bluuebunny/crossref_metadata_2025_split huggingface dataset:
Antioxidant Effects of Lycopene in African American Men with Prostate Cancer or Benign Prostate Hyperplasia: A Randomized, Controlled Trial
Authors: van Breemen Richard B. , Sharifi Roohollah , Viana Marlos , Pajkovic Natasa , Zhu Dongwei , Yuan Long , Yang Yanan , Bowen Phyllis E. , Stacewicz-Sapuntzakis Maria 
Published: March 2011

Abstract
Consumption of tomato products is associated with a decreased risk of developing prostate cancer, and lycopene, the red carotenoid in the tomato, is a potent antioxidant that might contribute to this chemoprevention activity. A double-blind, randomized, placebo-controlled trial of 105 African American men veterans, recommended for prostate biopsy to detect cancer, was carried out to investigate whether oral administration of lycopene increases lycopene levels in blood and prostate tissue and lowers markers of oxidative stress. Urology patients were randomly assigned to receive 30 mg/d of lycopene as a tomato oleoresin or placebo for 21 days prior to prostate biopsy for possible diagnosis of prostate cancer. A total of 47 men had a diagnosis of prostate cancer, and 58 men had a diagnosis of benign prostate hyperplasia. Diet, smoking, and drinking habits were assessed. For the men receiving lycopene, the mean lycopene concentration increased from 0.74 ± 0.39 to 1.43 ± 0.61 μmol/L in plasma (P &lt; 0.0001) and from 0.45 ± 0.53 to 0.59 ± 0.47 pmol/mg in prostate tissue (P = 0.005). No significant changes in the DNA oxidation product 8-oxo-deoxyguanosine and the lipid peroxidation product malondialdehyde were observed in prostate tissue and plasma, respectively, as a result of lycopene administration. Cancer Prev Res; 4(5); 711–8. ©2011 AACR.
Percutaneous Transatrial Access to the Pericardial Space for Epicardial Mapping and Ablation
Authors: Scanavacca Mauricio I. , Venancio Ana Claudia , Pisani Cristiano F. , Lara Sissy , Hachul Denise , Darrieux Francisco , Hardy Carina , Paola Edna , Aiello Vera D. , Mahapatra Srijoy , Sosa Eduardo 
Published: March 2011

Background—
Puncture of the atrial appendage may provide access to the pericardial space. The aim of this study was to evaluate the feasibility of epicardial mapping and ablation through an endocardial transatrial access in a swine model.

Methods and Results—

An 8-F Mullins sheath was used to perforate the right (n=16) or left (n=1) atrial appendage in 17 pigs (median weight, 27.5 kg; first and third quartiles [Q1, Q3], 25.2, 30.0 kg). A 7-F ablation catheter was introduced into the pericardial space to perform epicardial mapping and deliver radiofrequency pulses on the atria. The pericardial space was entered in all 17 animals. In 15 (88%) animals, there was no hemodynamic instability (mean blood pressure monitoring, initial median, 80 mm Hg; Q1, Q3, 70, 86 mm Hg; final median, 88 mm Hg; Q1, Q3, 80, 96 mm Hg;
P
=0.426). In these 15, a mild hemorrhagic pericardial effusion was identified and aspirated (median, 20 mL; Q1, Q3, 15, 30 mL) during the procedure, and postmortem gross analysis revealed that the atrial perforation was closed in these animals. In 2 (12%) of the 17 animals, there was major pericardial bleeding with hemodynamic collapse. On gross examination, it was found that pericardial space was accessed through right ventricular perforation in 1 animal and the tricuspid annulus in the other. After the initial study, we used an occlusion device in 3 other animals to attempt to seal the puncture (2 at the right atrial appendage and 1 at the right ventricle). These 3 animals had no significant pericardial bleeding.

Conclusions—
Transatrial endovascular right atrial appendage puncture may provide a potential alternative route for pericardial access. Further studies are needed to evaluate its safety with longer and more-complex procedures before being applied in clinical settings.
Coexistence of Left-Sided Atrioventricular Accessory Pathways With a Common Inferior Pulmonary Vein Ostium
Authors: Ihara Kensuke , Nitta Junichi , Sato Akira , Iwai Shinsuke , Asano Mitsutoshi , Kanoh Miki , Muramatsu Kenichi , Yamato Tsunehiro , Matsumura Yutaka , Takei Kazuyasu , Asakawa Kihiro , Hirao Kenzo , Isobe Mitsuaki 
Published: March 2011

Background—
As the technique for radiofrequency catheter ablation for atrial fibrillation (AF) has progressed, so has our knowledge of both normal and abnormal anatomy of the left atrium and pulmonary veins (PV). We treated several AF patients with accessory conduction pathways (ACP) who were also found to have a common ostium of inferior PVs (CIPV), a relatively rare PV anomaly. No relation between ACP and PV anomalies has ever been reported, and the aim of our study was to study this association.

