bluuebunny/crossref_metadata_2025_split huggingface dataset:
Complete Genome Sequence of Brucella canis Strain 118, a Strain Isolated from Canine
Authors: Gao Guangjun , Li Jing , Li Tiefeng , Zhang Zhengfang , Wang Liping , Yuan Xitong , Wang Yufei , Xu Jie , Ke Yuehua , Huang Liuyu , Wang Dali , Chen Zeliang , Xu Xingran 
Published: November 2012

ABSTRACTBrucella canisinfects several species of animals, and canine is the preferred host. Genome sequences of strains from different hosts are valuable for comparative analysis of host adaptation and microevolution. Here, we report the genome sequence ofBrucella canisstrain 118, a strain isolated from canine.
Draft Genome Sequence of the Thermophilic Bacterium Anoxybacillus kamchatkensis G10
Authors: Lee Sang-Jae , Lee Yong-Jik , Ryu Naeun , Park Seulki , Jeong Haeyoung , Lee Sang Jun , Kim Byoung-Chan , Lee Dong-Woo , Lee Han-Seung 
Published: November 2012

ABSTRACT

Anoxybacillus kamchatkensis
G10 is a spore-forming thermophilic bacterium isolated from a hot spring in Indonesia. Here, we report the draft genome sequence of
A. kamchatkensis
G10 that may reveal insights into aerobic/anaerobic metabolisms and carbon utilization in moderate thermophiles.
Copeptin in acute chest pain: identification of acute coronary syndrome and obstructive coronary artery disease on coronary CT angiography
Authors: Dedic Admir , ten Kate Gert-Jan , Rood Pleunie P M , Galema Tjebbe W , Ouhlous Mohamed , Moelker Adriaan , de Feyter Pim J , de Rijke Yolanda B , Nieman Koen 
Published: November 2012

ObjectiveTo determine the diagnostic accuracy of copeptin in patients with suspected acute coronary syndrome (ACS) and its correlation with obstructive coronary artery disease (CAD) on coronary CT angiography (CTA).MethodsCopeptin was measured at arrival in 65 consecutive patients (56±10 years, 45 men) suspected of ACS and no indication for immediate invasive angiography. All patients underwent coronary CTA without disclosure of the results to the treating physician, and outcomes were classified as obstructive CAD (>50% stenosis) or no obstructive CAD (≤50%) in one or more vessel.ResultsThe final diagnosis of ACS was established in 10 (15%) patients, 6 myocardial infarctions and 4 unstable angina pectoris. Coronary CTA detected obstructive CAD in all patients with ACS and in 10 (15%) patients with no ACS. Copeptin concentrations were higher in patients with ACS (median 7.42 pmol/l (IQR 3.71–18.72)) vs patients with no ACS (3.40 pmol/l (1.13–6.27), p=0.02). Copeptin was not higher in patients with obstructive CAD on coronary CTA (4.87 pmol/l (2.90–8.51) vs 3.60 pmol/l (1.21–6.23), p=0.20) compared with patients with no obstructive CAD.ConclusionsCopeptin seems to be elevated in patients with ACS while there is no strong correlation with obstructive coronary disease on CTA.
Determinants of patient satisfaction in an Australian emergency department fast-track setting
Authors: Dinh Michael M , Enright Nicholas , Walker Andrew , Parameswaran Ahilan , Chu Matthew 
Published: November 2012

ObjectivesTo describe the relationship between waiting time and patient satisfaction, and to determine predictors of overall care rating in an emergency department (ED) fast-track setting.MethodsA convenience sample of patients triaged to a fast-track unit were surveyed. Patient satisfaction was scored using a validated survey instrument, as well as a single overall care rating (poor to excellent). Median satisfaction scores were compared between each incremental hour of waiting time. Bivariate analysis was conducted between those who waited 1 h or less, and those who waited longer. Ordered logistic regression was used to determine predictors of improved overall care rating.Results236 patients completed surveys (response rate of 74%). Of these, 84% rated their care as either very good or excellent. There was a linear decrease in median satisfaction scores for each incremental hour of waiting time associated with half the odds of higher overall care rating after adjusting for presenting problem type, triage category, and treating clinician type (OR 0.53 95% CI 0.37 to 0.75 p<0.001). English language (OR 2.43 95% CI 1.33 to 4.42 p=0.004) and initial consultation by a nurse practitioner (NP) (OR 1.81 95% CI 1.03 to 3.31 p=0.038) were also found to be significant predictors of improved overall care rating.ConclusionsWaiting time was found to be highly predictive of patient satisfaction in an emergency fast-track unit with English language and NPs also associated with improved overall care rating. Future measures to improve patient satisfaction in fast-track units should focus on these factors.
Influence of social networking websites on medical school and residency selection process
Authors: Schulman Carl I , Kuchkarian Fernanda M , Withum Kelly F , Boecker Felix S , Graygo Jill M 
Published: November 2012

