bluuebunny/crossref_metadata_2025_split huggingface dataset:
Endovascular treatment in patients with acute ischemic stroke and apparent occlusion of the extracranial internal carotid artery on CTA
Authors: Duijsens Hanneke M , Spaander Fianne , van Dijk Lukas C , Treurniet Frank E , Keunen Rudolf W , Mosch Arne , Majoie Charles B , van Overhagen Hans 
Published: August 2014

BackgroundIntra-arterial treatment is gaining importance in acute ischemic stroke, but its role in patients with apparent occlusion of the extracranial internal carotid artery (ICA) on computed tomographic angiography (CTA) is inconclusive.ObjectiveTo review retrospectively the results of intra-arterial treatment in patients with stroke and apparent extracranial ICA occlusion.MethodsIn more than 3000 patients with stroke admitted to our institution during 2008–2013, and the subgroup with suboptimal results after intravenous thrombolysis (IVT), CTA showed the absence of contrast in the extracranial ICA in 16 patients. Angiography showed true occlusion of the extracranial ICA in 10 and pseudo-occlusion in 6 patients. Treatment was considered technically successful when Thrombolysis in Cerebral Infarction scale (TICI) scores improved to 2 or 3 and clinically successful when the National Institutes of Health Stroke Scale (NIHSS) improved by at least 10 points or a NIHSS score of 0 or 1 was found at discharge.ResultsRecanalization was achieved in 5 of 6 patients with pseudo-occlusions and in 6 of 10 patients with true occlusion of the extracranial ICA. Favorable clinical outcomes were seen in 3 of 6 patients with pseudo-occlusions and in 4 of 10 patients with true occlusions. Four patients died, and in these patients infarction of >15% of the affected hemisphere had been seen on admission CT.ConclusionsIn cases of acute stroke and apparent occlusion of the extracranial ICA, intra-arterial treatment should be considered, especially when IVT fails and <15% of the hemisphere is infarcted on CT. Endovascular treatment may be beneficial especially in pseudo-occlusions but also in true occlusions of the extracranial ICA.
Transfer of residents to hospital prior to cardiac death: the influence of nursing home quality and ownership type
Authors: Anic Gabriella M , Pathak Elizabeth Barnett , Tanner Jean Paul , Casper Michele L , Branch Laurence G 
Published: August 2014

ObjectivesWe hypothesised that among nursing home decedents, nursing home for-profit status and poor quality-of-care ratings, as well as patient characteristics, would lower the likelihood of transfer to hospital prior to heart disease death.MethodsUsing death certificates from a large metropolitan area (Tampa Florida Metropolitan Statistical Area) for 1998–2002, we geocoded residential street addresses of heart disease decedents to identify 2172 persons who resided in nursing homes (n=131) at the time of death. We analysed decedent place of death as an indicator of transfer prior to death. Multilevel logistic regression modelling was used for analysis. Cause of death and decedent characteristics were obtained from death certificates. Nursing home characteristics, including state inspector ratings for multiple time points, were obtained from Florida's Agency for Healthcare Administration.ResultsNursing home for-profit status, level of nursing care and quality-of-care ratings were not associated with the likelihood of transfer to hospital prior to heart disease death. Nursing homes >5 miles from a hospital were more likely to transfer decedents, compared with facilities located close to a hospital. Significant predictors of no transfer for nursing home residents were being white, female, older, less educated and widowed/unmarried.ConclusionsIn this study population, contrary to our hypotheses, sociodemographic characteristics of nursing home decedents were more important predictors of no transfer prior to cardiac death than quality rankings or for-profit status of nursing homes.
Novel cardiac pacemaker-based human model of periodic breathing to develop real-time, pre-emptive technology for carbon dioxide stabilisation
Authors: Baruah Resham , Giannoni Alberto , Willson Keith , Manisty Charlotte H , Mebrate Yoseph , Kyriacou Andreas , Yadav Hemang , Unsworth Beth , Sutton Richard , Mayet Jamil , Hughes Alun D , Francis Darrel P 
Published: August 2014

