bluuebunny/crossref_metadata_2025_split huggingface dataset:
Statin Use and Prostate Cancer Aggressiveness: Results from the Population-Based North Carolina–Louisiana Prostate Cancer Project
Authors: Allott Emma H. , Farnan Laura , Steck Susan E. , Arab Lenore , Su L. Joseph , Mishel Merle , Fontham Elizabeth T.H. , Mohler James L. , Bensen Jeannette T. 
Published: January 2016

Abstract
Background: Although statin use has been associated with reduced prostate cancer aggressiveness, the impact of race and patient characteristics on this association is not well understood. We examined the association between statin use and prostate cancer aggressiveness in Caucasians (CA) and African Americans (AA) and explored effect modification by health-seeking behaviors associated with statin use.
Methods: Of 1,930 cases from The North Carolina-Louisiana Prostate Cancer Project, 344 (18%) were classified as aggressive based on clinical criteria. Utilizing nonaggressive cases as referent, logistic regression was used to examine the association between statin use and prostate cancer aggressiveness, overall and stratified by race. Smoking and prostate cancer screening were examined as effect modifiers of this association.
Results: There was an inverse association between statin use and prostate cancer aggressiveness [OR, 0.74; 95% confidence interval (CI), 0.56–0.96], with comparable effect estimates in both races. Although not statistically significant, statin use was associated with reduced ORs for aggressive prostate cancer in never-screened men (OR, 0.79; 95% CI, 0.45–1.39), men screened at low/recommended frequency (≤once/year; OR, 0.66; 95% CI, 0.41–1.06), and men screened at high frequency (&gt;once/year; OR, 0.78; 95% CI, 0.53–1.15). Inverse associations between statins and aggressive prostate cancer were strongest in never smokers (OR, 0.42; 95% CI, 0.25–0.72), attenuated in former smokers (OR, 0.84; 95% CI, 0.59–1.19), and absent in current smokers (OR, 1.36; 95% CI, 0.70–2.64).
Conclusions: Statin use was associated with reduced prostate cancer aggressiveness in CA and AAs, with strongest inverse associations in nonsmokers.
Impact: Health-seeking behaviors associated with statin use should be considered when examining the impact of statins on prostate cancer aggressiveness. Cancer Epidemiol Biomarkers Prev; 25(4); 670–7. ©2016 AACR.
7-(2-Thienyl)-7-Deazaadenosine (AB61), a New Potent Nucleoside Cytostatic with a Complex Mode of Action
Authors: Perlíková Pavla , Rylová Gabriela , Nauš Petr , Elbert Tomáš , Tloušťová Eva , Bourderioux Aurelie , Slavětínská Lenka Poštová , Motyka Kamil , Doležal Dalibor , Znojek Pawel , Nová Alice , Harvanová Monika , Džubák Petr , Šiller Michal , Hlaváč Jan , Hajdúch Marián , Hocek Michal 
Published: January 2016

Abstract7-(2-Thienyl)-7-deazaadenosine (AB61) showed nanomolar cytotoxic activities against various cancer cell lines but only mild (micromolar) activities against normal fibroblasts. The selectivity of AB61 was found to be due to inefficient phosphorylation of AB61 in normal fibroblasts. The phosphorylation of AB61 in the leukemic CCRF-CEM cell line proceeds well and it was shown that AB61 is incorporated into both DNA and RNA, preferentially as a ribonucleotide. It was further confirmed that a triphosphate of AB61 is a substrate for both RNA and DNA polymerases in enzymatic assays. Gene expression analysis suggests that AB61 affects DNA damage pathways and protein translation/folding machinery. Indeed, formation of large 53BP1 foci was observed in nuclei of AB61-treated U2OS-GFP-53BP1 cells indicating DNA damage. Random incorporation of AB61 into RNA blocked its translation in an in vitro assay and reduction of reporter protein expression was also observed in mice after 4-hour treatment with AB61. AB61 also significantly reduced tumor volume in mice bearing SK-OV-3, BT-549, and HT-29 xenografts. The results indicate that AB61 is a promising compound with unique mechanism of action and deserves further development as an anticancer agent. Mol Cancer Ther; 15(5); 922–37. ©2016 AACR.
Post-Sepsis State Induces Tumor-Associated Macrophage Accumulation through CXCR4/CXCL12 and Favors Tumor Progression in Mice
Authors: Mota José M. , Leite Caio A. , Souza Lucas E. , Melo Paulo H. , Nascimento Daniele C. , de-Deus-Wagatsuma Virginia M. , Temporal Jessica , Figueiredo Florêncio , Noushmehr Houtan , Alves-Filho José C. , Cunha Fernando Q. , Rego Eduardo M. 
Published: January 2016