Methods and Results—

This study included 137 consecutive patients (104 men; mean age, 60±9 years) who underwent AF ablation for paroxysmal and persistent AF at our institution from March 2009 to August 2010. We analyzed coexisting supraventricular tachycardias and left atrium and PV morphology by multidetector row CT. Thirty-eight of 137 patients (27.7%) were found to have some PV anomaly, consisting of 13 with a common trunk of left PV, 19 with right additional PV, 3 with a common trunk of right PV, and 3 with CIPV. Thirty-one patients (22.6%) had supraventricular tachycardias. They were 26 cases of atrial flutter, 4 of Wolff-Parkinson-White syndrome, and 3 of atrioventricular nodal reentrant tachycardia. The prevalence of a coexisting ACP was significantly higher in patients with CIPV than in those without CIPV (3 of 3 [100%] versus 1 in 134 [0.7%];
P
<0.0001). All ACPs with CIPV were located in the left side. The other supraventricular tachycardias were not associated with any PV anomalies.

Conclusions—
There is a possible association between CIPV and left-sided ACP in AF patients. This suggests that there is a likelihood of developmental association between them.
Patterns of Care and Outcomes Differ for Urban Versus Rural Patients With Newly Diagnosed Heart Failure, Even in a Universal Healthcare System
Authors: Gamble John-Michael , Eurich Dean T. , Ezekowitz Justin A. , Kaul Padma , Quan Hude , McAlister Finlay A. 
Published: March 2011

Background—
Access to medical care differs between urban and rural residents, but the magnitude of these differences and whether they affect outcomes are unknown. We aimed to determine whether outcomes differ for patients with incident heart failure (HF) by urban-rural status.

Methods and Results—

This cohort study used administrative data from Alberta, Canada. Patients with incident HF were identified from April 1, 1999, to December 31, 2005, and followed for 1-year. Multivariable logistic regression was used to assess differences in 1-year outcomes after initial HF diagnosis in patients living in rural versus urban settings. We identified 72 043 patients with incident HF (mean age, 72±14; male sex, 50%) of whom 12 173 (17%) died and 29 074 (39%) were hospitalized within 1 year. Although crude all-cause 1-year mortality rates were higher in urban than in rural residents (17.3% versus 15.6%,
P
<0.001), after adjustment for comorbidities, no significant differences were observed (adjusted odds ratio [aOR], 0.95; 95% CI, 0.90 to 1.00). However, sex-specific analyses indicated that urban men had a significantly lower risk of mortality than rural men (aOR, 0.89; 95% CI, 0.83 to 0.96). In contrast, no difference was observed between urban and rural women (aOR, 1.02; 95% CI, 0.94 to 1.10). Urban patients were more likely to have office-based physician visits in the first year after HF diagnosis (aOR, 1.09; 95% CI, 1.02 to 1.17) and exhibited lower rates of hospitalization (aOR, 0.71; 95% CI, 0.68 to 0.74) and emergency department visits (aOR, 0.62; 95% CI, 0.60 to 0.65) than rural patients.

Conclusions—
Even within a universal healthcare system, there are differences in outcomes after HF diagnosis based on location of residence. Urban patients with HF are more likely to receive outpatient care and less likely to be hospitalized or present to the emergency department in the first year after diagnosis than rural patients with HF.
How to Tame the Elusive: Lessons from the Revision of the EU Flexibility Clause
Authors: Engström Viljam 
Published: March 2011

AbstractThe mechanism established in what has now become Article 352 of the Treaty on the Functioning of the European Union (formerly known as Article 235 and 308) has many names. One of the more common is to refer to the mechanism as the 'flexibility clause'. As the notion indicates, the basic purpose of the mechanism is to provide the European Union with a possibility of (flexibly) adjusting legislative powers to arising needs. Since the very purpose of the flexibility clause is to provide for the exercise of legal powers where none is to be found in the EU Treaties, the clause hereby defines the ultimate reach of EU competence. Remarkably, although use of the clause has often been contentious, the wording of the clause has remained unchanged ever since the Treaty of Rome. The aim of the article is to outline the function and development of the flexibility clause especially in light of the Treaty of Lisbon, which for the first time in the history of the EC/EU rewrites the flexibility clause.
Rethinking deliberative democracy: From deliberative discourse to transformative dialogue
Authors: Healy Paul 
Published: March 2011

