In 1961, Crick, Barnett, Brenner, and Watts-Tobin (Crick et al., 1961) designed an elegant experimental strategy to determine the nature of the genetic code. Remarkably, they reached the correct conclusion despite the absence of technology to analyze and compare DNA and protein sequences.

Johann Rudi∗, Hari Sundar†, Tobin Isaac∗, Georg Stadler∗, Michael Gurnis‡, and Omar Ghattas∗§¶ ∗Institute for Computational Engineering and Sciences, The University of Texas at Austin, USA †School of Computing, The University of Utah, USA ‡Seismological Laboratory, California Institute of Technology, USA §Department of Mechanical Engineering, The University of Texas at Austin, USA ¶Jackson Scho...

QUESTIONS Does inspiratory muscle training improve maximal inspiratory pressure in intubated older people? Does it improve breathing pattern and time to wean from mechanical ventilation? DESIGN Randomised trial with concealed allocation and intention-to-treat analysis. PARTICIPANTS 41 elderly, intubated adults who had been mechanically ventilated for at least 48 hr in an intensive care unit...

We investigate how a positive relation between inflation and capital investment (the Mundell–Tobin effect, MT-E) affects optimal monetary policy in framework that combines overlapping generations new Monetarist models. find rates above the Friedman rule are if only there is an MT-E. In absence of MT-E, optimal. With increasing leads to first-order welfare gain from investment, second-order loss...

Classical mean variance utility of Markowitz [1952] and Tobin [1958] have relied on objective expected utility hypothesis. This paper presents a choice-based axiomatization of mean variance utility, in a Savage-type setting of ambiguity, which neither assumes nor implies that individual’s preferences over portfolios conform to the expected utility hypothesis.

Tobin and colleagues show that both inhibition and excessive production of the inflammatory mediator TNFα impact the pathogenesis of tuberculosis (TB) and the response to therapy. Identifying a critical role for the genetically determined balance between pro- and anti-inflammatory eicosanoids in regulating TNFα levels provides a roadmap to tailored TB treatment based on host genotype.