Silent reading of direct versus indirect speech activates voice-selective areas in the auditory cortex

In human communication, direct speech (e.g., Mary said: “I'm hungry”) is perceived to be more vivid than indirect speech (e.g., Mary said [that] she was hungry). However, for silent reading, the representational consequences of this distinction are still unclear. Although many of us share the intuition of an “inner voice,” particularly during silent reading of direct speech statements in text, there has been little direct empirical confirmation of this experience so far. Combining fMRI with eye tracking in human volunteers, we show that silent reading of direct versus indirect speech engenders differential brain activation in voice-selective areas of the auditory cortex. This suggests that readers are indeed more likely to engage in perceptual simulations (or spontaneous imagery) of the reported speaker's voice when reading direct speech as opposed to meaning-equivalent indirect speech statements as part of a more vivid representation of the former. Our results may be interpreted in line with embodied cognition and form a starting point for more sophisticated interdisciplinary research on the nature of auditory mental simulation during reading

Intermittency and the Slow Approach to Kolmogorov Scaling

From a simple path integral involving a variable volatility in the velocity differences, we obtain velocity probability density functions with exponential tails, resembling those observed in fully developed turbulence. The model yields realistic scaling exponents and structure functions satisfying extended self-similarity. But there is an additional small scale dependence for quantities in the inertial range, which is linked to a slow approach to Kolmogorov (1941) scaling occurring in the large distance limit.Comment: 10 pages, 5 figures, minor changes to mirror version to appear in PR

Transitions and Probes in Turbulent Helium

Previous analysis of a Paris turbulence experiment \cite{zoc94,tab95} shows a transition at the Taylor Reynolds number \rel \approx 700. Here correlation function data is analyzed which gives further evidence for this transition. It is seen in both the power spectrum and in structure function measurements. Two possible explanations may be offered for this observed transition: that it is intrinsic to the turbulence flow in this closed box experiment or that it is an effect of a change in the flow around the anemometer. We particularly examine a pair of ``probe effects''. The first is a thermal boundary layer which does exist about the probe and does limit the probe response, particularly at high frequencies. Arguments based on simulations of the response and upon observations of dissipation suggests that this effect is only crucial beyond \rel\approx 2000. The second effect is produced by vortex shedding behind the probe. This has been seen to produce a large modification in some of the power spectra for large \rel. It might also complicate the interpretation of the experimental results. However, there seems to be a remaining range of data for \rel < 1300 uncomplicated by these effects, and which are thus suggestive of an intrinsic transition.Comment: uuencoded .ps files. submitted to PRE. 12 figures are sent upon request to jane wang ([email protected]

Chiral 1,4-Benzodiazepines. X. Further Investigations of Configurational Stability of the Chiral Centre C(3)

For various at C(3)-chiral 1,4-benzodiazepin-2-ones rate determinations of racemisation (ka.- for C(3)-0CH3 derivative ( + )-1), degenerate nucleophilic exchange (k0 - for rac. 1 and rac. 2), and solvolysis (k5 - for C(3)-hemisuccinyl derivative 4) have been performed. These investigations revealed; (a) retention of .configuration during methanolysis of ( + )-3, (b) slow racemisation of ( + )-1 during solvolytic degenerate nucleophilic substitution (kefko. - - 4), (c} no participation of SNl retentive reaction, possible via intramolecular transfer of the methoxy group within intermediary compounds 4-6, (d) thermodi:namic parameters for racemisation of ( + )-1 between 20-40 °c; liH"" = 18.0 ± 0.8 kcal/moll**, liS"" = = - 7.2 ± 2.5 e. u.*** Mechanistic scheme is offered which accounts for all experimental results. The effect of the electrocyclic equilibrium on the electronic structure of N(4) protonated benzodiazepines, and its possible consequences for their mechanisms of biological activity on the central nervous system (CNS), have briefly been discussed

Cyclooxygenase-2 preserves flow-mediated remodelling in old obese Zucker rat mesenteric arteries

AIMS: Resistance arteries have a key role in the control of local blood flow and pressure, and chronic increases in blood flow induce endothelium-dependent outward hypertrophic remodelling. The incidence of metabolic syndrome increases with age, and the combination of these two risk factors impairs endothelium integrity, in part through an inflammatory process. We hypothesized that cyclooxygenase-2 (COX2) would affect remodelling in 12-month-old obese rats compared with young rats. METHODS AND RESULTS: Mesenteric arteries of obese and lean Zucker rats were alternatively ligated to generate high flow (HF) in the median artery. After 21 days, arteries were isolated for in vitro analysis. After 21 days, outward hypertrophic remodelling occurred in HF arteries in obese (498 +/- 20 vs. 443 +/- 18 mum intraluminal diameter in normal flow (NF) arteries, P &lt; 0.01), but not in lean rats (454 +/- 17 vs. 432 +/- 14, NS; n = 12 per group). Endothelium-dependent (acetylcholine)-mediated relaxation (AMR) was lower in obese than in lean rats. AMR was reduced by NO-synthase blockade in all groups, and eNOS expression was higher in HF than in NF arteries without difference between lean and obese rats. Indomethacin further reduced AMR in HF arteries from obese rats only. Obesity increased COX2 immunostaining in mesenteric arteries. Acute COX2 inhibition (NS398) significantly reduced AMR in HF arteries from obese rats only, suggesting production of vasodilator prostanoid(s). In obese rats chronically treated with the COX2 inhibitor celecoxib, outward remodelling did not occur in HF arteries and AMR was improved without reaching the level found in lean rats. CONCLUSION: COX2 preserved in part flow-mediated arterial remodelling in old obese rats. Nevertheless, this effect was not sufficient to keep endothelium-dependent relaxation to the level obtained in lean rats

From impulses to maladaptive actions: the insula is a neurobiological gate for the development of compulsive behavior.

