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- Original Volume Four: Therapeutic Promise: Cardiovascular Diseases, Regenerative & Translational Medicine
-
NEW GENRE Volume Four: Therapeutic Promise: Cardiovascular Diseases, Regenerative & Translational Medicine
This volume has the following three parts:
PART A: The eTOCs in Spanish in Audio format
PART B: The eTOCs in Bi-lingual format: Spanish and English in Text format
PART C: The Editorials of the original e-Books in English in Audio format
PART A: The eTOCs in Spanish in Audio format
Serie A: libros electrónicos acerca de las enfermedades cardiovasculares
CUARTO VOLUMEN
Medicina regenerativa y Medicina traslativa
La promesa terapéutica para las
enfermedades cardiovasculares
(LIBRO 4 DE LA SERIE DE LIBROS ELECTRÓNICOS SOBRE BIOMEDICINA)
Traducción a español Montero Language Services
Disponible en Amazon.com desde el 26/12/2015
http://www.amazon.com/dp/B019UM909A
y
Leaders in Pharmaceutical Business Intelligence
avivalev-ari@alum.berkeley.edu
Redactora jefe
Indice de contenidos electrónico (IDCe)
Los enlaces indicados llevan al contenido original en inglés
| MD | Licenciado/a en medicina y cirugía (Estados Unidos) |
| PhD | Doctorado/a |
| RN | Enfermero/a titulado/a |
| FCAP | Miembro distinguido del Colegio de anatomopatólogos de los Estados Unidos |
| FACC | Miembro distinguido del Colegio de cardiólogos de los Estados Unidos |
Introducción al cuarto volumen
Introduction to Volume Four
Primera parte:
Enfermedades cardiovasculares, medicina traslativa (MT) y post-MT
Introducción a la primera parte
Enfermedades cardiovasculares, medicina traslativa (MT) y post-MT
Author and Curator: Larry H Bernstein, MD, FCAP and Curator: Aviva Lev-Ari, PhD, RN
Capítulo 1: Conceptos de la medicina traslativa
1.0 Modificación postraslativa de las proteínas
https://pharmaceuticalintelligence.com/2014/04/21/posttranslational-modification-of-proteins/
Larry H Bernstein, MD, FCAP
1.1 Identificación de la ciencia traslativa dentro del triángulo de la biomedicina
Griffin M Weber, Journal of Translational Medicine 2013, 11:126 (24 de mayo de 2013)
1.2 Estado de la cardiología con respecto al estrés parietal, la carga ventricular y la reserva contráctil del miocardio: aspectos de la medicina traslativa (MT)
Justin Pearlman, MD, PhD, FACC and Aviva Lev-Ari, PhD, RN
1.3 Riesgo de sesgo en la ciencia traslativa
https://pharmaceuticalintelligence.com/2013/11/03/risk-of-bias-in-translational-science/
Larry H Bernstein, MD, FCAP
1.4 Biosimilares: creación y protección de la propiedad intelectual por parte del descubridor y de los fabricantes de biosimilares
Aviva Lev-Ari, PhD, RN
Capítulo 2: Causas y etiología de las enfermedades cardiovasculares. Enfoques traslativos para la medicina cardiotorácica
2.1 Genómica
2.1.1 Clasificación basada en la genómica
https://pharmaceuticalintelligence.com/2013/11/01/genomics-based-classification/
Larry H Bernstein, MD, FCAP y Aviva Lev-Ari, PhD, RN
2.1.2 Uso como diana de protooncogenes no utilizables como diana terapéutica
https://pharmaceuticalintelligence.com/2013/11/01/targeting-untargetable-proto-oncogenes/
Larry H Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN
2.1.3 Genoma consultable para el desarrollo de fármacos
https://pharmaceuticalintelligence.com/2013/12/01/searchable-genome-for-drug-development/
Larry H Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN
2.1.4 Herramienta de estudio del pez cebra
https://pharmaceuticalintelligence.com/2013/11/01/zebrafish-study-tool/
Larry H Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN
2.1.5 Ya se ha secuenciado la secuencia eucromática del genoma humano. ¿Qué viene a continuación?
Larry H Bernstein, MD, FCAP
2.2 Proteómica
2.2.1 El papel de las proteínas de la unión estrecha en el transporte de agua y electrolitos
Larry H Bernstein, MD, FCAP
2.2.2 Conducción selectiva de iones
https://pharmaceuticalintelligence.com/2013/10/07/selective-ion-conduction/
Larry H Bernstein, MD, FCAP
2.2.3 Investigación traslativa sobre el mecanismo de los movimientos de entrada de agua y electrolitos en la célula
Larry H. Bernstein, MD, FACP
2.2.4 Inhibición de la cinasa específica de los cardiomiocitos TNNI3K. Estrés oxidativo
Larry H Bernstein, MD, FCAP
Una cinasa específica de los cardiomiocitos limita la lesión por reperfusión
2.2.5 Calcio/calmodulina-cinasa oxidada y fibrilación auricular
Larry H. Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN
Papel del receptor acoplado a la proteína G con S-nitrosilación en el síndrome coronario agudo
2.2.6 La S-nitrosilación en la isquemia cardíaca y el síndrome coronario agudo
2.2.6.1 Señalización de la S-nitrosilación
https://pharmaceuticalintelligence.com/2014/04/21/s-nitrosylation-signaling/
Larry H Bernstein, MD, FCAP
2.2.7 Acetilación y desacetilación
2.2.7.1 Histona-desacetilasa Sir2 (proteína de silenciamiento transcripcional y longevidad).
Larry H Bernstein, MD, FCAP
2.2.7.2 Acetilación y desacetilación de proteínas distintas de las histonas
Larry H Bernstein, MD, FCAP
2.2.8 Inhibidores de la óxido nítrico-sintasa (NOS-I)
https://pharmaceuticalintelligence.com/2013/11/02/nitric-oxide-synthase-inhibitors/
Larry H Bernstein, MD, FCAP, Stephen J. Williams, PhD and Aviva Lev-Ari, PhD, RN
2.3 Señalización cardíaca y vascular
2.3.1 La centralidad de la señalización del Ca(2+) y del citoesqueleto, con implicación de las calmodulina-cinasas y los receptores de rianodina, en la insuficiencia cardíaca, el músculo liso arterial y la arritmia postisquémica; similitudes, diferencias y dianas farmacéuticas
Larry H Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN
2.3.2 Señalización de la leptina en la mediación de la hipertrofia cardíaca asociada a la obesidad
Larry H Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN
2.3.3 Desencadenamiento de la ruptura de la placa de ateroma y la trombosis arterial
Larry H Bernstein, MD, FCAP
2.3.4 Sensores y señalización en el estrés oxidativo
https://pharmaceuticalintelligence.com/2013/11/01/sensors-and-signaling-in-oxidative-stress/
Larry H. Bernstein, MD, FCAP
2.3.5 Resistencia al receptor de tirosina-cinasa
https://pharmaceuticalintelligence.com/2013/11/01/resistance-to-receptor-of-tyrosine-kinase/
Larry H. Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN
2.3.6 Gaston B. M. et al. (2003) Señalización de la S-nitrosilación en la biología celular. Mol Interv. 3, 253-63.
2.4 Interacción plaqueto-endotelial
2.4.1 Las plaquetas en la investigación traslativa. Parte 1
https://pharmaceuticalintelligence.com/2013/10/07/platelets-in-translational-research-1/
Larry H Bernstein, MD, FCAP
2.4.2 Las plaquetas en la investigación traslativa. 2: Descubrimiento de posibles dianas antiplaquetarias
https://pharmaceuticalintelligence.com/2013/10/07/platelets-in-translational-research-2/
Larry H. Bernstein, MD, FCAP
2.4.3 Consideraciones finales sobre el papel de las plaquetas y las reacciones plaqueto-endoteliales en la ateroesclerosis, y nuevos tratamientos
Larry H. Bernstein, MD, FCAP
2.4.4 Función endotelial y enfermedades cardiovasculares
https://pharmaceuticalintelligence.com/2012/10/25/endothelial-function-and-cardiovascular-disease/
Larry H Bernstein, MD, FCAP
2.5 Modificaciones postraslativas (MPT)
2.5.1 Modificaciones postraslativas
https://pharmaceuticalintelligence.com/2014/04/21/posttranslational-modifications/
Larry H Bernstein, MD, FCAP
2.5.2. Análisis de las proteínas S-nitrosiladas
https://pharmaceuticalintelligence.com/2014/04/21/analysis-of-s-nitrosylated-proteins/
Larry H Bernstein, MD, FCAP
2.5.2.1 Análisis de las proteínas S-nitrosiladas: cambio de biotina sin detergente combinado con cromatografía líquida/espectrometría de masas en tándem
Larry H Bernstein, MD, FACP
2.5.3 Mecanismos de la enfermedad: transducción de señales. Akt fosforila a HK-II en Thr-473 y aumenta la asociación mitocondrial de HK-II para proteger a los cardiomiocitos.
David J. Roberts, Valerie P. Tan-Sah, Jeffery M. Smith and Shigeki Miyamoto, J. Biol. Chem. 2013, 288:23798-23806. http://dx.doi.org/10.1074/jbc.M113.482026
2.5.4 Acetilación y desacetilación de proteínas no histónicas
Larry H Bernstein, MD, FCAP
2.5.5 Un estudio descubre regiones de baja metilación propensas a presentar mutaciones estructurales
Aviva Lev-Ari, PhD, RN
2.6 Epigenética y ARN largos no codificantes (ARNlnc)
2.6.1 La magia de la caja de Pandora: epigenética y pluripotencialidad con los ARN largos no codificantes (ARNlnc)
Demet Sag, Ph.D., CRA, GCP
2.6.2 “El SILENCIO de los corderos”. Presentación del poder del ARN no codificado
Demet Sag, Ph.D., CRA, GCP
2.6.3 La red de ARN largos no codificantes regula la transcripción de PTEN
Larry H Bernstein, MD, FACP
2.6.4 Cómo promueven el cáncer los elementos móviles del ADN “basura”. Parte 1: tumorigénesis mediada por transposones
Stephen J. Williams, Ph.D.
2.6.5 La terapia génica mediada por transposones mejora la hemodinámica pulmonar y atenúa la hipertrofia de ventrículo derecho: la terapia génica con eNOS reduce la remodelación vascular pulmonar y la hiperplasia de la pared arterial
Aviva Lev-Ari, PhD, RN
2.6.6 El ADN basura codifica valiosos miARN: el ADN no codificante controla la diabetes
https://pharmaceuticalintelligence.com/2012/09/24/junk-dna-codes-for-valuable-mirnas/
Margaret Baker, PhD, Registered Patent Agent
2.6.7 Nucleasas dirigidas
https://pharmaceuticalintelligence.com/2013/03/02/targeted-nucleases/
Larry H Bernstein, MD, FACP
2.6.8 La aparición tardía de la enfermedad de Alzheimer y el metabolismo monocarbonado
https://pharmaceuticalintelligence.com/2013/05/06/alzheimers-disease-and-one-carbon-metabolism/
Dr. Sudipta Saha
2.6.9 Amiloidosis con miocardiopatía
https://pharmaceuticalintelligence.com/2013/03/31/amyloidosis-with-cardiomyopathy/
Larry H Bernstein, MD, FACP
2.6.10 ARN largos no codificantes: reguladores moleculares del destino celular. Conferencia de la profesora Laurie Boyer en el MIT – Simposio de verano 2014: Biología del ARN, cáncer e implicaciones terapéuticas, 13 de junio de 2014, Instituto Koch @MIT http://ki.mit.edu/news/symposium
Conference Reporter: Aviva Lev-Ari, PhD, RN
2.7 Metabolómica
2.7.1 Ampliación del alfabeto genético y vinculación del genoma con el metaboloma
Larry Bernstein, MD, FCAP
2.7.2 Cómo causa hiperhomocisteinemia el desequilibrio de la metionina con insuficiencia de azufre
https://pharmaceuticalintelligence.com/2013/04/04/sulfur-deficiency-leads_to_hyperhomocysteinemia/
Larry H Bernstein, MD, FACP
2.7.3 Una segunda mirada al enigma inflamatorio de la nutrición y la transtiretina
Larry H. Bernstein, MD, FACP
2.7.4 Transtiretina y masa corporal magra en estado estable y de estrés
Larry Bernstein, MD, FCAP
2.7.5 Interacción de la hiperhomocisteinemia con la proteína C y aumento del riesgo trombótico
https://pharmaceuticalintelligence.com/2013-12-3/larryhbern/Hyperhomocysteinemia
Larry H Bernstein, MD, FCAP
2.7.6 Cómo decir NO al riesgo cardíaco
https://pharmaceuticalintelligence.com/2012/12/10/telling-no-to-cardiac-risk/
Stephen J. Williams, PhD
2.8 Mitocondrias y estrés oxidativo
2.8.1 Reversión de la disfunción mitocondrial cardíaca
https://pharmaceuticalintelligence.com/2013/04/14/reversal-of-cardiac-mitochondrial-dysfunction/
Larry H. Bernstein, MD, FCAP
2.8.2 Señalización del calcio, mitocondrias cardíacas y síndrome metabólico
Larry H. Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN
2.8.3 Disfunción mitocondrial y trastornos cardíacos
https://pharmaceuticalintelligence.com/2013/04/14/mitochondrial-dysfunction-and-cardiac-disorders/
Larry H. Bernstein, MD, FCAP
2.8.4 Metabolismo mitocondrial y función cardíaca
https://pharmaceuticalintelligence.com/2013/04/14/mitochondrial-metabolism-and-cardiac-function/
Larry H. Bernstein, MD, FCAP
2.8.5 Las mitocondrias y las enfermedades cardiovasculares: homenaje a Richard Bing
https://pharmaceuticalintelligence.com/2013/04/14/chapter-5-mitochondria-and-cardiovascular-disease/
Larry H. Bernstein, MD, FCAP
2.8.6 Científicos del MIT y proteómica: identificadas todas las proteínas de la matriz mitocondrial
Aviva Lev-Ari, PhD, RN
2.8.7 La dinámica mitocondrial y enfermedades cardiovasculares
Ritu Saxena, Ph.D.
