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  • 1
    Language: English
    In: American journal of health behavior, July 2016, Vol.40(4), pp.523-33
    Description: We investigated the relationship between financial literacy and patient engagement while considering the possible interaction effects due to patient financial responsibility and patient-physician shared decision making, and the impact of personal attributes. Participants consisted of an Internet-based sample of American adults (N = 160). Hierarchical multiple linear regression analysis was conducted to examine the relationship of the study variables on patient engagement. We found that patient financial responsibility (β = -.19, p 〈 .05) and patient-physician shared decision-making (β = .17, p 〈 .05) predicted patient engagement. However, there was no statistically significant relationship between patient financial literacy and patient engagement; moreover, the moderation effects of patient financial responsibility and shared decision making with financial literacy also were not statistically significant. Increasing patient financial responsibility and patient-physician shared decision making can impact patient engagement. Understanding the predictors of patient engagement and the factors that influence financial behaviors may allow for the development of interventions to enable patients to make better healthcare decisions, and ultimately, improve health outcomes.
    Keywords: Financing, Personal ; Patient Participation -- Economics
    ISSN: 10873244
    E-ISSN: 1945-7359
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  • 2
    Language: English
    In: PLoS ONE, 01 January 2016, Vol.11(2), p.e0149053
    Description: This study aimed to assess the association of clinical factors with P2Y12-dependent platelet inhibition as monitored by the ratio of ADP- to TRAP-induced platelet aggregation and conventional ADP-induced aggregation, respectively.Controversial findings to identify and overcome high platelet reactivity (HPR) after coronary stent-implantation and to improve clinical outcome by tailored anti-platelet therapy exist. Monitoring anti-platelet therapy ex vivo underlies several confounding parameters causing that ex vivo platelet aggregation might not reflect in vivo platelet inhibition.In a single centre observational study, multiple electrode aggregometry was performed in whole blood of patients after recent coronary stent-implantation. Relative ADP-induced aggregation (r-ADP-agg) was defined as the ratio of ADP- to TRAP- induced aggregation reflecting the individual degree of P2Y12-mediated platelet reactivity.Platelet aggregation was assessed in 359 patients. Means (± SD) of TRAP-, ADP-induced aggregation and r-ADP-agg were 794 ± 239 AU*min, 297 ± 153 AU*min and 37 ± 14%, respectively. While ADP- and TRAP-induced platelet aggregation correlated significantly with platelet count (ADP: r = 0.302; p〈0.001; TRAP: r = 0.509 p〈0.001), r-ADP-agg values did not (r = -0.003; p = 0.960). These findings were unaltered in multivariate analyses adjusting for a range of factors potentially influencing platelet aggregation. The presence of an acute coronary syndrome and body weight were found to correlate with both ADP-induced platelet aggregation and r-ADP-agg.The ratio of ADP- to TRAP-induced platelet aggregation quantifies P2Y12-dependent platelet inhibition independently of the platelet count in contrast to conventional ADP-induced aggregation. Furthermore, r-ADP-agg was associated with the presence of an acute coronary syndrome and body weight as well as ADP-induced aggregation. Thus, the r-ADP-agg is a more valid reflecting platelet aggregation and potentially prognosis after coronary stent-implantation in P2Y12-mediated HPR than conventional ADP-induced platelet aggregation.
    Keywords: Sciences (General)
    E-ISSN: 1932-6203
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  • 3
    Language: English
    In: Science (New York, N.Y.), 22 September 2006, Vol.313(5794), pp.1781-4
    Description: Protein aggregation is an established pathogenic mechanism in Alzheimer's disease, but little is known about the initiation of this process in vivo. Intracerebral injection of dilute, amyloid-beta (Abeta)-containing brain extracts from humans with Alzheimer's disease or beta-amyloid precursor protein (APP) transgenic mice induced cerebral beta-amyloidosis and associated pathology in APP transgenic mice in a time- and concentration-dependent manner. The seeding activity of brain extracts was reduced or abolished by Abeta immunodepletion, protein denaturation, or by Abeta immunization of the host. The phenotype of the exogenously induced amyloidosis depended on both the host and the source of the agent, suggesting the existence of polymorphic Abeta strains with varying biological activities reminiscent of prion strains.
