Injectable extracellular matrix hydrogels contribute to native cell infiltration in a rat partial nephrectomy model.

Decellularized extracellular matrix (dECM) hydrogels have cytocompatibility, and are currently being investigated for application in soft tissues as a material that promotes native cell infiltration and tissue reconstruction. A dECM hydrogel has broad potential for application in organs with complex structures or various tissue injury models. In this study, we investigated the practical application of a dECM hydrogel by injecting a kidney-derived dECM hydrogel into a rat partial nephrectomy model.

[Operational management in our hospice ward-from the viewpoint of supporting a patient's recuperation at home].

Although many terminally ill cancer patients desire to receive medical treatment in palliative care units(PCUs or hospices), very few patients are actually able to receive such treatment. Our aim is to provide palliative care to as many people as possible. We have practiced palliative care in general wards and prioritized care according to the patient's prognosis on admission to our hospice.

MM-1 facilitates degradation of c-Myc by recruiting proteasome and a novel ubiquitin E3 ligase.

We have reported that a novel c-Myc-binding protein, MM-1, repressed the E-box-dependent transcription activity of c-Myc by recruiting the HDAC1 complex via TIF1beta/KAP1, a transcriptional corepressor. We have also reported that a mutation of A157R in MM-1, which is often observed in patients with leukemia or lymphoma, abrogated all of the repressive activities of MM-1 toward c-Myc, indicating that MM-1 is a novel tumor suppressor. In this study, we found that MM-1 was bound to a component of proteasome and stimulated degradation of c-Myc in human cells.

Repression of the c-fms gene in fibroblast cells by c-Myc-MM-1-TIF1beta complex.

MM-1 has been reported to repress the E-box-dependent transcription activity of c-Myc by recruiting histone deacetylase 1 complex via TIF1beta/KAP1. In this study, to identify target genes for c-Myc-MM-1-TIF1beta, we established rat-1 cells harboring the dominant-negative form of TIF1beta to abrogate the pathway from TIF1beta to MM-1-c-Myc. This cell line, in which transcription activity of c-Myc was activated, was found to be tumorigenic.