Abstract
Survivors from sepsis are in an immunosuppressed state that is associated with higher long-term mortality and risk of opportunistic infections. Whether these factors contribute to neoplastic proliferation, however, remains unclear. Tumor-associated macrophages (TAM) can support malignant cell proliferation, survival, and angiogenesis. We addressed the relationship between the post-sepsis state, tumor progression and TAM accumulation, and phenotypic and genetic profile, using a mouse model of sepsis resolution and then B16 melanoma in mice. In addition, we measured the serum concentrations of TNFα, TGFβ, CCL2, and CXCL12 and determined the effect of in vivo CXCR4/CXCL12 inhibition in this context. Mice that survived sepsis showed increased tumor progression both in the short and long term, and survival times were shorter. TAM accumulation, TAM local proliferation, and serum concentrations of TGFβ, CXCL12, and TNFα were increased. Naïve mice inoculated with B16 together with macrophages from post-sepsis mice also had faster tumor progression and shorter survival. Post-sepsis TAMs had less expression of MHC-II and leukocyte activation-related genes. Inhibition of CXCR4/CXCL12 prevented the post-sepsis–induced tumor progression, TAM accumulation, and TAM in situ proliferation. Collectively, our data show that the post-sepsis state was associated with TAM accumulation through CXCR4/CXCL12, which contributed to B16 melanoma progression. Cancer Immunol Res; 4(4); 312–22. ©2016 AACR.
D-dimer and factor VIIa in atrial fibrillation – prognostic values for cardiovascular events and effects of anticoagulation therapy
Authors: Siegbahn Agneta , Oldgren Jonas , Andersson Ulrika , Ezekowitz Michael D. , Reilly Paul A. , Connolly Stuart J. , Yusuf Salim , Wallentin Lars , Eikelboom John W. 
Published: January 2016

SummaryCoagulation markers may improve monitoring the risk of stroke and bleeding in patients with atrial fibrillation (AF) during anticoagulant treatment. We examined baseline levels of D-dimer and their association with stroke, cardiovascular death and major bleeding in 6,202 AF patients randomised to dabigatran or warfarin in the RE-LY trial. The effects of treatment on serial levels of D-dimer and coagulation factor (F) VIIa in 2,567 patients were also analysed. Baseline D-dimer levels were related to the rate of stroke/systemic embolism (SEE) with 0.64 % in the lowest quartile (Q1, as reference) (D-dimer < 298 μg/l), 1.38 % Q2 (D-dimer 298–473 μg/l), 1.71 % Q3 (D-dimer 474–822 μg/l) and 2.00 % in Q4 (D-dimer > 822 μg/l) (p=0.0007). Similar associations were shown for cardiovascular death and major bleeding. Addition of baseline D-dimer to established clinical risk factors improved prediction of stroke/SEE, cardiovascular death and major bleeding (C-index increased from 0.66 to 0.68, 0.71 to 0.73 and 0.66 to 0.67, respectively). Dabigatran provided a greater reduction of D-dimer levels than warfarin regardless of baseline anticoagulant treatment. Ontreatment levels of FVIIa were markedly reduced by warfarin (median 12.1–13.8 mU/ml) but significantly higher with dabigatran (median 39.4–49.0 mU/ml) at all-time points. Dabigatran is associated with greater reduction in D-dimer without the pronounced reduction of FVIIa seen with warfarin. These different effects on the coagulation system might explain the better efficacy and less intracranial bleeding observed with dabigatran compared with warfarin.Clinical Trial Registration: NCT00262600 (www.clinicaltrials.gov).Supplementary Material to this article is available online at www.thrombosis-online.com.
The Failing Heart Relies on Ketone Bodies as a Fuel
Authors: Aubert Gregory , Martin Ola J. , Horton Julie L. , Lai Ling , Vega Rick B. , Leone Teresa C. , Koves Timothy , Gardell Stephen J. , Krüger Marcus , Hoppel Charles L. , Lewandowski E. Douglas , Crawford Peter A. , Muoio Deborah M. , Kelly Daniel P. 
Published: January 2016

Background—
Significant evidence indicates that the failing heart is energy starved. During the development of heart failure, the capacity of the heart to utilize fatty acids, the chief fuel, is diminished. Identification of alternate pathways for myocardial fuel oxidation could unveil novel strategies to treat heart failure.