    Keywords: Amyloid Beta-Peptides -- Administration & Dosage ; Amyloid Beta-Protein Precursor -- Administration & Dosage ; Amyloidosis -- Metabolism ; Brain Diseases -- Metabolism ; Hippocampus -- Chemistry
    ISSN: 00368075
    E-ISSN: 1095-9203
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  • 4
    Language: English
    In: Thrombosis Research, February 2016, Vol.138, pp.63-68
    Description: Novel (or non-vitamin K antagonist) oral anti-coagulants (NOACs) are antagonists of coagulation factors (F) Xa (rivaroxaban) or IIa (dabigatran), and their non-inferiority compared with vitamin K antagonists has been demonstrated in patients with non-valvular atrial fibrillation. However, it is still not fully understood if and how dabigatran and rivaroxaban impact platelet function. This observational study aimed to assess platelet function in patients receiving dabigatran or rivaroxaban. This was a single centre, observational study quantifying platelet aggregation in 90 patients treated with NOACs by multiple electrode aggregometry. The thrombin receptor activating peptide (TRAP)-induced platelet aggregation was significantly higher in 35 patients receiving dabigatran (d) compared with control (c) patients (d 108 ± 31 vs. c 85 ± 30 arbitrary units [AU]∗ min, p 〈 0.001). Patients receiving rivaroxaban (r) showed no differences compared with the control group (r 88 ± 32 vs. c 85 ± 30 AU ∗ min, p = 0.335). In intraindividual time courses of 16 patients, a significantly higher aggregation was found after the administration of dabigatran (before vs. after; 83 ± 29 vs. 100 ± 31 AU ∗ min, p = 0.009). In this observational study, the TRAP-induced platelet aggregation was enhanced in cardiovascular patients receiving dabigatran. This might be explained by a change in the expression profile of thrombin receptors on the surface of platelets. Rivaroxaban had no influence on platelet aggregation.
    Keywords: Dabigatran ; Rivaroxaban ; Platelet ; Aggregation ; Medicine
    ISSN: 0049-3848
    E-ISSN: 1879-2472
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  • 5
    Language: English
    In: Journal of Thrombosis and Thrombolysis, 2016, Vol.42(4), pp.558-565
    Description: High platelet reactivity (HPR) after P2Y 12 -inhibition in patients undergoing coronary stenting is associated with an increased risk for thromboembolic events and coronary death. So far it is not known how HPR affects the clinical outcome of different treatment strategies in patients with atrial fibrillation (AF) undergoing coronary stenting. In this single centre, observational study the antiplatelet effect of P2Y 12 -inhibitors in AF patients undergoing coronary stenting was investigated using impedance aggregometry. Patients received either dual antiplatelet therapy (DAPT) or triple therapy (TT). HPR was defined as the ratio of ADP-to TRAP-induced aggregation (r-ADP-agg) ≥50 %. Thromboembolic and bleeding events were assessed within the first 30 days after stenting. Out of 910 screened patients 167 patients were available for the present analysis. HPR was found in 5 of 43 (12 %) patients treated with DAPT and in 18 of 124 (15 %) patients treated with TT. In patients receiving TT, HPR was not a risk factor for thromboembolic events compared to patients with adequate response to P2Y 12 -inhibitors (6 vs. 8 %, p = 0.712). There was a trend for less bleeding events in patients with HPR compared to r-ADP-agg 〈50 % in the TT group (0 vs. 16 %, p = 0.077). Our data suggest that HPR after P2Y 12 -antagonism in patients receiving TT due to AF and coronary stenting might protect from bleeding without increasing thromboembolic risk. Future studies will need to investigate if patients with AF receiving coronary stenting benefit from a reduction of antithrombotic therapy.