Abstract

Background
Social networking (SN) has become ubiquitous in modern culture. The potential consequences of revealing personal information through SN websites are not fully understood.

Objective
To assess familiarity with, usage of, and attitudes towards, SN websites by admissions offices at US medical schools and residency programmes.

Methods
A 26-question survey was distributed in autumn 2009 to 130 US medical school admissions officers and 4926 residency programme directors accredited by the Accreditation Council for Graduate Medical Education.

Results
A total of 600 surveys were completed, with 46 (8%) respondents who self-identified as reviewing only medical school applications, 511 (85%) who reported reviewing residency programme applications and 43 (7%) who reported reviewing both. 90/600 (15%) medical schools or programmes maintain profiles on SN websites and 381/600 (64%) respondents reported being somewhat or very familiar with searching individual profiles on SN websites. While a minority of medical schools and residency programmes routinely use SN websites in the selection process (53/600; 9%), more than half of respondents felt that unprofessional information on applicants' SN websites could compromise their admission into medical school or residency (315/600; 53%).

Conclusions
SN websites will affect selection of medical students and residents. Formal guidelines for professional behaviour on SN websites might help applicants avoid unforeseen bias in the selection process.
Characterization of Rearrangements Involving the ALK Gene Reveals a Novel Truncated Form Associated with Tumor Aggressiveness in Neuroblastoma
Authors: Cazes Alex , Louis-Brennetot Caroline , Mazot Pierre , Dingli Florent , Lombard Bérangère , Boeva Valentina , Daveau Romain , Cappo Julie , Combaret Valérie , Schleiermacher Gudrun , Jouannet Stéphanie , Ferrand Sandrine , Pierron Gaëlle , Barillot Emmanuel , Loew Damarys , Vigny Marc , Delattre Olivier , Janoueix-Lerosey Isabelle 
Published: November 2012

Abstract
Activating mutations of the ALK gene have been identified in sporadic and familial cases of neuroblastoma (NB), a cancer of the peripheral nervous system, and are thought to be the primary mechanism of oncogenic activation of this receptor in this pediatric neoplasm. To address the possibility that ALK activation may occur through genomic rearrangements as detected in other cancers, we first took advantage of high-resolution array-comparative genomic hybridization to search for ALK rearrangements in NB samples. Using complementary experiments by capture/paired-end sequencing and FISH experiments, various types of rearrangements were fully characterized, including partial gains or amplifications, in several NB cell lines and primary tumors. In the CLB-Bar cell line, we described a genomic rearrangement associated with an amplification of the ALK locus, leading to the expression of a 170 kDa protein lacking part of the extracellular domain encoded by exons 4 to 11, named ALKΔ4-11. Analysis of genomic DNA from the tumor at diagnosis and relapse revealed that the ALK gene was amplified at diagnosis but that the rearranged ALK allele was observed at the relapse stage only, suggesting that it may be implicated in tumor aggressiveness. Consistently, oncogenic and tumorigenic properties of the ALKΔ4-11 variant were shown after stable expression in NIH3T3 cells. Moreover, we documented an increased constitutive kinase activity of this variant, as well as an impaired maturation and retention into intracellular compartments. These results indicate that genomic rearrangements constitute an alternative mechanism to ALK point mutations resulting in receptor activation. Cancer Res; 73(1); 195–204. ©2012 AACR.
Oncostatin M Modulates the Mesenchymal–Epithelial Transition of Lung Adenocarcinoma Cells by a Mesenchymal Stem Cell-Mediated Paracrine Effect
Authors: Wang Mong-Lien , Pan Chih-Ming , Chiou Shih-Hwa , Chen Wen-Hsin , Chang Hsiang-Yi , Lee Oscar Kuang-Sheng , Hsu Han-Sui , Wu Cheng-Wen 
Published: November 2012

