Cost of College

We propose that we should alter the way public post-secondary institutions are funded in Ohio and suggest that the state of Ohio should subsidize some cost for the institution. In return, we hope this would trigger the institutions to cut tuition cost and in return, so students will have less of a financial burden when considering higher education.https://corescholar.libraries.wright.edu/raider_academy/1008/thumbnail.jp

Early detection of anthracycline- and trastuzumab-induced cardiotoxicity: value and optimal timing of serum biomarkers and echocardiographic parameters.

Aims To evaluate echocardiographic and biomarker changes during chemotherapy, assess their ability to early detect and predict cardiotoxicity and to define the best time for their evaluation. Methods and results Seventy-two women with breast cancer (52 ± 9.8 years) treated with anthracyclines (26 also with trastuzumab), were evaluated for 14 months (6 echocardiograms/12 laboratory tests). We analysed: high-sensitivity cardiac troponin T, NT-proBNP, global longitudinal strain (GLS), left ventricle end-systolic volume (LVESV), left ventricle end-diastolic volume (LVEDV), and left ventricular ejection fraction (LVEF). Cardiotoxicity was defined as a reduction in LVEF>10% compared with baseline with LVEF<53%. High-sensitivity troponin T levels rose gradually reaching a maximum peak at 96 ± 13 days after starting chemotherapy (P < 0.001) and 62.5% of patients presented increased values during treatment. NT-proBNP augmented after each anthracycline cycle (mean pre-cycle levels of 72 ± 68 pg/mL and post-cycle levels of 260 ± 187 pg/mL; P < 0.0001). Cardiotoxicity was detected in 9.7% of patients (mean onset at 5.2 months). In the group with cardiotoxicity, the LVESV was higher compared with those without cardiotoxicity (40 mL vs. 29.5 mL; P = 0.045) at 1 month post-anthracycline treatment and the decline in GLS was more pronounced ( 17.6% vs. 21.4%; P = 0.03). Trastuzumab did not alter serum biomarkers, but it was associated with an increase in LVESV and LVEDV (P < 0.05). While baseline LVEF was an independent predictor of later cardiotoxicity (P = 0.039), LVESV and GLS resulted to be early detectors of cardiotoxicity [odds ratio = 1.12 (1.02–1.24), odds ratio = 0.66 (0.44–0.92), P < 0.05] at 1 month post-anthracycline treatment. Neither high-sensitivity troponin T nor NT-proBNP was capable of predicting subsequent cardiotoxicity. Conclusions One month after completion of anthracycline treatment is the optimal time to detect cardiotoxicity by means of imaging parameters (LVESV and GSL) and to determine maximal troponin rise. Baseline LVEF was a predictor of later cardiotoxicity. Trastuzumab therapy does not affect troponin values hence imaging techniques are recommended to detect trastuzumab-induced cardiotoxicity.post-print3194 K

Evaluación del rendimiento de un modelo clínico-genético en la estimación del tiempo en rango terapéutico de pacientes con fibrilación auricular no valvular tratados con acenocumarol