BackgroundConstant flow and concentration CO2has previously been efficacious in attenuating ventilatory oscillations in periodic breathing (PB) where oscillations in CO2drive ventilatory oscillations. However, it has the undesirable effect of increasing end-tidal CO2, and ventilation. We tested, in a model of PB, a dynamic CO2therapy that aims to attenuate pacemaker-induced ventilatory oscillations while minimising CO2dose.MethodsFirst, pacemakers were manipulated in 12 pacemaker recipients, 6 with heart failure (ejection fraction (EF)=23.7±7.3%) and 6 without heart failure, to experimentally induce PB. Second, we applied a real-time algorithm of pre-emptive dynamic exogenous CO2administration, and tested different timings.ResultsWe found that cardiac output alternation using pacemakers successfully induced PB. Dynamic CO2therapy, when delivered coincident with hyperventilation, attenuated 57% of the experimentally induced oscillations in end-tidal CO2: SD/mean 0.06±0.01 untreated versus 0.04±0.01 with treatment (p<0.0001) and 0.02±0.01 in baseline non-modified breathing. This translated to a 56% reduction in induced ventilatory oscillations: SD/mean 0.19±0.09 untreated versus 0.14±0.06 with treatment (p=0.001) and 0.10±0.03 at baseline. Of note, end-tidal CO2did not significantly rise when dynamic CO2was applied to the model (4.84±0.47 vs 4.91± 0.45 kPa, p=0.08). Furthermore, mean ventilation was also not significantly increased by dynamic CO2compared with untreated (7.8±1.2 vs 8.4±1.2 L/min, p=0.17).ConclusionsCardiac pacemaker manipulation can be used to induce PB experimentally. In this induced PB, delivering CO2coincident with hyperventilation, ventilatory oscillations can be substantially attenuated without a significant increase in end-tidal CO2or ventilation. Dynamic CO2administration might be developed into a clinical treatment for PB.Trial Registration numberISRCTN29344450.
Reducing patient delay with symptoms of acute coronary syndrome: a research protocol for a systematic review of previous interventions to investigate which behaviour change techniques are associated with effective interventions
Authors: Farquharson Barbara , Dombrowski Stephan , Pollock Alex , Johnston Marie , Treweek Shaun , Williams Brian , Smith Karen , Dougall Nadine , Jones Claire , Pringle Stuart 
Published: August 2014

IntroductionDelay to presentation with symptoms of acute coronary syndrome (ACS) is common meaning many fail to achieve optimal benefit from treatments. Interventions have had variable success in reducing delay. Evidence suggests inclusion of behaviour change techniques (BCTs) may improve effectiveness of interventions but this has not yet been systematically evaluated. Data from other time-critical conditions may be relevant.Methods and analysisA systematic review will be undertaken to identify which BCTs are associated with effective interventions to reduce patient delay (or prompt rapid help-seeking) among people with time-critical conditions (eg, chest pain, ACS, lumps, stroke, cancer and meningitis). A systematic search of a wide range of databases (including Cochrane Library, MEDLINE, EMBASE, CINAHL, PsycInfo) and grey literature will be undertaken to identify all relevant intervention studies (randomised controlled trials, controlled clinical trials and cohort studies). Two independent reviewers will screen abstracts to identify relevant studies, apply inclusion criteria to full papers, assess methodological quality and extract data.Primary outcome measureChange in patient decision time BCTs reported in each of the included studies will be categorised and presented according to the latest reliable taxonomy. Results of included studies will be synthesised, exploring relationships between inclusion of each BCT and effectiveness of the overall intervention. Where possible, means and SDs for differences in delay time will be calculated and combined within meta-analyses to derive a standardised mean difference and 95% CI. Analysis of (1) all time-critical and (2) ACS-only interventions will be undertaken.Ethics and disseminationNo ethical issues are anticipated. Results will be submitted for publication in a relevant peer-reviewed journal.
The effect of bivalirudin and closure device on bleeding outcomes after percutaneous coronary interventions
Authors: Dobies David R , Barber Kimberly R , Cohoon Amanda L 
Published: August 2014