2.8.8 Daño y reparación mitocondrial bajo estrés oxidativo
Larry H Bernstein, MD, FCAP
2.8.9 El óxido nítrico tiene un papel omnipresente en la regulación de la glucólisis, con la consiguiente influencia en la función mitocondrial
Larry H. Bernstein, MD, FACP
2.8.10 Mecanismos patogénicos mitocondriales en la diabetes mellitus
Aviva Lev-Ari, PhD, RN
2.8.11 Disfunción mitocondrial y enfermedades cardiovasculares. Las mitocondrias: no solo son la “central energética de la célula”
Ritu Saxena, PhD
Capítulo 3: Riesgos y biomarcadores del diagnóstico y el pronóstico en la medicina cardiotorácica traslativa
3.1 Biomarcadores, diagnóstico y tratamiento: presente y futuro de los biomarcadores
https://pharmaceuticalintelligence.com/2013/11/10/biomarkers-diagnosis-and-management/
Larry Bernstein, MD, FCAP
3.2 Panorama de los biomarcadores cardíacos para una mejor utilización clínica
Larry H Bernstein, MD, FCAP
3.3 Lograr la automatización de la serología: nueva frontera de las prácticas óptimas
Larry H Bernstein, MD, FCAP
3.4 Identificación y tratamiento precisos de los episodios cardíacos urgentes
Larry Bernstein, MD, FCAP
3.5 Importancia de la troponina I como marcador pronóstico en la insuficiencia cardíaca aguda descompensada (ICAD)
https://pharmaceuticalintelligence.com/2013/06/30/troponin-i-in-acute-decompensated-heart-failure/
Larry H Bernstein, MD, FCAP
3.6 Análisis de troponina cardíaca de alta sensibilidad. Preparando a los Estados Unidos para los análisis de troponina cardíaca de alta sensibilidad
https://pharmaceuticalintelligence.com/2013/06/13/high-sensitivity-cardiac-troponin-assays/
Larry Bernstein, MD, FCAP
3.7 Voces de la Clínica Cleveland sobre la apoA1 circulante: biomarcador de proceso proaterogénico en la pared arterial
Aviva Lev-Ari, PhD, RN
3.8 Desencadenamiento de la ruptura de la placa de ateroma y la trombosis arterial
Larry H Bernstein, MD, FCAP
3.9 Descubierta la relación entre adiposidad y consumo elevado de fructosa
Larry Bernstein, MD, FCAP
3.10 El síndrome cardio-renal (SCR) en la insuficiencia cardíaca (IC)
https://pharmaceuticalintelligence.com/2013/06/30/the-cardiorenal-syndrome-in-heart-failure/
Larry H. Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN
3.11 Aneuploidía y carcinogénesis
https://pharmaceuticalintelligence.com/2013/10/31/aneuploidy-and-carcinogenesis/
Larry H. Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN
3.12 “La muerte súbita cardíaca”, SudD, está en la serie de pruebas genéticas cardiovasculares de Ferrer inCode que se comercializarán en EE. UU.
Aviva Lev-Ari, PhD, RN
Capítulo 4: Aspectos terapéuticos en la medicina cardiotorácica traslativa
4.1 Cardiología molecular y celular
4.1.1 Los antagonistas de αllbβ3 como ejemplo de agentes terapéuticos de la medicina traslativa
Larry H Bernstein, MD, FCAP
4.1.2 La matriz tridimensional de fibroblastos mejora la función del ventrículo izquierdo tras un IM
Larry H. Bernstein, MD. FCAP and Aviva Lev-Ari, PhD, RN
4.1.3 Tecnología de los biomateriales: modelos de ingeniería tisular para la reperfusión y dispositivos implantables para la revascularización
https://pharmaceuticalintelligence.com/2013/05/05/bioengineering-of-vascular-and-tissue-models/
Larry H Bernstein, MD, FACP and Aviva Lev-Ari, PhD, RN
4.1.4 Ensayo clínico aleatorizado CELLWAVE: modesta mejora de la FEVI a los 4 meses. “Administración intracoronaria de CMO facilitada por ondas de choque” frente al “tratamiento solo con ondas de choque”
Aviva Lev-Ari, PhD, RN
4.1.5 Prostaciclina y óxido nítrico: aventuras de la biología vascular, la historia de dos mediadores
Aviva Lev-Ari, PhD, RN
4.1.6 Contractilidad cardíaca y función miocárdica: arritmias ventriculares e insuficiencia cardíaca no isquémica. Implicaciones terapéuticas de la rianodinopatía (disfunción contráctil relacionada con la liberación de calcio) y respuestas de catecolaminas. Parte VII
Justin Pearlman, MD, PhD, FACC, Larry H Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN
4.1.7 Publicaciones sobre la insuficiencia cardíaca del profesor William Gregory Stevenson, M.D., BWH
Aviva Lev-Ari, PhD, RN
4.2 Cardiología Intervencionista y cirugía cardíaca. Soporte circulatorio mecánico y reparación vascular
4.2.1 Sistema de soporte circulatorio mecánico, DAVI, DAVD, biventricular como puente al trasplante cardíaco o como “terapia de destino”: opciones para los pacientes con insuficiencia cardíaca avanzada
https://pharmaceuticalintelligence.com/2013/06/30/advanced-heart-failure/
Larry H. Bernstein, MD, FACP
4.2.2 Trasplante de corazón: plan estratégico de investigación a diez años del NHLBI para lograr resultados basados en la evidencia
Larry H. Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN
4.2.3 Resultados mejorados para el tratamiento de las endofugas persistentes de tipo 2 tras la reparación endovascular de un aneurisma: embolización con pegamento Onyx
Larry H. Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN
4.2.4 Endarteriectomía carotídea (EAC) frente a colocación de stent en la arteria carótida (CAS): comparación de los criterios de alto riesgo de la CMMS en los resultados después de la cirugía. Análisis de los datos del registro vascular de la Sociedad de Cirugía Vascular (SVS)
Larry H. Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN
4.2.5 Efecto de las características hospitalarias en los resultados de la reparación endovascular de aneurismas de aorta descendente en la población estadounidense cubierta por Medicare
Larry H. Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN
4.2.6 Hipertensión y distensibilidad vascular: Frontera del pensamiento en 2013: el foco está en la elasticidad arterial
Justin D. Pearlman, MD, PhD, FACC and Aviva Lev-Ari, PhD, RN
4.2.7 Filosofía de la medicina preventiva: ejercicio frente a fármacos. Cuanto más de lo primero, menos de lo segundo
Aviva Lev-Ari, PhD, RN
4.2.8 Programas de cardiooncología y oncocardiología: tratamiento de pacientes con cáncer y antecedentes de enfermedades cardiovasculares
Aviva Lev-Ari, PhD, RN
Resumen – Cuarto volumen – Parte 1
Author and Curator: Larry H Bernstein, MD, FCAP and Curator: Aviva Lev-Ari, PhD, RN
Cuarto volumen – Segunda parte
Enfermedades cardiovasculares y medicina regenerativa
Introducción a la segunda parte
Enfermedades cardiovasculares y medicina regenerativa
Author: Larry H. Bernstein, MD. FCAP and Curator: Aviva Lev-Ari, PhD, RN
Capítulo 1: Células madre en las enfermedades cardiovasculares
1.1 Regeneración: sistema cardíaco (cardiomiogénesis) y vasculatura (angiogénesis)
https://pharmaceuticalintelligence.com/2014/01/15/regeneration-cardiac-system-and-vasculature/
Aviva Lev-Ari, PhD, RN
1.2 Contribuciones notables a la cardiología regenerativa por Richard T. Lee (laboratorio de Lee, parte I)
https://pharmaceuticalintelligence.com/2013/10/20/notable-contributions-to-regenerative-cardiology/
Larry H Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN
1.3 Contribuciones a las interacciones y la señalización de los cardiomiocitos (laboratorio de Lee, parte II)
Larry H Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN
1.4 Jmjd3 y diferenciación cardiovascular de las células madre embrionarias
Larry H Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN
1.5 Terapia con células madre para la arteriopatía coronaria (AC)
https://pharmaceuticalintelligence.com/2013/11/02/stem-cell-therapy-for-coronary-heart-disease/
Larry H. Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN
1.6 Trasplante intracoronario de células progenitoras tras un IM agudo
https://pharmaceuticalintelligence.com/2013/11/02/progenitor-cells-coronary-graft-after-ami/
Larry H. Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN
1.7 El trasplante de células progenitoras para el IM y la cardiogénesis (parte 1)
Larry H. Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN
1.8 Fuente de células madre para mejorar el miocardio dañado (parte 2)
Larry H. Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN
1.9 Efecto neoangiogénico del injerto de una armazón de colágeno tridimensional acelular en el miocardio (parte 3)
Larry H. Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN
1.10 Trasplante de células estromales derivadas del tejido adiposo humano modificadas que expresan VEGF165
Larry H. Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN
1.11 La matriz tridimensional de fibroblastos mejora la función del ventrículo izquierdo tras un IM
Larry H. Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN
Capítulo 2: Biología celular y molecular regenerativa
2.1 Células progenitoras endoteliales circulantes (CPEc) como biomarcadores
Larry H. Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN
2.2 Investigación con células madre. La frontera en el Technion de Israel
Aviva Lev-Ari, PhD, RN
2.3 El descubrimiento de las células madre generadoras de vasos sanguíneos
https://pharmaceuticalintelligence.com/2012/10/22/blood-vessel-generating-stem-cells-discovered/
Ritu Saxena, PhD
2.4 Renovación del corazón por los cardiomiocitos preexistentes: descubierta la fuente de crecimiento de nuevas células cardíacas
Aviva Lev-Ari, PhD, RN
2.5 El corazón: protección de la vasculatura. Tratamiento farmacológico conceptual con inclusión de una timosina
Aviva Lev-Ari, PhD, RN
2.6 Innovaciones en la bioinstrumentación para la medición de las células endoteliales progenitoras circulantes en la sangre humana.
Sudipta Saha, PhD
2.7 Diferenciación endotelial y morfogénesis de los precursores cardíacos
Sudipta Saha, PhD
Capítulo 3: Niveles terapéuticos en cardiología molecular
3.1 Los secretos de tus células. Descubre la inteligencia interior de tu cuerpo (Sounds True, a la venta el 1 de mayo de 2013) de Sondra Barrett
Aviva Lev-Ari, PhD, RN
3.2 Células progenitoras cardíacas derivadas de embriones humanos para la reparación del miocardio
Sudipta Saha, PhD
3.3 Reparación con CPi o células madre
3.3.1 Reprogramación celular en la reparación de tejidos
https://pharmaceuticalintelligence.com/2013/11/28/reprogramming-cell-in-tissue-repair/
Larry H Bernstein, MD, FCAP
3.3.2 La conversión de las células de la piel de los pacientes cardíacos en células sanas de músculo cardíaco
Aviva Lev-Ari, PhD, RN
3.4 Arteriogénesis y reparación cardíaca: dos biomateriales: timosina beta4 inyectable e hidrogel de matriz miocárdica
Aviva Lev-Ari, PhD, RN
3.5 Resultados cardiovasculares: función de las células progenitoras endoteliales circulantes (CPEc): exploración de la farmacoterapia dirigida al aumento endógeno de las CPEc
Aviva Lev-Ari, PhD, RN
3.6 El ciclo del calcio (bomba ATPasa) en la terapia génica cardíaca: terapia génica inhalable para la hipertensión arterial pulmonar e infusión intracoronaria percutánea para la insuficiencia cardíaca. Las aportaciones del Dr. Roger J. Hajjar
Aviva Lev-Ari, PhD, RN
Capítulo 4: Propuestas de investigación para el aumento endógeno de las células progenitoras endoteliales circulantes (cEPC)
4.1 Receptor activado por el proliferador de peroxisomas (PPAR-gamma). Activación de los receptores: transrepresión del PPARγ para la angiogénesis en las enfermedades cardiovasculares y transactivación del PPARγ para el tratamiento de la diabetes
Aviva Lev-Ari, PhD, RN
4.2 Resultados de ensayos clínicos acerca del sistema de la endotelina: función fisiopatológica en la insuficiencia cardíaca crónica, los síndromes coronarios agudos y el IM. ¿Marcador de la gravedad de la enfermedad o la determinación genética?
