bluuebunny/crossref_metadata_2025_split huggingface dataset:
Dietary Fat, Fatty Acids, and Risk of Prostate Cancer in the NIH-AARP Diet and Health Study
Authors: Pelser Colleen , Mondul Alison M. , Hollenbeck Albert R. , Park Yikyung 
Published: April 2013

AbstractBackground: Observational studies report inconsistent associations of fat and fatty acids with prostate cancer.Methods: We investigated associations between dietary fats and fatty acids and risk of prostate cancer in the NIH-American Association of Retired Persons (AARP) Diet and Health Study. Diet was assessed at baseline with self-administered food-frequency questionnaires. Cases were determined by linkage with state cancer registries. HR and 95% confidence intervals (CI) were estimated with Cox proportional hazards models.Results: Among 288,268 men with average follow-up of nine years, 23,281 prostate cancer cases (18,934 nonadvanced and 2,930 advanced including 725 fatal cases) were identified. Total fat and mono- and polyunsaturated fat intakes were not associated with incidence of prostate cancer. Saturated fat intake was related to increased risk of advanced prostate cancer (HRQuintile 5 vs. Qunitile 1 (Q1 vs. Q5), 1.21; 95% CI, 1.00–1.46; Ptrend = 0.03) and fatal prostate cancer (HRQ5 vs. Q1, 1.47; 95% CI, 1.01–2.15; Ptrend = 0.04). α-Linolenic acid (ALA) intake was related to increased risk of advanced prostate cancer (HRQ5 vs. Q1, 1.17; 95% CI, 1.04–1.31; Ptrend = 0.01). Eicosapentanoic acid (EPA) intake was related to decreased risk of fatal prostate cancer (HRQ5 vs. Q1, 0.82; 95% CI, 0.64–1.04; Ptrend = 0.02).Conclusion: Our study suggests that the associations of fat and fatty acids differ by prostate cancer severity. Saturated fat, ALA, and EPA intakes were related to the risk of advanced or fatal prostate cancer but not to nonadvanced prostate cancer.Impact: Identifying factors associated with advanced prostate cancer could reduce morbidity and mortality. Cancer Epidemiol Biomarkers Prev; 22(4); 697–707. ©2013 AACR.
Dysplastic Nevi and Melanoma
Authors: Goldstein Alisa M. , Tucker Margaret A. 
Published: April 2013

Abstract
Dysplastic nevi are described as being on a continuum between common acquired nevi and melanoma because they are morphologically and biologically intermediate between these 2 entities. Since initially being reported as histologic lesions observed in melanoma-prone families, there has been considerable debate about the definition of dysplastic nevi, the histologic and clinical criteria used to define them, and their biologic importance. Their role as precursor lesions for melanoma is not their primary role in their relationship to melanoma because of the rarity of transformation of any individual nevus to a melanoma. Although there is still no single, universally agreed upon histologic or clinical definition or even name for these nevi, dysplastic nevi should be considered important because of their association with an increased risk for melanoma. Cancer Epidemiol Biomarkers Prev; 22(4); 528–32. ©2013 AACR.
MicroRNA-150
Authors: Devaux Yvan , Vausort Melanie , McCann Gerry P. , Zangrando Jennifer , Kelly Dominic , Razvi Naveed , Zhang Lu , Ng Leong L. , Wagner Daniel R. , Squire Iain B. 
Published: April 2013

Background—
Left ventricular (LV) remodeling after acute myocardial infarction is associated with adverse prognosis. MicroRNAs (miRNAs) regulate the expression of several genes involved in LV remodeling. Our aim was to identify miRNAs associated with LV remodeling after acute myocardial infarction.

Methods and Results—

We studied 90 patients after first ST-segment–elevation acute myocardial infarction. A derivation cohort consisted of 60 patients characterized by echocardiography predischarge and at 6-month follow-up. Thirty patients characterized by magnetic resonance imaging predischarge and at 4-month follow-up were the validation cohort. Remodeling was defined as an increase in LV end-diastolic volume (ΔEDV>0) between discharge and follow-up. Circulating miRNAs were measured by microarrays and polymerase chain reaction. Using a systems-based approach, we identified several miRNAs potentially involved in LV remodeling. In the derivation cohort, one of these miRNAs, miR-150, was downregulated in patients with remodeling (ΔEDV>0) compared with patients without remodeling (ΔEDV≤0). In the validation cohort, patients with remodeling had 2-fold lower levels of miR-150 than those without (
P
=0.03). miR-150 outperformed N-terminal pro-brain natriuretic peptide to predict remodeling (area under the receiver-operating characteristic curve of 0.74 and 0.60, respectively). miR-150 reclassified 54% (95% confidence interval, 5–102;
P
=0.03) of patients misclassified by N-terminal pro-brain natriuretic peptide and 59% (95% confidence interval, 9–108;
P
=0.02) of patients misclassified by a multiparameter clinical model, including age, sex, and admission levels of troponin I, creatine kinase, and N-terminal pro-brain natriuretic peptide.