IntroductionStudies have demonstrated bivalirudin efficacy in some patients at increased risk of bleeding. The aim of this study was to determine the extent to which bleeding reduction is achieved among all patients using bivalirudin as compared with a heparin with or without 2B3A inhibitor strategy.MethodsThis is a real-world, large-scale retrospective study utilising the American College of Cardiology (ACC) data from a 37-hospital Ascension Health System. The registry represents routine clinical practice between 1 June 2009 and 30 June 2012. End points included major bleeding, major adverse cardiac events and death. Multivariate regression analysis modelled on predictors of end points.ResultsThis study included 58 862 PCI procedures. Major bleeding rates were lowest for bivalirudin plus closure device overall (OR=0.53, CI 0.21 to 0.84, p=0.001). The use of a device for access closure contributed to the greatest declines in major bleeding. Compared with heparin with device, bivalirudin with device had a significantly lower rate of bleeding (OR=0.37, CI 0.18 to 0.74, p=0.005). The use of device had a greater effect on decreasing bleeding among patients receiving bivalirudin compared with heparin, especially among women (p=0.001). After adjustment for 2B3A use, this advantage was no longer significant in ST segment elevation myocardial infarction patients (OR=1.8, CI 0.5 to 6.0, p=0.34).ConclusionsAll risk groups in this real world database representing current clinical practice benefited from the use of bivalirudin and device closure with lower risk groups benefiting the most. This robust analysis of real-world clinical data supports a combined treatment strategy of bivalirudin and closure device.
Enhanced thermoelectric properties of n-type Bi2Te2.7Se0.3 by indium and sodium co-doping
Authors: Duan Xingkai , Hu Konggang , Ding Shifeng , Man Dahu , Zhang Wangnian , Ma Mingliang 
Published: August 2014

Bi (1.98-x) In 0.02 Na x Te 2.7 Se 0.3 (x = 0, 0.02, 0.04, 0.06) and Bi 2 Te 2.7 Se 0.3 alloys were prepared by vacuum melting and hot pressing methods. The phase structure of the bulk samples were characterized by X-ray diffraction. Effects of indium and sodium co-substitutions for bismuth on the electrical and thermal transport properties were investigated in the temperature range of 298–473 K. Indium and sodium co-doping can enhance the carrier concentration, and accordingly the electrical conductivity can be improved effectively. The Seebeck coefficients of the co-doped samples have not been derogated strongly. The power factors are enhanced for the Bi (1.98-x) In 0.02 Na x Te 2.7 Se 0.3 (x = 0.02) within the whole testing temperature range. The Bi (1.98-x) In 0.02 Na x Te 2.7 Se 0.3 (x = 0.02) samples have the lower thermal conductivity due to reduction in lattice thermal conductivity, which leads to a great improvement in the thermoelectric figure of merit ZT. The highest ZT of the sample can reach 0.87 at 398 K.
EFA6B Antagonizes Breast Cancer
Authors: Zangari Joséphine , Partisani Mariagrazia , Bertucci François , Milanini Julie , Bidaut Ghislain , Berruyer-Pouyet Carole , Finetti Pascal , Long Elodie , Brau Frédéric , Cabaud Olivier , Chetaille Bruno , Birnbaum Daniel , Lopez Marc , Hofman Paul , Franco Michel , Luton Frédéric 
Published: August 2014

Abstract
One of the earliest events in epithelial carcinogenesis is the dissolution of tight junctions and cell polarity signals that are essential for normal epithelial barrier function. Here, we report that EFA6B, a guanine nucleotide exchange factor for the Ras superfamily protein Arf6 that helps assemble and stabilize tight junction, is required to maintain apico-basal cell polarity and mesenchymal phenotypes in mammary epithelial cells. In organotypic three-dimensional cell cultures, endogenous levels of EFA6B were critical to determine epithelial–mesenchymal status. EFA6B downregulation correlated with a mesenchymal phenotype and ectopic expression of EFA6B hampered TGFβ-induced epithelial-to-mesenchymal transition (EMT). Transcriptomic and immunohistochemical analyses of human breast tumors revealed that the reduced expression of EFA6B was associated with loss of tight junction components and with increased signatures of EMT, cancer stemness, and poor prognosis. Accordingly, tumors with low levels of EFA6B were enriched in the aggressive triple-negative and claudin-low breast cancer subtypes. Our results identify EFA6B as a novel antagonist in breast cancer and they point to its regulatory and signaling pathways as rational therapeutic targets in aggressive forms of this disease. Cancer Res; 74(19); 5493–506. ©2014 AACR.
Anti-CCR4 Monoclonal Antibody Mogamulizumab for the Treatment of EBV-Associated T- and NK-Cell Lymphoproliferative Diseases
Authors: Kanazawa Tetsuhiro , Hiramatsu Yutaka , Iwata Seiko , Siddiquey Mohammed , Sato Yoshitaka , Suzuki Michio , Ito Yoshinori , Goshima Fumi , Murata Takayuki , Kimura Hiroshi 
Published: August 2014