Given its contribution to enhancing the inclusiveness, responsiveness, transparency and accountability of socio-political decision-making, the deliberative model has achieved considerable prominence in recent times as a basis for revitalizing democracy. But notwithstanding its strengths, it has also become clear that the deliberative proposal exhibits certain weaknesses that stand in need of correction if it is to realize its potential for revitalizing democracy in our contemporary pluralistic and multicultural world. Not surprisingly, then, there have been calls for significant modifications to the core proposal. Of particular interest for present purposes is Iris Marion Young’s call for a ‘communicative’ reappropriation of the standard model with a view to rendering it more inclusive of and responsive to difference. While Young’s call for reconfiguring the deliberative template in a manner conducive to treating difference as a resource rather than as a barrier to unity is judicious and timely, the present article contends that her communicative proposal does not go far enough to achieve the envisaged outcomes. Instead, to enhance inclusiveness and responsiveness to difference in a manner conducive to promoting mutual understanding and potentially transformative learning, a thoroughgoing dialogical reappropriation is called for, along the lines defended here. Only in this way can the deliberative proposal live up to its pluralistic as well as inclusive intent. Moreover, far from being an external imposition, a dialogical reconfiguration of the requisite sort is rather a means of liberating potentials inherent in the deliberative proposal from the outset but typically suppressed by an undue emphasis on homogeneity, uniformity and consensus.
Guidelines for the Design and Conduct of Clinical Studies in Knee Articular Cartilage Repair
Authors: Mithoefer Kai , Saris Daniel B.F. , Farr Jack , Kon Elizaveta , Zaslav Kenneth , Cole Brian J. , Ranstam Jonas , Yao Jian , Shive Matthew , Levine David , Dalemans Wilfried , Brittberg Mats 
Published: March 2011

Objective: To summarize current clinical research practice and develop methodological standards for objective scientific evaluation of knee cartilage repair procedures and products. Design: A comprehensive literature review was performed of high-level original studies providing information relevant for the design of clinical studies on articular cartilage repair in the knee. Analysis of cartilage repair publications and synopses of ongoing trials were used to identify important criteria for the design, reporting, and interpretation of studies in this field. Results: Current literature reflects the methodological limitations of the scientific evidence available for articular cartilage repair. However, clinical trial databases of ongoing trials document a trend suggesting improved study designs and clinical evaluation methodology. Based on the current scientific information and standards of clinical care, detailed methodological recommendations were developed for the statistical study design, patient recruitment, control group considerations, study endpoint definition, documentation of results, use of validated patient-reported outcome instruments, and inclusion and exclusion criteria for the design and conduct of scientifically sound cartilage repair study protocols. A consensus statement among the International Cartilage Repair Society (ICRS) and contributing authors experienced in clinical trial design and implementation was achieved. Conclusions: High-quality clinical research methodology is critical for the optimal evaluation of current and new cartilage repair technologies. In addition to generally applicable principles for orthopedic study design, specific criteria and considerations apply to cartilage repair studies. Systematic application of these criteria and considerations can facilitate study designs that are scientifically rigorous, ethical, practical, and appropriate for the question(s) being addressed in any given cartilage repair research project.
Correction of murine β-thalassemia after minimal lentiviral gene transfer and homeostatic in vivo erythroid expansion
Authors: Negre Olivier , Fusil Floriane , Colomb Charlotte , Roth Shoshannah , Gillet-Legrand Beatrix , Henri Annie , Beuzard Yves , Bushman Frederic , Leboulch Philippe , Payen Emmanuel 
Published: March 2011

