The phosphatidylinositol (PI)-specific phospholipase C (PLC) of Bacillus cereus was cloned into Escherichia coli by using monoclonal antibody probes raised against the purified protein. Phosphoinositide-specific phospholipases C (PLCs) are important enzymes in the regulation of the cellular metabolism of eucaryotic cells. These enzymes have been shown to generate intracellular second messenger molecules in re-

The authors analyzed data from 134 responses from communities in 42 states and the District of Columbia. Communities are enthusiastic about moving forward with health information exchange to create LHIIs to improve the efficiency, quality, and safety of care. They have identified significant local sources of investment and plan to use some clinical data standards but not as broadly as was expected. The communities have not yet developed the specific technical approaches or the sustainable business models that will be required. Many communities are interested in creating an LHII and are developing the leadership commitment needed to translate that interest into an operational reality. Clinical information standards can be incorporated into a community's plans as often as they need to be. Communities have to overcome funding issues, develop deeper understanding of the technical and organizational issues, and aggressively share their learning to succeed within their community and to help other communities succeed.

The β‐amyloid peptides, Aβ1‐42 and Aβ1‐40, were quantified in ventricular CSF taken daily for up to 3 weeks from six individuals with severe traumatic brain injury (TBI). There was considerable interindividual variability in the levels of Aβ peptides, but in general Aβ1‐42 levels equalled or exceeded those of Aβ1‐40. Averaging the daily totals of our trauma cohort revealed that the levels of Aβ1‐42 and Aβ1‐40 rose after injury, peaking in the first week and then declining toward control levels over the next 2 weeks. Aβ1‐42 levels were on average two to three times higher in the trauma cohort than in CSF from nontrauma samples. Compared with nontrauma samples, the Aβ1‐40/Aβ1‐42 ratio decreased about fivefold in the trauma patients, further indicative of increased Aβ1‐42 levels. The ratio remained low at all time points studied. No change was measured in the levels of β‐amyloid precursor protein during the same interval. These results suggest that Aβ1‐42 becomes elevated in the CSF after severe brain trauma.