Abstract
Mesenchymal stem cells (MSC) are strongly associated with tumor progression and have been used as novel cell-based agents to deliver anticancer drugs to tumors. However, controversies about the direct involvement of MSCs in tumor progression suggest that MSCs mediate tumor progression in a cancer type-dependent manner. In this report, we analyzed the functional interactions between human MSCs and lung adenocarcinoma (LAC) cells to determine the therapeutic potential of MSCs in lung cancer. We showed that MSCs effectively inhibited the migration, invasion, and cell-cycle progression of several LAC cell lines. MSCs also enhanced the mesenchymal–epithelial transition (MET) pathway, as evidenced by the reduction of several epithelial–mesenchymal transition-related markers in LAC cells cocultured with MSCs or in MSC-conditioned medium (MSC-CM). By cytokine array analysis, we determined that Oncostatin M (OSM), a differentiation-promoting cytokine, was elevated in the MSC-CM derived from primary MSC cultures. Furthermore, OSM treatment had the same effects as MSC-CM on LAC, whereas neutralizing antibodies to OSM reversed them. Notably, short hairpin RNAs against STAT1, an important downstream target of OSM, hindered the OSM-dependent induction of MET. In vivo xenograft tumor studies indicated that OSM inhibited tumor formation and metastasis of LAC cells, whereas neutralizing OSM in the MSC-CM hampered its inhibitory effects. In conclusion, this study showed that OSM is a paracrine mediator of MSC-dependent inhibition of tumorigenicity and activation of MET in LAC cells. These effects of OSM may serve as a basis for the development of new drugs and therapeutic interventions targeting cancer cells. Cancer Res; 72(22); 6051–64. ©2012 AACR.
RANKL Expression, Function, and Therapeutic Targeting in Multiple Myeloma and Chronic Lymphocytic Leukemia
Authors: Schmiedel Benjamin Joachim , Scheible Carolin Andrea , Nuebling Tina , Kopp Hans-Georg , Wirths Stefan , Azuma Miyuki , Schneider Pascal , Jung Gundram , Grosse-Hovest Ludger , Salih Helmut Rainer 
Published: November 2012

Abstract
Bone destruction is a prominent feature of multiple myeloma, but conflicting data exist on the expression and pathophysiologic involvement of the bone remodeling ligand RANKL in this disease and the potential therapeutic benefits of its targeted inhibition. Here, we show that RANKL is expressed by primary multiple myeloma and chronic lymphocytic leukemia (CLL) cells, whereas release of soluble RANKL was observed exclusively with multiple myeloma cells and was strongly influenced by posttranscriptional/posttranslational regulation. Signaling via RANKL into multiple myeloma and CLL cells induced release of cytokines involved in disease pathophysiology. Both the effects of RANKL on osteoclastogenesis and cytokine production by malignant cells could be blocked by disruption of RANK–RANKL interaction with denosumab. As we aimed to combine neutralization of RANKL with induction of antibody-dependent cellular cytotoxicity of natural killer (NK) cells against RANKL-expressing malignant cells and as denosumab does not stimulate NK reactivity, we generated RANK-Fc fusion proteins with modified Fc moieties. The latter displayed similar capacity compared with denosumab to neutralize the effects of RANKL on osteoclastogenesis in vitro, but also potently stimulated NK cell reactivity against primary RANKL-expressing malignant B cells, which was dependent on their engineered affinity to CD16. Our findings introduce Fc-optimized RANK-Ig fusion proteins as attractive tools to neutralize the detrimental function of RANKL while at the same time potently stimulating NK cell antitumor immunity. Cancer Res; 73(2); 683–94. ©2012 AACR.
Comparison of two methods for selection of out of hospital treatment in patients with acute pulmonary embolism
Authors: Crobach Monique J. T. , Dolsma Anneke , Donker Marjolein L. , Eijsvogel Michiel , Faber Laura M. , Hofstee Herman M. A. , Kaasjager Karin A. H. , Kruip Marieke J. H. A. , Labots Geert , Melissant Christian F. , Sikkens Michelle S. G. , Huisman Menno V. , Zondag Wendy , den Exter Paul L. 
Published: November 2012