Abstract
A challenge for gene therapy of genetic diseases is to maintain corrected cell populations in subjects undergoing transplantation in cases in which the corrected cells do not have intrinsic selective advantage over nontransduced cells. For inherited hematopoietic disorders, limitations include inefficient transduction of stem cell pools, the requirement for toxic myelosuppression, and a lack of optimal methods for cell selection after transduction. Here, we have designed a lentiviral vector that encodes human β-globin and a truncated erythropoietin receptor, both under erythroid-specific transcriptional control. This truncated receptor confers enhanced sensitivity to erythropoietin and a benign course in human carriers. Transplantation of marrow transduced with the vector into syngenic thalassemic mice, which have elevated plasma erythropoietin levels, resulted in long-term correction of the disease even at low ratios of transduced/untransduced cells. Amplification of the red over the white blood cell lineages was self-controlled and averaged ∼ 100-fold instead of ∼ 5-fold for β-globin expression alone. There was no detectable amplification of white blood cells or alteration of hematopoietic homeostasis. Notwithstanding legitimate safety concerns in the context of randomly integrating vectors, this approach may prove especially valuable in combination with targeted integration or in situ homologous recombination/repair and may lower the required level of pretransplantation myelosuppression.
The development of inflammatory joint disease is attenuated in mice expressing the anticoagulant prothrombin mutant W215A/E217A
Authors: Flick Matthew J. , Chauhan Anil K. , Frederick Malinda , Talmage Kathryn E. , Kombrinck Keith W. , Miller Whitney , Mullins Eric S. , Palumbo Joseph S. , Zheng Xunzhen , Esmon Naomi L. , Esmon Charles T. , Thornton Sherry , Becker Ann , Pelc Leslie A. , Di Cera Enrico , Wagner Denisa D. , Degen Jay L. 
Published: March 2011

Abstract
Thrombin is a positive mediator of thrombus formation through the proteolytic activation of protease-activated receptors (PARs), fibrinogen, factor XI (fXI), and other substrates, and a negative regulator through activation of protein C, a natural anticoagulant with anti-inflammatory/cytoprotective properties. Protease-engineering studies have established that 2 active-site substitutions, W215A and E217A (fIIWE), result in dramatically reduced catalytic efficiency with procoagulant substrates while largely preserving thrombomodulin (TM)–dependent protein C activation. To explore the hypothesis that a prothrombin variant favoring antithrombotic pathways would be compatible with development but limit inflammatory processes in vivo, we generated mice carrying the fIIWE mutations within the endogenous prothrombin gene. Unlike fII-null embryos, fIIWE/WE mice uniformly developed to term. Nevertheless, these mice ultimately succumbed to spontaneous bleeding events shortly after birth. Heterozygous fIIWT/WE mice were viable and fertile despite a shift toward an antithrombotic phenotype exemplified by prolonged tail-bleeding times and times-to-occlusion after FeCl3 vessel injury. More interestingly, prothrombinWE expression significantly ameliorated the development of inflammatory joint disease in mice challenged with collagen-induced arthritis (CIA). The administration of active recombinant thrombinWE also suppressed the development of CIA in wild-type mice. These studies provide a proof-of-principle that pro/thrombin variants engineered with altered substrate specificity may offer therapeutic opportunities for limiting inflammatory disease processes.
Limited stage I disease is not necessarily indicative of an excellent prognosis in childhood anaplastic large cell lymphoma
Authors: Attarbaschi Andishe , Mann Georg , Rosolen Angelo , Williams Denise , Uyttebroeck Anne , Marky Ildiko , Lamant Laurence , Horibe Keizo , Wrobel Grazyna , Beishuizen Auke , Wössmann Wilhelm , Reiter Alfred , Mauguen Audrey , Le Deley Marie-Cecile , Brugières Laurence ,   for the European Intergroup for Childhood Non-Hodgkin Lymphoma (EICNHL) ALCL99 Trial
Published: March 2011

Abstract
Data on incidence, characteristics, and prognosis in stage I childhood anaplastic large cell lymphoma are scarce. Of 463 patients enrolled in the international ALCL99 trial, 36 (8%) had stage I disease and were treated with a prephase chemotherapy, followed by either 3 chemotherapy courses in case of initial complete resection (6 patients) or otherwise by 6 courses of chemotherapy (30 patients). Disease localization was to the peripheral lymph nodes in 26, soft tissue mass in 8, and solitary bone and bronchial disease in 1 patient each. Of the 6 patients with complete resection, none experienced relapse, whereas of the 30 remaining stage I patients, 9 (30%) relapsed, including in all cases a new site of disease involvement and including 3 of 5 anaplastic lymphoma kinase–negative patients. In summary, the failure rate for incompletely resected stage I disease was similar to that for patients with stage II and stage III/IV disease. Whether anaplastic lymphoma kinase negativity contributed to this moderate outcome has to be proven prospectively. This study was registered at www.clinicaltrials.gov as NCT00006455.
Overexpression of the UGT73C6 alters brassinosteroid glucoside formation in Arabidopsis thaliana
Authors: Husar Sigrid , Berthiller Franz , Fujioka Shozo , Rozhon Wilfried , Khan Mamoona , Kalaivanan Florian , Elias Luisa , Higgins Gillian S , Li Yi , Schuhmacher Rainer , Krska Rudolf , Seto Hideharu , Vaistij Fabian E , Bowles Dianna , Poppenberger Brigitte 
Published: March 2011