Methods and Results—
Quantitative mitochondrial proteomics was used to identify energy metabolic derangements that occur during the development of cardiac hypertrophy and heart failure in well-defined mouse models. As expected, the amounts of proteins involved in fatty acid utilization were downregulated in myocardial samples from the failing heart. Conversely, expression of β-hydroxybutyrate dehydrogenase 1, a key enzyme in the ketone oxidation pathway, was increased in the heart failure samples. Studies of relative oxidation in an isolated heart preparation using ex vivo nuclear magnetic resonance combined with targeted quantitative myocardial metabolomic profiling using mass spectrometry revealed that the hypertrophied and failing heart shifts to oxidizing ketone bodies as a fuel source in the context of reduced capacity to oxidize fatty acids. Distinct myocardial metabolomic signatures of ketone oxidation were identified.

Conclusions—
These results indicate that the hypertrophied and failing heart shifts to ketone bodies as a significant fuel source for oxidative ATP production. Specific metabolite biosignatures of in vivo cardiac ketone utilization were identified. Future studies aimed at determining whether this fuel shift is adaptive or maladaptive could unveil new therapeutic strategies for heart failure.
Reanalyses and Observations: What’s the Difference?
Authors: Parker Wendy S. 
Published: January 2016

Abstract
Are there important differences between reanalysis data and familiar observations and measurements? If so, what are they? This essay evaluates four possible answers that relate to: the role of inference, reliance on forecasts, the need to solve an ill-posed inverse problem, and understanding of errors and uncertainties. The last of these is argued to be most significant. The importance of characterizing uncertainties associated with results—whether those results are observations or measurements, analyses or reanalyses, or forecasts—is emphasized.
Sea Surface Temperature Climate Data Record for the North Sea and Baltic Sea
Authors: Høyer Jacob L. , Karagali Ioanna 
Published: January 2016

Abstract
A 30-yr climate data record (CDR) of sea surface temperature (SST) has been produced with daily gap-free analysis fields for the North Sea and the Baltic Sea region from 1982 to 2012 by combining the Pathfinder AVHRR satellite data record with the Along-Track Scanning Radiometer (ATSR) Reprocessing for Climate (ARC) dataset and with in situ observations. A dynamical bias correction scheme adjusts the Pathfinder observations toward the ARC and in situ observations. Largest Pathfinder–ARC differences are found in the summer months, when the Pathfinder observations are up to 0.4°C colder than the ARC observations on average. Validation against independent in situ observations shows a very stable performance of the data record, with a mean difference of −0.06°C compared to moored buoys and a 0.46°C standard deviation of the differences. The mean annual biases of the SST CDR are small for all years, with a negligible temporal trend when compared against drifting and moored buoys. Analysis of the SST CDR reveals that the monthly anomalies for the North Sea, the Danish straits, and the central Baltic Sea regions show a high degree of correlation for interannual and decadal time scales, whereas the monthly variability differs from one region to another. The linear trends of the 1982–2012 SST anomaly time series range from 0.037°C yr−1 for the North Sea to 0.041°C yr−1 for the Baltic Sea.
Reducing inequalities in care for patients with non-malignant diseases: Insights from a realist evaluation of an integrated palliative care pathway
Authors: Dalkin Sonia Michelle , Lhussier Monique , Philipson Pete , Jones Diana , Cunningham William 
Published: January 2016

Background: The need for palliative care is growing internationally with an increasing prevalence of non-malignant diseases. The integrated care pathway was implemented in primary care by multidisciplinary teams from 2009 in a locality in the North East of England. Fourteen general practitioner practices provided data for the study. Aim: To find whether, how, and under what circumstances palliative care registrations are made for patients with non-malignant diseases in primary care. Design: General practitioner practice data were analysed statistically and qualitative data were collected from health care professionals and members of relevant organisations. Findings: A mixed-effects logistic model indicated a significant difference beyond the 0.1% level ( p < 0.001) in registrations between the malignant and non-malignant groups in 2011, with an odds ratio of 0.09 (=exp(−2.4266)), indicating that patients in the non-malignant group are around 11 times (1/0.09) less likely to be registered than patients in the malignant group. However, patients with non-malignant diseases were significantly more likely to be registered in 2012 than in 2011 with an odds ratio of 1.46, significant beyond the 1% level. Qualitative analyses indicate that health care professionals find registering patients with non-malignant diseases stressful, yet feel that their confidence in treating this population is increasing. Conclusion: The integrated care pathway began to enable the reduction in inequalities in care by identifying, registering and managing an increasing number of palliative patients with non-malignant diseases. Consensual and inclusive definitions of palliative care were developed in order to legitimise the registration of such patients.
Latarjet Procedure for Anterior Shoulder Instability Due to Tramadol-Induced Seizures
Authors: Khater Ahmad Hany , Sobhy Mohamed H. , Said Hatem G. , Kandil Ahmed , Reda Walid , Seifeldin Ahmed Fouad , Moustafa Ramez , Elassal Maher A. , Kamel Ezzat M. 
Published: January 2016

