bluuebunny/crossref_metadata_2025_split huggingface dataset:
Intraoperative cell salvage is associated with reduced postoperative blood loss and transfusion requirements in cardiac surgery: a cohort study
Authors: Vonk Alexander B.A. , Meesters Michael I. , Garnier Robert P. , Romijn Johannes W.A. , van Barneveld Lerau J.M. , Heymans Martijn W. , Jansen Evert K. , Boer Christa 
Published: February 2013

BackgroundThis study investigated whether implementation of cell salvage of shed mediastinal and residual blood in all patients undergoing low‐to‐moderate–risk cardiac surgery reduces the need for allogeneic red blood cell (RBC) transfusion compared to patients not subjected to cell salvage.Study Design and MethodsThis retrospective cohort study included patients undergoing low‐to‐moderate–risk cardiac surgery with cardiopulmonary bypass without (control; n = 531) or with cell salvage (n = 433; Autolog, Medtronic). Study endpoints, including 24‐hour blood loss and RBC requirements, were evaluated using adjusted logistic regression.ResultsBaseline characteristics were similar between groups. The cell saver group received 568 ± 267 mL of autologous blood. Median number of allogeneic RBC transfusions was higher in the control group (2 [1‐5]) compared with the cell salvage group (1 [0‐3]; p < 0.001). There were no clinically relevant differences in postoperative coagulation test results between groups. The relative risk (RR) for postoperative RBC transfusion was reduced to 0.76 (95% confidence interval [CI], 0.70‐0.83; p < 0.0001) in the cell salvage group. Moreover, patients in the cell salvage group had a lower chance for myocardial infarction (RR, 0.26; 95% CI, 0.08‐0.91; p = 0.035), whereas the cell salvage group was associated with a higher probability for intensive care discharge within 24 hours after surgery (RR, 1.08; 95% CI, 1.02‐1.14; p = 0.009).ConclusionThe use of cell salvage throughout the entire procedure reduces postoperative blood loss and allogeneic RBC transfusion. These findings advocate implementation of cell salvage in all patients undergoing on‐pump cardiac surgery, irrespective of anticipated surgery‐related blood loss.
Multiple Human Papillomavirus Infections with High Viral Loads Are Associated with Cervical Lesions but Do Not Differentiate Grades of Cervical Abnormalities
Authors: Schmitt Markus , Depuydt Christophe , Benoy Ina , Bogers Johannes , Antoine Jerome , Arbyn Marc , Pawlita Michael 
Published: February 2013

ABSTRACT

Multiple human papillomavirus (HPV) genotypes often coexist within cervical epithelia and are frequently detected together in smears of different grades of cervical neoplasia. Describing the association between multiple infections and cervical disease is important in generating hypotheses regarding its pathogenesis. We analyzed the prevalence of multiple HPV infections and their attribution to cervical disease in a screening population of 999 consecutive BD SurePath liquid-based cervical cytology samples enriched with atypical squamous cells of undetermined significance (ASCUS) (
n
= 100), low-grade squamous intraepithelial lesions (LSIL) (
n
= 100), and high-grade squamous intraepithelial lesions (HSIL) (
n
= 97). HPV genotyping was performed only on cytology specimens using a broad-spectrum GP5
+
/6
+
-PCR/multiplex HPV genotyping (BSGP5
+
/6
+
-PCR/MPG) assay that detects and quantifies 51 HPV genotypes and 3 subtypes. Using a recently defined high viral load cutoff, the quantitative data were scored as high or low viral load. In the 36-month follow-up, 79 histologically confirmed cervical intraepithelial neoplasia grade 2 or greater (CIN2+) cases were identified. In the screening population, there was a trend of having more multiple infections at a younger age. Multiple HPV infections were common. Multiple HPV types were most prevalent in LSIL (75.9% of HPV positives), followed by HSIL (65.5%), ASCUS (64.6%), and negative for intraepithelial lesion or malignancy (NILM) (36.8%). On average, 3.2 and 2.5 HPV types were detected per LSIL and HSIL sample, respectively. Multiple HPV types with high viral loads were most prevalent in LSIL (62.6% of high viral load positives), followed by HSIL (51.9%), ASCUS (40.7%), and NILM (19.3%). Patients with multiple high viral loads showed a 4- to 6-fold-higher risk of having cervical precancerous cytological lesions than did patients with single high viral loads. Compared to NILM, multiple infections, especially with multiple high viral loads, were significantly associated with cytological precancerous lesions. However, the presence of multiple infections did not distinguish low-grade from high-grade cytological lesions.
Injury rates, types, mechanisms and risk factors in female youth ice hockey
Authors: Decloe Melissa D , Meeuwisse Willem H , Hagel Brent E , Emery Carolyn A 
Published: February 2013