    Keywords: Atrial fibrillation ; Percutaneous coronary intervention ; Antithrombotic therapy ; High platelet reactivity ; r-ADP-agg
    ISSN: 0929-5305
    E-ISSN: 1573-742X
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  • 6
    Language: English
    In: Breast Cancer Research and Treatment, 2013, Vol.138(1), pp.99-108
    Description: A comprehensive, blinded, pathology evaluation of HER2 testing in HER2-positive/negative breast cancers was performed among three central laboratories. Immunohistochemistry (IHC) and fluorescence in situ hybridization (FISH) analyses were performed on 389 tumor blocks from three large adjuvant trials: N9831, BCIRG-006, and BCIRG-005. In 123 cases, multiple blocks were examined. HER2 status was defined according to FDA-approved guidelines and was independently re-assessed at each site. Discordant cases were adjudicated at an on-site, face-to-face meeting. Results across three independent pathologists were concordant by IHC in 351/381 (92 %) and FISH in 343/373 (92 %) blocks. Upon adjudication, consensus was reached on 16/30 and 18/30 of discordant IHC and FISH cases, respectively, resulting in overall concordance rates of 96 and 97 %. Among 155 HER2-negative blocks, HER2 status was confirmed in 153 (99 %). In the subset of 102 HER2-positive patients from N9831/BCIRG-006, primary blocks from discordant cases were selected, especially those with discordant test between local and central laboratories. HER2 status was confirmed in 73 (72 %) of these cases. Among 118 and 113 cases with IHC and FISH results and 〉1 block evaluable, block-to-block variability/heterogeneity in HER2 results was seen in 10 and 5 %, respectively. IHC−/FISH− was confirmed for 57/59 (97 %) primary blocks from N9831 (locally positive, but centrally negative); however, 5/22 (23 %) secondary blocks showed HER2 positivity. Among 53 N9831 patients with HER2-normal disease adjudicated as IHC−/FISH—(although locally positive), there was a non-statistically significant improvement in disease-free survival with concurrent trastuzumab compared to chemotherapy alone (adjusted hazard ratio 0.34; 95 % CI, 0.11–1.05; p  = 0.06). There were similar agreements for IHC and FISH among pathologists (92 % each). Agreement was improved at adjudication (96 %). HER2 tumor heterogeneity appears to partially explain discordant results in cases initially tested as positive and subsequently called negative.
    Keywords: Breast cancer ; HER2 testing ; FISH ; IHC ; Concordance
    ISSN: 0167-6806
    E-ISSN: 1573-7217
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  • 7
    In: The New England Journal of Medicine, 2013, Vol.369(26), pp.2492-2503
    Description: Background Although inhibitors of the renin–angiotensin–aldosterone system can slow the progression of diabetic kidney disease, the residual risk is high. Whether nuclear 1 factor (erythroid-derived 2)–related factor 2 activators further reduce this risk is unknown. Methods We randomly assigned 2185 patients with type 2 diabetes mellitus and stage 4 chronic kidney disease (estimated glomerular filtration rate [GFR], 15 to 〈30 ml per minute per 1.73 m 2 of body-surface area) to bardoxolone methyl, at a daily dose of 20 mg, or placebo. The primary composite outcome was end-stage renal disease (ESRD) or death from cardiovascular causes. Results The sponsor and the steering committee terminated the trial on the recommendation of the independent data and safety monitoring committee; the median follow-up was 9 months. A total of 69 of 1088 patients (6%) randomly assigned to bardoxolone methyl and 69 of 1097 (6%) randomly assigned to placebo had a primary composite outcome (hazard ratio in the bardoxolone methyl group vs. the placebo group, 0.98; 95% confidence interval [CI], 0.70 to 1.37; P=0.92). In