Introducción: La eficacia y seguridad del tratamiento con antagonistas de la vitamina K (AVK) en pacientes con fibrilación auricular (FA) depende en gran medida de la capacidad de alcanzar y mantener un adecuado nivel de anticoagulación. A pesar de la introducción de los anticoagulantes orales directos, los AVK continúan siendo el tratamiento anticoagulante más empleado en pacientes con FA a nivel mundial. La calidad de la anticoagulación se evalúa mediante tiempo en rango terapéutico (TRT) definido por Rosendaal. Si bien en los ensayos clínicos se obtiene un TRT relativamente elevado, en el mundo real se sospecha que el control de la anticoagulación no es tan estricto. Además, con el fin de identificar aquellos pacientes que serían buenos respondedores al tratamiento con AVK, se ha propuesto la escala SAMeTT2R2. En el estudio inicial, esta escala presentó un razonable nivel de discriminación, esto es una adecuada capacidad para identificar los pacientes con un TRT adecuado. Sin embargo, dicha escala fue elaborada a partir de una población de pacientes con FA incluidos en un ensayo clínico, por lo que el sesgo de selección y otras limitaciones metodológicas, suscitan dudas sobre su aplicabilidad en práctica clínica real. Finalmente, algunos autores han propuesto que la predicción del TRT podía mejorar con la determinación de polimorfismos genéticos que se han visto implicados en el mecanismo de biotransformación de los AVK. Objetivos: - Estudiar la calidad de la anticoagulación de pacientes con FA no valvular bajo tratamiento con acenocumarol en nuestro medio calculando el TRT mediante el método de Rosendaal. - Estimar el rendimiento de la escala SAMeTT2R2 en la predicción del TRT en nuestra población. - Identificar aquellos factores clínicos y genéticos implicados en un adecuado nivel de anticoagulación con antagonistas de la vitamina K que potencialmente podrían mejorar la capacidad discriminativa de la escala SAMeTT2R2. Métodos: se incluyeron 212 pacientes atendidos en consultas externas de Cardiología diagnosticados de FA no valvular, bajo tratamiento con acenocumarol durante al menos 6 meses y catalogados como adherentes al tratamiento anticoagulante. Elaboramos un modelo de regresión multivariable con el fin de identificar aquellas variables independientes predictoras de un buen control de anticoagulación. Los polimorfismos genéticos VKORC1, CYP2C9*2, CYP2C9*3 y MIR133A2 fueron analizados en todos los pacientes. Resultados: un total de 128 pacientes (60.4%) presentaron un TRT < 70% (TRT medio= 63.2). Identificamos el índice de masa corporal (OR 0.94, IC 95% 0.89 - 0.99, p=0.032) y la ingesta regular de vitamina K (OR 0.53, IC 95% 0.28 - 0.99, p= 0.046) como predictores independientes de un pobre control de anticoagulación. La capacidad discriminativa de un modelo clínico-genético derivado de nuestra cohorte (que incluyó el índice de masa corporal, la ingesta de vitamina K y los polimorfismos analizados) fue significativamente superior comparado con la escala SAMeTT2R2 (estadístico-C 0.658 frente a 0.524, p<0.001). Conclusiones: El estudio de la calidad de anticoagulación con acenocumarol en pacientes con FA no valvular reveló una elevada proporción de pacientes con mal control de dicha terapia en nuestro medio. La escala SAMeTT2R2 presentó muy pobre capacidad predictiva de un TRT adecuado. El índice de masa corporal, la ingesta de vitamina K y los polimorfismos analizados fueron capaces de mejorar la capacidad discriminativa de la escala SAMeTT2R2.Introduction: The efficacy and safety of treatment with vitamin K antagonists (VKA) in patients with atrial fibrillation (AF) strongly depends on the ability of achieving and maintaining an adequate level of anticoagulation. In spite of the introduction of direct oral anticoagulants, VKA remain the most used anticoagulant treatment in patients with AF world-wide. Quality of anticoagulation is assessed with time in therapeutic range (TTR) defined by Rosendaal, and although clinical trials present relatively high TTR, it seems that “real-world” control is not that strict. The SAMeTT2R2 score was proposed in order to identify those patients that would present a good response to VKA treatment. In the initial study the SAMeTT2R2 score showed a reasonable discrimination, that is a correct ability to identify patients with an adequate TTR. However, this score was elaborated from a group of patients with AF included in a clinical trial, and therefore a potential selection bias and other methodological limitations raise doubts about its applicability in clinical practice. Finally, some authors have proposed that TTR prediction could improve with the identification of genetic polymorphisms that have been found to be involved in the biotransformation mechanisms o VKA. Aims: - To analyze the quality of anticoagulation in patients with non-valvular AF in our cohort treated with acenocoumarol by means of TTR calculated by the Rosendaal method. - To assess the performance of the SAMeTT2R2 score in the prediction of TTR in our cohort. - To identify the clinical and genetic factors involved in a correct level of anticoagulation with VKA that could potentially improve the diagnostic performance of SAMeTT2R2 score. Methods: we included 212 consecutive patients with non-valvular atrial fibrillation under treatment with acenocoumarol for at least 6 months, that were attended in a Cardiology outpatient clinic and were categorized as adherent to medication. We carried out a multivariate regression analysis to detect the independent predictive factors of good anticoagulation control. In all patients VKORC1, CYP2C9*2, CYP2C9*3 and MIR133A2 genotyping was performed. Results: a total of 128 (60.4%) patients presented TTR <70% (average TTR = 63.2). We identified body mass index (OR 0.94, 95%CI 0.89 - 0.99, p=0.032) and regular vitamin K intake (OR 0.53, 95%CI 0.28 - 0.99, p= 0.046) as independent predictors of poor anticoagulation control. The discriminatory power of a clinical-genetic model derived from our cohort (that included body mass index, vitamin K intake and the analysed polymorphisms) was significantly better compared to the SAMeTT2R2score (C- statistic 0.658 vs. 0.524, p<0.001). Conclusions: the analysis of quality of anticoagulation with acenocoumarol in patients with non-valvular AF revealed a high proportion of patients with suboptimal control of such therapy in our cohort. The SAMeTT2R2 score revealed a poor ability to predict an adequate TTR. Clinical factors such as body mass index and vitamin K intake as well as the analysed genetic polymorphisms were capable of improving the discriminatory power of SAMeTT2R2 score