BackgroundThe objectives of this cohort study were to examine the rate, types, mechanisms and risk factors for injury in female youth (ages 9–17) ice hockey players in the Girls Hockey Calgary Association.MethodsThe main outcome was ice hockey injury, defined as any injury occurring during the 2008/2009 season that required medical attention, and/or removal from a session and/or missing a subsequent session. Potential risk factors included age group, level of play, previous injury, ice hockey experience, physical activity level, weight, height, position of play and menarche. Incidence rate ratios (IRR) were estimated with Poisson Regression adjusted for cluster (team). Exposure data were collected for every session for each participating player.ResultsTwenty-eight teams (n=324) from Atom (ages 9–10), PeeWee (11–12), Bantam (13–14) and Midget (15–17) participated with 53 reported injuries. The overall injury rate was 1.9 injuries/1000 player-hours (95% CI 1.4 to 2.7). Previous injury (IRR=2.7, 95% CI 1.7 to 4.3), games (IRR=2.1, 95% CI 1.1 to 4.2), menarche (PeeWee) (IRR=4.1, 95% CI 1.0 to 16.8) were significant risk factors. In Midget, the more elite divisions were associated with a lower injury risk (A-IRR=0.2, 95% CI 0.1 to 0.5) (AAA-IRR=0.5, 95% CI 0.2 to 0.9).ConclusionsInjury rates were lower in this study than previously found in male youth and women's ice hockey populations. Previous injury and game play as risk factors are consistent with the literature. Menarche as a risk factor is a new finding in this study. This research will inform future studies of the development of injury prevention strategies in this population.
Facies and climate changes across the Permian–Triassic boundary in the North German Basin: insights from a high-resolution organic carbon isotope record
Authors: Hiete Michael , Röhling Heinz-Gerd , Heunisch Carmen , Berner Ulrich 
Published: February 2013

Abstract
The transition from the uppermost Permian Zechstein Group to the lowermost Triassic Lower Buntsandstein Subgroup in the North German Basin is characterized by a shift from sabkha to playa and to fluviatile facies indicative of a shift to a more humid climate and associated with a major reorganization of the sedimentary system. These changes are recorded in a high-resolution carbon isotope profile of bulk organic matter spanning from the upper Zechstein Group of Changhsingian age to the Calvörde Formation of the Lower Buntsandstein Subgroup of Changhsingian–Indusian age. The organic carbon isotopes reflect a varying composition of the organic matter. Dependent on the facies type, which is mainly controlled by humidity, the proportions of cyanobacterial, phytoplankton and land-plant-derived organic matter with differing organic carbon isotope values change in the samples. A negative organic carbon isotope excursion shortly below the supposed Permian–Triassic Boundary (PTB) is interpreted as a horizon rich in isotopically light phytoplankton, representing a perennial playa lake stage. Although certain effects of global carbon cycle perturbations around the PTB on the analysed organic carbon isotope profile cannot be excluded, the facies and climatic changes associated with the PTB events are thought to be more important.
Kinetic Modeling–Based Detection of Genetic Signatures That Provide Chemoresistance via the E2F1-p73/DNp73-miR-205 Network
Authors: Vera Julio , Schmitz Ulf , Lai Xin , Engelmann David , Khan Faiz M. , Wolkenhauer Olaf , Pützer Brigitte M. 
Published: February 2013