Aviva Lev-Ari, PhD, RN
4.3 Receptores de endotelina en las enfermedades cardiovasculares: el papel de la estimulación de la eNOS
Aviva Lev-Ari, PhD, RN
4.4 Inhibición de ET-1, ETA y ETA-ETB, inducción de la producción de óxido nítrico, estimulación de la eNOS y régimen de tratamiento con agonistas del PPAR-gamma (TZD): revisión bibliográfica sobre el aumento endógeno de las CPEe para reducir el riesgo cardiovascular
Aviva Lev-Ari, PhD, RN
4.5 Posicionamiento de un concepto terapéutico para el aumento endógeno de las CPEc: indicaciones terapéuticas en las enfermedades macrovasculares: coronarias, cerebrovasculares y periféricas
Aviva Lev-Ari, PhD, RN
4.6 Disfunción endotelial, disponibilidad disminuida de CPEc y aumento del riesgo de enfermedades macrovasculares: el potencial terapéutico de las CPEc
Aviva Lev-Ari, PhD, RN
4.7 Medicina y biología vascular: CLASIFICACIÓN DEL TRATAMIENTO DE ACCIÓN RÁPIDA PARA PACIENTES CON ALTO RIESGO DE EPISODIOS MACROVASCULARES. Enfermedad macrovascular y potencial terapéutico de las CPEc
Aviva Lev-Ari, PhD, RN
4.8 Las enfermedades cardiovasculares (ECV) y el papel de los fármacos alternativos en la activación de la óxido nítrico-sintasa endotelial (eNOS) y la producción de óxido nítrico
Aviva Lev-Ari, PhD, RN
4.9 Tratamiento basado en células residentes de la cardiopatía isquémica humana: evolución de los datos prometedores sobre la timosina beta4 para la reparación cardíaca
https://pharmaceuticalintelligence.com/2012/04/30/93/
Aviva Lev-Ari, PhD, RN
4.10 Enfermedades macrovasculares. Potencial terapéutico de las CPEc: métodos de reducción del riesgo CV
Aviva Lev-Ari, PhD, RN
4.11 Nebivolol genérico de Bystolic. Efecto positivo sobre el aumento endógeno de las células progenitoras endoteliales en circulación
Aviva Lev-Ari, PhD, RN
4.12 Vasculatura del corazón. Regeneración y protección del endotelio y el músculo liso de las arterias coronarias: tratamiento farmacológico conceptual mediante un régimen combinado de tres fármacos, incluida una TIMOSINA
Aviva Lev-Ari, PhD, RN
Resumen de la segunda parte
Autor: Larry H. Bernstein, MD. Miembro distinguido del Colegio de anatomopatólogos de los Estados Unidos
Epílogo del cuarto volumen
Larry H Bernstein, MD, FCAP, autor y editor, cuarto volumen, coeditor
Justin Pearlman, MD, PhD, FACC, consultor de contenidos para la Serie A: enfermedades cardiovasculares
Aviva Lev-Ari, PhD, RN, coeditora del cuarto volumen y redactora jefe de la serie electrónica BioMed
Medicina regenerativa y traslativa:
la promesa terapéutica para las enfermedades cardiovasculares
Regenerative and Translational Medicine
The Therapeutic Promise for Cardiovascular Diseases
en Amazon.com desde el 26/12/2015
2015
http://www.amazon.com/dp/B019UM909A
PART B: The eTOCs in Bi-lingual format:
Spanish and English in Text format
Serie A: libros electrónicos acerca de las enfermedades cardiovasculares
CUARTO VOLUMEN
Medicina regenerativa y Medicina traslativa
La promesa terapéutica para las
enfermedades cardiovasculares
(LIBRO 4 DE LA SERIE DE LIBROS ELECTRÓNICOS SOBRE BIOMEDICINA)
Traducción a español Montero Language Services
Disponible en Amazon.com desde el 26/12/2015
http://www.amazon.com/dp/B019UM909A
y
Leaders in Pharmaceutical Business Intelligence
avivalev-ari@alum.berkeley.edu
Redactora jefe
Series A: e-Books on Cardiovascular Diseases
VOLUME FOUR
Regenerative and Translational Medicine
The Therapeutic Promise for Cardiovascular Diseases
(BIOMED E-BOOKS BOOK 4)
Available on Amazon.com since 12/26/2015
2015
http://www.amazon.com/dp/B019UM909A
and
Leaders in Pharmaceutical Business Intelligence
avivalev-ari@alum.berkeley.edu
Editor-in-Chief
Indice de contenidos electrónico (IDCe)
electronic Table of Contents
Los enlaces indicados llevan al contenido original en inglés
| MD | Licenciado/a en medicina y cirugía (Estados Unidos) |
| PhD | Doctorado/a |
| RN | Enfermero/a titulado/a |
| FCAP | Miembro distinguido del Colegio de anatomopatólogos de los Estados Unidos |
| FACC | Miembro distinguido del Colegio de cardiólogos de los Estados Unidos |
Listado de colaboradores
List of Contributors
Justin D. Pearlman MD ME PhD MA FACC, Content Consultant to Series A: Cardiovascular Diseases
Part One
1.2, 4.1.6, 4.2.6
Epilogue to Volume Four
Larry H Bernstein, MD, FCAP, Volume Editor, Author and Article Curator
Part One:
Introduction, 1.0, 1.3, 2.1.1, 2.1.2, 2.1.3, 2.1.4, 2.1.5, 2.2.1, 2.2.2, 2.2.3, 2.2.4, 2.2.5, 2.2.6.1, 2.2.7.1, 2.2.7.2, 2.2.8, 2.3.1, 2.3.2, 2.3.3, 2.3.4, 2.3.5, 2.4.1, 2.4.2, 2.4.3, 2.4.4, 2.5.1, 2.5.2, 2.5.2.1, 2.5.4, 2.6.3, 2.6.7, 2.6.9, 2.7.1, 2.7.2, 2.7.3, 2.7.4, 2.7.5, 2.8.1, 2.8.2, 2.8.3, 2.8.4, 2.8.5, 2.8.8, 2.8.9, 3.1, 3.2, 3.3, 3.4, 3.5, 3.6, 3.8, 3.9, 3.10, 3.11, 4.1.1, 4.1.2, 4.1.3, 4.1.6, 4.2.1, 4.2.2, 4.2.3, 4.2.4, 4.2.5, Summary
Part Two:
Introduction, 1.2, 1.3, 1.4, 1.5, 1.6, 1.7, 1.8, 1.9, 1.10, 1.11, 2.1, 3.3.1, Summary
Epilogue to Volume Four
Aviva Lev-Ari, PhD, RN, Volume Editor, Article Curator, Editor-in-Chief, BioMed e-Series
Part One:
Introduction, 1.2, 1.4, 2.1.1, 2.1.2, 2.1.3, 2.1.4, 2.2.5, 2.2.8, 2.3.1, 2.3.2, 2.3.5, 2.5.5, 2.6.5, 2.6.10, 2.8.2, 2.8.6, 2.8.10, 3.7, 3.10, 3.11, 3.12, 4.1.2, 4.1.3, 4.1.4, 4.1.5, 4.1.6, 4.1.7, 4.2.2, 4.2.3, 4.2.4, 4.2.5, 4.2.6, 4.2.7, 4.2.8, Summary
Part Two:
Introduction, 1.1, 1.2, 1.3, 1.4, 1.5, 1.6, 1.7, 1.8, 1.9, 1.10, 1.11, 2.1, 2.2, 2.4, 2.5, 3.1, 3.3.2, 3.4, 3.5, 3.6, 4.1, 4.2, 4.3, 4.4, 4.5, 4.6, 4.7, 4.8, 4.9, 4.10, 4.11, 4.12
Epilogue to Volume Four
Ritu Saxena, PhD, Article Author & Curator
Part One:
2.8.7, 2.8.11
Part Two:
2.3
Sudipta Saha, PhD, Article Curator
Part One:
2.6.8
Part Two:
2.6, 2.7, 3.2
Dr. Demet Sag, Article Author & Curator
Part One:
2.6.1, 2.6.2
Dr. Stephen J Williams, Article Author & Curator
Part One:
2.2.8, 2.6.4, 2.7.6
Dr. Margaret Baker, Article Author & Curator
Part One:
2.6.6
Introducción al cuarto volumen
Introduction to Volume Four
Primera parte:
Enfermedades cardiovasculares, medicina traslativa (MT) y
post-MT
Part One:
Cardiovascular Diseases, Translational Medicine (TM) and Post TM
Introducción a la primera parte
Introduction to Part One
Enfermedades cardiovasculares, medicina traslativa (MT) y post-MT
Cardiovascular Diseases, Translational Medicine (TM) and Post TM
Author and Curator: Larry H Bernstein, MD, FCAP and Curator: Aviva Lev-Ari, PhD, RN
Capítulo 1: Conceptos de la medicina traslativa
Chapter 1: Translational Medicine Concepts
1.0 Modificación postraslativa de las proteínas
1.0 Post-Translational Modification of Proteins
https://pharmaceuticalintelligence.com/2014/04/21/posttranslational-modification-of-proteins/
Larry H Bernstein, MD, FCAP
1.1 Identificación de la ciencia traslativa dentro del triángulo de la biomedicina
1.1 Identifying Translational Science within the Triangle of Biomedicine
Griffin M Weber, Journal of Translational Medicine 2013, 11:126 (24 de mayo de 2013)
Griffin M Weber, Journal of Translational Medicine 2013, 11:126 (24 May 2013)
1.2 Estado de la cardiología con respecto al estrés parietal, la carga ventricular y la reserva contráctil del miocardio: aspectos de la medicina traslativa (MT)
1.2 State of Cardiology on Wall Stress, Ventricular Workload and Myocardial Contractile Reserve: Aspects of Translational Medicine (TM)
Justin Pearlman, MD, PhD, FACC and Aviva Lev-Ari, PhD, RN
1.3 Riesgo de sesgo en la ciencia traslativa
1.3 Risk of Bias in Translational Science
https://pharmaceuticalintelligence.com/2013/11/03/risk-of-bias-in-translational-science/
Larry H Bernstein, MD, FCAP
1.4 Biosimilares: creación y protección de la propiedad intelectual por parte del descubridor y de los fabricantes de biosimilares
1.4 Biosimilars: Intellectual Property Creation and Protection by Pioneer and by Biosimilar Manufacturers
Aviva Lev-Ari, PhD, RN
Capítulo 2: Causas y etiología de las enfermedades cardiovasculares. Enfoques traslativos para la medicina cardiotorácica
Chapter 2: Causes and the Etiology of Cardiovascular Diseases – Translational Approaches for Cardiothoracic Medicine
2.1 Genómica
2.1 Genomics
2.1.1 Clasificación basada en la genómica
2.1.1 Genomics-Based Classification
https://pharmaceuticalintelligence.com/2013/11/01/genomics-based-classification/
Larry H Bernstein, MD, FCAP y Aviva Lev-Ari, PhD, RN
2.1.2 Uso como diana de protooncogenes no utilizables como diana terapéutica
2.1.2 Targeting Untargetable Proto-Oncogenes
https://pharmaceuticalintelligence.com/2013/11/01/targeting-untargetable-proto-oncogenes/
Larry H Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN
2.1.3 Genoma consultable para el desarrollo de fármacos
2.1.3 Searchable Genome for Drug Development
https://pharmaceuticalintelligence.com/2013/12/01/searchable-genome-for-drug-development/
Larry H Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN
2.1.4 Herramienta de estudio del pez cebra
2.1.4 Zebrafish Study Tool
https://pharmaceuticalintelligence.com/2013/11/01/zebrafish-study-tool/
Larry H Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN
2.1.5 Ya se ha secuenciado la secuencia eucromática del genoma humano. ¿Qué viene a continuación?
2.1.5 What comes after finishing the Euchromatic Sequence of the Human Genome?
Larry H Bernstein, MD, FCAP
2.2 Proteómica
2.2 Proteomics
2.2.1 El papel de las proteínas de la unión estrecha en el transporte de agua y electrolitos
2.2.1 The Role of Tight Junction Proteins in Water and Electrolyte Transport
Larry H Bernstein, MD, FCAP
2.2.2 Conducción selectiva de iones
2.2.2 Selective Ion Conduction
https://pharmaceuticalintelligence.com/2013/10/07/selective-ion-conduction/
Larry H Bernstein, MD, FCAP
2.2.3 Investigación traslativa sobre el mecanismo de los movimientos de entrada de agua y electrolitos en la célula
2.2.3 Translational Research on the Mechanism of Water and Electrolyte Movements into the Cell
Larry H. Bernstein, MD, FACP
2.2.4 Inhibición de la cinasa específica de los cardiomiocitos TNNI3K. Estrés oxidativo
2.2.4 Inhibition of the Cardiomyocyte-Specific Kinase TNNI3K Oxidative Stress
Larry H Bernstein, MD, FCAP
Una cinasa específica de los cardiomiocitos limita la lesión por reperfusión
A cardiomyocyte-specific kinase limits reperfusion injury
2.2.5 Calcio/calmodulina-cinasa oxidada y fibrilación auricular
2.2.5 Oxidized Calcium Calmodulin Kinase and Atrial Fibrillation
Larry H. Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN
Papel del receptor acoplado a la proteína G con S-nitrosilación en el síndrome coronario agudo
Role of G-protein-coupled receptor with S-nitrosylation in acute coronary syndrome