Conclusions—
Low circulating levels of miR-150 are associated with LV remodeling after first ST-segment–elevation acute myocardial infarction. miR-150 has potential as a novel biomarker in this setting.
Is the Washington Consensus Dead? Growth, Openness, and the Great Liberalization, 1970s–2000s
Authors: Estevadeordal Antoni , Taylor Alan M. 
Published: April 2013

Abstract
According to the Washington Consensus, developing countries' growth would benefit from reductions in barriers to trade. However, the empirical basis for judging trade reforms is weak. Econometrics are mostly ad hoc, results are typically not judged against models, policies are poorly measured, and most studies are based on pre-1990 experience. We address these concerns by employing a model with capital and intermediate goods, compiling new disaggregated tariff measures, and employing treatment and control regression analysis with differences-in-differences. We find that a specific treatment, liberalizing tariffs on imported capital and intermediate goods, led to faster growth, consistent with the model.
Are Household Surveys Like Tax Forms? Evidence from Income Underreporting of the Self-Employed
Authors: Hurst Erik , Li Geng , Pugsley Benjamin 
Published: April 2013

Abstract
A large literature shows that the self-employed underreport their income to tax authorities. In this paper, we quantify the extent to which the self-employed also systematically underreport their income in U.S. household surveys. We use the Engel curve describing the relationship between income and expenditures of wage and salary workers to infer the actual income, and thus the reporting gap, of the self-employed based on their reported expenditures. On average, the self-employed underreport their income by about 25%. We show that failing to account for such income underreporting leads to biased conclusions in a variety of settings.
Competition and Innovation: The Inverted-U Relationship Revisited
Authors: Hashmi Aamir Rafique 
Published: April 2013

Abstract
I reexamine the inverted-U relationship between competition and innovation (modeled and tested by Aghion et al. (2005)) by using data from publicly traded manufacturing firms in the United States. I control for the possible endogeneity of competition by using a trade-weighted average of industry exchange rates as an instrument. I find a mildly negative relationship between competition (as measured by the inverse of markups) and innovation (as measured by citation-weighted patents). The negative relationship is robust to many alternative assumptions and specifications. To reconcile the mildly negative relationship in the U.S. data with the inverted-U relationship that Aghion et al. (2005) find in the U.K. data, I modify their theoretical model and show that the modified model can explain both negative and inverted-U relationships. The key theoretical assumption is that the U.K. manufacturing industries are technologically more neck-and-neck than their counterparts in the United States. I find support for this assumption in the data. The different empirical results between the two countries may also arise because of differences in data and samples.
Determining the Influence of Type 1 Diabetes on Two Common Eating Disorder Questionnaires
Authors: Powers Margaret A. , Richter Sara , Ackard Diann , Critchley Stephanie , Meier Marcia , Criego Amy 
Published: April 2013

Purpose This research evaluated the level of influence that having type 1 diabetes (T1DM) has on responses to questions about food choices, eating concerns, dietary restraint, and others that are included on two widely used, validated eating disorder (ED) questionnaires and examined responses to these two questionnaires from patients with T1DM and an eating disorder (ED-T1DM) and an ED-no-diabetes. Method An expert panel rated each item on the Eating Disorders Examination Questionnaire (EDE-Q) and Eating Disorders Inventory, version 3 (EDI-3) regarding T1DM level of influence on item interpretation. These questionnaires were completed by 2 matched samples (ED-T1DM, n = 48 and ED-no-diabetes, n = 96); responses were compared between the samples with particular attention to items of high T1DM influence. Results The expert panel identified that 50% (19/38) of the items on the EDE-Q and 6.6% (6/91) on the EDI-3 could be highly influenced by having T1DM. Before Bonferroni correction, the 2 groups responded statistically different on 9 out of 38 items on the EDE-Q and 27 out of 91 items on the EDI-3; generally responses were healthier for those with ED-T1DM than ED-no-diabetes. Of these items, on the EDE-Q, 5 were rated high T1DM influence and on the EDI-3, 3 were rated high. Conclusion Having T1DM influences responses on ED questionnaires developed for the general population. This influence may be greater when questionnaires focus on eating, weight, and shape and result in misinterpretation of total and subscale scores by even well-trained clinicians. A careful review of individual item responses by the treatment team is warranted.
Ir más allá de los “grupos vulnerables”: contextos y dinámica de la vulnerabilidad
Authors: Zarowsky Christina , Haddad Slim , Nguyen Vinh-Kim 
Published: April 2013