Abstract
Drug resistance is a major cause of deaths from cancer. E2F1 is a transcription factor involved in cell proliferation, apoptosis. and metastasis through an intricate regulatory network, which includes other transcription factors like p73 and cancer-related microRNAs like miR-205. To investigate the emergence of drug resistance, we developed a methodology that integrates experimental data with a network biology and kinetic modeling. Using a regulatory map developed to summarize knowledge on E2F1 and its interplay with p73/DNp73 and miR-205 in cancer drug responses, we derived a kinetic model that represents the network response to certain genotoxic and cytostatic anticancer drugs. By perturbing the model parameters, we simulated heterogeneous cell configurations referred to as in silico cell lines. These were used to detect genetic signatures characteristic for single or double drug resistance. We identified a signature composed of high E2F1 and low miR-205 expression that promotes resistance to genotoxic drugs. In this signature, downregulation of miR-205, can be mediated by an imbalance in the p73/DNp73 ratio or by dysregulation of other cancer-related regulators of miR-205 expression such as TGFβ-1 or TWIST1. In addition, we found that a genetic signature composed of high E2F1, low miR-205, and high ERBB3 can render tumor cells insensitive to both cytostatic and genotoxic drugs. Our model simulations also suggested that conventional genotoxic drug treatment favors selection of chemoresistant cells in genetically heterogeneous tumors, in a manner requiring dysregulation of incoherent feedforward loops that involve E2F1, p73/DNp73, and miR-205. Cancer Res; 73(12); 3511–24. ©2013 AACR.
TNRC9 Downregulates BRCA1 Expression and Promotes Breast Cancer Aggressiveness
Authors: Shan Jingxuan , DSouza Shoba P. , Bakhru Sasha , Al-Azwani Eman K. , Ascierto Maria L. , Sastry Konduru S. , Bedri Shahinaz , Kizhakayil Dhanya , Aigha Idil I. , Malek Joel , Al-Bozom Issam , Gehani Salah , Furtado Stacia , Mathiowitz Edith , Wang Ena , Marincola Francesco M. , Chouchane Lotfi 
Published: February 2013

Abstract
Although the linkage between germline mutations of BRCA1 and hereditary breast/ovarian cancers is well established, recent evidence suggests that altered expression of wild-type BRCA1 might contribute to the sporadic forms of breast cancer. The breast cancer gene trinucleotide-repeat-containing 9 (TNRC9; TOX3) has been associated with disease susceptibility but its function is undetermined. Here, we report that TNRC9 is often amplified and overexpressed in breast cancer, particularly in advanced breast cancer. Gene amplification was associated with reduced disease-free and metastasis-free survival rates. Ectopic expression of TNRC9 increased breast cancer cell proliferation, migration, and survival after exposure to apoptotic stimuli. These phenotypes were associated with tumor progression in a mouse model of breast cancer. Gene expression profiling, protein analysis, and in silico assays of large datasets of breast and ovarian cancer samples suggested that TNRC9 and BRCA1 expression were inversely correlated. Notably, we found that TNRC9 bound to both the BRCA1 promoter and the cAMP-responsive element-binding protein (CREB) complex, a regulator of BRCA1 transcription. In support of this connection, expression of TNRC9 downregulated expression of BRCA1 by altering the methylation status of its promoter. Our studies unveil a function for TNRC9 in breast cancer that highlights a new paradigm in BRCA1 regulation. Cancer Res; 73(9); 2840–9. ©2013 AACR.
Aberrant Expression of Mucin Core Proteins and O-Linked Glycans Associated with Progression of Pancreatic Cancer
Authors: Remmers Neeley , Anderson Judy M. , Linde Erin M. , DiMaio Dominick J. , Lazenby Audrey J. , Wandall Hans H. , Mandel Ulla , Clausen Henrik , Yu Fang , Hollingsworth Michael A. 
Published: February 2013

AbstractPurpose: Mucin expression is a common feature of most adenocarcinomas and features prominently in current attempts to improve diagnosis and therapy for pancreatic cancer and other adenocarcinomas. We investigated the expression of a number of mucin core proteins and associated O-linked glycans expressed in pancreatic adenocarcinoma—sialyl Tn (STn), Tn, T antigen, sialyl Lewis A (CA19-9), sialyl Lewis C (SLeC), Lewis X (LeX), and sialyl LeX (SLeX)—during the progression of pancreatic cancer from early stages to metastatic disease.Experimental Design: Immunohistochemical analyses of mucin and associated glycan expression on primary tumor and liver metastatic tumor samples were conducted with matched sets of tissues from 40 autopsy patients diagnosed with pancreatic adenocarcinoma, 14 surgically resected tissue samples, and 8 normal pancreata.Results: There were significant changes in mucin expression patterns throughout disease progression. MUC1 and MUC4 were differentially glycosylated as the disease progressed from early pancreatic intraepithelial neoplasias to metastatic disease. De novo expression of several mucins correlated with increased metastasis indicating a potentially more invasive phenotype, and we show the expression of MUC6 in acinar cells undergoing acinar to ductal metaplasia. A “cancer field-effect” that included changes in mucin protein expression and glycosylation in the adjacent normal pancreas was also seen.Conclusions: There are significant alterations in mucin expression and posttranslational processing during progression of pancreatic cancer from early lesions to metastasis. The results are presented in the context of how mucins influence the biology of tumor cells and their microenvironment during progression of pancreatic cancer. Clin Cancer Res; 19(8); 1981–93. ©2013 AACR.
Serum levels of vitamin D are not associated with future risk of venous thromboembolism
Authors: Lerstad Gunhild , Grimnes Guri , Brækkan Sigrid K. , Vik Anders , Brox Jan , Svartberg Johan , Jorde Rolf , Hansen John-Bjarne , Brodin Ellen E. 
Published: February 2013