2.2.6 La S-nitrosilación en la isquemia cardíaca y el síndrome coronario agudo
2.2.6 S-Nitrosylation in Cardiac Ischemia and Acute Coronary Syndrome
2.2.6.1 Señalización de la S-nitrosilación
2.2.6.1 S-nitrosylation signaling
https://pharmaceuticalintelligence.com/2014/04/21/s-nitrosylation-signaling/
Larry H Bernstein, MD, FCAP
2.2.7 Acetilación y desacetilación
2.2.7 Acetylation and Deacetylation
2.2.7.1 Histona-desacetilasa Sir2 (proteína de silenciamiento transcripcional y longevidad).
2.2.7.1 Transcriptional Silencing and Longevity Protein Sir2 histone deacetylase.
Larry H Bernstein, MD, FCAP
2.2.7.2 Acetilación y desacetilación de proteínas distintas de las histonas
2.2.7.2 Acetylation and Deacetylation of non-Histone Proteins
Larry H Bernstein, MD, FCAP
2.2.8 Inhibidores de la óxido nítrico-sintasa (NOS-I)
2.2.8 Nitric Oxide Synthase Inhibitors (NOS-I)
https://pharmaceuticalintelligence.com/2013/11/02/nitric-oxide-synthase-inhibitors/
Larry H Bernstein, MD, FCAP, Stephen J. Williams, PhD and Aviva Lev-Ari, PhD, RN
2.3 Señalización cardíaca y vascular
2.3 Cardiac and Vascular Signaling
2.3.1 La centralidad de la señalización del Ca(2+) y del citoesqueleto, con implicación de las calmodulina-cinasas y los receptores de rianodina, en la insuficiencia cardíaca, el músculo liso arterial y la arritmia postisquémica; similitudes, diferencias y dianas farmacéuticas
2.3.1 The Centrality of Ca(2+) Signaling and Cytoskeleton Involving Calmodulin Kinases and Ryanodine Receptors in Cardiac Failure, Arterial Smooth Muscle, Post-ischemic Arrhythmia, Similarities and Differences, and Pharmaceutical Targets
Larry H Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN
2.3.2 Señalización de la leptina en la mediación de la hipertrofia cardíaca asociada a la obesidad
2.3.2 Leptin Signaling in Mediating the Cardiac Hypertrophy associated with Obesity
Larry H Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN
2.3.3 Desencadenamiento de la ruptura de la placa de ateroma y la trombosis arterial
2.3.3 Triggering of Plaque Disruption and Arterial Thrombosis
Larry H Bernstein, MD, FCAP
2.3.4 Sensores y señalización en el estrés oxidativo
2.3.4 Sensors and Signaling in Oxidative Stress
https://pharmaceuticalintelligence.com/2013/11/01/sensors-and-signaling-in-oxidative-stress/
Larry H. Bernstein, MD, FCAP
2.3.5 Resistencia al receptor de tirosina-cinasa
2.3.5 Resistance to Receptor of Tyrosine Kinase
https://pharmaceuticalintelligence.com/2013/11/01/resistance-to-receptor-of-tyrosine-kinase/
Larry H. Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN
2.3.6 Gaston B. M. et al. (2003) Señalización de la S-nitrosilación en la biología celular. Mol Interv. 3, 253-63.
2.3.6 Gaston B. M. et al. (2003) S-nitrosylation signaling in cell biology. Mol Interv. 3, 253-63.
2.4 Interacción plaqueto-endotelial
2.4 Platelet Endothelial Interaction
2.4.1 Las plaquetas en la investigación traslativa. Parte 1
2.4.1 Platelets in Translational Research – Part 1
https://pharmaceuticalintelligence.com/2013/10/07/platelets-in-translational-research-1/
Larry H Bernstein, MD, FCAP
2.4.2 Las plaquetas en la investigación traslativa. 2: Descubrimiento de posibles dianas antiplaquetarias
2.4.2 Platelets in Translational Research 2: Discovery of Potential Anti-platelet Targets
https://pharmaceuticalintelligence.com/2013/10/07/platelets-in-translational-research-2/
Larry H. Bernstein, MD, FCAP
2.4.3 Consideraciones finales sobre el papel de las plaquetas y las reacciones plaqueto-endoteliales en la ateroesclerosis, y nuevos tratamientos
2.4.3 The Final Considerations of the Role of Platelets and Platelet Endothelial Reactions in Atherosclerosis and Novel Treatments
Larry H. Bernstein, MD, FCAP
2.4.4 Función endotelial y enfermedades cardiovasculares
2.4.4 Endothelial Function and Cardiovascular Disease
https://pharmaceuticalintelligence.com/2012/10/25/endothelial-function-and-cardiovascular-disease/
Larry H Bernstein, MD, FCAP
2.5 Modificaciones postraslativas (MPT)
2.5 Post-translational modifications (PTMs)
2.5.1 Modificaciones postraslativas
2.5.1 Post-Translational Modifications
https://pharmaceuticalintelligence.com/2014/04/21/posttranslational-modifications/
Larry H Bernstein, MD, FCAP
2.5.2. Análisis de las proteínas S-nitrosiladas
2.5.2. Analysis of S-nitrosylated Proteins
https://pharmaceuticalintelligence.com/2014/04/21/analysis-of-s-nitrosylated-proteins/
Larry H Bernstein, MD, FCAP
2.5.2.1 Análisis de las proteínas S-nitrosiladas: cambio de biotina sin detergente combinado con cromatografía líquida/espectrometría de masas en tándem
2.5.2.1 Analysis of S-nitrosylated Proteins: Detergent-free biotin switch combined with liquid chromatography/tandem mass spectrometry
Larry H Bernstein, MD, FACP
2.5.3 Mecanismos de la enfermedad: transducción de señales. Akt fosforila a HK-II en Thr-473 y aumenta la asociación mitocondrial de HK-II para proteger a los cardiomiocitos. David J. Roberts, Valerie P. Tan-Sah, Jeffery M. Smith and Shigeki Miyamoto, J. Biol. Chem. 2013, 288:23798-23806.
2.5.3 Mechanisms of Disease: Signal Transduction – Akt Phosphorylates HK-II at Thr-473 and Increases Mitochondrial HK-II Association to Protect Cardiomyocytes, David J. Roberts, Valerie P. Tan-Sah, Jeffery M. Smith and Shigeki Miyamoto, J. Biol. Chem. 2013, 288:23798-23806.
http://dx.doi.org/10.1074/jbc.M113.482026
2.5.4 Acetilación y desacetilación de proteínas no histónicas
2.5.4 Acetylation and Deacetylation of non-Histone Proteins
Larry H Bernstein, MD, FCAP
2.5.5 Un estudio descubre regiones de baja metilación propensas a presentar mutaciones estructurales
2.5.5 Study Finds Low Methylation Regions Prone to Structural Mutation
Aviva Lev-Ari, PhD, RN
2.6 Epigenética y ARN largos no codificantes (ARNlnc)
2.6 Epigenetics and Long non-coding RNAs (lncRNAs)
2.6.1 La magia de la caja de Pandora: epigenética y pluripotencialidad con los ARN largos no codificantes (ARNlnc)
2.6.1 The Magic of the Pandora’s Box: Epigenetics and Stemness with Long non-coding RNAs (lincRNA)
Demet Sag, Ph.D., CRA, GCP
2.6.2 “El SILENCIO de los corderos”. Presentación del poder del ARN no codificado
2.6.2 “The SILENCE of the Lambs” Introducing The Power of Uncoded RNA
Demet Sag, Ph.D., CRA, GCP
2.6.3 La red de ARN largos no codificantes regula la transcripción de PTEN
2.6.3 Long Noncoding RNA Network regulates PTEN Transcription
Larry H Bernstein, MD, FACP
2.6.4 Cómo promueven el cáncer los elementos móviles del ADN “basura”. Parte 1: tumorigénesis mediada por transposones
2.6.4 How Mobile Elements in “Junk” DNA Promote Cancer – Part 1: Transposon-mediated Tumorigenesis
Stephen J. Williams, Ph.D.
2.6.5 La terapia génica mediada por transposones mejora la hemodinámica pulmonar y atenúa la hipertrofia de ventrículo derecho: la terapia génica con eNOS reduce la remodelación vascular pulmonar y la hiperplasia de la pared arterial
2.6.5 Transposon-mediated Gene Therapy improves Pulmonary Hemodynamics and attenuates Right Ventricular Hypertrophy: eNOS gene therapy reduces Pulmonary vascular remodeling and Arterial Wall hyperplasia
Aviva Lev-Ari, PhD, RN
2.6.6 El ADN basura codifica valiosos miARN: el ADN no codificante controla la diabetes
2.6.6 Junk DNA codes for valuable miRNAs: non-coding DNA controls Diabetes
https://pharmaceuticalintelligence.com/2012/09/24/junk-dna-codes-for-valuable-mirnas/
Margaret Baker, PhD, Registered Patent Agent
2.6.7 Nucleasas dirigidas
2.6.7 Targeted Nucleases
https://pharmaceuticalintelligence.com/2013/03/02/targeted-nucleases/
Larry H Bernstein, MD, FACP
2.6.8 La aparición tardía de la enfermedad de Alzheimer y el metabolismo monocarbonado
2.6.8 Late Onset of Alzheimer’s Disease and One-carbon Metabolism
https://pharmaceuticalintelligence.com/2013/05/06/alzheimers-disease-and-one-carbon-metabolism/
Dr. Sudipta Saha
2.6.9 Amiloidosis con miocardiopatía
2.6.9 Amyloidosis with Cardiomyopathy
https://pharmaceuticalintelligence.com/2013/03/31/amyloidosis-with-cardiomyopathy/
Larry H Bernstein, MD, FACP
2.6.10 ARN largos no codificantes: reguladores moleculares del destino celular. Conferencia de la profesora Laurie Boyer en el MIT – Simposio de verano 2014: Biología del ARN, cáncer e implicaciones terapéuticas, 13 de junio de 2014, Instituto Koch @MIT http://ki.mit.edu/news/symposium
2.6.10 Long non-coding RNAs: Molecular Regulators of Cell Fate – Lecture by Prof. Laurie Boyer @MIT – Summer Symposium 2014: RNA Biology, Cancer and Therapeutic Implications, June 13, 2014, Koch Institute @MIT http://ki.mit.edu/news/symposium
Conference Reporter: Aviva Lev-Ari, PhD, RN
2.7 Metabolómica
2.7 Metabolomics
2.7.1 Ampliación del alfabeto genético y vinculación del genoma con el metaboloma
2.7.1 Expanding the Genetic Alphabet and Linking the Genome to the Metabolome
Larry Bernstein, MD, FCAP
2.7.2 Cómo causa hiperhomocisteinemia el desequilibrio de la metionina con insuficiencia de azufre
2.7.2 How Methionine Imbalance with Sulfur-Insufficiency Leads to Hyperhomocysteinemia
https://pharmaceuticalintelligence.com/2013/04/04/sulfur-deficiency-leads_to_hyperhomocysteinemia/
Larry H Bernstein, MD, FACP
2.7.3 Una segunda mirada al enigma inflamatorio de la nutrición y la transtiretina
2.7.3 A Second Look at the Transthyretin Nutrition Inflammatory Conundrum
Larry H. Bernstein, MD, FACP
2.7.4 Transtiretina y masa corporal magra en estado estable y de estrés
2.7.4 Transthyretin and Lean Body Mass in Stable and Stressed State
Larry Bernstein, MD, FCAP
2.7.5 Interacción de la hiperhomocisteinemia con la proteína C y aumento del riesgo trombótico
2.7.5 Hyperhomocysteinemia interaction with Protein C and Increased Thrombotic Risk
https://pharmaceuticalintelligence.com/2013-12-3/larryhbern/Hyperhomocysteinemia
Larry H Bernstein, MD, FCAP
2.7.6 Cómo decir NO al riesgo cardíaco
2.7.6 Telling NO to Cardiac Risk
https://pharmaceuticalintelligence.com/2012/12/10/telling-no-to-cardiac-risk/
Stephen J. Williams, PhD
2.8 Mitocondrias y estrés oxidativo
2.8 Mitochondria and Oxidative Stress
2.8.1 Reversión de la disfunción mitocondrial cardíaca
2.8.1 Reversal of Cardiac Mitochondrial Dysfunction
https://pharmaceuticalintelligence.com/2013/04/14/reversal-of-cardiac-mitochondrial-dysfunction/
Larry H. Bernstein, MD, FCAP
2.8.2 Señalización del calcio, mitocondrias cardíacas y síndrome metabólico
2.8.2 Calcium Signaling, Cardiac Mitochondria and Metabolic Syndrome
Larry H. Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN
2.8.3 Disfunción mitocondrial y trastornos cardíacos
2.8.3 Mitochondrial Dysfunction and Cardiac Disorders
https://pharmaceuticalintelligence.com/2013/04/14/mitochondrial-dysfunction-and-cardiac-disorders/
Larry H. Bernstein, MD, FCAP
2.8.4 Metabolismo mitocondrial y función cardíaca
2.8.4 Mitochondrial Metabolism and Cardiac Function
https://pharmaceuticalintelligence.com/2013/04/14/mitochondrial-metabolism-and-cardiac-function/
Larry H. Bernstein, MD, FCAP
2.8.5 Las mitocondrias y las enfermedades cardiovasculares: homenaje a Richard Bing
2.8.5 Mitochondria and Cardiovascular Disease: A Tribute to Richard Bing
https://pharmaceuticalintelligence.com/2013/04/14/chapter-5-mitochondria-and-cardiovascular-disease/
Larry H. Bernstein, MD, FCAP
2.8.6 Científicos del MIT y proteómica: identificadas todas las proteínas de la matriz mitocondrial
2.8.6 MIT Scientists on Proteomics: All the Proteins in the Mitochondrial Matrix Identified
Aviva Lev-Ari, PhD, RN
2.8.7 La dinámica mitocondrial y enfermedades cardiovasculares
2.8.7 Mitochondrial Dynamics and Cardiovascular Diseases
Ritu Saxena, Ph.D.
