Fetal testosterone (2D:4D) as predictor of cognitive reflection

The Cognitive Reflection Test (CRT) is a test introduced by S. Frederick (2005) Cognitive reflection and decision making, J Econ Perspect 19(4): 25-42. The task is designed to measure the tendency to override an intuitive response that is incorrect and to engage in further reflection that leads to the correct response. The consistent sex differences in CRT performance may suggest a role for gonadal hormones, particularly testosterone. A now widely studied putative marker for fetal testosterone is the second-to-fourth digit ratio (2D:4D). This paper tests to what extent 2D:4D, as a proxy for prenatal exposure to testosterone, can predict CRT scores in a sample of 623 students. After controlling for sex, we observe that a lower 2D:4D (reflecting a higher exposure to testosterone) is significantly associated with a higher number of correct answers. The result holds for both hands? 2D:4Ds. In addition, the effect appears to be sharper for females than for males. We also control for patience and math proficiency, which are significantly related to performance in the CRT. But the effect of 2D:4D on performance in CRT is not reduced with these controls, implying that these variables are not mediating the relationship between digit ratio and CRT.

Circadian glomerular function: from physiology to molecular and therapeutical aspects.

Life on earth is rhythmic by essence due to day/night alternation, and many biological processes are also cyclic. The kidney has a special role in the organism, controlling electrolytes and water balance, blood pressure, elimination of metabolic waste and xenobiotics and the production of several hormones. The kidney is submitted to changes throughout 24 h with periods of intense activity followed by calmer periods. Filtration, reabsorption and secretion are the three components determining renal function. Here, we review circadian changes related to glomerular function and proteinuria and emphasize the role of the clock in these processes.

Glucagon-like peptide-1 and control of insulin secretion.

Although glucose is the major regulator of insulin secretion by pancreatic beta cells, its action is modulated by several neural and hormonal stimuli. In particular, hormones secreted by intestinal endocrine cells stimulate glucose-induced insulin secretion very potently after nutrient absorption. These hormones, called gluco-incretins or insulinotropic hormones, are major regulators of postprandial glucose homeostasis. The main gluco-incretins are GIP (gastric inhibitory polypeptide or glucose-dependent insulinotropic polypeptide) and GLP-1 (glucagon-like polypeptide-1). The secretion of GIP, a 42 amino acid polypeptide secreted by duodenal K cells, is triggered by fat and glucose. GIP stimulation of insulin secretion depends on the presence of specific beta-cell receptors and requires glucose at a concentration at least equal to or higher than the normoglycaemic level of approximately 5 mM. GIP accounts for about 50% of incretin activity, and the rest may be due to GLP-1 which is produced by proteolytic processing of the preproglucagon molecule in intestinal L cells. GLP-1 is the most potent gluco-incretin characterized so far. As with GIP, its stimulatory action requires a specific membrane receptor and normal or elevated glucose concentrations. Contrary to GIP, the incretin effect of GLP-1 is maintained in non-insulin-dependent diabetic patients. This peptide or agonists of its beta-cell receptor could provide new therapeutic tools for the treatment of Type II diabetic hyperglycaemia.

Acute post-exercise oxygen uptake, hormone and plasma metabolite response in obese men.

This study aimed to compare oxygen uptake (  V˙O2), hormone and plasma metabolite responses during the 30 min after submaximal incremental exercise (Incr) performed at the same relative/absolute exercise intensity and duration in lean (L) and obese (O) men. Eight L and 8 O men (BMI: 22.9±0.4; 37.2±1.8 kg · m(-2)) completed Incr and were then seated for 30 min.   V˙O2 was monitored during the first 10 min and from the 25-30(th) minutes of recovery. Blood samples were drawn for the determination of hormone (catecholamines, insulin) and plasma metabolite (NEFA, glycerol) concentrations. Excess post-exercise oxygen consumption (EPOC) magnitude during the first 10 min was similar in O and in L (3.5±0.4; 3.4±0.3 liters, respectively, p=0.86). When normalized to percent change (  V˙O2END=100%), %   V˙O2END during recovery was significantly higher from 90-120 s in O than in L (p≤0.04). There were no significant differences in catecholamines (p≥0.24), whereas insulin was significantly higher in O than in L during recovery (p=0.01). The time-course of glycerol was similar from 10-30 min of recovery (-42% for L; -41% for O, p=0.85), whereas significantly different patterns of NEFA were found from 10-30 min of recovery between groups (-18% for L; +8% for O, p=0.03). Despite similar EPOC, a difference in   V˙O2 modulation between groups was observed, likely due to faster initial rates of   V˙O2 decline in L than in O. The different patterns of NEFA between groups may suggest a lower NEFA reesterification during recovery in O, which was not involved in the rapid EPOC component.