the bardoxolone methyl group, ESRD developed in 43 patients, and 27 patients died from cardiovascular causes; in the placebo group, ESRD developed in 51 patients, and 19 patients died from cardiovascular causes. A total of 96 patients in the bardoxolone methyl group were hospitalized for heart failure or died from heart failure, as compared with 55 in the placebo group (hazard ratio, 1.83; 95% CI, 1.32 to 2.55; P〈0.001). Estimated GFR, blood pressure, and the urinary albumin-to-creatinine ratio increased significantly and body weight decreased significantly in the bardoxolone methyl group, as compared with the placebo group. Conclusions Among patients with type 2 diabetes mellitus and stage 4 chronic kidney disease, bardoxolone methyl did not reduce the risk of ESRD or death from cardiovascular causes. A higher rate of cardiovascular events with bardoxolone methyl than with placebo prompted termination of the trial. (Funded by Reata Pharmaceuticals; BEACON ClinicalTrials.gov number, NCT01351675 .) Among patients with type 2 diabetes and stage 4 chronic kidney disease, bardoxolone methyl, as compared with placebo, did not reduce the risk of end-stage renal disease or cardiovascular death. Cardiovascular events in the bardoxolone group prompted trial termination. Type 2 diabetes mellitus is the most important cause of progressive chronic kidney disease in the developed and developing worlds. Various therapeutic approaches to slow progression, including restriction of dietary protein, glycemic control, and control of hypertension, have yielded mixed results.1–3 Several randomized clinical trials have shown that inhibitors of the renin–angiotensin–aldosterone system significantly reduce the risk of progression,4–6 although the residual risk remains high.7 None of the new agents tested during the past decade have proved effective in late-stage clinical trials.8–12 Oxidative stress and impaired antioxidant capacity intensify with the progression of chronic kidney disease.13 In . . .
    Keywords: Medicine;
    ISSN: 0028-4793
    E-ISSN: 1533-4406
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  • 8
    Language: English
    In: Hearing Research, March 2018, Vol.359, pp.40-49
    Description: The effort required to listen to and understand noisy speech is an important factor in the evaluation of noise reduction schemes. This paper introduces a model for Listening Effort prediction from Acoustic Parameters (LEAP). The model is based on methods from automatic speech recognition, specifically on performance measures that quantify the degradation of phoneme posteriorgrams produced by a deep neural net: Noise or artifacts introduced by speech enhancement often result in a temporal smearing of phoneme representations, which is measured by comparison of phoneme vectors. This procedure does not require a priori knowledge about the processed speech, and is therefore single-ended. The proposed model was evaluated using three datasets of noisy speech signals with listening effort ratings obtained from normal hearing and hearing impaired subjects. The prediction quality was compared to several baseline models such as the ITU-T standard P.563 for single-ended speech quality assessment, the American National Standard ANIQUE+ for single-ended speech quality assessment, and a single-ended SNR estimator. In all three datasets, the proposed new model achieved clearly better prediction accuracies than the baseline models; correlations with subjective ratings were above 0.9. So far, the model is trained on the specific noise types used in the evaluation. Future work will be concerned with overcoming this limitation by training the model on a variety of different noise types in a multi-condition way in order to make it generalize to unknown noise types.