2.8.8 Daño y reparación mitocondrial bajo estrés oxidativo
2.8.8 Mitochondrial Damage and Repair under Oxidative Stress
Larry H Bernstein, MD, FCAP
2.8.9 El óxido nítrico tiene un papel omnipresente en la regulación de la glucólisis, con la consiguiente influencia en la función mitocondrial
2.8.9 Nitric Oxide has a Ubiquitous Role in the Regulation of Glycolysis -with a Concomitant Influence on Mitochondrial Function
Larry H. Bernstein, MD, FACP
2.8.10 Mecanismos patogénicos mitocondriales en la diabetes mellitus
2.8.10 Mitochondrial Mechanisms of Disease in Diabetes Mellitus
Aviva Lev-Ari, PhD, RN
2.8.11 Disfunción mitocondrial y enfermedades cardiovasculares. Las mitocondrias: no solo son la “central energética de la célula”
2.8.11 Mitochondria Dysfunction and Cardiovascular Disease – Mitochondria: More than just the “Powerhouse of the Cell”
Ritu Saxena, PhD
Capítulo 3: Riesgos y biomarcadores del diagnóstico y el pronóstico en la medicina cardiotorácica traslativa
Chapter 3: Risks and Biomarkers for Diagnosis and Prognosis in Translational Cardiothoracic Medicine
3.1 Biomarcadores, diagnóstico y tratamiento: presente y futuro de los biomarcadores
3.1 Biomarkers, Diagnosis and Management: Biomarkers, Present and Future
https://pharmaceuticalintelligence.com/2013/11/10/biomarkers-diagnosis-and-management/
Larry Bernstein, MD, FCAP
3.2 Panorama de los biomarcadores cardíacos para una mejor utilización clínica
3.2 Landscape of Cardiac Biomarkers for Improved Clinical Utilization
Larry H Bernstein, MD, FCAP
3.3 Lograr la automatización de la serología: nueva frontera de las prácticas óptimas
3.3 Achieving Automation in Serology: A New Frontier in Best Practices
Larry H Bernstein, MD, FCAP
3.4 Identificación y tratamiento precisos de los episodios cardíacos urgentes
3.4 Accurate Identification and Treatment of Emergent Cardiac Events
Larry Bernstein, MD, FCAP
3.5 Importancia de la troponina I como marcador pronóstico en la insuficiencia cardíaca aguda descompensada (ICAD)
3.5 Prognostic Marker Importance of Troponin I in Acute Decompensated Heart Failure (ADHF)
https://pharmaceuticalintelligence.com/2013/06/30/troponin-i-in-acute-decompensated-heart-failure/
Larry H Bernstein, MD, FCAP
3.6 Análisis de troponina cardíaca de alta sensibilidad. Preparando a los Estados Unidos para los análisis de troponina cardíaca de alta sensibilidad
3.6 High-Sensitivity Cardiac Troponin Assays Preparing the United States for High-Sensitivity Cardiac Troponin Assays
https://pharmaceuticalintelligence.com/2013/06/13/high-sensitivity-cardiac-troponin-assays/
Larry Bernstein, MD, FCAP
3.7 Voces de la Clínica Cleveland sobre la apoA1 circulante: biomarcador de proceso proaterogénico en la pared arterial
3.7 Voices from the Cleveland Clinic On Circulating apoA1: A Biomarker for a Proatherogenic Process in the Artery Wall
Aviva Lev-Ari, PhD, RN
3.8 Desencadenamiento de la ruptura de la placa de ateroma y la trombosis arterial
3.8 Triggering of Plaque Disruption and Arterial Thrombosis
Larry H Bernstein, MD, FCAP
3.9 Descubierta la relación entre adiposidad y consumo elevado de fructosa
3.9 Relationship between Adiposity and High Fructose Intake Revealed
Larry Bernstein, MD, FCAP
3.10 El síndrome cardio-renal (SCR) en la insuficiencia cardíaca (IC)
3.10 The Cardio-Renal Syndrome (CRS) in Heart Failure (HF)
https://pharmaceuticalintelligence.com/2013/06/30/the-cardiorenal-syndrome-in-heart-failure/
Larry H. Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN
3.11 Aneuploidía y carcinogénesis
3.11 Aneuploidy and Carcinogenesis
https://pharmaceuticalintelligence.com/2013/10/31/aneuploidy-and-carcinogenesis/
Larry H. Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN
3.12 “La muerte súbita cardíaca”, SudD, está en la serie de pruebas genéticas cardiovasculares de Ferrer inCode que se comercializarán en EE. UU.
3.12 “Sudden Cardiac Death,” SudD is in Ferrer inCode’s Suite of Cardiovascular Genetic Tests to be Commercialized in the US
Aviva Lev-Ari, PhD, RN
Capítulo 4: Aspectos terapéuticos en la medicina cardiotorácica traslativa
Chapter 4: Therapeutic Aspects in Translational Cardiothoracic Medicine
4.1 Cardiología molecular y celular
4.1 Molecular and Cellular Cardiology
4.1.1 Los antagonistas de αllbβ3 como ejemplo de agentes terapéuticos de la medicina traslativa
4.1.1 αllbβ3 Antagonists As An Example of Translational Medicine Therapeutics
Larry H Bernstein, MD, FCAP
4.1.2 La matriz tridimensional de fibroblastos mejora la función del ventrículo izquierdo tras un IM
4.1.2 Three-Dimensional Fibroblast Matrix Improves Left Ventricular Function post MI
Larry H. Bernstein, MD. FCAP and Aviva Lev-Ari, PhD, RN
4.1.3 Tecnología de los biomateriales: modelos de ingeniería tisular para la reperfusión y dispositivos implantables para la revascularización
4.1.3 Biomaterials Technology: Models of Tissue Engineering for Reperfusion and Implantable Devices for Revascularization
https://pharmaceuticalintelligence.com/2013/05/05/bioengineering-of-vascular-and-tissue-models/
Larry H Bernstein, MD, FACP and Aviva Lev-Ari, PhD, RN
4.1.4 Ensayo clínico aleatorizado CELLWAVE: modesta mejora de la FEVI a los 4 meses. “Administración intracoronaria de CMO facilitada por ondas de choque” frente al “tratamiento solo con ondas de choque”
4.1.4 CELLWAVE Randomized Clinical Trial: Modest improvement in LVEF at 4 months “Shock wave facilitated intracoronary administration of BMCs” vs “Shock wave treatment alone”
Aviva Lev-Ari, PhD, RN
4.1.5 Prostaciclina y óxido nítrico: aventuras de la biología vascular, la historia de dos mediadores
4.1.5 Prostacyclin and Nitric Oxide: Adventures in Vascular Biology – a Tale of Two Mediators
Aviva Lev-Ari, PhD, RN
4.1.6 Contractilidad cardíaca y función miocárdica: arritmias ventriculares e insuficiencia cardíaca no isquémica. Implicaciones terapéuticas de la rianodinopatía (disfunción contráctil relacionada con la liberación de calcio) y respuestas de catecolaminas. Parte VII
4.1.6 Cardiac Contractility & Myocardium Performance: Ventricular Arrhythmias and Non-ischemic Heart Failure – Therapeutic Implications for Cardiomyocyte Ryanopathy (Calcium Release-related Contractile Dysfunction) and Catecholamine Responses – Part VII
Justin Pearlman, MD, PhD, FACC, Larry H Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN
4.1.7 Publicaciones sobre la insuficiencia cardíaca del profesor William Gregory Stevenson, M.D., BWH
4.1.7 Publications on Heart Failure by Prof. William Gregory Stevenson, M.D., BWH
Aviva Lev-Ari, PhD, RN
4.2 Cardiología Intervencionista y cirugía cardíaca. Soporte circulatorio mecánico y reparación vascular
4.2 Interventional Cardiology and Cardiac Surgery – Mechanical Circulatory Support and Vascular Repair
4.2.1 Sistema de soporte circulatorio mecánico, DAVI, DAVD, biventricular como puente al trasplante cardíaco o como “terapia de destino”: opciones para los pacientes con insuficiencia cardíaca avanzada
4.2.1 Mechanical Circulatory Support System, LVAD, RVAD, Biventricular as a Bridge to Heart Transplantation or as “Destination Therapy”: Options for Patients in Advanced Heart Failure
https://pharmaceuticalintelligence.com/2013/06/30/advanced-heart-failure/
Larry H. Bernstein, MD, FACP
4.2.2 Trasplante de corazón: plan estratégico de investigación a diez años del NHLBI para lograr resultados basados en la evidencia
4.2.2 Heart Transplantation: NHLBI’s Ten Year Strategic Research Plan to Achieving Evidence-based Outcomes
Larry H. Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN
4.2.3 Resultados mejorados para el tratamiento de las endofugas persistentes de tipo 2 tras la reparación endovascular de un aneurisma: embolización con pegamento Onyx
4.2.3 Improved Results for Treatment of Persistent type 2 Endoleak after Endovascular Aneurysm Repair: Onyx Glue Embolization
Larry H. Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN
4.2.4 Endarteriectomía carotídea (EAC) frente a colocación de stent en la arteria carótida (CAS): comparación de los criterios de alto riesgo de la CMMS en los resultados después de la cirugía. Análisis de los datos del registro vascular de la Sociedad de Cirugía Vascular (SVS)
4.2.4 Carotid Endarterectomy (CEA) vs. Carotid Artery Stenting (CAS): Comparison of CMMS high-risk criteria on the Outcomes after Surgery: Analysis of the Society for Vascular Surgery (SVS) Vascular Registry Data
Larry H. Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN
4.2.5 Efecto de las características hospitalarias en los resultados de la reparación endovascular de aneurismas de aorta descendente en la población estadounidense cubierta por Medicare
4.2.5 Effect of Hospital Characteristics on Outcomes of Endovascular Repair of Descending Aortic Aneurysms in US Medicare Population
Larry H. Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN
4.2.6 Hipertensión y distensibilidad vascular: Frontera del pensamiento en 2013: el foco está en la elasticidad arterial
4.2.6 Hypertension and Vascular Compliance: 2013 Thought Frontier – An Arterial Elasticity Focus
Justin D. Pearlman, MD, PhD, FACC and Aviva Lev-Ari, PhD, RN
4.2.7 Filosofía de la medicina preventiva: ejercicio frente a fármacos. Cuanto más de lo primero, menos de lo segundo
4.2.7 Preventive Medicine Philosophy: Excercise vs. Drug, IF More of the First THEN Less of the Second
Aviva Lev-Ari, PhD, RN
4.2.8 Programas de cardiooncología y oncocardiología: tratamiento de pacientes con cáncer y antecedentes de enfermedades cardiovasculares
4.2.8 Cardio-oncology and Onco-Cardiology Programs: Treatments for Cancer Patients with a History of Cardiovascular Disease
Aviva Lev-Ari, PhD, RN
Resumen – Cuarto volumen – Parte 1
Summary – Volume Four – Part 1
Author and Curator: Larry H Bernstein, MD, FCAP and Curator: Aviva Lev-Ari, PhD, RN
Cuarto volumen – Segunda parte
Enfermedades cardiovasculares y medicina regenerativa
Volume Four – Part Two
Cardiovascular Diseases and Regenerative Medicine
Introducción a la segunda parte
Introduction to Part Two
Enfermedades cardiovasculares y medicina regenerativa
Cardiovascular Diseases and Regenerative Medicine
Author: Larry H. Bernstein, MD. FCAP and Curator: Aviva Lev-Ari, PhD, RN
Capítulo 1: Células madre en las enfermedades cardiovasculares
Chapter 1: Stem Cells in Cardiovascular Diseases
1.1 Regeneración: sistema cardíaco (cardiomiogénesis) y vasculatura (angiogénesis)
1.1 Regeneration: Cardiac System (cardiomyogenesis) and Vasculature (angiogenesis)
https://pharmaceuticalintelligence.com/2014/01/15/regeneration-cardiac-system-and-vasculature/
Aviva Lev-Ari, PhD, RN
1.2 Contribuciones notables a la cardiología regenerativa por Richard T. Lee (laboratorio de Lee, parte I)
1.2 Notable Contributions to Regenerative Cardiology by Richard T. Lee (Lee’s Lab, Part I)
https://pharmaceuticalintelligence.com/2013/10/20/notable-contributions-to-regenerative-cardiology/
Larry H Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN
1.3 Contribuciones a las interacciones y la señalización de los cardiomiocitos (laboratorio de Lee, parte II)
1.3 Contributions to Cardiomyocyte Interactions and Signaling (Lee’s Lab, Part II)
Larry H Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN
1.4 Jmjd3 y diferenciación cardiovascular de las células madre embrionarias
1.4 Jmjd3 and Cardiovascular Differentiation of Embryonic Stem Cells
Larry H Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN
1.5 Terapia con células madre para la arteriopatía coronaria (AC)
1.5 Stem Cell Therapy for Coronary Artery Disease (CAD)
https://pharmaceuticalintelligence.com/2013/11/02/stem-cell-therapy-for-coronary-heart-disease/
Larry H. Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN
1.6 Trasplante intracoronario de células progenitoras tras un IM agudo
1.6 Intracoronary Transplantation of Progenitor Cells after Acute MI
https://pharmaceuticalintelligence.com/2013/11/02/progenitor-cells-coronary-graft-after-ami/
Larry H. Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN
1.7 El trasplante de células progenitoras para el IM y la cardiogénesis (parte 1)
1.7 Progenitor Cell Transplant for MI and Cardiogenesis (Part 1)
Larry H. Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN
1.8 Fuente de células madre para mejorar el miocardio dañado (parte 2)
1.8 Source of Stem Cells to Ameliorate Damage Myocardium (Part 2)
Larry H. Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN
1.9 Efecto neoangiogénico del injerto de una armazón de colágeno tridimensional acelular en el miocardio (parte 3)
1.9 Neoangiogenic Effect of Grafting an Acellular 3-Dimensional Collagen Scaffold Onto Myocardium (Part 3)
Larry H. Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN
1.10 Trasplante de células estromales derivadas del tejido adiposo humano modificadas que expresan VEGF165
1.10 Transplantation of Modified Human Adipose Derived Stromal Cells Expressing VEGF165
Larry H. Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN
1.11 La matriz tridimensional de fibroblastos mejora la función del ventrículo izquierdo tras un IM
1.11 Three-Dimensional Fibroblast Matrix Improves Left Ventricular Function Post MI
Larry H. Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN
Capítulo 2: Biología celular y molecular regenerativa
Chapter 2: Regenerative Cell and Molecular Biology
2.1 Células progenitoras endoteliales circulantes (CPEc) como biomarcadores
2.1 Circulating Endothelial Progenitors Cells (cEPCs) as Biomarkers
Larry H. Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN
2.2 Investigación con células madre. La frontera en el Technion de Israel
2.2 Stem Cell Research — The Frontier at the Technion in Israel
Aviva Lev-Ari, PhD, RN
2.3 El descubrimiento de las células madre generadoras de vasos sanguíneos
2.3 Blood vessel-generating stem cells discovered
https://pharmaceuticalintelligence.com/2012/10/22/blood-vessel-generating-stem-cells-discovered/
Ritu Saxena, PhD
2.4 Renovación del corazón por los cardiomiocitos preexistentes: descubierta la fuente de crecimiento de nuevas células cardíacas
2.4 Heart Renewal by pre-existing Cardiomyocytes: Source of New Heart Cell Growth Discovered
Aviva Lev-Ari, PhD, RN
2.5 El corazón: protección de la vasculatura. Tratamiento farmacológico conceptual con inclusión de una timosina
2.5 The Heart: Vasculature Protection – A Concept-based Pharmacological Therapy including THYMOSIN
Aviva Lev-Ari, PhD, RN
2.6 Innovaciones en la bioinstrumentación para la medición de las células endoteliales progenitoras circulantes en la sangre humana.