Abstract
Purpose: Epstein–Barr virus (EBV) infects not only B cells but also T cells and natural killer (NK) cells, and T- and NK-cell lymphoproliferative diseases (T/NK-LPD) that are refractory to conventional chemotherapies may develop. To identify a molecular-targeted therapy for EBV-associated T/NK-LPDs, we investigated whether CC chemokine receptor 4 (CCR4) was expressed on EBV-infected T and/or NK cells and whether a humanized anti-CCR4 monoclonal antibody, mogamulizumab, was effective.
Experimental Design: CCR4 expression was examined in various cell lines. In vitro, the effects of mogamulizumab on cell lines were evaluated in the presence of peripheral blood mononuclear cells from volunteers. In vivo, the effects of mogamulizumab were evaluated using a murine xenograft model. CCR4 expression was examined on EBV-infected cells from patients with EBV-associated T/NK-LPDs. Ex vivo, the effects of mogamulizumab were evaluated using patient lymphocytes.
Results: CCR4 expression was confirmed in most EBV-positive T and NK cell lines. Mogamulizumab induced antibody-dependent cellular cytotoxicity (ADCC) activity against CCR4-positive cell lines, and inhibited the growth of EBV-positive NK-cell lymphomas in a murine xenograft model. Furthermore, CCR4 was expressed on EBV-infected cells in 8 of 17 patients with EBV-associated T/NK-LPDs. Interestingly, CCR4 was positive in 5 of 5 patients with hydroa vacciniforme, a photodermatosis caused by the clonal expansion of EBV-infected γδT cells. EBV-positive γδT cells were obtained from a patient with hydroa vacciniforme and subjected to an antibody-dependent cell-mediated cytotoxicity (ADCC) assay. The γδT cells that were positive for CCR4 were killed by mogamulizumab via ADCC.
Conclusions: These results indicate that mogamulizumab may be a therapeutic option against EBV-associated T/NK-LPDs. Clin Cancer Res; 20(19); 5075–84. ©2014 AACR.
Contemporary Patterns of Discharge Aspirin Dosing After Acute Myocardial Infarction in the United States
Authors: Hall Hurst M. , de Lemos James A. , Enriquez Jonathan R. , McGuire Darren K. , Peng S. Andrew , Alexander Karen P. , Roe Matthew T. , Desai Nihar , Wiviott Stephen D. , Das Sandeep R. 
Published: August 2014

Background—
Accumulated data suggest that low-dose aspirin after myocardial infarction (MI) may offer similar efficacy to higher dose aspirin with reduced risk of bleeding. Few data are available on contemporary aspirin dosing patterns after MI in the United States

Methods and Results—
Aspirin dosing from 221 199 patients with MI (40.2% ST-segment–elevation MI) from 525 US hospitals enrolled in the National Cardiovascular Data Registry’s (NCDR’s) Acute Coronary Treatment and Intervention Outcomes Network Registry-Get with the Guidelines were described, overall and in clinically relevant subgroups. High-dose aspirin was defined as 325 mg and low dose as 81 mg. Between January 2007 and March 2011, 60.9% of patients with acute MI were discharged on high-dose aspirin, 35.6% on low-dose aspirin, and 3.5% on other doses. High-dose aspirin was prescribed at discharge to 73.0% of patients treated with percutaneous coronary intervention and 44.6% of patients managed medically. Among 9075 patients discharged on aspirin, thienopyridine, and warfarin, 44.0% were prescribed high-dose aspirin. Patients with an in-hospital major bleeding event were also frequently discharged on high-dose aspirin (56.7%). A 25-fold variation in the proportion prescribed high-dose aspirin at discharge was observed across participating centers.

Conclusions—
Most US patients with MI continue to be discharged on high-dose aspirin. Although aspirin dosing after percutaneous coronary intervention largely reflected prevailing guidelines before 2012, high-dose aspirin was prescribed with similar frequency in medically managed patients and to those in categories expected to be at high risk for bleeding. Wide variability in the proportional use of high-dose aspirin across centers suggests significant influence from local practice habits and uncertainty about appropriate aspirin dosing.
Alternatively Spliced Tissue Factor Promotes Plaque Angiogenesis Through the Activation of Hypoxia-Inducible Factor-1α and Vascular Endothelial Growth Factor Signaling
Authors: Giannarelli Chiara , Alique Matilde , Rodriguez David T. , Yang Dong Kwon , Jeong Dongtak , Calcagno Claudia , Hutter Randolph , Millon Antoine , Kovacic Jason C. , Weber Thomas , Faries Peter L. , Soff Gerald A. , Fayad Zahi A. , Hajjar Roger J. , Fuster Valentin , Badimon Juan J. 
Published: August 2014

Background—
Alternatively spliced tissue factor (asTF) is a novel isoform of full-length tissue factor, which exhibits angiogenic activity. Although asTF has been detected in human plaques, it is unknown whether its expression in atherosclerosis causes increased neovascularization and an advanced plaque phenotype.