SummaryPrevious studies have provided indirect evidence for a possible association between vitamin D status and risk of venous thromboembolism (VTE). However, no study has so far investigated the association between serum levels of 25-hydroxyvitamin D (25(OH)D), the biomarker of vitamin D status, and risk of VTE. The aim of our study was to investigate whether high levels of 25(OH)D were associated with decreased risk of VTE in a prospective population-based study. Serum levels of 25(OH)D were measured in 6,021 men and women, aged 25–84 years, who participated in the Tromsø Study in 1994–1995. Incident VTE-events were registered from date of inclusion through the end of follow-up, September 1, 2007. Cox-regression models were used to calculate hazard ratios (HR) with 95% confidence interval (CI) for VTE. There were 201 incident VTE-events during a median of 10.7 years of follow-up. The risk of VTE did not decrease per one standard deviation (SD) (19.8 nmol/l) increase in serum 25(OH)D (multivariable HR 1.02; 95% CI 0.91–1.22). Moreover, subjects with serum 25(OH)D ≥ 70 nmol/l (upper quartile) did not have decreased risk of VTE compared to those ≤ 44 nmol/l (lower quartile) in age- and sex-adjusted analysis (HR 0.91, 95% CI: 0.60–1.37, p for trend across quartiles 0.9) or multivariable analysis adjusted for age, sex, body mass index, smoking, and physical activity (HR 0.76, 95% CI: 0.45–1.28, p for trend across quartiles 0.9). Subgroup analyses showed no associations between serum levels of 25(OH)D and unprovoked or provoked VTE. In conclusion, in our study, normal serum levels of 25(OH)D were not associated with future risk of VTE, suggesting that vitamin D status does not play an important role in the pathogenesis of VTE. However, our findings did not apply to subjects with vitamin D deficiency (< 30 nmol/l) due to lack of statistical power among these subjects.
CD4+ T cells in atherosclerosis: Regulation by platelets
Authors: Li Nailin 
Published: February 2013

SummaryAtherosclerosis is an inflammatory and thrombotic disease, in which both CD4+ T cells and platelets play important roles throughout all stages of atherogenesis. CD4+ T cells are the most abundant T cells present in atherosclerotic lesions. They are primarily seen as type 1 T helper (Th1) cells, while the other CD4+ T cell subsets Th2, Th17, and regulatory T (Treg) cells are also found in the lesions with lower frequencies. CD4+ T effector cells release various cytokines, which exert paracrine or autocrine effects among different CD4+ T cell subsets and other lesional cells and subsequently modulate inflammatory processes in the lesions. Platelets are instrumental in thrombosis and haemostasis, but also play important regulatory roles in immune response, inflammation, and angiogenesis. The present review summarises the current knowledge and/or understanding on how platelets regulate recruitment, activation, differentiation, and cytokine production of different CD4+ T cell subsets, as well as impacts of the platelet-CD4+ T cell interactions on atherogenesis. The research perspectives of platelet-CD4+ T cell interaction in atherosclerosis are also discussed.
From mice to men – mouse models in obesity research: What can we learn?
Authors: Scroyen Ilse , Hemmeryckx Bianca , Lijnen H. Roger 
Published: February 2013

summaryObesity has become a world-wide epidemic and is associated with diseases such as diabetes, dyslipidaemia, cardiovascular disease and certain types of cancers. Understanding the adipose tissue developmental process, involving adipogenesis, angiogenesis and extracellular matrix remodelling, is therefore crucial to reveal the pathobiology of obesity. Experimental mouse models are extensively used to gain new insights into these processes and to evaluate the role of new key players, in particular proteolytic system components, in adipose tissue development and obesity. In this paper, we will review available in vitro and in vivo murine models of obesity and discuss their value in understanding the mechanisms contributing to obesity.
Rapid Feature-driven Changes in the Attentional Window
Authors: Leonard Carly J. , Lopez-Calderon Javier , Kreither Johanna , Luck Steven J. 
Published: February 2013