2.6 Innovations in Bio instrumentation for Measurement of Circulating Progenetor Endothelial Cells in Human Blood.
Sudipta Saha, PhD
2.7 Diferenciación endotelial y morfogénesis de los precursores cardíacos
2.7 Endothelial Differentiation and Morphogenesis of Cardiac Precursor
Sudipta Saha, PhD
Capítulo 3: Niveles terapéuticos en cardiología molecular
Chapter 3: Therapeutics Levels in Molecular Cardiology
3.1 Los secretos de tus células. Descubre la inteligencia interior de tu cuerpo (Sounds True, a la venta el 1 de mayo de 2013) de Sondra Barrett
3.1 Secrets of Your Cells: Discovering Your Body’s Inner Intelligence (Sounds True, on sale May 1, 2013) by Sondra Barrett
Aviva Lev-Ari, PhD, RN
3.2 Células progenitoras cardíacas derivadas de embriones humanos para la reparación del miocardio
3.2 Human Embryonic-Derived Cardiac Progenitor Cells for Myocardial Repair
Sudipta Saha, PhD
3.3 Reparación con CPi o células madre
3.3 Repair using iPPCs or Stem Cells
3.3.1 Reprogramación celular en la reparación de tejidos
3.3.1 Reprogramming cell in Tissue Repair
https://pharmaceuticalintelligence.com/2013/11/28/reprogramming-cell-in-tissue-repair/
Larry H Bernstein, MD, FCAP
3.3.2 La conversión de las células de la piel de los pacientes cardíacos en células sanas de músculo cardíaco
3.3.2 Heart patients’ skin cells turned into healthy heart muscle cells
Aviva Lev-Ari, PhD, RN
3.4 Arteriogénesis y reparación cardíaca: dos biomateriales: timosina beta4 inyectable e hidrogel de matriz miocárdica
3.4 Arteriogenesis and Cardiac Repair: Two Biomaterials – Injectable Thymosin beta4 and Myocardial Matrix Hydrogel
Aviva Lev-Ari, PhD, RN
3.5 Resultados cardiovasculares: función de las células progenitoras endoteliales circulantes (CPEc): exploración de la farmacoterapia dirigida al aumento endógeno de las CPEc
3.5 Cardiovascular Outcomes: Function of circulating Endothelial Progenitor Cells (cEPCs): Exploring Pharmaco-therapy targeted at Endogenous Augmentation of cEPCs
Aviva Lev-Ari, PhD, RN
3.6 El ciclo del calcio (bomba ATPasa) en la terapia génica cardíaca: terapia génica inhalable para la hipertensión arterial pulmonar e infusión intracoronaria percutánea para la insuficiencia cardíaca. Las aportaciones del Dr. Roger J. Hajjar
3.6 Calcium Cycling (ATPase Pump) in Cardiac Gene Therapy: Inhalable Gene Therapy for Pulmonary Arterial Hypertension and Percutaneous Intra-coronary Artery Infusion for Heart Failure: Contributions by Roger J. Hajjar, MD
Aviva Lev-Ari, PhD, RN
Capítulo 4: Propuestas de investigación para el aumento endógeno de las células progenitoras endoteliales circulantes (cEPC)
Chapter 4: Research Proposals for Endogenous Augmentation of circulating Endothelial Progenitor Cells (cEPCs)
4.1 Receptor activado por el proliferador de peroxisomas (PPAR-gamma). Activación de los receptores: transrepresión del PPARγ para la angiogénesis en las enfermedades cardiovasculares y transactivación del PPARγ para el tratamiento de la diabetes
4.1 Peroxisome proliferator-activated receptor (PPAR-gamma) Receptors Activation: PPARγ transrepression for Angiogenesis in Cardiovascular Disease and PPARγ transactivation for Treatment of Diabetes
Aviva Lev-Ari, PhD, RN
4.2 Resultados de ensayos clínicos acerca del sistema de la endotelina: función fisiopatológica en la insuficiencia cardíaca crónica, los síndromes coronarios agudos y el IM. ¿Marcador de la gravedad de la enfermedad o la determinación genética?
4.2 Clinical Trials Results for Endothelin System: Pathophysiological role in Chronic Heart Failure, Acute Coronary Syndromes and MI – Marker of Disease Severity or Genetic Determination?
Aviva Lev-Ari, PhD, RN
4.3 Receptores de endotelina en las enfermedades cardiovasculares: el papel de la estimulación de la eNOS
4.3 Endothelin Receptors in Cardiovascular Diseases: The Role of eNOS Stimulation
Aviva Lev-Ari, PhD, RN
4.4 Inhibición de ET-1, ETA y ETA-ETB, inducción de la producción de óxido nítrico, estimulación de la eNOS y régimen de tratamiento con agonistas del PPAR-gamma (TZD): revisión bibliográfica sobre el aumento endógeno de las CPEe para reducir el riesgo cardiovascular
4.4 Inhibition of ET-1, ETA and ETA-ETB, Induction of NO production, stimulation of eNOS and Treatment Regime with PPAR-gamma agonists (TZD): cEPCs Endogenous Augmentation for Cardiovascular Risk Reduction – A Bibliography
Aviva Lev-Ari, PhD, RN
4.5 Posicionamiento de un concepto terapéutico para el aumento endógeno de las CPEc: indicaciones terapéuticas en las enfermedades macrovasculares: coronarias, cerebrovasculares y periféricas
4.5 Positioning a Therapeutic Concept for Endogenous Augmentation of cEPCs — Therapeutic Indications for Macrovascular Disease: Coronary, Cerebrovascular and Peripheral
Aviva Lev-Ari, PhD, RN
4.6 Disfunción endotelial, disponibilidad disminuida de CPEc y aumento del riesgo de enfermedades macrovasculares: el potencial terapéutico de las CPEc
4.6 Endothelial Dysfunction, Diminished Availability of cEPCs, Increasing CVD Risk for Macrovascular Disease – Therapeutic Potential of cEPCs
Aviva Lev-Ari, PhD, RN
4.7 Medicina y biología vascular: CLASIFICACIÓN DEL TRATAMIENTO DE ACCIÓN RÁPIDA PARA PACIENTES CON ALTO RIESGO DE EPISODIOS MACROVASCULARES. Enfermedad macrovascular y potencial terapéutico de las CPEc
4.7 Vascular Medicine and Biology: CLASSIFICATION OF FAST ACTING THERAPY FOR PATIENTS AT HIGH RISK FOR MACROVASCULAR EVENTS Macrovascular Disease – Therapeutic Potential of cEPCs
Aviva Lev-Ari, PhD, RN
4.8 Las enfermedades cardiovasculares (ECV) y el papel de los fármacos alternativos en la activación de la óxido nítrico-sintasa endotelial (eNOS) y la producción de óxido nítrico
4.8 Cardiovascular Disease (CVD) and the Role of agent alternatives in endothelial Nitric Oxide Synthase (eNOS) Activation and Nitric Oxide Production
Aviva Lev-Ari, PhD, RN
4.9 Tratamiento basado en células residentes de la cardiopatía isquémica humana: evolución de los datos prometedores sobre la timosina beta4 para la reparación cardíaca
4.9 Resident-cell-based Therapy in Human Ischaemic Heart Disease: Evolution in the PROMISE of Thymosin beta4 for Cardiac Repair
https://pharmaceuticalintelligence.com/2012/04/30/93/
Aviva Lev-Ari, PhD, RN
4.10 Enfermedades macrovasculares. Potencial terapéutico de las CPEc: métodos de reducción del riesgo CV
4.10 Macrovascular Disease – Therapeutic Potential of cEPCs: Reduction Methods for CV Risk
Aviva Lev-Ari, PhD, RN
4.11 Nebivolol genérico de Bystolic. Efecto positivo sobre el aumento endógeno de las células progenitoras endoteliales en circulación
4.11 Bystolic’s generic Nebivolol – positive effect on circulating Endothelial Proginetor Cells endogenous augmentation
Aviva Lev-Ari, PhD, RN
4.12 Vasculatura del corazón. Regeneración y protección del endotelio y el músculo liso de las arterias coronarias: tratamiento farmacológico conceptual mediante un régimen combinado de tres fármacos, incluida una TIMOSINA
4.12 Heart Vasculature – Regeneration and Protection of Coronary Artery Endothelium and Smooth Muscle: A Concept-based Pharmacological Therapy of a Combination Three Drug Regimen including THYMOSIN
Aviva Lev-Ari, PhD, RN
Resumen de la segunda parte
Summary to Part Two
Autor: Larry H. Bernstein, MD. Miembro distinguido del Colegio de anatomopatólogos de los Estados Unidos
Author: Larry H. Bernstein, MD. FCAP
Epílogo del cuarto volumen
Epilogue to Volume Four
Larry H Bernstein, MD, FCAP, autor y editor, cuarto volumen, coeditor
Larry H Bernstein, MD, FCAP, Author and Curator, Volume Four, Co-Editor
Justin Pearlman, MD, PhD, FACC, consultor de contenidos para la Serie A: enfermedades cardiovasculares
Justin Pearlman, MD, PhD, FACC, Content Consultant for Series A: Cardiovascular Diseases
Aviva Lev-Ari, PhD, RN, coeditora del cuarto volumen y redactora jefe de la serie electrónica BioMed
Aviva Lev-Ari, PhD, RN, Co-Editor of Volume Four and Editor-in-Chief, BioMed e-Series
Medicina regenerativa y traslativa:
la promesa terapéutica para las enfermedades cardiovasculares
Regenerative and Translational Medicine
The Therapeutic Promise for Cardiovascular Diseases
en Amazon.com desde el 26/12/2015
2015
http://www.amazon.com/dp/B019UM909A
PART C: The Editorials of the original e-Books in
English in Audio format
Introduction to Part One: Cardiovascular Diseases,Translational Medicine (TM) and Post TM
Author and Curator: Larry H Bernstein, MD, FCAP
and
Curator: Aviva Lev-Ari, PhD, RN
This document in the Series A: Cardiovascular Diseases e-Series Volume 4: Translational and Regenerative Medicine, is a measure of the post-genomic and proteomic advances in the laboratory to the practice of clinical medicine. The Chapters are preceded by several videos by prominent figures in the emergence of this transformative change. When I was a medical student, a large body of the current language and technology that has extended the practice of medicine did not exist, but a new foundation, predicated on the principles of modern medical education set forth by Abraham Flexner, was sprouting. The highlights of this evolution were:
- Requirement for premedical education in biology, organic chemistry, physics, and genetics.
- Medical education included two years of basic science education in anatomy, physiology, pharmacology, and pathology prior to introduction into the clinical course sequence of the last two years.
- Post medical graduate education was an internship year followed by residency in pediatrics, OBGyn, internal medicine, general surgery, psychiatry, neurology, neurosurgery, pathology, radiology, and anesthesiology, emergency medicine.
- Academic teaching centers were developing subspecialty centers in ophthalmology, ENT and head and neck surgery, cardiology and cardiothoracic surgery, and hematology, hematology/oncology, and neurology.
- The expansion of postgraduate medical programs included significant postgraduate funding for programs by the National Institutes of Health, and the NIH had faculty development support in a system of peer-reviewed research grant programs in medical and allied sciences.
The period after the late 1980s saw a rapid expansion of research in genomics and drug development to treat emerging threats of infectious diseases as US had a large worldwide involvement after the end of the Vietnam War, and drug resistance was increasingly encountered (malaria, tick borne diseases, salmonellosis, pseudomonas aeruginosa, staphylococcus aureus, etc.).
Moreover, the post-millenium found a large, dwindling population of veterans who had served in WWII and Vietnam, and cardiovascular, musculoskeletal, dementias, and cancer were now more common. The Human Genome Project was undertaken to realign the existing knowledge of gene structure and genetic regulation with the needs for drug development, which was languishing in development failures due to unexpected toxicities.
A substantial disconnect existed between diagnostics and pharmaceutical development, which had been over-reliant on modification of known organic structures to increase potency and reduce toxicity. This was about to change with changes in medical curricula, changes in residency programs and physicians cross-training in disciplines, and the emergence of bio-pharma, based on the emerging knowledge of the cell function, and at the same time, the medical profession was developing an evidence-base for therapeutics, and more pressure was placed on informed decision-making.
The great improvement in proteomics came from GCLC/MS-MS and is described in the video interview with Dr. Gyorgy Marko-Varga, Sweden, in video 1 of 3 (Advancing Translational Medicine). This is a discussion that is focused on functional proteomics role in future diagnostics and therapy, involving a greater degree of accuracy in mass spectrometry (MS) than can be obtained by antibody-ligand binding, and is illustrated below, the last emphasizing the importance of information technology and predictive analytics
Thermo Scientific Immunoassays and LC–MS/MS have emerged as the two main approaches for quantifying peptides and proteins in biological samples. ELISA kits are available for quantification, but inherently lack the discriminative power to resolve isoforms and PTMs.
To address this issue we have developed and applied a mass spectrometry immunoassay–selected reaction monitoring (Thermo Scientific™ MSIA™ SRM technology) research method to quantify PCSK9 (and PTMs), a key player in the regulation of circulating low density lipoprotein cholesterol (LDL-C).
A Day in the (Future) Life of a Predictive Analytics Scientist
By Lars Rinnan, CEO, NextBridge April 22, 2014
A look into a normal day in the near future, where predictive analytics is everywhere, incorporated in everything from household appliances to wearable computing devices.