SummaryThe aim of this study is to compare the performance of two clinical decision rules to select patients with acute pulmonary embolism (PE) for outpatient treatment: the Hestia criteria and the simplified Pulmonary Embolism Severity Index (sPESI). From 2008 to 2010, 468 patients with PE were triaged with the Hestia criteria for outpatient treatment: 247 PE patients were treated at home and 221 were treated as inpatients. The outcome of interest was all-cause 30-day mortality. In a post-hoc fashion, the sPESI items were scored and patients were classified according to the sPESI in low and high risk groups. Of the 247 patients treated at home, 189 (77%) patients were classified as low risk according to the sPESI and 58 patients (23%) as high risk. In total, 11 patients died during the first month; two patients treated at home and nine patients treated in-hospital. None of the patients treated at home died of fatal PE. Both the Hestia criteria and sPESI selected >50% of patients as low risk, with good sensitivity and negative predictive values for 30-day mortality: 82% and 99% for the Hestia criteria and 91% and 100% for the sPESI, respectively. The Hestia criteria and the sPESI classified different patients eligible for out-patient treatment, with similar low risks for 30-day mortality. This study suggests that the Hestia criteria may identify a proportion of high risk sPESI patiennts who can be safely treated at home, this however requires further validation.
Differential expression of T-cell genes in blood and bone marrow between ITP patients and controls
Authors: Nookaew Intawat , Wadenvik Hans , Olsson Bob , Jernås Margareta 
Published: November 2012

SummaryPrimary immune thrombocytopenia (ITP) is an autoimmune disease characterised by premature platelet destruction in spleen, liver and bone marrow and a diminished production of platelets. T-cells are important in all forms of autoimmunity including ITP; however, very little is known about T-cells in organs where platelets are destroyed. Our aim was to investigate differences in gene expression in peripheral blood-derived T-cells and bone marrow-derived T-cells between ITP patients and controls. T-cells and subsequent RNA were isolated from blood and bone marrow from chronic ITP patients and healthy controls followed by DNA microarray analysis. There were 1554 differentially expressed genes in peripheral blood-derived T-cells and 976 in bone marrow-derived T-cells between ITP patients and controls and three genes were verified with real-time PCR. Using Gene Ontology functional enrichment analysis we found that genes involved in growth, development, migration, chemotaxis, adhesion and apoptosis were enriched in bone marrow-derived T-cells in ITP. Immune-related genes involved in T-helper cell differentiation, T-cell chemotaxis, migration, immunoglobulin-mediated immune response and classical and alternative pathway complement activation were also enriched in bone marrow-derived T-cells in ITP. Only 213 T-cell genes were differentially expressed in both blood and bone marrow between ITP patients and controls. In conclusion, our findings show that genes involved in major pathophysiologic pathways in ITP such as T-helper cell differentiation, autoantibody response and complement activation are altered in bone marrow-derived T-cells in ITP patients compared with controls. This further supports the concept that bone marrow is an important compartment in ITP.
ACAT Inhibition Reduces the Progression of Preexisting, Advanced Atherosclerotic Mouse Lesions Without Plaque or Systemic Toxicity
Authors: Rong James X. , Blachford Courtney , Feig Jonathan E. , Bander Ilda , Mayne Jeffrey , Kusunoki Jun , Miller Christine , Davis Matthew , Wilson Martha , Dehn Shirley , Thorp Edward , Tabas Ira , Taubman Mark B. , Rudel Lawrence L , Fisher Edward A. 
Published: November 2012

Objective—
Acyl-CoA:cholesterol acyltransferase (ACAT) converts cholesterol to cholesteryl esters in plaque foam cells. Complete deficiency of macrophage ACAT has been shown to increase atherosclerosis in hypercholesterolemic mice because of cytotoxicity from free cholesterol accumulation, whereas we previously showed that partial ACAT inhibition by Fujirebio compound F1394 decreased early atherosclerosis development. In this report, we tested F1394 effects on preestablished, advanced lesions of apolipoprotein-E–deficient mice.

Methods and Results—
Apolipoprotein-E–deficient mice on Western diet for 14 weeks developed advanced plaques, and were either euthanized (Baseline), or continued on Western diet with or without F1394 and euthanized after 14 more weeks. F1394 was not associated with systemic toxicity. Compared with the baseline group, lesion size progressed in both groups; however, F1394 significantly retarded plaque progression and reduced plaque macrophage, free and esterified cholesterol, and tissue factor contents compared with the untreated group. Apoptosis of plaque cells was not increased, consistent with the decrease in lesional free cholesterol. There was no increase in plaque necrosis and unimpaired efferocytosis (phagocytic clearance of apoptotic cells). The effects of F1394 were independent of changes in plasma cholesterol levels.

