Euchologium Sinaiticum. 03 / [éd.] R. Graffin ; [trad.] Jean Frcek,...

[Euchologe (français). 1933-1939 fac-sim.]

Euchologium Sinaiticum. 05 / [éd.] R. Graffin ; [trad.] Jean Frcek,...

[Euchologe (français). 1933-1939 fac-sim.]

Preparación examen P.I.R

Este proyecto final de carrera, consiste en la creación de un blog que gira en torno de una misma temática: el P.I.R (Psicólogo interno residente). Este título se crea en diciembre de 1998 mediante el Real Decreto 2490/1998. Se obtiene realizando la formación especializada en una plaza sanitaria de psicólogo interno residente o por un proceso de solicitud, de acuerdo con lo previsto en las disposiciones transitorias, para quienes ejercen antes de la creación del mismo.

Oxidized LDL modulates apoptosis of regulatory T cells in patients with ESRD.

Increased levels of oxidized low-density lipoproteins (oxLDL) contribute to the increased risk for atherosclerosis, which persists even after adjusting for traditional risk factors, among patients with ESRD. Regulatory T cells (CD4+/CD25+ Tregs), which down-regulate T cell responses to foreign and self-antigens, are protective in murine atherogenesis, but whether similar immunoregulation occurs in humans with ESRD is unknown. Because cellular defense systems against oxLDL involve proteolytic degradation, the authors investigated the role of oxLDL on proteasome activity of CD4+/CD25+ Tregs in patients with ESRD. CD4+/CD25+ Tregs isolated from uremic patients' peripheral blood, especially that of chronically hemodialyzed patients, failed to suppress cell proliferation, exhibited cell-cycle arrest, and entered apoptosis by altering proteasome activity. Treating CD4+/CD25+ Tregs with oxLDL or uremic serum ex vivo decreased the number and suppressive capacity of CD4+/CD25+ Tregs. In vitro, oxLDL promoted the accumulation of p27Kip1, the cyclin-dependent kinase inhibitor responsible for G1 cell cycle arrest, and increased apoptosis in a time- and concentration-dependent manner. In summary, proteasome inhibition by oxLDL leads to cell cycle arrest and apoptosis, dramatically affecting the number and suppressive capacity of CD4+/CD25+ Tregs in chronically hemodialyzed patients. This response may contribute to the immune dysfunction, microinflammation, and atherogenesis observed in patients with ESRD.