During the test drive (of an automobile), the extreme acceleration makes your heart beat so fast that your personal health data sensor triggers an alarm. The health data sensor is integrated into the strap of your wrist watch. This data is transferred to your health insurance company, so you say a prayer that their data scientists are clever enough to exclude these abnormal values from your otherwise impressive health data. Based on such data, your health insurance company’s consulting unit regularly gives you advice about diet, exercise, and sleep. You have followed their advice in the past, and your performance has increased, which automatically reduced your insurance premiums. Win-win, you think to yourself, as you park the car, and decide to buy it.
In the clinical presentation at Harlan Krumholtz’ Yale Symposium, Prof. Robert Califf, Director of the Duke University Translational Medicine Clinical Research Institute, defines translational medicine as effective translation of science to clinical medicine in two segments:
- Adherence to current standards
- Improving the enterprise by translating knowledge
He says that discrepancies between outcomes and medical science will bridge a gap in translation by traversing two parallel systems.
- Physician-health organization
- Personalized medicine
He emphasizes that the new basis for physician standards will be legitimized in the following:
- Comparative effectiveness (Krumholtz)
- Accountability
An interesting sidebar to the scientific medical advances is the huge shift in pressure on an insurance system that has coexisted with a public system in Medicare and Medicaid, initially introduced by the health insurance industry for worker benefits (Kaiser Permanente, IBM, Rockefeller), and we are undertaking a formidable change in the ACA.
The current reality is that actuarially, the twin system that has existed was unsustainable in the long term because it is necessary to have a very large pool of the population to spread the costs, and in addition, the cost of pharmaceutical development has driven consolidation in the industry, and has relied on the successes from public and privately funded research.
https://www.youtube.com/watch?v=X6J_7PvWoMw#t=57 Corbett Report Nov 2013
(1979 ER Brown) UCPress Rockefeller Medicine Men
https://www.youtube.com/watch?v=X6J_7PvWoMw#t=57
Liz Fowler VP of Wellpoint (designed ACA)
I shall digress for a moment and insert a video history of DNA, that hits the high points very well, and is quite explanatory of the genomic revolution in medical science, biology, infectious disease and microbial antibiotic resistance, virology, stem cell biology, and the undeniability of evolution.
DNA History
https://www.youtube.com/watch?v=UUDzN4w8mKI&list=UUoHRSQ0ahscV14hlmPabkVQ
As I have noted above, genomics is necessary, but not sufficient. The story began as replication of the genetic code, which accounted for variation, but the accounting for regulation of the cell and for metabolic processes was, and remains in the domain of an essential library of proteins. Moreover, the functional activity of proteins, at least but not only if they are catalytic, shows structural variants that is characterized by small differences in some amino acids that allow for separation by net charge and have an effect on protein-protein and other interactions.
Protein chemistry is so different from DNA chemistry that it is quite safe to consider that DNA in the nucleotide sequence does no more than establish the order of amino acids in proteins. On the other hand, proteins that we know so little about their function and regulation, do everything that matters including to set what and when to read something in the DNA.
Chapters 2, 3, and 4 sequentially examine:
- The causes and etiologies of cardiovascular diseases
- The diagnosis, prognosis and risks determined by – biomarkers in serum, circulating cells, and solid tissue by contrast radiography
- Treatment of cardiovascular diseases by translation of science from bench to bedside, including interventional cardiology and surgical repair
These are systematically examined within a framework of:
- Genomics
- Proteomics
- Cardiac and Vascular Signaling
- Platelet and Endothelial Signaling
- Cell-protein interactions
- Protein-protein interactions
- Post-Translational Modifications (PTMs)
- Epigenetics
- Noncoding RNAs and regulatory considerations
- Metabolomics (the metabolome)
- Mitochondria and oxidative stress
Summary
e-Series A: Cardiovascular Diseases, Volume Four
Part 1: Translational Medicine
Author and Curator: Larry H Bernstein, MD, FCAP
and
Curator: Aviva Lev-Ari, PhD, RN
Part 1 of Volume 4 in the e-series A: Cardiovascular Diseases and Translational Medicine, provides a foundation for grasping a rapidly developing surging scientific endeavor that is transcending laboratory hypothesis testing and providing guidelines to:
- Target genomes and multiple nucleotide sequences involved in either coding or in regulation that might have an impact on complex diseases, not necessarily genetic in nature.
- Target signaling pathways that are demonstrably maladjusted, activated or suppressed in many common and complex diseases, or in their progression.
- Enable a reduction in failure due to toxicities in the later stages of clinical drug trials as a result of this science-based understanding.
- Enable a reduction in complications from the improvement of machanical devices that have already had an impact on the practice of interventional procedures in cardiology, cardiac surgery, and radiological imaging, as well as improving laboratory diagnostics at the molecular level.
- Enable the discovery of new drugs in the continuing emergence of drug resistance.
- Enable the construction of critical pathways and better guidelines for patient management based on population outcomes data, that will be critically dependent on computational methods and large data-bases.
What has been presented can be essentially viewed in the following Table:
There are some developments that deserve additional development:
- The importance of mitochondrial function in the activity state of the mitochondria in cellular work (combustion) is understood, and impairments of function are identified in diseases of muscle, cardiac contraction, nerve conduction, ion transport, water balance, and the cytoskeleton – beyond the disordered metabolism in cancer. A more detailed explanation of the energetics that was elucidated based on the electron transport chain might also be in order.
- The processes that are enabling a more full application of technology to a host of problems in the environment we live in and in disease modification is growing rapidly, and will change the face of medicine and its allied health sciences.
Electron Transport and Bioenergetics
Deferred for metabolomics topic
Synthetic Biology
Introduction to Synthetic Biology and Metabolic Engineering
Kristala L. J. Prather: Part-1 <iBiology > iBioSeminars > Biophysics & Chemical Biology >
http://www.ibiology.org Lecturers generously donate their time to prepare these lectures. The project is funded by NSF and NIGMS, and is supported by the ASCB and HHMI.
Dr. Prather explains that synthetic biology involves applying engineering principles to biological systems to build “biological machines”.
Dr. Prather has received numerous awards both for her innovative research and for excellence in teaching. Learn more about how Kris became a scientist at
| Prather 1: Synthetic Biology and Metabolic Engineering 2/6/14 Introduction Lecture Overview In the first part of her lecture, Dr. Prather explains that synthetic biology involves applying engineering principles to biological systems to build “biological machines”. The key material in building these machines is synthetic DNA. Synthetic DNA can be added in different combinations to biological hosts, such as bacteria, turning them into chemical factories that can produce small molecules of choice. In Part 2, Prather describes how her lab used design principles to engineer E. coli that produce glucaric acid from glucose. Glucaric acid is not naturally produced in bacteria, so Prather and her colleagues “bioprospected” enzymes from other organisms and expressed them in E. coli to build the needed enzymatic pathway. Prather walks us through the many steps of optimizing the timing, localization and levels of enzyme expression to produce the greatest yield. Speaker Bio: Kristala Jones Prather received her S.B. degree from the Massachusetts Institute of Technology and her PhD at the University of California, Berkeley both in chemical engineering. Upon graduation, Prather joined the Merck Research Labs for 4 years before returning to academia. Prather is now an Associate Professor of Chemical Engineering at MIT and an investigator with the multi-university Synthetic Biology Engineering Reseach Center (SynBERC). Her lab designs and constructs novel synthetic pathways in microorganisms converting them into tiny factories for the production of small molecules. Dr. Prather has received numerous awards both for her innovative research and for excellence in teaching. |
Where Will the Century of Biology Lead Us?
By Randall Mayes
A technology trend analyst offers an overview of synthetic biology, its potential applications, obstacles to its development, and prospects for public approval.
- In addition to boosting the economy, synthetic biology projects currently in development could have profound implications for the future of manufacturing, sustainability, and medicine.
- Before society can fully reap the benefits of synthetic biology, however, the field requires development and faces a series of hurdles in the process. Do researchers have the scientific know-how and technical capabilities to develop the field?
Biology + Engineering = Synthetic Biology
Bioengineers aim to build synthetic biological systems using compatible standardized parts that behave predictably. Bioengineers synthesize DNA parts—oligonucleotides composed of 50–100 base pairs—which make specialized components that ultimately make a biological system. As biology becomes a true engineering discipline, bioengineers will create genomes using mass-produced modular units similar to the microelectronics and computer industries.
Currently, bioengineering projects cost millions of dollars and take years to develop products. For synthetic biology to become a Schumpeterian revolution, smaller companies will need to be able to afford to use bioengineering concepts for industrial applications. This will require standardized and automated processes.
A major challenge to developing synthetic biology is the complexity of biological systems. When bioengineers assemble synthetic parts, they must prevent cross talk between signals in other biological pathways. Until researchers better understand these undesired interactions that nature has already worked out, applications such as gene therapy will have unwanted side effects. Scientists do not fully understand the effects of environmental and developmental interaction on gene expression. Currently, bioengineers must repeatedly use trial and error to create predictable systems.
Similar to physics, synthetic biology requires the ability to model systems and quantify relationships between variables in biological systems at the molecular level.
The second major challenge to ensuring the success of synthetic biology is the development of enabling technologies. With genomes having billions of nucleotides, this requires fast, powerful, and cost-efficient computers. Moore’s law, named for Intel co-founder Gordon Moore, posits that computing power progresses at a predictable rate and that the number of components in integrated circuits doubles each year until its limits are reached. Since Moore’s prediction, computer power has increased at an exponential rate while pricing has declined.
DNA sequencers and synthesizers are necessary to identify genes and make synthetic DNA sequences. Bioengineer Robert Carlson calculated that the capabilities of DNA sequencers and synthesizers have followed a pattern similar to computing. This pattern, referred to as the Carlson Curve, projects that scientists are approaching the ability to sequence a human genome for $1,000, perhaps in 2020. Carlson calculated that the costs of reading and writing new genes and genomes are falling by a factor of two every 18–24 months. (see recent Carlson comment on requirement to read and write for a variety of limiting conditions).
Part Two
Cardiovascular Diseases and Regenerative Medicine
Introduction to Part Two
Author: Larry H. Bernstein, MD. FCAP
and
Curator: Aviva Lev-Ari, PhD, RN
This document is entirely devoted to medical and surgical therapies that have made huge strides in
- simplification of interventional procedures,
- reduced complexity, resulting in procedures previously requiring surgery are now done, circumstances permitting, by medical intervention.
This revolution in cardiovascular interventional therapy is regenerative medicine. It is regenerative because it is largely driven by
- the introduction into the impaired vasculature of an induced pleuripotent cell, called a stem cell, although
- the level of differentiation may not be a most primitive cell line.
There is also a very closely aligned development in cell biology that extends beyond and including vascular regeneration that is called synthetic biology. These developments have occurred at an accelerated rate in the last 15 years. The methods of interventional cardiology were already well developed in the mid 1980s. This was at the peak of cardiothoracic bypass surgery.
Research on the endothelial cell,
- endothelial cell proliferation,
- shear flow in small arteries, especially at branch points, and
- endothelial-platelet interactions
led to insights about plaque formation and vessel thrombosis.
Much was learned in biomechanics about the shear flow stresses on the luminal surface of the vasculature, and there was also
- the concomitant discovery of nitric oxide,
- oxidative stress, and
- the isoenzymes of nitric oxide synthase (eNOS, iNOS, and nNOS).
It became a fundamental tenet of vascular biology that
- atherogenesis is a maladjustment to oxidative stress not only through genetic, but also
- non-genetic nutritional factors that could be related to the balance of omega (ω)-3 and omega (ω)-6 fatty acids,
- a pro-inflammatory state that elicits inflammatory cytokines, such as, interleukin-6 (IL6) and c-reactive protein (CRP),
- insulin resistance with excess carbohydrate associated with type 2 diabetes and beta (β) cell stress,
- excess trans- and saturated fats, and perhaps
- the now plausible colonic microbial population of the gastrointestinal tract (GIT).
There is also an association of abdominal adiposity,
- including the visceral peritoneum, with both T2DM and with arteriosclerotic vessel disease,
- which is presenting at a young age, and has ties to
- the effects of an adipokine, adiponectin.
Much important work has already been discussed in the domain of cardiac catheterization and research done to
- prevent athero-embolization and beyond that,
- research done to implant an endothelial growth matrix.
Even then, dramatic work had already been done on
- the platelet structure and metabolism, and
- this has transformed our knowledge of platelet biology.
The coagulation process has been discussed in detailed in a previous document. The result was the development of a
- new class of platelet aggregation inhibitors designed to block the activation of protein on the platelet surface that
- is critical in the coagulation cascade.
In addition, the term long used to describe atherosclerosis, atheroma notwithstanding, is “hardening of the arteries”. This is particularly notable with respect to mid-size arteries and arterioles that feed the heart and kidneys. Whether it is preceded by or develops concurrently with chronic renal insufficiency and lowered glomerular filtration rate is perhaps arguable. However, there is now a body of evidence that points to
- a change in the vascular muscularis and vessel stiffness, in addition to the endothelial features already mentioned.
This has provided a basis for
- targeted pharmaceutical intervention, and
- reduction in salt intake.
So we have a group of metabolic disorders, which may alone or in combination,
- lead to and be associated with the long-term effects of cardiovascular disease, including
- congestive heart failure.
This has been classically broken down into forward and backward Heart Failure
- depending on decrease outflow through the aorta (ejection fraction), or
- Venous return refers to the flow of blood from the periphery back to the right atrium, and except for periods of a few seconds, it is equal to cardiac output
- decreased venous return through the vena cava involves an increased pulmonary vascular resistance and decreased return into the left atrium.
This also has ties to several causes, which may be cardiac or vascular. This document, as the previous, has four parts. They are broadly:
- Stem Cells in Cardiovascular Diseases
- Regenerative Cell and Molecular Biology
- Therapeutics Levels in Molecular Cardiology
- Research Proposals for Endogenous Augmentation of circulating Endothelial Progenitor Cells (cEPCs)
As in the previous section, we start with the biology of the stem cell and the degeneration in cardiovascular diseases, then proceed to regeneration, then therapeutics, and finally – proposals for augmenting therapy with circulating endogenous endothelial progenitor cells (cEPCs).
