Multipotent mesenchymal stem cells (MSCs), first identified in the bone marrow, have subsequently been found in many other tissues, including fat, cartilage, muscle, and bone. Adipose tissue has been identified as an alternative to bone marrow as a source for the isolation of MSCs, as it is neither limited in volume nor as invasive in the harvesting. This study compares the multipotentiality of bone marrow-derived mesenchymal stem cells (BMSCs) with that of adiposederived mesenchymal stem cells (AMSCs) from 12 age-and sex-matched donors. Phenotypically, the cells are very similar, with only three surface markers, CD106, CD146, and HLA-ABC, differentially expressed in the BMSCs. Although colony-forming units-fibroblastic numbers in BMSCs were higher than in AMSCs, the expression of multiple stem cell-related genes, like that of fibroblast growth factor 2 (FGF2), the Wnt pathway effectors FRAT1 and frizzled 1, and other self-renewal markers, was greater in AMSCs. Furthermore, AMSCs displayed enhanced osteogenic and adipogenic potential, whereas BMSCs formed chondrocytes more readily than AMSCs. However, by removing the effects of proliferation from the experiment, AMSCs no longer out-performed BMSCs in their ability to undergo osteogenic and adipogenic differentiation. Inhibition of the FGF2/fibroblast growth factor receptor 1 signaling pathway demonstrated that FGF2 is required for the proliferation of both AMSCs and BMSCs, yet blocking FGF2 signaling had no direct effect on osteogenic differentiation. STEM CELLS

Large-scale treatment of oily water arising from frequent marine oil spills presents a major challenge to scientists and engineers. Although the recently emerged phase-selective organogelators (PSOG) do offer very best promises for oil spill treatment, there still exists a number of technical barriers to overcome collectively, including gelators’ high solubility, high gelling ability, general applicability toward crude oil of various types, rapid gelation with room temperature operation, low toxicity, and low cost. Here, a denovo-designed unusually robust molecular gelling scaffold is used for facile construction of a PSOG library and for rapid identification of PSOGs with the most sought-after practical traits. The identified gelators concurrently overcome the existing technical hurdles, and for the first time enable instant room-temperature gelation of crude oil of various types in the presence of seawater. Remarkably, these excellent gelations were achieved with the use of only 0.058–0.18 L of environmentally benign carrier solvents and 7–35 g of gelator per liter of crude oil. Significantly, 2 out of 20 gelators could further congeal crude oil in the powder form at room temperature, highlighting another excellent potential of the developed modularly tunable system in searching for more powerful powder-based gelators for oil spill treatment.

Tumor necrosis factor-α (TNF)-induced RIP1/RIP3-mediated necroptosis has been proposed to be an alternative strategy for treating apoptosis-resistant leukemia. However, we found that most acute myeloid leukemia (AML) cells, especially M4 and M5 subtypes, produce TNF and show basal level activation of RIP1/RIP3/MLKL signaling, yet do not undergo necroptosis. TNF, through RIP1/RIP3 signaling, prevents degradation of SOCS1, a key negative regulator of interferon-γ (IFN-γ) signaling. Using both pharmacologic and genetic assays, we show here that inactivation of RIP1/RIP3 resulted in reduction of SOCS1 protein levels and partial differentiation of AML cells. AML cells with inactivated RIP1/RIP3 signaling show increased sensitivity to IFN-γ-induced differentiation. RIP1/RIP3 inactivation combined with IFN-γ treatment significantly attenuated the clonogenic capacity of both primary AML cells and AML cell lines. This combination treatment also compromised the leukemogenic ability of murine AML cells in vivo. Our studies suggest that inhibition of RIP1/RIP3-mediated necroptotic signaling might be a novel strategy for the treatment of AML when combined with other differentiation inducers.

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