Resumen Este artículo repasa los enfoques a la vulnerabilidad en el campo de la salud pública y presenta 10 trabajos sobre cómo abordarla en África. Entendemos la vulnerabilidad a la vez como situación y como proceso. Las desigualdades sociales son evidentes y se exacerban en tres dimensiones clave de la vulnerabilidad: el nivel inicial de bienestar, el grado de exposición al riesgo y la capacidad de gestionar el riesgo de manera efectiva. Subrayamos las interacciones dinámicas en virtud de las cuales se genera una relación entre la privación material y social, la pobreza, la impotencia y la mala salud: los riesgos o percances (shocks) y sus repercusiones sobre la salud están íntimamente interrelacionados y se refuerzan mutuamente en un círculo que multiplica la vulnerabilidad a menos que se realicen intervenciones eficaces. Gracias a un proceso inductivo que no empieza con una definición o una medición a priori de la “vulnerabilidad” y que no presupone la existencia de “grupos vulnerables” fijos, pudimos por un lado reafirmar los aspectos centrales de los marcos conceptuales existentes y por otro considerar de forma diferente la literatura que aborda específicamente la vulnerabilidad y la resiliencia a nivel de la población así como otro tipo de literatura - por ejemplo, en materia de ecología y en torno al concepto de fragilidad en los estudios sobre envejecimiento - con la que posiblemente no estén familiarizados los investigadores sobre salud y pobreza en África. Invitamos a realizar una labor conceptual y empírica sobre la vulnerabilidad en marcos de sistemas complejos. Estas perspectivas subrayan los contextos y la causalidad no lineal, dando más peso por lo tanto a los análisis de vulnerabilidad y de resiliencia en tanto que marcadores de las interacciones dinámicas y como propiedades emergentes de estas interacciones. Aceptamos una definición operativa de vulnerabilidad y reconocemos que algunos grupos de personas susceptibles de ser definidos tienen más probabilidades que otros de sufrir perjuicio como consecuencia de su exposición a los riesgos para la salud. Pero sugerimos que de lo que se trata en realidad – tanto a nivel intelectual como político y en materia de elaboración de políticas- es de comprender la dinámica, los significados y las relaciones de poder que subyacen a las instancias y procesos reales de vulnerabilidad y perjuicio y darles respuesta.
Incidence, risk factors, and outcomes of sclerosis in patients with chronic graft-versus-host disease
Authors: Inamoto Yoshihiro , Storer Barry E. , Petersdorf Effie W. , Nelson J. Lee , Lee Stephanie J. , Carpenter Paul A. , Sandmaier Brenda M. , Hansen John A. , Martin Paul J. , Flowers Mary E. D. 
Published: April 2013

Key Points
Incidence of sclerotic GVHD is 20% by 3 years after initial systemic treatment for chronic GVHD. The use of mobilized blood cell graft and total body irradiation conditioning are associated with an increased risk of sclerotic GVHD.
Tribbles in acute leukemia
Authors: Liang Kai Ling , Rishi Loveena , Keeshan Karen 
Published: April 2013

Abstract
There is growing research interest in the mammalian Tribbles (Trib) family of serine/threonine pseudokinases and their oncogenic association with acute leukemias. This review is to understand the role of Trib genes in hematopoietic malignancies and their potential as targets for novel therapeutic strategies in acute myeloid leukemia and acute lymphoblastic leukemia. We discuss the role of Tribs as central signaling mediators in different subtypes of acute leukemia and propose that inhibition of dysregulated Trib signaling may be therapeutically beneficial.
Alcohol ingestion disrupts alveolar epithelial barrier function by activation of macrophage-derived transforming growth factor beta1
Authors: Curry-McCoy Tiana V , Venado Aida , Guidot David M , Joshi Pratibha C 
Published: April 2013

Abstract

Background
Chronic alcohol abuse causes oxidative stress and impairs alveolar epithelial barrier integrity, thereby rendering the lung susceptible to acute edematous injury. Experimentally, alcohol-induced oxidative stress increases the expression of transforming growth factor β1 (TGFβ1) in the lung; however, we do not know the precise contribution of various alveolar cells in this process. In the present study, we focused on cell-cell interactions between alveolar macrophages and epithelial cells and the potential mechanisms by which TGFβ1 may become activated in the alveolar space of the alcoholic lung.

