To improve fuel efficiency, advanced combustion engines are being designed to minimize the amount of heat wasted in the exhaust. Hence, future generations of catalysts must perform at temperatures that are 100°C lower than current exhaust-treatment catalysts. Achieving low-temperature activity, while surviving the harsh conditions encountered at high engine loads, remains a formidable challenge. In this study, we demonstrate how atomically dispersed ionic platinum (Pt) on ceria (CeO), which is already thermally stable, can be activated via steam treatment (at 750°C) to simultaneously achieve the goals of low-temperature carbon monoxide (CO) oxidation activity while providing outstanding hydrothermal stability. A new type of active site is created on CeO in the vicinity of Pt, which provides the improved reactivity. These active sites are stable up to 800°C in oxidizing environments.

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Hematopoietic stem cells (HSC) can be harmed by disease, chemotherapy, radiation and normal aging. We now show that damage also occurs in mice repeatedly treated with very low doses of lipopolysaccharide (LPS). Overall health of the animals was good, and there were relatively minor changes in marrow hematopoietic progenitors. However, HSC were unable to maintain quiescence, and transplantation revealed them to be myeloid skewed. Moreover, HSC from treated mice were not sustained in serial transplants and produced lymphoid progenitors with low levels of the E47 transcription factor. This phenomenon was previously seen in normal aging. Screening identified monoclonal antibodies that resolve HSC subsets, and relative proportions of these HSC changed with age and/or chronic LPS treatment. For example, minor CD150Hi CD48− populations lacking CD86 or CD18 expanded. Simultaneous loss of CD150Lo/− CD48− HSC and gain of the normally rare subsets, in parallel with diminished transplantation potential would be consistent with age or Tolllike receptor (TLR) related injury. On the other hand, HSC in old mice differed from those in LPS treated animals with respect to VCAM-1 or CD41 expression, and lacked proliferation abnormalities. HSC can be exposed to endogenous and pathogen derived TLR ligands during persistent low-grade infections. This stimulation might contribute in part to HSC senescence and ultimately compromise immunity.

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