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La utilización de la terapia de ultrasonidos pulsados de baja intensidad para la cicatrización ósea y el tratamiento de fracturas es considerada cada vez más como una alternativa terapéutica de coste económico moderado y con efectos adversos nulos o mínimos (p. ej. leve reacción al gel conductor).

El objetivo del estudio fue analizar qué características de tipo individual (factores sociodemográficos, actitudinales y políticos) condicionan la elección sanitaria en España en relación con una alternativa de sanidad privada frente a una pública para los casos de médico de familia, médico especialista, ingreso hospitalario y urgencias durante el año 2022.

Phorbol esters, the activators of protein kinase C (PKC), induce apoptosis in androgen-sensitive LNCaP prostate cancer cells. The role of individual PKC isozymes as mediators of this effect has not been thoroughly examined to date. To study the involvement of the novel isozyme PKCdelta, we used a replication-deficient adenovirus (PKCdeltaAdV), which allowed for a tightly controlled expression of PKCdelta in LNCaP cells. A significant reduction in cell number was observed after infection of LNCaP cells with PKCdeltaAdV. Overexpression of PKCdelta markedly enhanced the apoptotic effect of phorbol 12-myristate 13-acetate in LNCaP cells. PKCdelta-mediated apoptosis was substantially reduced by the pan-caspase inhibitor z-VAD and by Bcl-2 overexpression. Importantly, and contrary to other cell types, PKCdelta-mediated apoptosis does not involve its proteolytic cleavage by caspase-3, suggesting that allosteric activation of PKCdelta is sufficient to trigger apoptosis in LNCaP cells. In addition, phorbol ester-induced apoptosis was blocked by a kinase-deficient mutant of PKCdelta, supporting the concept that PKCdelta plays an important role in the regulation of apoptotic cell death in LNCaP prostate cancer cells.

The objectives of this research were to determine the effects of β-mercaptoethanol (β-ME) and fetal bovine serum (FBS) on in vitro development of bovine embryos derived from oocytes matured and fertilized in vitro and to examine the mechanism through which β-ME may influence embryo development. A 2 × 2 factorial treatment arrangement was used to evaluate the effect of 0 or 100 µM β-ME and 0% or 10% FBS on embryos cultured in Medium 199 (M199) in the absence of somatic cells. Embryos were randomly allocated within stage of development (< 8 cells or 8–16 cells) to one of four treatment combinations and were cultured for 6 days. Both β-ME and FBS promoted increased (p< 0.01) development of embryos to the blastocyst stage, and their effects were greater (p< 0.01) in 8- to 16-cell embryos than in embryos having fewer than 8 cells at the initiation of treatment. The cysteine and cystine content of M199, with and without β-ME, were determined by HPLC. Medium supplemented with β-ME contained neither cysteine nor cystine, and it is suggested that these compounds were converted into a mixed disulfide between cysteine and PI-ME. These results indicate that β-ME is capable of enhancing bovine embryo development in a cell-free, serum-free culture system.

Previous studies have indicated that Bcl-3 interacts through its ankyrin repeats with the transcriptional factors NF-kappaB1 (p50) and NF-kappaB2 (p52), affecting their biological activities. To further investigate the role of Bcl-3 in vivo and its association with the NF-kappaB proteins, we have generated transgenic mice constitutively expressing Bcl-3 in thymocytes. The results indicate that Bcl-3 is associated with endogenous p50 and p52 in nuclear extracts from transgenic animals. Remarkably, constitutive expression of Bcl-3 in these cells augments the DNA binding activity of p52 homodimers. This effect could be reproduced in vitro and is blocked by anti-Bcl-3 antibodies. We have also shown that Bcl-3 is phosphorylated in thymocytes and that its dephosphorylation greatly decreases the effect on p50 homodimers.