Large-Scale Simulations of Melting in Two-Dimensional Lennard-Jones Systems: Evidence for a Metastable Hexatic Phase

In 1995, North Americans installed $5 billion in efficiency equipment in their buildings in order to save money and conserve energy and water. But this covers only a small fraction of the existing cost-effective opportunities for energy savings investments. If all cost-effective efficiency investments were made in public and commercial buildings, the United States would save$20 billion per year on energy bills, create over 100,000 jobs, and significantly cut pollution. When firms invest in energy efficiency, they naturally want to know how much they have saved and how long their savings will last. If the installation had been made to generate energy, measurements would be trivial - install a meter. But to measure savings is a challenge, and requires both metering and a methodology, known as a measurement and verification protocol. To determine energy savings, the parties (the building owner, the installer and perhaps the financier) must first agree on the {open_quotes}base case{close_quotes} (what the building used before retrofit), and then must measure energy use after retrofit. They may want to adjust the savings for variations in the weather or changes in occupancy or work schedules. And they should keep up the measurements to ensure that their savings persist

microRNA-155, Induced by Interleukin-1ß, Represses the Expression of Microphthalmia-Associated Transcription Factor (MITF-M) in Melanoma Cells

Loss of expression of surface antigens represents a significant problem for cancer immunotherapy. Microphthalmia-associated transcription factor (MITF-M) regulates melanocyte fate by driving expression of many differentiation genes, whose protein products can be recognized by cytolytic T lymphocytes. We previously reported that interleukin-1ß (IL-1ß) can downregulate MITF-M levels. Here we show that downregulation of MITF-M expression by IL-1ß was paralleled by an upregulation of miR-155 expression in four melanoma lines. We confirmed that miR-155 was able to target endogenous MITF-M in melanoma cells and demonstrated a role for miR-155 in the IL-1ß-induced repression of MITF-M by using an antagomiR. Notably, we also observed a strong negative correlation between MITF-M and miR-155 levels in a mouse model of melanoma. Taken together, our results indicate that MITF-M downregulation by inflammatory stimuli might be partly due to miR-155 upregulation. This could represent a novel mechanism of melanoma immune escape in an inflammatory microenvironment