Evaluación de necesidades y diseño de la intervención para la reintegración social de los delincuentes sexuales de alto riesgo

Informe ejecutivo del estudio de adaptación "Evaluación de necesidades y diseño de la intervención para la reinserción social de los delincuentes sexuales de alto riesgo: Adaptación de los Círculos de Apoyo y Responsabilidad al sistema de ejecución penal de Cataluña".

Needs assessment and design of the intervention for high risk sex offenders social reintegration

Executive report of the adaptation study "Needs assessment and design of the intervention for high risk sex offenders social reintegration: Adaptation of the Circles of Support and Accountability to the Penal Enforcement System of Catalonia".

Metabolic and physiologic effects of an endotoxin challenge in healthy obese subjects.

Aim: The obesity epidemic has increased the number of obese patients admitted to the ICU. In vitro studies suggest that adipose tissue response to inflammation is enhanced: in vivo data are not conclusive yet. The aim of this study was to test the physiologic response of healthy obese subjects to a standardized intravenous LPS challenge.Methods: Prospective single-blind, randomized, cross-over study in eight subjects (four men, four women), aged 34 +/- 7 years, BMI 34.7 +/- 4.2, without glucose intolerance and lipid abnormalities, testing the impact of intravenous LPS (2 ng kg(-1) of actual body weight) versus placebo.Results: Temperature, hemodynamic variables, indirect calorimetry and blood samples (TNF-alpha, IL-6, stress hormones, hs-CRP) were collected. After LPS temperature, heart rate. TNF-alpha and IL-6 concentrations and stress hormones (cortisol and glucagon) increased significantly, with maximal responses between 120 and 240 min after the injection. The pattern, the timing and the magnitude of change were similar to those observed in lean subjects.Conclusion: This study shows that healthy obese subjects have a similar response pattern to intravenous LPS as described in lean subjects.

Modulation in Wistar rats of blood corticosterone compartmentation by sex and prior exposure to a cafeteria diet

In the metabolic syndrome, glucocorticoid activity is increased, but circulating levels show little change. Most of blood glucocorticoids are bound to corticosteroid-binding globulin (CBG), which liver expression and circulating levels are higher in females than in males. Since blood hormones are also bound to blood cells, and the size of this compartment is considerable for androgens and estrogens, we analyzed whether sex or eating a cafeteria diet altered the compartmentation of corticosterone in rat blood. The main corticosterone compartment in rat blood is that specifically bound to plasma proteins, with smaller compartments bound to blood cells or free. Cafeteria diet increased the expression of liver CBG gene, binding plasma capacity and the proportion of blood cell-bound corticosterone. There were marked sex differences in blood corticosterone compartmentation in rats, which were unrelated to testosterone. The use of a monoclonal antibody ELISA and a polyclonal Western blot for plasma CBG compared with both specific plasma binding of corticosterone and CBG gene expression suggested the existence of different forms of CBG, with varying affinities for corticosterone in males and females, since ELISA data showed higher plasma CBG for males, but binding and Western blot analyses (plus liver gene expression) and higher physiological effectiveness for females. Good cross- reactivity to the antigen for polyclonal CBG antibody suggests that in all cases we were measuring CBG.The different immunoreactivity and binding affinity may help explain the marked sex-related differences in plasma hormone binding as sex-linked different proportions of CBG forms.

Small but thick enough-the Arabidopsis hypocotyl as a model to study secondary growth.

The continuous production of vascular tissues through secondary growth results in radial thickening of plant organs and is pivotal for various aspects of plant growth and physiology, such as water transport capacity or resistance to mechanical stress. It is driven by the vascular cambium, which produces inward secondary xylem and outward secondary phloem. In the herbaceous plant Arabidopsis thaliana (Arabidopsis), secondary growth occurs in stems, in roots and in the hypocotyl. In the latter, radial growth is most prominent and not obscured by parallel ongoing elongation growth. Moreover, its progression is reminiscent of the secondary growth mode of tree trunks. Thus, the Arabidopsis hypocotyl is a very good model to study basic molecular mechanisms of secondary growth. Genetic approaches have succeeded in the identification of various factors, including peptides, receptors, transcription factors and hormones, which appear to participate in a complex network that controls radial growth. Many of these players are conserved between herbaceous and woody plants. In this review, we will focus on what is known about molecular mechanisms and regulators of vascular secondary growth in the Arabidopsis hypocotyl.

