The Kepler Mission, launched on Mar 6, 2009 was designed with the explicit capability to detect Earth-size planets in the habitable zone of solar-like stars using the transit photometry method. Results from just forty-three days of data along with ground-based follow-up observations have identified five new transiting planets with measurements of their masses, radii, and orbital periods. Many aspects of stellar astrophysics also benefit from the unique, precise, extended and nearly continuous data set for a large number and variety of stars. Early results for classical variables and eclipsing stars show great promise. To fully understand the methodology, processes and eventually the results from the mission, we present the underlying rationale that ultimately led to the flight and ground system designs used to achieve the exquisite photometric performance. As an example of the initial photometric results, we present variability measurements that can be used to distinguish dwarf stars from red giants.

Most of the new drugs reaching the market today are single enantiomers, rather than the racemic mixtures that dominated up to ten years ago. Many of the new single-enantiomer drugs were developed as such, but there are also important examples of new single-enantiomer drugs derived from 'chiral switches' of established racemates. Indeed, a well-timed chiral switch can offer enhanced therapy and further profitability as a 'line extension' of a major racemic drug with patents that are expiring.

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Diclofenac is a nonsteroidal anti-inflammatory drug that causes rare but serious hepatotoxicity, the mechanism of which is unclear. The purpose of the present study was to explore the potential role played by the immune processes. Antibodies to diclofenac metabolite-modified liver protein adducts were detected in the sera of seven out of seven patients with diclofenac-induced hepatotoxicity, 12 of 20 subjects on diclofenac without hepatotoxicity, and none of four healthy controls. The antibodies recognized adducts expressed in livers from rats treated with multiple doses of diclofenac, but not in those given single doses. In addition, several potential diclofenac adducts were identified in the liver of a patient with diclofenac-induced hepatic failure, but not from a normal human donor liver, by immunoblotting with an adduct-selective rabbit antiserum. To determine whether or not polymorphisms in genes encoding cytokine-related proteins influence susceptibility to hepatotoxicity, genotyping for the polymorphisms -627 in the interleukin (