Methods
Primary alveolar macrophages and epithelial cells were isolated from control- and alcohol-fed Sprague–Dawley rats. Expression of TGFβ1 and the epithelial integrin αvβ6 were examined by real time PCR and either immunocytochemistry or flow cytometry. Alveolar epithelial cells were cultured on transwell supports in the presence of macrophage cell lysate from control- or alcohol-fed rats or in the presence of viable macrophages ± alcohol. Epithelial barrier function was assessed by transepithelial resistance (TER) and paracellular flux of Texas Red dextran.

Results
TGFβ1 expression was increased in alveolar macrophages from alcohol-fed rats, and TGFβ1 protein was predominantly membrane-bound. Importantly, alveolar macrophage cellular lysate from alcohol-fed rats decreased TER and increased paracellular dextran flux in primary alveolar epithelial cell monolayers as compared to the lysates from control-fed rats. Alcohol-induced epithelial barrier dysfunction was prevented by anti-TGFβ1 antibody treatment, indicating the presence of bioactive TGFβ1 in the macrophage lysate. In addition, co-culturing macrophages and epithelial cells in the presence of alcohol decreased epithelial barrier function, which also was prevented by anti-TGFβ1 and anti-αvβ6 treatment. In parallel, chronic alcohol ingestion in vivo, or direct treatment with active TGFβ1 in vitro, increased the expression of αvβ6 integrin, which is known to activate TGFβ1, in alveolar epithelial cells.

Conclusions
Taken together, these data suggest that interactions between alveolar epithelial cells and macrophages contribute to the alcohol-mediated disruption of epithelial barrier function via the expression and activation of TGFβ1 at points of cell-cell contact.
CAMTA 1 regulates drought responses in Arabidopsis thaliana
Authors: Pandey Neha , Ranjan Alok , Pant Poonam , Tripathi Rajiv K , Ateek Farha , Pandey Haushilla P , Patre Uday V , Sawant Samir V 
Published: April 2013

Abstract

Background
Transcription factors (TF) play a crucial role in regulating gene expression and are fit to regulate diverse cellular processes by interacting with other proteins. A TF named calmodulin binding transcription activator (CAMTA) was identified in Arabidopsis thaliana (AtCAMTA1-6). To explore the role of CAMTA1 in drought response, the phenotypic differences and gene expression was studied between camta1 and Col-0 under drought condition.

Results
In camta1, root development was abolished showing high-susceptibility to induced osmotic stress resulting in small wrinkled rosette leaves and stunted primary root. In camta1 under drought condition, we identified growth retardation, poor WUE, low photosystem II efficiency, decline in RWC and higher sensitivity to drought with reduced survivability. The microarray analysis of drought treated camta1 revealed that CAMTA1 regulates “drought recovery” as most indicative pathway along with other stress response, osmotic balance, apoptosis, DNA methylation and photosynthesis. Interestingly, majority of positively regulated genes were related to plasma membrane and chloroplast. Further, our analysis indicates that CAMTA1 regulates several stress responsive genes including RD26, ERD7, RAB18, LTPs, COR78, CBF1, HSPs etc. and promoter of these genes were enriched with CAMTA recognition cis-element. CAMTA1 probably regulate drought recovery by regulating expression of AP2-EREBP transcription factors and Abscisic acid response.

