows.
Autocrine Motility Factor Modulates EGF-Mediated Invasion Signaling
Authors: Kho Dhong Hyo , Zhang Tianpeng , Balan Vitaly , Wang Yi , Ha Seung-Wook , Xie Youming , Raz Avraham 
Published: February 2014

Abstract
Autocrine motility factor (AMF) enhances invasion by breast cancer cells, but how its secretion and effector signaling are controlled in the tumor microenvironment is not fully understood. In this study, we investigated these issues with a chimeric AMF that is secreted at high levels through a canonical endoplasmic reticulum (ER)/Golgi pathway. Using this tool, we found that AMF enhances tumor cell motility by activating AKT/ERK, altering actin organization, and stimulating β-catenin/TCF and activating protein 1 transcription. EGF enhanced secretion of AMF through its casein kinase II–mediated phosphorylation. RNA interference–mediated attenuation of AMF expression inhibited EGF-induced invasion by suppressing extracellular signal–regulated kinase signaling. Conversely, exogenous AMF overcame the inhibitory effect of EGF receptor inhibitor gefitinib on invasive motility by activating HER2 signaling. Taken together, our findings show how AMF modulates EGF-induced invasion while affecting acquired resistance to cytotoxic drugs in the tumor microenvironment. Cancer Res; 74(8); 2229–37. ©2014 AACR.
Identification and Initial Functional Characterization of a Human Vascular Cell–Enriched Long Noncoding RNA
Authors: Bell Robert D. , Long Xiaochun , Lin Mingyan , Bergmann Jan H. , Nanda Vivek , Cowan Sarah L. , Zhou Qian , Han Yu , Spector David L. , Zheng Deyou , Miano Joseph M. 
Published: February 2014

Objective—
Long noncoding RNAs (lncRNAs) represent a rapidly growing class of RNA genes with functions related primarily to transcriptional and post-transcriptional control of gene expression. There is a paucity of information about lncRNA expression and function in human vascular cells. Thus, we set out to identify novel lncRNA genes in human vascular smooth muscle cells and to gain insight into their role in the control of smooth muscle cell phenotypes.

Approach and Results—

RNA sequencing (RNA-seq) of human coronary artery smooth muscle cells revealed 31 unannotated lncRNAs, including a vascular cell–enriched lncRNA (Smooth muscle and Endothelial cell–enriched migration/differentiation-associated long NonCoding RNA [
SENCR
]). Strand-specific reverse transcription polymerase chain reaction (PCR) and rapid amplification of cDNA ends indicate that
SENCR
is transcribed antisense from the 5′ end of the
FLI1
gene and exists as 2 splice variants. RNA fluorescence in situ hybridization and biochemical fractionation studies demonstrate
SENCR
is a cytoplasmic lncRNA. Consistent with this observation, knockdown studies reveal little to no
cis
-acting effect of
SENCR
on
FLI1
or neighboring gene expression. RNA-seq experiments in smooth muscle cells after
SENCR
knockdown disclose decreased expression of Myocardin and numerous smooth muscle contractile genes, whereas several promigratory genes are increased. Reverse transcription PCR and Western blotting experiments validate several differentially expressed genes after
SENCR
knockdown. Loss-of-function studies in scratch wound and Boyden chamber assays support
SENCR
as an inhibitor of smooth muscle cell migration.

Conclusions—

SENCR
is a new vascular cell–enriched, cytoplasmic lncRNA that seems to stabilize the smooth muscle cell contractile phenotype.
Overexpression of C1q/Tumor Necrosis Factor–Related Protein-3 Promotes Phosphate-Induced Vascular Smooth Muscle Cell Calcification Both In Vivo and In Vitro
Authors: Zhou Yun , Wang Jin-Yu , Feng Han , Wang Cheng , Li Li , Wu Dan , Lei Hong , Li Hao , Wu Li-Ling 
Published: February 2014

Objective—
Vascular calcification is highly correlated with increased cardiovascular morbidity and mortality. C1q/tumor necrosis factor–related protein-3 (CTRP3) is a newly identified adipokine that plays important roles in cardiovascular system. Here, we investigated the role of CTRP3 in vascular calcification and its underlying mechanism.

Approach and Results—

Adenine-induced chronic renal failure rat model was used to mimic the process of arterial medial calcification. The level of CTRP3 was elevated in serum and abdominal aorta of chronic renal failure rats. Periadventitial gene delivery of CTRP3 significantly accelerated the calcification of abdominal aorta and arterial ring. In cultured vascular smooth muscle cells (VSMCs), CTRP3 increased β-glycerophosphate–induced calcium deposition and alkaline phosphatase activity. Although CTRP3 alone was not sufficient to induce calcification in VSMCs, it upregulated the expression of osteogenic marker genes including runt-related transcription factor 2 (
Runx2
), bone morphogenetic protein 2, and osteopontin. CTRP3 further enhanced β-glycerophosphate–induced downregulation of smooth muscle α-actin and smooth muscle 22α, while augmenting osteogenic marker expression in VSMCs induced by β-glycerophosphate. In contrast, knockdown of CTRP3 in VSMCs potently suppressed β-glycerophosphate–induced calcification. Mechanistically, knockdown of Runx2 inhibited CTRP3-promoted VSMC calcification. CTRP3 increased extracellular signal–regulated kinase 1/2 phosphorylation and reactive oxygen species production. Preincubation with U0126, an extracellular signal–regulated kinase 1/2 upstream kinase inhibitor, had no effect on CTRP3-induced reactive oxygen species production. However, pretreatment with N-acetyl-
l
-cysteine, a reactive oxygen species scavenger, suppressed CTRP3-induced extracellular signal–regulated kinase 1/2 phosphorylation. Both N-acetyl-
l
-cysteine and U0126 significantly inhibited CTRP3-induced upregulation of Runx2 and calcified nodule formation.