    Keywords: Automatic Speech Recognition ; Deep Neural Networks ; Listening Effort Prediction ; Medicine ; Anatomy & Physiology
    ISSN: 0378-5955
    E-ISSN: 1878-5891
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  • 9
    Language: English
    In: New England journal of medicine, 2013, Vol.369(9), pp.799-808
    Description: Background Apixaban, an oral factor Xa inhibitor administered in fixed doses, may simplify the treatment of venous thromboembolism. Methods In this randomized, double-blind study, we compared apixaban (at a dose of 10 mg twice daily for 7 days, followed by 5 mg twice daily for 6 months) with conventional therapy (subcutaneous enoxaparin, followed by warfarin) in 5395 patients with acute venous thromboembolism. The primary efficacy outcome was recurrent symptomatic venous thromboembolism or death related to venous thromboembolism. The principal safety outcomes were major bleeding alone and major bleeding plus clinically relevant nonmajor bleeding. Results The primary efficacy outcome occurred in 59 of 2609 patients (2.3%) in the apixaban group, as compared with 71 of 2635 (2.7%) in the conventional-therapy group (relative risk, 0.84; 95% confidence interval [CI], 0.60 to 1.18; difference in risk [apixaban minus conventional therapy], -0.4 percentage points; 95% CI, -1.3 to 0.4). Apixaban was noninferior to conventional therapy (P 〈0.001) for predefined upper limits of the 95% confidence intervals for both relative risk ( 〈1.80) and difference in risk ( 〈3.5 percentage points). Major bleeding occurred in 0.6% of patients who received apixaban and in 1.8% of those who received conventional therapy (relative risk, 0.31; 95% CI, 0.17 to 0.55; P 〈0.001 for superiority). The composite outcome of major bleeding and clinically relevant nonmajor bleeding occurred in 4.3% of the patients in the apixaban group, as compared with 9.7% of those in the conventional-therapy group (relative risk, 0.44; 95% CI, 0.36 to 0.55; P 〈0.001). Rates of other adverse events were similar in the two groups. Conclusions A fixed-dose regimen of apixaban alone was noninferior to conventional therapy for the treatment of acute venous thromboembolism and was associated with significantly less bleeding (Funded by Pfizer and Bristol-Myers Squibb; ClinicalTrials.gov number, NCT00643201)
    Keywords: Life Sciences ; Sciences Du Vivant;
    ISSN: 0028-4793
    ISSN: 1533-4406
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  • 10
    Language: English
    In: New England journal of medicine, 2013, Vol.368(8), pp.699-708
    Description: BACKGROUND Apixaban, an oral factor Xa inhibitor that can be administered in a simple, fixed-dose regimen, may be an option for the extended treatment of venous thromboembolism. METHODS In this randomized, double-blind study, we compared two doses of apixaban (2.5 mg and 5 mg, twice daily) with placebo in patients with venous thromboembolism who had completed 6 to 12 months of anticoagulation therapy and for whom there was clinical equipoise regarding the continuation or cessation of anticoagulation therapy. The study drugs were administered for 12 months. RESULTS A total of 2486 patients underwent randomization, of whom 2482 were included in the intention-to-treat analyses. Symptomatic recurrent venous thromboembolism or death from venous thromboembolism occurred in 73 of the 829 patients (8.8%) who were receiving placebo, as compared with 14 of the 840 patients (1.7%) who were receiving 2.5 mg of apixaban (a difference of 7.2 percentage points; 95% confidence interval [CI], 5.0 to 9.3) and 14 of the 813 patients (1.7%) who were receiving 5 mg of apixaban (a difference of 7.0 percentage points; 95% CI, 4.9 to 9.1) (P 〈0.001 for both comparisons). The rates of major bleeding were 0.5% in the placebo group, 0.2% in the 2.5-mg apixaban group, and 0.1% in the 5-mg apixaban group. The rates of clinically relevant nonmajor bleeding were 2.3% in the placebo group, 3.0% in the 2.5-mg apixaban group, and 4.2% in the 5-mg apixaban group. The rate of death from any cause was 1.7% in the placebo group, as compared with 0.8% in the 2.5-mg apixaban group and 0.5% in the 5-mg apixaban group. CONCLUSIONS Extended anticoagulation with apixaban at either a treatment dose (5 mg) or a thromboprophylactic dose (2.5 mg) reduced the risk of recurrent venous thromboembolism without increasing the rate of major bleeding. (Funded by Bristol-Myers Squibb and Pfizer; AMPLIFY-EXT ClinicalTrials.gov number, NCT00633893.)
    Keywords: Medicine;
    ISSN: 0028-4793
    ISSN: 1533-4406
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