The Cost of College: Today and the 70s

When starting to look at college\u27s we look at the price of what everything cost: dorms, class credit prices, meal tickets, and books. Well what if everything was lowered in price? What if our tuition could be free? What if more people would go to college if these things were true. With debt being a major cause of why young adults and adults don\u27t want to go back to school after starting in the real world. Public university in the United States have periodically increased the cost of tuition which have resulted in drastic amounts of student debt.https://corescholar.libraries.wright.edu/raider_academy/1004/thumbnail.jp

Low Performance of a Clinical-Genetic Model in the Estimation of Time in Therapeutic Range in Acenocoumarol-Adherent Patients with Nonvalvular Atrial Fibrillation: The Quality of Anticoagulation Challenge

Background. Anticoagulation with vitamin K antagonists continues to be a challenging task given the difficulty of achieving a correct time in therapeutic range (TTR). The SAMeTT2R2 score has been proposed to identify patients that will be good responders. In this study we aimed to analyse clinical and genetic factors involved in a correct level of anticoagulation in patients with atrial fibrillation and thereby potentially improve the diagnostic performance of SAMeTT2R2 score. Methods. We prospectively included 212 consecutive patients with nonvalvular atrial fibrillation under treatment with acenocoumarol for at least 6 months that were attended in a cardiology outpatient clinic and were categorized as adherent to medication. We carried out a multivariate regression analysis to detect the independent predictive factors of good control. In all patients VKORC1, CYP2C9⁎2, CYP2C9⁎3, and MIR133A2 genotyping was performed. Results. A total of 128 (60.4%) patients presented TTR <70% (average TTR = 63.2). We identified body mass index (OR 0.94, 95%CI 0.89-0.99, p=0.032) and regular vitamin K intake (OR 0.53, 95%CI 0.28-0.99, p= 0.046) as independent predictors of poor anticoagulation control. The discriminatory power of a clinical-genetic model derived from our cohort was significantly better compared to the SAMeTT2R2 score (C-statistic 0.658 versus 0.524, p<0.001). Conclusions. In our study the SAMeTT2R2 score revealed a poor ability in the prediction of TTR. Besides SAMeTT2R2, body mass index and possibly vitamin K intake should be taken into account when deciding the optimal anticoagulation strategy. The information provided by the identified genotypes was marginal

Low Performance of a Clinical-Genetic Model in the Estimation of Time in Therapeutic Range in Acenocoumarol-Adherent Patients with Nonvalvular Atrial Fibrillation: The Quality of Anticoagulation Challenge

