NEWS OF TH E WEEK
SHALE GAS DRAWS JAPANESE PLANT
technology, a new production process originally developed by Lucite International that uses ethylene as its main feedstock. Most MMA production starts with hydrogen cyanide and acetone. Mitsubishi Rayon acquired Lucite in 2009 and was itself acquired by Mitsubishi Chemical soon thereafter. Trading company Mitsui is part of the venture because of its ability to raise financing and ship materials to buyers worldwide. Mitsubishi Chemical declined to disclose a cost estimate for the project, which it expects will open by the end of 2018. Shigeki Okazaki, a stock analyst at the brokerage firm Nomura Securities, reckons the investment required will be in the neighborhood of $500 million. Like other Japanese companies faced with high raw material costs in their home country, Mitsubishi Chemical is looking to the U.S. as a preferred investment site. When announcing its fiscal 2014 earnings earlier this year, the company said its management strategy includes “responding to the shale gas revolution.” In April, the U.S. arm of the Japanese polyvinyl chloride producer Shin-Etsu Chemical filed permits with Louisiana authorities to build what would be the firm’s first U.S. ethylene cracker. And earlier this year, Japan’s Toray Industries acquired a 400-acre site in Spartanburg County, S.C., to set up new plants. At the time Toray said it anticipates investing about $1 billion in the U.S. because it sees the country regaining industrial competitiveness on the back of its abundant shale gas supply.—JEAN-FRANÇOIS TREMBLAY
FEEDSTOCK: Cheap ethylene convinces Mitsubishi to make acrylic monomer in U.S. ITSUBISHI RAYON and the trading firm Mitsui
M
& Co. are planning a large acrylic plant in the U.S. that would use as feedstock low-cost ethylene supplied by Dow Chemical. The project is in keeping with a Japanese corporate strategy to take advantage of cheap shale-derived energy and raw materials in the U.S. The proposed Japanese joint venture would build a 250,000-metric-ton-per-year plant making methyl methacrylate (MMA), a material used in acrylic plastics. Some of the plant’s output would be sold to Dow, which itself is a producer and user of MMA. The venture would likely be based on the Gulf Coast where Dow is building new shale-gas-fed ethylene capacity. The MMA plant will implement Mitsubishi’s Alpha MITSUBISHI RAYON
Lucite, later bought by Mitsubishi Rayon, opened this ethylene-based MMA plant in Singapore in 2008.
SHEDDING LIGHT ON LUNG DISEASE IMMUNOCHEMISTRY: Engineered
antibody reduces inflammation in mice with lung condition
A
NEW STUDY REVEALS the key role a protein
plays in chronic obstructive pulmonary disease (COPD) and provides a potential lead for treating the incurable lung disease (Sci. Transl. Med. 2014, DOI: 10.1126/scitranslmed.3008074). Stephen L. Nishimura, a professor in the pathology department at the University of California, San Francisco, and colleagues have engineered a monoclonal antibody that prevents the activation of a destructive protein in COPD mouse models and have explored in detail how the antibody binds to its target. COPD, which makes it hard to breathe, is caused by a cascade of biochemical events that begin with exposure to an irritant such as cigarette smoke or with repeated infections. These insults are associated with the increased CEN.ACS.ORG
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SCI. TRANS L. MED.
A deadly protein is thwarted by the binding of an engineered antibody (gray) to integrin ανβ8 (binding site in red) in this computer model.
expression of a protein, TGF-β, which creates scar tissue that in time begins to block small airways, a process known as airway remodeling. For TGF-β to do its damage, it needs to be activated by a class of signaling proteins known as integrins, in particular, ανβ6 and ανβ8. The integrin ανβ6 has been well studied, but not much has been known about how integrin ανβ8 contributes to the TGF-β activation process. Now, Nishimura’s group has engineered the first antibody to integrin ανβ8, called B5. The group engineered mice to produce human integrin ανβ8, exposed them to cigarette smoke, and then treated them with B5. They show that in these mice, TGF-β activation is inhibited and airway inflammation and scarring are reduced. The authors examined the antibody-integrin binding system in detail, uncovering how the two species adjust their shapes to form a stable complex. Enid R. Neptune, professor in the Division of Pulmonary & Critical Care Medicine at Johns Hopkins School of Medicine, says the paper is “mechanistically revealing about the conformational changes that underlie integrin/TGF-β signaling.” Like many animal models of human disease, the COPD mouse model has some shortcomings, as mice have shorter airways and shorter life spans. The next step, Nishimura says, will be to test the antibody’s toxicity, with hopes of leading to a human clinical trial.— ELIZABETH WILSON
JUNE 23, 2014