Abstract

Background
Brassinosteroids (BRs) are signaling molecules that play essential roles in the spatial regulation of plant growth and development. In contrast to other plant hormones BRs act locally, close to the sites of their synthesis, and thus homeostatic mechanisms must operate at the cellular level to equilibrate BR concentrations. Whilst it is recognized that levels of bioactive BRs are likely adjusted by controlling the relative rates of biosynthesis and by catabolism, few factors, which participate in these regulatory events, have as yet been identified. Previously we have shown that the UDP-glycosyltransferase UGT73C5 of Arabidopsis thaliana catalyzes 23-O-glucosylation of BRs and that glucosylation renders BRs inactive. This study identifies the closest homologue of UGT73C5, UGT73C6, as an enzyme that is also able to glucosylate BRs in planta.

Results
In a candidate gene approach, in which homologues of UGT73C5 were screened for their potential to induce BR deficiency when over-expressed in plants, UGT73C6 was identified as an enzyme that can glucosylate the BRs CS and BL at their 23-O-positions in planta. GUS reporter analysis indicates that UGT73C6 shows over-lapping, but also distinct expression patterns with UGT73C5 and YFP reporter data suggests that at the cellular level, both UGTs localize to the cytoplasm and to the nucleus. A liquid chromatography high-resolution mass spectrometry method for BR metabolite analysis was developed and applied to determine the kinetics of formation and the catabolic fate of BR-23-O-glucosides in wild type and UGT73C5 and UGT73C6 over-expression lines. This approach identified novel BR catabolites, which are considered to be BR-malonylglucosides, and provided first evidence indicating that glucosylation protects BRs from cellular removal. The physiological significance of BR glucosylation, and the possible role of UGT73C6 as a regulatory factor in this process are discussed in light of the results presented.

Conclusion
The present study generates essential knowledge and molecular and biochemical tools, that will allow for the verification of a potential physiological role of UGT73C6 in BR glucosylation and will facilitate the investigation of the functional significance of BR glucoside formation in plants.
Enhancement of heat transfer and entropy generation analysis of nanofluids turbulent convection flow in square section tubes
Authors: Bianco Vincenzo , Nardini Sergio , Manca Oronzio 
Published: March 2011

AbstractIn this article, developing turbulent forced convection flow of a water-Al2O3 nanofluid in a square tube, subjected to constant and uniform wall heat flux, is numerically investigated. The mixture model is employed to simulate the nanofluid flow and the investigation is accomplished for particles size equal to 38 nm.An entropy generation analysis is also proposed in order to find the optimal working condition for the given geometry under given boundary conditions. A simple analytical procedure is proposed to evaluate the entropy generation and its results are compared with the numerical calculations, showing a very good agreement.A comparison of the resulting Nusselt numbers with experimental correlations available in literature is accomplished. To minimize entropy generation, the optimal Reynolds number is determined.
Aberrant Expression of Thyroid Hormone Receptor β Isoform May Cause Inappropriate Secretion of TSH in a TSH-Secreting Pituitary Adenoma
Authors: Tagami Tetsuya , Usui Takeshi , Shimatsu Akira , Beniko Mutsuo , Yamamoto Hiroyuki , Moriyama Kenji , Naruse Mitsuhide 
Published: March 2011

Context:Patients with TSH-secreting pituitary adenomas (TSHoma) show inappropriate secretion of TSH; serum TSH levels are not suppressed despite high serum free thyroid hormone levels. The mechanism of a defect in negative regulation of TSH in a TSHoma is still unclear.Objective:Recently, we cloned a novel thyroid hormone receptor β isoform (TRβ4) from a human pituitary library. To elucidate the clinical significance of TRβ4, we investigated the expression of this isoform in TSHoma.Methods:RT-PCR was performed to detect TRβ isoforms such as TRβ1, TRβ2, and TRβ4 using RNA obtained from surgically resected TSHoma. The effects of TRβ4 on the TSH gene expression were examined in the transient gene expression experiments.Results:Quantitative analysis using a real-time PCR revealed that relative expression of TRβ4 to TRβ1+2 was higher in three TSHoma than in a prolactinoma or a nonfunctioning pituitary adenoma. TRβ4 construct did not mediate T3-dependent gene regulation but inhibited the negative regulation of TSHα mediated by TRβ1 or TRβ2.Conclusions:Aberrant expression of TRβ4 may partly contribute to the inappropriate secretion of TSH in a TSHoma.