Conclusion
CAMTA1 rapidly changes broad spectrum of responsive genes of membrane integrity and photosynthetic machinery by generating ABA response for challenging drought stress. Our results demonstrate the important role of CAMTA1 in regulating drought response in Arabidopsis, thus could be genetically engineered for improving drought tolerance in crop.
Anti-tumor necrosis factor VNAR single domains reduce lethality and regulate underlying inflammatory response in a murine model of endotoxic shock
Authors: Bojalil Rafael , Mata-González María Teresa , Sánchez-Muñoz Fausto , Yee Yepci , Argueta Iván , Bolaños Lucía , Amezcua-Guerra Luis Manuel , Camacho-Villegas Tanya Amanda , Sánchez-Castrejón Edna , García-Ubbelohde Walter Jakob , Licea-Navarro Alexei Fedorovish , Márquez-Velasco Ricardo , Paniagua-Solís Jorge Fernando 
Published: April 2013

Abstract

Background
In sepsis, tumor necrosis factor (TNF) is the key factor triggering respiratory burst, tissue injury and disseminated coagulation. Anti-TNF strategies based on monoclonal antibodies or F(ab’)2 fragments have been used in sepsis with contradictory results. Immunoglobulin new antigen receptors (IgNAR) are a unique subset of antibodies consisting of five constant (CNAR) and one variable domains (VNAR). VNAR domains are the smallest, naturally occurring, antibody-based immune recognition units, having potential use as therapy.
Our aim was to explore the impact of an anti-TNF VNAR on survival in an experimental model of endotoxic shock. Also, mRNA expression and serum protein of several inflammatory molecules were measured.

Results
Endotoxic shock was induced by lipopolysaccharide (LPS) in male Balb/c mice. Animals were treated with anti-TNF VNAR domains, F(ab’)2 antibody fragments, or saline solution 15 minutes before, 2 h and 24 h after lethal dose100 (LD100) LPS administration. TNF blockade with either VNAR domains or F(ab’)2 fragments were associated with lower mortality (60% and 75%, respectively) compared to LD100. Challenge with LPS induced significant production of serum TNF and interleukins -10 and -6 at 3 h. After that, significant reduction of IL-6 at 24 h (vs 3 h) was shown only in the VNAR group. Nitrites level also increased in response to LPS.
In liver, TNF and IL-10 mRNA expression showed a pro-inflammatory imbalance in response to LPS. Blocking TNF was associated with a shift towards an anti-inflammatory status; however, polarization was more pronounced in animals receiving F(ab’)2 fragments than in those with VNAR therapy. With regard to IL-6, gene expression was increased at 3 h in all groups. TNF blockade was associated with rapid and sustained suppression of IL-6 expression, even more evident in the VNAR group. Finally, expression of inducible-nitric oxide synthase (iNOS) increased in response to LPS at 3 h, but this was decreased at 24 h only in the anti-TNF VNAR group.

Conclusions
Anti-TNF VNAR single domains improved survival in a murine model of endotoxic shock. Protection was associated with regulation in the TNF/IL-10 balance, attenuation of IL-6 and iNOS gene expression in the liver as well as decreased serum IL-6 concentration.
Chronic kidney diseases in mixed ancestry south African populations: prevalence, determinants and concordance between kidney function estimators
Authors: Matsha Tandi E , Yako Yandiswa Y , Rensburg Megan A , Hassan Mogamat S , Kengne Andre P , Erasmus Rajiv T 
Published: April 2013

Abstract

Background
Population-based data on the burden of chronic kidney disease (CKD) in sub-Saharan Africa is still very limited. We assessed the prevalence and determinants of CKD, and evaluated the concordance of commonly advocated estimators of glomerular filtration rate (eGFR) in a mixed ancestry population from South Africa.

Methods
Participants were a population-based sample of adults selected from the Bellville-South community in the metropolitan city of Cape Town. eGFR was based on the Cockroft-Gault (CG), Modification of Diet in Kidney Disease (MDRD) and CKD Epidemiology Collaboration (CKD-EPI) equations (with and without adjustment for ethnicity). Kidney function staging used the Kidney Disease Outcome Quality Initiative (KDOQI) classification. Logistic regressions and kappa statistic were used to investigate determinants of CKD and assess the agreement between different estimators.

Results
The crude prevalence of CKD stage 3–5 was 14.8% for Cockcroft-Gault, 7.6% and 23.9% respectively for the MDRD with and without ethnicity correction, and 7.4% and 17.3% for the CKD-EPI equations with and without ethnicity correction. The highest agreement between GFR estimators was between MDRD and CKD-EPI equations, both with ethnicity correction, Kappa 0.91 (95% CI: 0.86-0.95), correlation coefficient 0.95 (95% CI: 0.94-0.96). In multivariable logistic regression models, sex, age and known hypertension were consistently associated with CKD stage 3–5 across the 5 estimators.

Conclusions
The prevalence of CKD stages greater than 3 is the highest reported in Africa. This study provides evidence for support of the CKD-EPI equation for eGFR reporting and CKD classification.