Background. Anticoagulation with vitamin K antagonists continues to be a challenging task given the difficulty of achieving a correct time in therapeutic range (TTR). The SAMeTT2R2 score has been proposed to identify patients that will be good responders. In this study we aimed to analyse clinical and genetic factors involved in a correct level of anticoagulation in patients with atrial fibrillation and thereby potentially improve the diagnostic performance of SAMeTT2R2 score. Methods. We prospectively included 212 consecutive patients with nonvalvular atrial fibrillation under treatment with acenocoumarol for at least 6 months that were attended in a cardiology outpatient clinic and were categorized as adherent to medication. We carried out a multivariate regression analysis to detect the independent predictive factors of good control. In all patients VKORC1, CYP2C9⁎2, CYP2C9⁎3, and MIR133A2 genotyping was performed. Results. A total of 128 (60.4%) patients presented TTR <70% (average TTR = 63.2). We identified body mass index (OR 0.94, 95%CI 0.89-0.99, p=0.032) and regular vitamin K intake (OR 0.53, 95%CI 0.28-0.99, p= 0.046) as independent predictors of poor anticoagulation control. The discriminatory power of a clinical-genetic model derived from our cohort was significantly better compared to the SAMeTT2R2 score (C-statistic 0.658 versus 0.524, p<0.001). Conclusions. In our study the SAMeTT2R2 score revealed a poor ability in the prediction of TTR. Besides SAMeTT2R2, body mass index and possibly vitamin K intake should be taken into account when deciding the optimal anticoagulation strategy. The information provided by the identified genotypes was marginal

Early detection of anthracycline- and trastuzumab-induced cardiotoxicity: value and optimal timing of serum biomarkers and echocardiographic parameters.

To evaluate echocardiographic and biomarker changes during chemotherapy, assess their ability to early detect and predict cardiotoxicity and to define the best time for their evaluation. Seventy-two women with breast cancer (52 ± 9.8 years) treated with anthracyclines (26 also with trastuzumab), were evaluated for 14 months (6 echocardiograms/12 laboratory tests). We analysed: high-sensitivity cardiac troponin T, NT-proBNP, global longitudinal strain (GLS), left ventricle end-systolic volume (LVESV), left ventricle end-diastolic volume (LVEDV), and left ventricular ejection fraction (LVEF). Cardiotoxicity was defined as a reduction in LVEF>10% compared with baseline with LVEF<53%. High-sensitivity troponin T levels rose gradually reaching a maximum peak at 96 ± 13 days after starting chemotherapy (P < 0.001) and 62.5% of patients presented increased values during treatment. NT-proBNP augmented after each anthracycline cycle (mean pre-cycle levels of 72 ± 68 pg/mL and post-cycle levels of 260 ± 187 pg/mL; P < 0.0001). Cardiotoxicity was detected in 9.7% of patients (mean onset at 5.2 months). In the group with cardiotoxicity, the LVESV was higher compared with those without cardiotoxicity (40 mL vs. 29.5 mL; P = 0.045) at 1 month post-anthracycline treatment and the decline in GLS was more pronounced (-17.6% vs. -21.4%; P = 0.03). Trastuzumab did not alter serum biomarkers, but it was associated with an increase in LVESV and LVEDV (P < 0.05). While baseline LVEF was an independent predictor of later cardiotoxicity (P = 0.039), LVESV and GLS resulted to be early detectors of cardiotoxicity [odds ratio = 1.12 (1.02-1.24), odds ratio = 0.66 (0.44-0.92), P < 0.05] at 1 month post-anthracycline treatment. Neither high-sensitivity troponin T nor NT-proBNP was capable of predicting subsequent cardiotoxicity. One month after completion of anthracycline treatment is the optimal time to detect cardiotoxicity by means of imaging parameters (LVESV and GSL) and to determine maximal troponin rise. Baseline LVEF was a predictor of later cardiotoxicity. Trastuzumab therapy does not affect troponin values hence imaging techniques are recommended to detect trastuzumab-induced cardiotoxicity.This work was supported by Fundación de Investigación HM hospitales (I Convocatoria Intramural para grupos emergentes, 2016). LFF and AM have received funding from Comunidad de Madrid (AORTASANA-CM; B2017/BMD3676), Fondo Social Europeo (FSE) and LFF from Instituto de Salud Carlos III, España (PI15/02019;PI20/01238).S