Background: Seizures, commonly due to epilepsy, are known to cause shoulder instability. Tramadol addiction has recently been found to induce seizures in patients who exceed the recommended dose. Because of the easy accessibility and low cost of tramadol, an increasingly alarming phenomenon of tramadol abuse has been demonstrated in recent years. Purpose/Hypothesis: The purpose of this multicenter study was to investigate shoulder instability resulting from tramadol-induced seizure (TIS) as well as to recommended management for such shoulder instability. The hypothesis was that TIS leads to anterior shoulder dislocations with major bony defects, which favors bony reconstructive procedures as a suitable method of treatment. Study Design: Case series; Level of evidence, 4. Methods: This prospective case series study was conducted on 73 patients (78 shoulders) who presented with anterior shoulder dislocations and a clear history of tramadol abuse. The mean age of the patients was 26.8 years, and the mean number of dislocations was 14. The mean duration of addiction was 17 months, with a mean dose of 752 mg of tramadol hydrochloride per day. Glenoid and humeral bone loss ranged from 15% to 35% and from 15% to 40%, respectively. The mean follow-up period was 28 months. All patients underwent an open Latarjet procedure. Results: Postoperative mean Rowe score and American Shoulder and Elbow Surgeons score at final follow-up (24 months) improved significantly from 20 to 84 and from 44 to 91, respectively ( P < .05). The patient satisfaction rate reached 95%, and the mean period of return to work was 12.8 weeks. Five patients (9%) had postoperative seizures due to relapse of the tramadol abuse, but only 3 patients (5%) had redislocations with nonunion or breakage of the graft or hardware. Conclusion: Tramadol addiction has evolved as an important cause of seizures that can result in shoulder dislocation. Anterior shoulder instability with TIS occurs mainly with higher levels of addiction and results in significant humeral and/or glenoid bone defects. The Latarjet procedure is recommended for these patients, after control of addiction, and provides 95% satisfaction at midterm follow-up.
Helping professionals and Border Force secrecy: effective asylum-seeker healthcare requires independence from callous policies
Authors: Dudley Michael 
Published: January 2016

Objective: To examine the Australian Border Force Act (BFA) and its context, its implications for asylum-seeker healthcare and professionals, and contemporary and historical parallels. Conclusions: Prolonged immigration detention and policies aiming to deter irregular migration cause maritime asylum-seekers undeniable, well-publicised harms and (notwithstanding claims about preventing drownings) show reckless indifference and calculated cruelty. Service personnel may be harmed. Such policies misuse helping professionals to underwrite state abuses and promote public numbing and indifference, resembling other state abuses in the ‘war on terror’ and (with qualification) historical counterparts, e.g. Nazi Germany. Human service practitioners and organisations recently denounced the BFA that forbids disclosure about these matters. Continuing asylum-seeker healthcare balances the likelihood of effective care and monitoring with lending credibility to abuses. Boycotting it might sacrifice scrutiny and care, fail to compel professionals and affect temporary overseas workers. Entirely transferring healthcare from immigration to Federal and/or State health departments, with resources augmented to adequate standard, would strengthen clinical independence and quality, minimise healthcare’s being securitised and politicised, and uphold ethical codes. Such measures will not resolve detention’s problems, but coupled with independent auditing, would expose and moderate detention’s worst effects, promoting changes in national conversation and policy-making.
First episode mania following cessation of varenicline (Champix)
Authors: Baker Richard , Gill Nav , Parker Gordon 
Published: January 2016

Objectives: To describe a case of first episode mania and in which varenicline (Champix) or its withdrawal appears to have been the precipitating factor. Methods: The clinical presentation and progress are detailed and the relevant literature in relation to varenicline is provided. Results: The case report adds to the literature indicating that varenicline may induce a range of mood states, albeit with reported incidents of mania being rare. Conclusions: In reviewing causes of mood states, including mania, seeking information on any exposure to varenicline would appear to be relevant.
Objects, images and texts: Archaeology and violence
Authors: Hall Martin 
Published: January 2016

