Author: CITLALLI TORNEZ BENITEZ

Marcadores de disfunción endotelial asociados con riesgo cardiovascular en jóvenes con obesidad y peso normal

Citlalli Tornéz Benítez (2013)

La obesidad favorece la disfunción endotelial causando el desprendimiento de las células endoteliales y la sobreexpresión de moléculas de adhesión celular. Objetivo. Evaluar la relación del número de células endoteliales en circulación y de los niveles de sICAM-1, sVCAM-1 y sE-selectina, con los factores de riesgo cardiovascular tradicionales en jóvenes con y sin obesidad.,

Consejo Nacional de Ciencia y Tecnología (CONACyT) de México

Obesity promotes endothelial dysfunction causing the detachment of endothelial cells and overexpression of cell adhesion molecules. Objective. To evaluate the ratio of the number of circulating endothelial cells and levels of sICAM-1, sVCAM-1 and sE-selectin, with traditional cardiovascular risk factors in youth with and without obesity

Master thesis

Células endoteliales Disfunción endotelial Obesidad Jóvenes MEDICINA Y CIENCIAS DE LA SALUD CIENCIAS MÉDICAS FISIOLOGÍA HUMANA FISIOLOGÍA CARDIOVASCULAR

Mycobacterium tuberculosis TLR-2 agonists LprA, LM and Man-LAM induce notch1 and socs3 transcription

MARIO ALBERTO FLORES VALDEZ VANIA ELVIRA BONIFAZ PENA ERIKA NAHOMY MARINO MARMOLEJO CITLALLI TORNEZ BENITEZ Mabel Guzmán Rodríguez Abel Gutiérrez Ortega Letícia Santos (2011)

"Mycobacterium tuberculosis employs a number of strategies to subvert host signaling events, leading to its persistence within macrophages. Upon infection, Mycobacterium bovis BCG induce the expression of suppressor of cytokine signaling 3 (socs3), in a Toll-like receptor 2 (TLR2)-Notch1- dependent manner. Purified phosphatidyl inositol di-mannosides (a TLR2 agonist) act as an inducer for the Notch1-socs3 pathway. This prompted us to analyze other TLR2 agonists seeking for additional molecules that may affect this pathway. We found that lipoprotein LprA, as well as glycolipids lipomannan (LM), and mannose-capped lipoarabinomannan (ManLAM) treatment of murine macrophages resulted in stimulation of notch1 and socs3 transcription".

Article

BIOLOGÍA Y QUÍMICA BIOLOGÍA Y QUÍMICA

Mycobacterium tuberculosis TLR2 agonists LprA, LM and Man-LAM induce notch1 and socs3 transcription

ERIKA NAHOMY MARINO MARMOLEJO CITLALLI TORNEZ BENITEZ VANIA ELVIRA BONIFAZ PENA MABEL GUZMAN RODRIGUEZ HUGO ENRIQUE LOPEZ GONZALEZ ABEL GUTIERREZ ORTEGA MARTHA LETICIA SANTOS MARTINEZ MARIO ALBERTO FLORES VALDEZ (2011)

"Mycobacterium tuberculosis employs a number of strategies to subvert host signaling events, leading to its persistence within macrophages. Upon infection, Mycobacterium bovis BCG induce the expression of suppressor of cytokine signaling 3 (socs3), in a Toll-like receptor 2 (TLR2)-Notch1-dependent manner. Purified phosphatidyl inositol di-mannosides (a TLR2 agonist) act as an inducer for the Notch1-socs3 pathway. This prompted us to analyze other TLR2 agonists seeking for additional molecules that may affect this pathway. We found that lipoprotein LprA, as well as glycolipids lipomannan (LM), and mannose-capped lipoarabinomannan (ManLAM) treatment of murine macrophages resulted in stimulation of notch1 and socs3 transcription."

Article

Mycobacterium tuberculosis Toll-like receptor 2 (TLR2) Notch1 Socs3 Innate immunity BIOLOGÍA Y QUÍMICA