Summary to Part Two
Author: Larry H. Bernstein, MD. FCAP
We have covered a large amount of material that involves
- the development,
- application, and
- validation of outcomes of medical and surgical procedures
that are based on translation of science from the laboratory to the bedside, improving the standards of medical practice at an accelerated pace in the last quarter century, and in the last decade. Encouraging enabling developments have been:
1. The establishment of national and international outcomes databases for procedures by specialist medical societies
Stent Design and Thrombosis: Bifurcation Intervention, Drug Eluting Stents (DES) and Biodegrable Stents
Aviva Lev-Ari, PhD, RN
Justin Pearlman, MD, PhD, FACC and Article Curator: Aviva Lev-Ari, PhD, RN
Mitral Valve Repair: Who is a Patient Candidate for a Non-Ablative Fully Non-Invasive Procedure?
Justin Pearlman, MD, PhD, FACC and Article Curator: Aviva Lev-Ari, PhD, RN
Justin D Pearlman, MD, PhD, FACC and Article Curator: Aviva Lev-Ari, PhD, RN
Survivals Comparison of Coronary Artery Bypass Graft (CABG) and Percutaneous Coronary Intervention (PCI) /Coronary Angioplasty
Larry H. Bernstein, MD, FCAP And Aviva Lev-Ari, PhD, RN
Revascularization: PCI, Prior History of PCI vs CABG
Aviva Lev-Ari, PhD, RN
Aviva Lev-Ari, PhD, RN
Aviva Lev-Ari, PhD, RN
and more
2. The identification of problem areas, particularly in activation of the prothrombotic pathways, infection control to an extent, and targeting of pathways leading to progression or to arrythmogenic complications
Anticoagulation genotype guided dosing
Larry H. Bernstein, MD, FCAP
Aviva Lev-Ari, PhD, RN
The Effects of Aprotinin on Endothelial Cell Coagulant Biology
Kamran Baig, MBBS, James Jaggers, MD, Jeffrey H. Lawson, MD, PhD
Pharmacogenomics – A New Method for Druggability
Demet Sag, PhD
Advanced Topics in Sepsis and the Cardiovascular System at its End Stage
Larry H Bernstein, MD, FCAP
3. Development of procedures that use a safer materials in vascular management
Stent Design and Thrombosis: Bifurcation Intervention, Drug Eluting Stents (DES) and Biodegrable Stents
Aviva Lev-Ari, PhD, RN
Biomaterials Technology: Models of Tissue Engineering for Reperfusion and Implantable Devices for Revascularization
Larry H Bernstein, MD, FACP and Aviva Lev-Ari, PhD, RN
Vascular Repair: Stents and Biologically Active Implants
Larry H Bernstein, MD, FACP and Aviva Lev-Ari, RN, PhD
Larry H Bernstein, MD, FACP and Aviva Lev-Ari, PhD, RN
MedTech & Medical Devices for Cardiovascular Repair
Aviva Lev-Ari, PhD, RN
4. Discrimination of cases presenting for treatment based on qualifications for medical versus surgical intervention
Treatment Options for Left Ventricular Failure – Temporary Circulatory Support: Intra-aortic balloon pump (IABP) – Impella Recover LD/LP 5.0 and 2.5, Pump Catheters (Non-surgical) vs Bridge Therapy: Percutaneous Left Ventricular Assist Devices (pLVADs) and LVADs (Surgical)
Larry H Bernstein, MD, FCAP and Justin D Pearlman, MD, PhD, FACC
Larry H. Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN
ACC/AHA Guidelines for Coronary Artery Bypass Graft Surgery
Aviva Lev-Ari, PhD, RN
Mitral Valve Repair: Who is a Patient Candidate for a Non-Ablative Fully Non-Invasive Procedure?
Justin Pearlman, MD, PhD, FACC and Article Curator: Aviva Lev-Ari, PhD, RN
5. This has become possible because of the advances in our knowledge of key related pathogenetic mechanisms involving gene expression and cellular regulation of complex mechanisms.
What is the key method to harness Inflammation to close the doors for many complex diseases?
Larry H Bernstein, MD, FCAP
CVD Prevention and Evaluation of Cardiovascular Imaging Modalities: Coronary Calcium Score by CT Scan Screening to justify or not the Use of Statin
Aviva Lev-Ari, PhD, RN
Pathophysiological Effects of Diabetes on Ischemic-Cardiovascular Disease and on Chronic Obstructive Pulmonary Disease (COPD)
Larry H. Bernstein, MD, FCAP
Larry H Bernstein, MD, CAP and Aviva Lev-Ari, PhD, RN
Notable Contributions to Regenerative Cardiology
Larry H Bernstein, MD, FCAP and Article Commissioner: Aviva Lev-Ari, PhD, RN
As noted in the introduction, any of the material can be found and reviewed by content, and the eTOC is to be found at
This completes what has been presented in Part 2, Vol 4 , and supporting references for the main points that are found in the Leaders in Pharmaceutical Intelligence Cardiovascular book. Part 1 was concerned with Posttranslational Modification of Proteins, vital for understanding cellular regulation and dysregulation. Part 2 was concerned with Translational Medical Therapeutics, the efficacy of medical and surgical decisions based on bringing the knowledge gained from the laboratory, and from clinical trials into the realm opf best practice. The time for this to occur in practice in the past has been through roughly a generation of physicians. That was in part related to the busy workload of physicians, and inability to easily access specialty literature as the volume and complexity increased. This had an effect of making access of a family to a primary care provider through a lifetime less likely than the period post WWII into the 1980s.
However, the growth of knowledge has accelerated in the specialties since the 1980′s so that the use of physician referral in time became a concern about the cost of medical care. This is not the place for or a matter for discussion here. It is also true that the scientific advances and improvements in available technology have had a great impact on medical outcomes. The only unrelated issue is that of healthcare delivery, which is not up to the standard set by serial advances in therapeutics, accompanied by high cost due to development costs, marketing costs, and development of drug resistance.
I shall identify continuing developments in cardiovascular diagnostics, therapeutics, and bioengineering that is and has been emerging in the last decade.
About Stem Cells and Regenerative Biology
Adult Stem Cells Reverse Muscle Atrophy In Elderly Mice http://www.science20.com/profile/news_staff
Bioengineers at the University of California, Berkeley in a new study published in Nature say they have identified two key regulatory pathways that control how well adult stem cells repair and replace damaged tissue. They then tweaked how those stem cells reacted to those biochemical signals to revive the ability of muscle tissue in old mice to repair itself nearly as well as the muscle in the mice’s much younger counterparts. Irina Conboy, an assistant professor of bioengineering and an investigator at the Berkeley Stem Cell Center and at the California Institute for Quantitative Biosciences (QB3), led the research team conducting this study. Because the findings relate to adult stem cells that reside in existing tissue, this approach to rejuvenating degenerating muscle eliminates the ethical and medical complications associated with transplanting tissues grown from embryonic stem cells. The researchers focused on
- the interplay of two competing molecular pathways that control the stem cells,
Regenerating heart tissue through stem cell therapy
http://www.mayo.edu/research/discoverys-edge/regenerating-heart-tissue-stem-cell-therapy
Summary
A groundbreaking study on repairing damaged heart tissue through stem cell therapy has given patients hope that they may again live active lives. An international team of Mayo Clinic researchers and collaborators has done it by discovering a way to regenerate heart tissue.
“It’s a paradigm shift,” says Andre Terzic, M.D., Ph.D., director of Mayo Clinic’sCenter for Regenerative Medicine and senior investigator of the stem cell trial. “We are moving from traditional medicine, which addresses the symptoms of disease to cure disease.” Treating patients with cardiac disease has typically involved managing heart damage with medication. In collaboration with European researchers, Mayo Clinic researchers have discovered a novel way to repair a damaged heart. In Mayo Clinic’s breakthrough process,
- stem cells are harvested from a patient’s bone marrow.
- undergo a laboratory treatment that guides them into becoming cardiac cells,
- which are then injected into the patient’s heart in an effort to grow healthy heart tissue.
The study is the first successful demonstration in people of the feasibility and safety of transforming adult stem cells into cardiac cells. Beyond heart failure, the Mayo Clinic research also is a milestone in the emerging field of regenerative medicine, which seeks to fully heal damaged tissue and organs.
Creating a heart repair kit
This image shows the process used in the clinical trials to repair damaged hearts. Cardio-progenitor cells is another term for cardiopoietic cells, those that were transformed into cardiac cells.
Transformation: The cardiopoietic cells on the left react to the cardiac environment, cluster together with like cells and form tissue.
Mayo Clinic researchers pursued this research, inspired by an intriguing discovery. In the early 2000s, they analyzed stem cells from 11 patients undergoing heart bypass surgery. The stem cells from two of the patients had an unusually high expression of certain transcription factors — the proteins that control the flow of genetic information between cells. Clinically, the two patients appeared no different from the others, yet their stem cells seemed to show unique capacity for heart repair.
That observation drove them to determine how to convert non-reparative stem cells to become reparative. Doing so required determining precisely how the human heart naturally develops, at a subcellular level. That painstaking work was led by Atta Behfar, M.D., Ph.D., a cardiovascular researcher at Mayo Clinic in Rochester, Minn. With other members of the Terzic research team, Dr. Behfar identified hundreds of proteins involved in the process of heart development (cardiogenesis). The researchers then set out to identify which of these proteins are essential in driving a stem cell to become a cardiac cell. Using computer models,
- They simulated the effects of eliminating proteins one by one from the process of heart development.
- That method yielded about 25 proteins.
- The team then pared that number down to 8 proteins that their data indicated were essential.
The research team was then able to develop the lab procedure that guides stem cells to become heart cells.
The treated stem cells were dubbed cardiopoietic, or heart creative. A proof of principle study about guided cardiopoiesis, whose results were published in the Journal of the American College of Cardiology in 2010, demonstrated that animal models with heart disease that had been injected with caridiopoietic cells had improved heart function compared with animals injected with untreated stem cells. Hailed as “landmark work,” by the journal’s editorial writer, the study showed it was indeed possible to teach stem cells to become cardiac cells. Stem cells from each patient in the cardiopoiesis group were successfully guided to become cardiac cells. The treated cells were injected into the heart wall of each of those patients without apparent complications.
“this new process of cardiopoiesis was achieved in 100 percent of cases, with a very good safety profile,” Dr.Terzic says. “We are enabling the heart to regain its initial structure and function,” Dr.Terzic says, “and we will not stop here.” The clinical trial findings are expected to be published in the Journal of the American College of Cardiology in 2013. Meanwhile, research to improve the injection process and effectiveness is underway.
Synthetic Biology
Artists and biologists team up to ush boundaries of synthetic biology
Kenrick Vezina | May 1, 2014 | Genetic Literacy Project
Synthetic biologists are often accused of “playing God,” of tampering with his Creation. Well, if you’re going to Create then you might as well do so with the help of some creative individuals? That’s just what the biologists in the pages of the new book Synthetic Aesthetics, from MIT Press, aims to do. Its arrival is well-timed, with the
Alun Anderson has reviewed the new book for New Scientist. Unlike the typically defensive posture found in biotech broadly, he writes, the spirit captured by this book is “freewheeling” and collaborative, with 20 authors ranging from the arts and sciences putting their minds together to generate original ideas. Anderson notes that parts of the book “may irritate conventional scientists – some of the ideas were dreamed up while ‘performing a dance based on the myth of the Golem’, for example. But it certainly explains the key ideas of the field and leads you to many lateral conversations about what it may become.” The book is itself an offshoot of a larger project, which you can check out at its official page. It describes itself as an “experimental, international research project between synthetic biology, art, design and social science” It has roots at the University of Edinburgh, Scotland, and Stanford University, California. And the main project team is comprised of bioengineers Drew Endy (Stanford) and Alistair Elfick (Edinburgh), social scientists Jane Calvert (Edinburgh) and Pablo Schyfter (Edinburgh), and designer/artist Alexandra Daisy Ginsberg.
In the book Synthetic Aesthetics, Ginsberg provides a thought-provoking counterpoint to the engineering definition of “design”. Anderson explains in his review: An engineer might think of designing a bridge to a particular specification; a synthetic biologist of designing a microorganism with a new commercial application, pumping out green gasoline for example; but a real designer, a fashion designer, for example, is doing something else. As artist Daisy Ginsberg puts it, design “is about possibility”, the unimagined things that life could be.
Synthetic biology, she writes, has been addressing “humanity’s needs” – limitless fuel, for example – rather than “our needs as individual, diverse and complex humans”. This is refreshing: worries about the separation between the top-down design of the future and those who must live with the results are quite rare in science. These words ring true, given the intensely “problem oriented” approach to most synthetic biology research. This approach extends to the coverage of this research in the media, where even a research achievement with sweeping potential like the synthetic yeast chromosome ends up broken down into pragmatic chunks. (Yeast could mass-produce medicines! Help process fuels!) Alistair Elfick, one of the leads on the Synthetics Aesthetics project, has written a fascinating opinion piece at The Conversation to accompany the release of his book. In it, he puts forth the idea it’s time for synthetic biologists to stop thinking “like scientists,” lest they hamstring themselves.
Kenrick Vezina is Gene-ius Editor for the Genetic Literacy Project
https://geneticliteracyproject.org/ and a freelance science writer, educator, and naturalist based in the Greater Boston area. Sources:
- ”Synthetic biology gets reborn as an aesthetic dream,” Alun Anderson | New Scientist
- “If synthetic biologists think like scientists, they may miss their eureka moment,” Alistair Elfick | The Conversation
- Synthetic Aesthetics project
- “Breakthrough biology: First synthetic chromosome for yeast created, capping month of biotech innovations,” Kenrick Vezina | Genetic Literacy Project
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