Conclusion—
Partial ACAT inhibition by F1394 lowered plaque cholesterol content and had other antiatherogenic effects in advanced lesions in apolipoprotein-E–deficient mice without overt systemic or plaque toxicity, suggesting the continued potential of ACAT inhibition for the clinical treatment of atherosclerosis, in spite of recent trial data.
Adiponectin and Long-Term Mortality in Coronary Artery Disease Participants and Controls
Authors: Hascoet Sébastien , Elbaz Meyer , Bongard Vanina , Bouisset Fréderic , Verdier Céline , Vindis Cécile , Genoux Annelise , Taraszkiewicz Dorota , Perret Bertrand , Galinier Michel , Carrié Didier , Ferrières Jean , Ruidavets Jean Bernard 
Published: November 2012

Objective—
Despite cardioprotective properties, studies investigating adiponectin as a cardiovascular disease marker led to conflicting results. We investigated in participants with stable coronary artery disease (CAD) and controls whether serum adiponectin was associated with long-term mortality, considering varying degrees of CAD severity.

Methods and Results—

A case–control design with prospective median follow-up of 8.1 years was used. Survival rates among 715 CAD men (aged 45–74 years) in increasing quartiles of serum adiponectin values were 87.5%, 85.6%, 76.4%, and 67.6%, respectively (
P
<0.001). Survival rates in 782 controls with adiponectin <9.1 µg/mL and ≥9.1 µg/mL (third quartile) were 95.3% and 91.0%, respectively (
P
=0.035). Adiponectin concentration above the highest quartile was associated with an increased risk of total and cardiovascular disease mortality in CAD patients (
P
=0.001 and
P
=0.001) and controls (
P
=0.02 and
P
=0.004). The associations among high adiponectin, total mortality, and cardiovascular disease mortality remained significant after multivariate adjustments for metabolic, cardiac, and CAD severity variables. No significant interaction was found among CAD patients, controls, and the relationship of adiponectin with mortality.

Conclusion—
High serum adiponectin is a predictor of mortality, particularly from cardiovascular disease. This prognostic value remains significant whatever the severity of the CAD and the metabolic status and is not different among people with and without CAD.
Integration of Genetics into a Systems Model of Electrocardiographic Traits Using HumanCVD BeadChip
Authors: Gaunt Tom R. , Shah Sonia , Nelson Christopher P. , Drenos Fotios , Braund Peter S. , Adeniran Ismail , Folkersen Lasse , Lawlor Debbie A. , Casas Juan-Pablo , Amuzu Antoinette , Kivimaki Mika , Whittaker John , Eriksson Per , Zhang Henggui , Hancox Jules C. , Tomaszewski Maciej , Burton Paul R. , Tobin Martin D. , Humphries Steve E. , Talmud Philippa J. , Macfarlane Peter W. , Hingorani Aroon D. , Samani Nilesh J. , Kumari Meena , Day Ian N.M. 
Published: November 2012

Background—
Electrocardiographic traits are important, substantially heritable determinants of risk of arrhythmias and sudden cardiac death.

Methods and Results—

In this study, 3 population-based cohorts (n=10 526) genotyped with the Illumina HumanCVD Beadchip and 4 quantitative electrocardiographic traits (PR interval, QRS axis, QRS duration, and QTc interval) were evaluated for single-nucleotide polymorphism associations. Six gene regions contained single nucleotide polymorphisms associated with these traits at
P
<10
−6
, including
SCN5A
(PR interval and QRS duration),
CAV1-CAV2
locus (PR interval),
CDKN1A
(QRS duration),
NOS1AP
,
KCNH2
, and
KCNQ1
(QTc interval). Expression quantitative trait loci analyses of top associated single-nucleotide polymorphisms were undertaken in human heart and aortic tissues.
NOS1AP
,
SCN5A, IGFBP3, CYP2C9
, and
CAV1
showed evidence of differential allelic expression. We modeled the effects of ion channel activity on electrocardiographic parameters, estimating the change in gene expression that would account for our observed associations, thus relating epidemiological observations and expression quantitative trait loci data to a systems model of the ECG.

Conclusions—
These association results replicate and refine the mapping of previous genome-wide association study findings for electrocardiographic traits, while the expression analysis and modeling approaches offer supporting evidence for a functional role of some of these loci in cardiac excitation/conduction.