Murali Ramachandran

Un externista epistémico debería admitir que, para cualquier proposición sobre el mundo, P, que se sepa verdadera, habrá algún otro hecho que uno no está en condiciones de conocer, pero que resulta necesario para que la creencia en P constituya conocimiento. Sostenemos que los sujetos cognoscentes ordinarios tienen noticia de tales «hacedores de conocimiento desconocidos». Sobre esta base, presentamos un argumento novedoso —que distinguimos de sus rivales— a favor del fracaso generalizado del principio KK: a saber, que, en términos muy generales, si alguien sabe que P, no estará en condiciones de saber que lo sabe.

In his influential paper ‘Speaker's Reference and Semantic Reference’, Kripke defends Russell's theory of descriptions against the charge that the existence of referential and attributive uses of descriptions reflects a semantic ambiguity. He presents a purely defensive argument to show that Russell's theory is not refuted by the referential usage and a number of methodological considerations which apparently tell in favour of Russell's unitary theory over an ambiguity theory. In this paper, I put forward a case for the ambiguity theory that thwarts Kripke's defensive strategy and argue that it is not undermined by any of his methodological points.

Both W9 and OP3‐4 were known to bind the receptor activator of NF‐κB ligand (RANKL), inhibiting osteoclastogenesis. Recently, both peptides were shown to stimulate osteoblast differentiation; however, the mechanism underlying the activity of these peptides remains to be clarified. A primary osteoblast culture showed that rapamycin, an mTORC1 inhibitor, which was recently demonstrated to be an important serine/threonine kinase for bone formation, inhibited the peptide‐induced alkaline phosphatase activity. Furthermore, both peptides promoted the phosphorylation of Akt and S6K1, an upstream molecule of mTORC1 and the effector molecule of mTORC1, respectively. In the in vivo calvarial defect model, W9 and OP3‐4 accelerated BMP‐2‐induced bone formation to a similar extent, which was confirmed by histomorphometric analyses using fluorescence images of undecalcified sections. Our data suggest that these RANKL‐binding peptides could stimulate the mTORC1 activity, which might play a role in the acceleration of BMP‐2‐induced bone regeneration by the RANKL‐binding peptides.