Methods and Results—

Carotid (n=10) and coronary (n=8) specimens from patients with stable or unstable angina were classified as complicated or uncomplicated on the basis of plaque morphology. Analysis of asTF expression and cell type–specific expression revealed a strong expression and colocalization of asTF with macrophages and neovessels within complicated, but not uncomplicated, human plaques. Our results showed that the angiogenic activity of asTF is mediated via hypoxia-inducible factor-1α upregulation through integrins and activation of phosphatidylinositol-3-kinase/Akt and mitogen-activated protein kinase pathways. Hypoxia-inducible factor-1α upregulation by asTF also was associated with increased vascular endothelial growth factor expression in primary human endothelial cells, and vascular endothelial growth factor–Trap significantly reduced the angiogenic effect of asTF in vivo. Furthermore, asTF gene transfer significantly increased neointima formation and neovascularization after carotid wire injury in ApoE
−/−
mice.

Conclusions—
The results of this study provide strong evidence that asTF promotes neointima formation and angiogenesis in an experimental model of accelerated atherosclerosis. Here, we demonstrate that the angiogenic effect of asTF is mediated via the activation of the hypoxia-inducible factor-1/vascular endothelial growth factor signaling. This mechanism may be relevant to neovascularization and the progression and associated complications of human atherosclerosis as suggested by the increased expression of asTF in complicated versus uncomplicated human carotid and coronary plaques.
Associations Between Estimated Glomerular Filtration Rate and Stroke Outcomes in Diabetic Versus Nondiabetic Patients
Authors: Luo Yang , Wang Xianwei , Matsushita Kunihiro , Wang Chunxue , Zhao Xingquan , Hu Bo , Liu Liping , Li Hao , Liu Gaifen , Jia Qian , Wang Yilong , Wang Yongjun 
Published: August 2014

Background and Purpose—
Low estimated glomerular filtration rate (eGFR) is known to be associated with clinical adverse outcomes. However, whether diabetes mellitus influences the association between eGFR and prognosis of stroke is still not elucidated.

Methods—
Prospective cohort of 17 280 (nondiabetic 12 498 and diabetic 4782) Chinese patients with acute stroke from the China National Stroke Registry and from abnormal glucose regulation in patients with acute stroke across China (ACROSS) between 2007 and 2009 were followed-up for 1 year for all-cause mortality, stroke recurrence, and stroke disability related to baseline eGFR in the presence and absence of diabetes mellitus.

Results—

Among nondiabetic patients, as compared with eGFR of 90 to 119 mL/min per 1.73 m
2
, the adjusted odds ratio of lower eGFR of < 45 mL/min per 1.73 m
2
was 2.79 (95% confidence interval, 2.09–3.73) for all-cause mortality, 2.28 (1.74–2.98) for stroke recurrence, and 1.53 (1.16–2.01) for stroke disability; higher eGFR of ≥120 mL/min per 1.73 m
2
was just significantly associated with higher risk of all-cause mortality (odds ratio, 1.38; 95% confidence interval, 1.02–1.86) but not with other outcomes. In diabetic patients, the adjusted odds ratios of all-cause mortality, stroke recurrence, and stroke disability in lower eGFR were 2.16 (1.51–3.08), 1.43 (1.02–2.00), and 1.38 (0.98–1.95), respectively; higher eGFR was significantly associated with higher risks of all stroke outcomes.

Conclusions—

Decreased eGFR (<45 mL/min per 1.73 m
2
) is a strong predictor of all-cause mortality, stroke recurrence, and stroke disability in diabetic and nondiabetic patients with acute stroke. Increased eGFR (≥120 mL/min per 1.73 m
2
) is associated with all of stroke outcomes in diabetic patients and linked to all-cause mortality in nondiabetic patients.