SMAD4-deficient intestinal tumors recruit CCR1+ myeloid cells that promote invasion

Inactivation of TGF-beta family signaling is implicated in colorectal tumor progression. Using cis-Apc(+/Delta716) Smad4(+/-) mutant mice (referred to as cis-Apc/Smad4), a model of invasive colorectal cancer in which TGF-beta family signaling is blocked, we show here that a new type of immature myeloid cell (iMC) is recruited from the bone marrow to the tumor invasion front. These CD34(+) iMCs express the matrix metalloproteinases MMP9 and MMP2 and the CC-chemokine receptor 1 (CCR1) and migrate toward the CCR1 ligand CCL9. In adenocarcinomas, expression of CCL9 is increased in the tumor epithelium. By deleting Ccr1 in the background of the cis-Apc/Smad4 mutant, we further show that lack of CCR1 prevents accumulation of CD34(+) iMCs at the invasion front and suppresses tumor invasion. These results indicate that loss of transforming growth factor-beta family signaling in tumor epithelium causes accumulation of iMCs that promote tumor invasion.     

One-step facile synthesis of Pd nanoclusters supported on carbon and their electrochemical property

Well-crystallized Pd nanoclusters supported on Ketjen Black(KB) were successfully fabricated when Pd wires were served as an electrode pair by a solution plasma technique at atmospheric pressure. The synthesis of Pd nanoclusters was almost simultaneous with their dispersion on KB.Pd nanoclusters with the average diameter of about 2 nm were equably distributed on KB, and showed good electrochemical property corresponding to their obvious characteristic peaks. Multi-scan cyclic voltammetry and chronoamperometry clarified that as-prepared Pd nanoclusters have better electrochemical stability in alkaline solution than that of in acidic solution. Thus as-obtained Pd nanoclusters would become a promising electrocatalyst for fuel cells or Li-air batteries.