Abstract
Spatial attention must adjust around an object of interest in a manner that reflects the object's size on the retina as well as the proximity of distracting objects, a process often guided by nonspatial features. This study used ERPs to investigate how quickly the size of this type of “attentional window” can adjust around a fixated target object defined by its color and whether this variety of attention influences the feedforward flow of subsequent information through the visual system. The task involved attending either to a circular region at fixation or to a surrounding annulus region, depending on which region contained an attended color. The region containing the attended color varied randomly from trial to trial, so the spatial distribution of attention had to be adjusted on each trial. We measured the initial sensory ERP response elicited by an irrelevant probe stimulus that appeared in one of the two regions at different times after task display onset. This allowed us to measure the amount of time required to adjust spatial attention on the basis of the location of the task-relevant feature. We found that the probe-elicited sensory response was larger when the probe occurred within the region of the attended dots, and this effect required a delay of approximately 175 msec between the onset of the task display and the onset of the probe. Thus, the window of attention is rapidly adjusted around the point of fixation in a manner that reflects the spatial extent of a task-relevant stimulus, leading to changes in the feedforward flow of subsequent information through the visual system.
Development of a short measure of psychological recovery in serious mental illness: the STORI-30
Authors: Andresen Retta , Caputi Peter , Oades Lindsay 
Published: February 2013

Objective: To develop a brief measure of stage of psychological recovery from mental illness by identifying the best-performing items of the 50-item Stages of Recovery Instrument (STORI). Method: Item response modelling was used to identify a short form of the full-length STORI. The resulting items were subjected to factor analysis to further refine the subscales. A second data set was used to confirm the construct validity of the new measure. A correlational analysis was conducted to examine relationships among the five subscale scores. Results: Analyses identified 30 items that represented the five stages of the full STORI. The five stage subscale scores of the shorter measure, the STORI-30, showed a pattern of correlations that demonstrated an ordinal relationship between the stages. Conclusions: There is a need for recovery-oriented measures to augment established clinical assessment tools. The shorter version of the STORI, the STORI-30, shows promise as a brief measure of stage of recovery, more feasible for routine clinical use. Further psychometric and longitudinal testing is recommended. Qualitative research would be valuable in establishing acceptability to consumers and the clinical usefulness of the STORI-30.
Novel diagnostic assays for heparin-induced thrombocytopenia
Authors: Cuker Adam , Rux Ann H. , Hinds Jillian L. , Dela Cruz May , Yarovoi Serge V. , Brown Isola A. M. , Yang Wei , Konkle Barbara A. , Arepally Gowthami M. , Watson Stephen P. , Cines Douglas B. , Sachais Bruce S. 
Published: February 2013

Key Points
The KKO-inhibition ELISA and DT40-luciferase tests are novel laboratory assays for HIT. They showed better discrimination than 2 commercial immunoassays and may improve the specificity and feasibility of HIT laboratory testing.
A Korpelevich-like algorithm for variational inequalities
Authors: Wu Zhitao , Yao Yonghong , Liou Yeong-Cheng , Li Hong-Jun 
Published: February 2013

Abstract
A Korpelevich-like algorithm has been introduced for solving a generalized variational inequality. It is shown that the presented algorithm converges strongly to a special solution of the generalized variational inequality.

MSC:47H05, 47J25.
Homology-based inference sets the bar high for protein function prediction
Authors: Hamp Tobias , Kassner Rebecca , Seemayer Stefan , Vicedo Esmeralda , Schaefer Christian , Achten Dominik , Auer Florian , Boehm Ariane , Braun Tatjana , Hecht Maximilian , Heron Mark , Hönigschmid Peter , Hopf Thomas A , Kaufmann Stefanie , Kiening Michael , Krompass Denis , Landerer Cedric , Mahlich Yannick , Roos Manfred , Rost Burkhard 
Published: February 2013

Abstract

Background
Any method that de novo predicts protein function should do better than random. More challenging, it also ought to outperform simple homology-based inference.

Methods
Here, we describe a few methods that predict protein function exclusively through homology. Together, they set the bar or lower limit for future improvements.

Results and conclusions
During the development of these methods, we faced two surprises. Firstly, our most successful implementation for the baseline ranked very high at CAFA1. In fact, our best combination of homology-based methods fared only slightly worse than the top-of-the-line prediction method from the Jones group. Secondly, although the concept of homology-based inference is simple, this work revealed that the precise details of the implementation are crucial: not only did the methods span from top to bottom performers at CAFA, but also the reasons for these differences were unexpected. In this work, we also propose a new rigorous measure to compare predicted and experimental annotations. It puts more emphasis on the details of protein function than the other measures employed by CAFA and may best reflect the expectations of users. Clearly, the definition of proper goals remains one major objective for CAFA.