Los Resultados Obtenidos por el Mount Sinaí de EEUU, el Instituto Pasteur de Corea y el CSIC de España en sus Respectivos Laboratorios
"" Confirman que la Hipótesis de que la Diana Terapéutica del Fármaco Antitumoral Aplidin ( Plitidepsina ), Que es el EF1A, es La Clave para la Multiplicación y Propagación del Virus "" .
El Covid-19 Necesita la Proteína EF1A, Presente en el Cuerpo Humano, Para que la Nucleoproteína N del Virus se Haga Visible y Consiga Reproducirse y Propagarse por las Células.
Aplidin Secuestraría el Virus, Formando un Complejo Estable que Haga que el Virus No sea Viable .
De la Misma Opinión es Nevan Krogan, Professor and Director of Quantitative Biosciences Institute, University of California, San Francisco e Investigador Principal en los Institutos J. David Gladstone.
Por lo Qué Hasta la Obtención de los Resultados Completos ... Más la Elaboración del Dossier ... Más la Evaluación de las Agencias ... Nos Podemos Ir al 2027 .
18 agosto 2020
PharmaMar Group . Genómica SAU Comercializa Exclusivamente los Reactivos Dirigidos a Diagnóstico Veterinario de la APHA en España y Portugal .
Por Recordar .
VETERINARIA (APHA)
APHA Scientific, laboratorio de referencia animal en Reino Unido, ofrece una amplia gama de reactivos biológicos especializados y eficaces kits de diagnóstico para laboratorio.La agencia tiene más de 100 años de experiencia en el diagnóstico y control de enfermedades del ganado de granja y otros animales. Estos productos están dirigidos a la industria de la salud animal y se distribuyen en laboratorios de diagnóstico veterinario de todo el mundo.
Los reactivos APHA Scientific, que incluyen antisueros y kits de diagnóstico de antígenos, están disponibles para:
- Enfermedades bacterianas.
- Enfermedades víricas aviares.
- Enfermedades víricas de mamíferos.
- Anticuerpos monoclonales.
- Antisuero de Salmonella.
- Aislamientos bacterianos.
Cáncer de Colon . ZepZelCa (TM) y Yondelis ® Prolongan la Supervivencia de Ratones Portadores de Adenocarcinoma de Colon C26, sin Afectar el Crecimiento Tumoral Ni la Caquexia .
Trabectedin and Lurbinectedin Extend Survival of Mice Bearing C26 Colon Adenocarcinoma, without Affecting Tumor Growth or Cachexia .
Published : 17 August 2020 .
Abstract
Trabectedin (ET743) and lurbinectedin (PM01183) limit the production of inflammatory cytokines that are elevated during cancer cachexia.
Mice carrying C26 colon adenocarcinoma display cachexia (i.e., premature death and body wasting with muscle, fat and cardiac tissue depletion), high levels of inflammatory cytokines and subsequent splenomegaly.
We tested whether such drugs protected these mice from cachexia. Ten-week-old mice were inoculated with C26 cells and three days later randomized to receive intravenously vehicle or 0.05 mg/kg ET743 or 0.07 mg/kg PM01183, three times a week for three weeks.
ET743 or PM01183 extended the lifespan of C26-mice by 30% or 85%, respectively, without affecting tumor growth or food intake. Within 13 days from C26 implant, both drugs did not protect fat, muscle and heart from cachexia.
Since PM01183 extended the animal survival more than ET743, we analyzed PM01183 further. In tibialis anterior of C26-mice, but not in atrophying myotubes, PM01183 restrained the NF-κB/PAX7/myogenin axis, possibly reducing the pro-inflammatory milieu, and failed to limit the C/EBPβ/atrogin-1 axis.
Inflammation-mediated splenomegaly of C26-mice was inhibited by PM01183 for as long as the treatment lasted, without reducing IL-6, M-CSF or IL-1β in plasma.
ET743 and PM01183 extend the survival of C26-bearing mice unchanging tumor growth or cachexia but possibly restrain muscle-related inflammation and C26-induced splenomegaly.
Published : 17 August 2020 .
Abstract
Trabectedin (ET743) and lurbinectedin (PM01183) limit the production of inflammatory cytokines that are elevated during cancer cachexia.
Mice carrying C26 colon adenocarcinoma display cachexia (i.e., premature death and body wasting with muscle, fat and cardiac tissue depletion), high levels of inflammatory cytokines and subsequent splenomegaly.
We tested whether such drugs protected these mice from cachexia. Ten-week-old mice were inoculated with C26 cells and three days later randomized to receive intravenously vehicle or 0.05 mg/kg ET743 or 0.07 mg/kg PM01183, three times a week for three weeks.
ET743 or PM01183 extended the lifespan of C26-mice by 30% or 85%, respectively, without affecting tumor growth or food intake. Within 13 days from C26 implant, both drugs did not protect fat, muscle and heart from cachexia.
Since PM01183 extended the animal survival more than ET743, we analyzed PM01183 further. In tibialis anterior of C26-mice, but not in atrophying myotubes, PM01183 restrained the NF-κB/PAX7/myogenin axis, possibly reducing the pro-inflammatory milieu, and failed to limit the C/EBPβ/atrogin-1 axis.
Inflammation-mediated splenomegaly of C26-mice was inhibited by PM01183 for as long as the treatment lasted, without reducing IL-6, M-CSF or IL-1β in plasma.
ET743 and PM01183 extend the survival of C26-bearing mice unchanging tumor growth or cachexia but possibly restrain muscle-related inflammation and C26-induced splenomegaly.
Suscribirse a:
Entradas (Atom)