Today, monuments and archaeological sites are often specific targets for violence. But rather than casting this as either collateral damage or the result of ignorance and incivility, it can be argued that the material world, in all its widely varied forms, is enmeshed in conflict and violence. This can be better understood in terms of the haptic significance of objects caught up in extreme and traumatic circumstances. The point of departure for this paper is W.J.T. Mitchell’s concept of the “traumatic gap” that emerges as “the unrepresentable space between words and images”. I show that where the normative breaks down, the haptic qualities of media can assume far greater significance. Books and pictures become objects as well as semiotic registers and graphic representations. Understanding this – the “X” that Mitchell uses to designate the emptiness between the normal meanings of words and images – requires and enables an archaeology of violence. Taking a cue from Mitchell’s formulation, I show how the particular qualities of this space can be expressed in a new algorithm, “image ←→ object ←→ text”. This space – Mitchell’s “presence of an absence” – can only be filled by things that are neither images nor texts in their conventional sense. This is demonstrated by the extreme of the torture cell, where the most mundane of everyday objects become both normalized in the careful, systematic records of the military operative, and terrifying in the experience of the prisoner. Here, the figure of the Hooded Man, leaked from the clandestine archive of Abu Ghraib, serves as an emblem for the horror of contemporary violence; both executioner and victim, torturer and prisoner, both the Christ-like posture of the saviour and the horror of beheading.
Markers of fibrinolysis may predict development of lower extremity arterial disease in patients with diabetes: A longitudinal prospective cohort study with 10 years of follow-up
Authors: Rautio Aslak , Boman Kurt , Eriksson Jan W , Svensson Maria K 
Published: January 2016

Background: A previous cross-sectional study suggested that tissue plasminogen activator–activity might be an early marker of asymptomatic lower extremity arterial disease, but the long-term relationship is unknown. Subjects and methods: This study included 96 diabetic (48 type 1/48 type 2) and 62 non-diabetic subjects aged 30–70 years without previously known lower extremity arterial disease (age: 50.3 ± 9.3 years, gender: M/W 47.5/52.5% and body mass index: 26.6 ± 4.5 kg/m2). The relationships between asymptomatic lower extremity arterial disease and fibrinolytic markers (tissue plasminogen activator–activity, tissue plasminogen activator–mass, plasminogen activator inhibitor-1 activity) at baseline and after 10 years were assessed by logistic regression analysis adjusting for age, hypertension, statin treatment, HbA1c, triglycerides and low-density lipoprotein cholesterol as fixed covariates. Results: The tissue plasminogen activator–activity at baseline and at the 10-year follow-up significantly predicted the presence of sign(s) of lower extremity arterial disease (odds ratio = 1.78, 95% confidence interval: 1.02–3.10, p = 0.043 and odds ratio = 1.78, 95% confidence interval: 1.12–2.23, p = 0.014, respectively). In addition, tissue plasminogen activator–mass at the 10-year follow-up was associated with signs of lower extremity arterial disease (odds ratio = 1.07, 95% confidence interval: 1.00–1.15, p = 0.046). Baseline age, hypertension and HbA1c were independently associated with sign(s) of lower extremity arterial disease at 10 years (odds ratio = 1.09, 95% confidence interval: 1.04–1.14, p = < 0.001; odds ratio = 3.68, 95% confidence interval: 1.67–8.12, p = 0.001 and odds ratio = 1.54, 95% confidence interval: 1.21–1.95, p = < 0.001, respectively). Conclusion: This long-term study supports previous findings of a significant association between asymptomatic lower extremity arterial disease and tissue plasminogen activator–activity. Thus, tissue plasminogen activator–activity may be an early marker of lower extremity arterial disease although the mechanism of this relationship remains unclear.
Lumbosacral agenesis in a cat
Authors: Hybki Gabrielle C , Murphy Lisa A , Marchi Joseph P , Patlogar Jeffrey E , Brisson Jennifer O , Nakamura Reid K 
Published: January 2016

Case summary Lumbosacral agenesis is a rare congenital condition reported in children. We report a 17-week-old female domestic shorthair cat with lumbosacral agenesis on whole-body radiographs. The cat was euthanized shortly thereafter presentation. A necropsy was not permitted. Relevance and novel information This is the first reported feline case of lumbosacral agenesis.