PrefaceThis manifesto bases its suggestions on a postmodern view of art in education with an emphasis on difference, plurality and independence of mind. The proposals derive from the rationale and argue for more decision-making and autonomy for teachers and learners within a climate that emphasises and expects enquiry, experiment and creative opportunity. For this to happen the subject matter of art, ways of approaching it, and improved means of encouraging diversity and innovation must be developed. This implies that the values within the current statutory Orders for Art, the initial education and in-service development of teachers, and the nature and purpose of assessment must be reconsidered. This manifesto addresses the areas that impinge on the activity of art in schools, makes critical comment on the effect of current ideology and practice, and provides a rationale and proposals for its implementation. RationaleThe rationale is based on three fundamental principles: difference, plurality, and independent thought. Through their application in © NSEAD, 1999 art practice and theory, knowledge and knowing will become understood as a negotiation of ideas which arise from asking pertinent questions, and testing provisional answers rather than seeking predetermined ones. The emphasis is on the learner and learning, negotiating what they learn, learning how to learn, and understanding knowledge as a multiplicity of changing hypotheses or theories which are subject to evidence, proof, argument and embodiment. As such difference becomes a locus for action and discussion at a personal and social level, plurality points to a variety of methods, means, solutions and awareness for any issue, and independent thought develops individuality, the capacity to challenge, and creativity through introspection into the nature of learning and teaching in art. These abilities are as vital for teachers as they are for learners.

Stem cells have important clinical and experimental potentials. Trophoblast stem (TS) cells possess the ability to differentiate into trophoblast subtypes in vitro and contribute to the trophoblast lineage in vivo.Suppressor of cytokine signaling 3 (SOCS3) is a negative regulator of cytokine signaling. Targeted disruption of SOCS3 revealed embryonic lethality on E12.5; it was caused by placental defect with enhanced leukemia inhibitory factor receptor signaling. A complementation of the wild-type (WT) placenta by using tetraploid rescue technique showed that the embryonic lethality in SOCS3-deficient embryo was due to the placental defect. Here we demonstrate that TS cells supplementation rescues placental defect in SOCS3-deficient embryos. In the rescued placenta, TS cells were integrated into the placental structure, and a substantial structural improvement was observed in the labyrinthine layer that was disrupted in the SOCS3-deficient placenta. Importantly, by supplying TS cells, living SOCS3-deficient embryos were detected at term. These results indicate a functional contribution of TS cells in the placenta and their potential application.In mammals, trophoblast cells in the placenta are essential for the growth and survival of the embryo. Trophoblast stem (TS) 3 cells have been established from either blastocysts or early postimplantation trophoblasts in the presence of fibroblast growth factor 4 (FGF4) (1). These cell lines differentiated into trophoblast subtypes in vitro and have the potential to contribute to the placenta in chimeras in vivo. However, it remains to be clarified whether the in vivo differentiated trophoblasts from TS cells are functional.SOCS3 is an essential negative regulator of leukemia inhibitory factor receptor signaling in trophoblast differentiation (2). Targeted disruption of SOCS3 demonstrates embryonic lethality with placental defect (2, 3). In the SOCS3-deficient placenta, an excess status of trophoblast giant cell differentiation is observed. The embryonic lethality in SOCS3Ϫ/Ϫ embryos is rescued by the complementation of wild-type tetraploid embryos, thus demonstrating an essential role of SOCS3 in placental development and a non-essential role in embryo development (2). To explore the potential of TS cells in rescuing the placental defect in SOCS3-deficient mice, we attempted to prepare a chimera by using SOCS3Ϫ/Ϫ embryo and WT TS cells. MATERIALS AND METHODSMice-The generation of SOCS3-disrupted mice was as described in a previous study (2). Using tail biopsies, genotyping was performed by PCR as described. Mutant phenotypes were analyzed in a mixed 129/Sve, C57Bl/6 background.TS Cell Injections-TS cell lines were derived from B5/enhanced green florescent protein (EGFP) transgenic mice (4) (kindly supplied by Dr. J. Rossant) that ubiquitously express EGFP. These cells had already been cultured for more than 30 passages and showed a typical colony (Fig. 1, left). TS cells were maintained in the presence of FGF4 and conditioned medium from mouse embryonic fibroblast cells...

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