Conclusions—
CTRP3 promotes vascular calcification by enhancing phosphate-induced osteogenic transition of VSMC through reactive oxygen species–extracellular signal–regulated kinase 1/2–Runx2 pathway.
Poor Long-Term Functional Outcome After Stroke Among Adults Aged 18 to 50 Years
Authors: Synhaeve Nathalie E. , Arntz Renate M. , Maaijwee Noortje A.M. , Rutten-Jacobs Loes C.A. , Schoonderwaldt Henny C. , Dorresteijn Lucille D.A. , de Kort Paul L.M. , van Dijk Ewoud J. , de Leeuw Frank-Erik 
Published: February 2014

Background and Purpose—
Stroke in young adults has a dramatic effect on life; therefore, we investigated the long-term functional outcome after transient ischemic attack, ischemic stroke, or intracerebral hemorrhage in adults aged 18 to 50 years.

Methods—
We studied 722 young patients with first-ever stroke admitted between January 1, 1980, and November 1, 2010. Functional outcome was assessed by stroke subtype with the modified Rankin Scale and Instrumental Activities of Daily Living scale.

Results—
After a mean follow-up of 9.1 (SD, 8.2) years, 32.0% of all patients had a poor functional outcome (modified Rankin Scale, >2); for ischemic stroke, this was 36.5%, for intracerebral hemorrhage 49.3%, and for transient ischemic attack 16.8%. At follow-up, 10.8% of transient ischemic attack, 14.6% of ischemic stroke, and 18.2% of intracerebral hemorrhage patients had a poor outcome as assessed by Instrumental Activities of Daily Living (<8).

Conclusions—
Ten years after ischemic stroke or intracerebral hemorrhage in young adults, 1 of 8 survivors is still dependent in daily life.
Genome-Wide Genotyping Demonstrates a Polygenic Risk Score Associated With White Matter Hyperintensity Volume in CADASIL
Authors: Opherk Christian , Gonik Mariya , Duering Marco , Malik Rainer , Jouvent Eric , Hervé Dominique , Adib-Samii Poneh , Bevan Steve , Pianese Luigi , Silvestri Serena , Dotti Maria Teresa , De Stefano Nicola , Liem Michael , Boon Elles M.J. , Pescini Francesca , Pachai Chahin , Bracoud Luc , Müller-Myhsok Bertram , Meitinger Thomas , Rost Natalia , Pantoni Leonardo , Lesnik Oberstein Saskia , Federico Antonio , Ragno Michele , Markus Hugh S. , Tournier-Lasserve Elisabeth , Rosand Jonathan , Chabriat Hugues , Dichgans Martin 
Published: February 2014

Background and Purpose—
White matter hyperintensities (WMH) on MRI are a quantitative marker for sporadic cerebral small vessel disease and are highly heritable. To date, large-scale genetic studies have identified only a single locus influencing WMH burden. This might in part relate to biological heterogeneity of sporadic WMH. The current study searched for genetic modifiers of WMH volume in cerebral autosomal-dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), a monogenic small vessel disease.

Methods—
We performed a genome-wide association study to identify quantitative trait loci for WMH volume by combining data from 517 CADASIL patients collected through 7 centers across Europe. WMH volumes were centrally analyzed and quantified on fluid attenuated inversion recovery images. Genotyping was performed using the Affymetrix 6.0 platform. Individuals were assigned to 2 distinct genetic clusters (cluster 1 and cluster 2) based on their genetic background.

Results—

Four hundred sixty-six patients entered the final genome-wide association study analysis. The phenotypic variance of WMH burden in CADASIL explained by all single nucleotide polymorphisms in cluster 1 was 0.85 (SE=0.21), suggesting a substantial genetic contribution. Using cluster 1 as derivation and cluster 2 as a validation sample, a polygenic score was significantly associated with WMH burden (
P
=0.001) after correction for age, sex, and vascular risk factors. No single nucleotide polymorphism reached genome-wide significance.

Conclusions—
We found a polygenic score to be associated with WMH volume in CADASIL subjects. Our findings suggest that multiple variants with small effects influence WMH burden in CADASIL. The identification of these variants and the biological pathways involved will provide insights into the pathophysiology of white matter disease in CADASIL and possibly small vessel disease in general.