‘The Great Fiasco’ of the 1948 presidential election polls: status recognition and norms conflict in social science

All three ‘scientific’ pollsters (Crossley, Gallup and Roper) wrongly predicted incumbent President Harry Truman’s defeat in the 1948 presidential election, and thus faced a potentially serious legitimacy crisis. This ‘fiasco’ occurred at a most inopportune time. Social science was embroiled in a policy debate taking place in the halls of Congress. It was fighting a losing battle to be included, along with the natural sciences, in the National Science Foundation, for which legislation was being drafted. Faced with the failure of the polls, the Social Science Research Council (SSRC) intervened quickly to prevent social science’s adversaries from using this event to degrade further its status. After all, many social scientists considered the sample survey as the paramount tool of social research, and sampling as one of social science’s greatest innovation. Concurrently, there was an ongoing conflict among polling practitioners themselves—between advocates of probability sampling and users of quotas, like the pollsters. The SSRC committee appointed to evaluate the polling debacle managed to keep this contentious issue of sampling from becoming the centre of attention. Given the inauspicious environment in which this event happened, the SSRC did not wish to advertise the fact that the house of social science was in turmoil.     

PYY modulation of cortical and hypothalamic brain areas predicts feeding behaviour in humans

The ability to maintain adequate nutrient intake is critical for survival. Complex interrelated neuronal circuits have developed in the mammalian brain to regulate many aspects of feeding behaviour, from food-seeking to meal termination. The hypothalamus and brainstem are thought to be the principal homeostatic brain areas responsible for regulating body weight. However, in the current 'obesogenic' human environment food intake is largely determined by non-homeostatic factors including cognition, emotion and reward, which are primarily processed in corticolimbic and higher cortical brain regions. Although the pleasure of eating is modulated by satiety and food deprivation increases the reward value of food, there is currently no adequate neurobiological account of this interaction between homeostatic and higher centres in the regulation of food intake in humans. Here we show, using functional magnetic resonance imaging, that peptide YY3-36 (PYY), a physiological gut-derived satiety signal, modulates neural activity within both corticolimbic and higher-cortical areas as well as homeostatic brain regions. Under conditions of high plasma PYY concentrations, mimicking the fed state, changes in neural activity within the caudolateral orbital frontal cortex predict feeding behaviour independently of meal-related sensory experiences. In contrast, in conditions of low levels of PYY, hypothalamic activation predicts food intake. Thus, the presence of a postprandial satiety factor switches food intake regulation from a homeostatic to a hedonic, corticolimbic area. Our studies give insights into the neural networks in humans that respond to a specific satiety signal to regulate food intake. An increased understanding of how such homeostatic and higher brain functions are integrated may pave the way for the development of new treatment strategies for obesity.     

Disposition of the portal vessels of the avian pituitary in relation to the median eminence and the pars distalis

Zusammenfassung Die ermittelte Gefässversorgung der Vogelhypophyse beweist die Existenz eines doppelten Portalsystems der Pars distalis, womit auf zwei hypothalamo-hypophysäre Mechanismen hingewiesen wird.     

A steady-state superradiant laser with less than one intracavity photon

The spectral purity of an oscillator is central to many applications, such as detecting gravity waves, defining the second, ground-state cooling and quantum manipulation of nanomechanical objects, and quantum computation. Recent proposals suggest that laser oscillators which use very narrow optical transitions in atoms can be orders of magnitude more spectrally pure than present lasers. Lasers of this high spectral purity are predicted to operate deep in the 'bad-cavity', or superradiant, regime, where the bare atomic linewidth is much less than the cavity linewidth. Here we demonstrate a Raman superradiant laser source in which spontaneous synchronization of more than one million rubidium-87 atomic dipoles is continuously sustained by less than 0.2 photons on average inside the optical cavity. By operating at low intracavity photon number, we demonstrate isolation of the collective atomic dipole from the environment by a factor of more than ten thousand, as characterized by cavity frequency pulling measurements. The emitted light has a frequency linewidth, measured relative to the Raman dressing laser, that is less than that of single-particle decoherence linewidths and more than ten thousand times less than the quantum linewidth limit typically applied to 'good-cavity' optical lasers, for which the cavity linewidth is much less than the atomic linewidth. These results demonstrate several key predictions for future superradiant lasers, which could be used to improve the stability of passive atomic clocks and which may lead to new searches for physics beyond the standard model.     

Critical role for the p110alpha phosphoinositide-3-OH kinase in growth and metabolic regulation

The eight catalytic subunits of the mammalian phosphoinositide-3-OH kinase (PI(3)K) family form the backbone of an evolutionarily conserved signalling pathway; however, the roles of most PI(3)K isoforms in organismal physiology and disease are unknown. To delineate the role of p110alpha, a ubiquitously expressed PI(3)K involved in tyrosine kinase and Ras signalling, here we generated mice carrying a knockin mutation (D933A) that abrogates p110alpha kinase activity. Homozygosity for this kinase-dead p110alpha led to embryonic lethality. Mice heterozygous for this mutation were viable and fertile, but displayed severely blunted signalling via insulin-receptor substrate (IRS) proteins, key mediators of insulin, insulin-like growth factor-1 and leptin action. Defective responsiveness to these hormones led to reduced somatic growth, hyperinsulinaemia, glucose intolerance, hyperphagia and increased adiposity in mice heterozygous for the D933A mutation. This signalling function of p110alpha derives from its highly selective recruitment and activation to IRS signalling complexes compared to p110beta, the other broadly expressed PI(3)K isoform, which did not contribute to IRS-associated PI(3)K activity. p110alpha was the principal IRS-associated PI(3)K in cancer cell lines. These findings demonstrate a critical role for p110alpha in growth factor and metabolic signalling and also suggest an explanation for selective mutation or overexpression of p110alpha in a variety of cancers.