Impulsivity is an endophenotype of vulnerability for compulsive behaviors. However, the neural mechanisms whereby impulsivity facilitates the development of compulsive disorders, such as addiction or obsessive compulsive disorder, remain unknown. We first investigated, in rats, anatomical and functional correlates of impulsivity in the anterior insular (AI) cortex by measuring both the thickness of, and cellular plasticity markers in, the AI with magnetic resonance imaging and in situ hybridization of the immediate early gene zif268, respectively. We then investigated the influence of bilateral AI cortex lesions on the high impulsivity trait, as measured in the five-choice serial reaction time task (5-CSRTT), and the associated propensity to develop compulsivity as measured by high drinking levels in a schedule-induced polydipsia procedure (SIP). We demonstrate that the AI cortex causally contributes to individual vulnerability to impulsive-compulsive behavior in rats. Motor impulsivity, as measured by premature responses in the 5-CSRTT, was shown to correlate with the thinness of the anterior region of the insular cortex, in which highly impulsive (HI) rats expressed lower zif268 mRNA levels. Lesions of AI reduced impulsive behavior in HI rats, which were also highly susceptible to develop compulsive behavior as measured in a SIP procedure. AI lesions also attenuated both the development and the expression of SIP. This study thus identifies the AI as a novel neural substrate of maladaptive impulse control mechanisms that may facilitate the development of compulsive disorders.This research was carried-out within the Department of Psychology and the Department of Pharmacology of the University of Cambridge as well as the INSERM AVENIR team Psychobiology of Compulsive Disorders of the University of Poitiers. It was supported by an INSERM AVENIR grant and a FYSSEN foundation grant to DB. MLD was supported by a PhD fellowship from the Fondation pour la Recherche Médicale (FRM) and ABR was supported by a post-doctoral fellowship from the INSERM. BJE was supported by the United Kingdom Medical Research Council (MRC) Grant 9536855.This is the author accepted manuscript. The final version is available from Nature Publishing Group via http://dx.doi.org/10.1038/mp.2015.14

Probability Density Function of Longitudinal Velocity Increment in Homogeneous Turbulence

Two conditional averages for the longitudinal velocity increment u_r of the simulated turbulence are calculated: h(u_r) is the average of the increment of the longitudinal Laplacian velocity field with u_r fixed, while g(u_r) is the corresponding one of the square of the difference of the gradient of the velocity field. Based on the physical argument, we suggest the formulae for h and g, which are quite satisfactorily fitted to the 512^3 DNS data. The predicted PDF is characterized as (1) the Gaussian distribution for the small amplitudes, (2) the exponential distribution for the large ones, and (3) a prefactor before the exponential function for the intermediate ones.Comment: 4 pages, 4 figures, using RevTeX3.

Longitudinal Structure Functions in Decaying and Forced Turbulence

In order to reliably compute the longitudinal structure functions in decaying and forced turbulence, local isotropy is examined with the aid of the isotropic expression of the incompressible conditions for the second and third order structure functions. Furthermore, the Karman-Howarth-Kolmogorov relation is investigated to examine the effects of external forcing and temporally decreasing of the second order structure function. On the basis of these investigations, the scaling range and exponents $\zeta_n$ of the longitudinal structure functions are determined for decaying and forced turbulence with the aid of the extended-self-similarity (ESS) method. We find that $\zeta_n$'s are smaller, for $n \geq 4$, in decaying turbulence than in forced turbulence. The reasons for this discrepancy are discussed. Analysis of the local slopes of the structure functions is used to justify the ESS method.Comment: 15 pages, 16 figure

Reactive oxygen species and cyclooxygenase 2-derived thromboxane A2 reduce angiotensin II type 2 receptor vasorelaxation in diabetic rat resistance arteries

Angiotensin II has a key role in the control of resistance artery tone and local blood flow. Angiotensin II possesses 2 main receptors. Although angiotensin II type 1 receptor is well known and is involved in the vasoconstrictor and growth properties of angiotensin II, the role of the angiotensin II type 2 receptor (AT2R) remains much less understood. Although AT2R stimulation induces vasodilatation in normotensive rats, it induces vasoconstriction in pathological conditions involving oxidative stress and cyclooxygenase 2 expression. Thus, we studied the influence of cyclooxygenase 2 on AT2R-dependent tone in diabetes mellitus. Mesenteric resistance arteries were isolated from Zucker diabetic fatty (ZDF) and lean Zucker rats and studied using in vitro using wire myography. In ZDF rats, AT2R-induced dilation was lower than in lean rats (11% versus 21% dilation). Dilation in ZDF rats returned to the control (lean rats) level after acute superoxide reduction (Tempol and apocynin), cyclooxygenase 2 inhibition (NS398), or thromboxane A(2) synthesis inhibition (furegrelate). Cyclooxygenase 2 expression and superoxide production were significantly increased in ZDF rat arteries compared with arteries of lean rats. After chronic treatment with Tempol, AT2R-dependent dilation was equivalent in ZDF and lean rats. Chronic treatment of ZDF rats with NS398 also restored AT2R-dependent dilation to the control (lean rats) level. Plasma thromboxane B(2) (thromboxane A(2) metabolite), initially high in ZDF rats, was decreased by chronic Tempol and by chronic NS398 to the level found in lean Zucker rats. Thus, in type 2 diabetic rats, superoxide and thromboxane A(2) reduced AT2R-induced dilation. These findings are important to take into consideration when choosing vasoactive drugs for diabetic patients