Circulating sex steroids during pregnancy and maternal risk of non-epithelial ovarian cancer.

BACKGROUND: Sex steroid hormones have been proposed to play a role in the development of non-epithelial ovarian cancers (NEOC) but so far no direct epidemiological data are available.METHODS: A case-control study was nested within the Finnish Maternity Cohort, the world's largest bio-repository of serum specimens from pregnant women. Study subjects were selected among women who donated a blood sample during a singleton pregnancy that led to the birth of their last child preceding diagnosis of NEOC. Case subjects were 41 women with sex-cord stromal tumors (SCST) and 21 with germ cell tumors (GCT). Three controls, matching the index case for age, parity at the index pregnancy, and date at blood donation were selected (n=171). Odds ratios (OR) and 95% confidence intervals (CI) associated with concentrations of testosterone, androstenedione, 17-OH-progesterone, progesterone, estradiol and sex hormone binding globulin (SHBG) were estimated through conditional logistic regression.RESULTS: For SCST, doubling of testosterone, androstenedione and 17-OH-progesterone concentrations were associated with about 2-fold higher risk of SCST [ORs and 95% CI of 2.16 (1.25-3.74), 2.16 (1.20-3.87), and 2.62 (1.27-5.38), respectively]. These associations remained largely unchanged after excluding women within 2, 4 or 6 years lag-time between blood donation and cancer diagnosis. Sex steroid hormones concentrations were not related to maternal risk of GCT.CONCLUSIONS: This is the first prospective study providing initial evidence that elevated androgens play a role in the pathogenesis of SCST. Impact: Our study may note a particular need for larger confirmatory investigations on sex steroids and NEOC.

Prise alimentaire: pas uniquement une question de volonté [Food intake: not only a question of will!]

During many years, we thought that food intake was only a question of will. Nevertheless, in the second part on the XXth century, we identified several hormones regulating food intake and energy expenditure. Furthermore, these hormones seem to be implicated in the pathogenesis of obesity and in weight loss following bariatric surgery. This short review highlights the main mechanisms implicated in food intake and energy expenditure and also their implication in obesity and bariatric surgery.

Mate availability and male dispersal in the Argentine ant Linepithema humile (Mayr) (=Iridomyrmex humilis)

In the Argentine ant Linepithema humile (=Iridomyrmex humilis) only males disperse whereas female sexuals (unmated winged queens) stay in their mother nest where they mate. This study investigated (1) whether dispersing males are accepted into foreign colonies, (2) whether they can mate with resident female sexuals, and (3) whether the propensity of males to disperse is affected by the expectation of mating in their mother nest. Field experiments demonstrated that males were accepted into foreign colonies only when these colonies contained female sexuals or queen pupae. Before and after the time of (sic) female sexuals, workers attacked and killed most of the foreign males. Laboratory experiments snowed that males that successfully enter foreign colonies can mate with resident female sexuals. The propensity of males to disperse was significantly influenced by the presence of female sexuals in their nest. Males were more likely to fly out from colonies containing no female sexuals than from those with them. These results are consistent with males preferentially dispersing when there is little or no opportunity to mate in their mother nest. Thus there are two mating strategies available for males: staying in their mother nest when an opportunity to mate arises or dispersing and attempting to mate in a foreign nest when there are no female sexuals in their mother nest. This latter behaviour could mediate gene flow between colonies and account for the lack of significant inbreeding previously documented in this species.

Role for JIP-1/IB1 in pancreatic β-cell and adipocyte dysfunctions in type 2 diabetes and obesity

L'insuline, produite par les cellules β du pancréas, joue un rôle central dans le contrôle de la glycémie. Un manque d'insuline entraine le diabète de type 2, une maladie répandue au stade d'épidémie au niveau mondial. L'augmentation du nombre de personnes obèses est une des causes principales du développement de la maladie. Avec l'obésité les tissus tels que le foie, le muscle, et le tissu adipeux deviennent résistants à l'insuline. En général, cette résistance est équilibrée par une augmentation de la sécrétion d'insuline. De ce fait, un grand nombre d'individus obèses ne deviennent pas diabétiques. Lorsque les cellules β ne produisent plus suffisamment d'insuline, alors le diabète se développe. Dans l'obésité, les cellules graisseuses sont résistantes à l'insuline et relâchent des lipides et autres produits qui affectent le bon fonctionnement et la vie des cellules β. «c-Jun Ν terminal Kinase» (JNK) est une enzyme qui joue un rôle important dans la résistance de l'insuline des cellules graisseuses. Cette même en2yme contribue aussi au déclin de la cellule β dans les conditions diabétogènes, et représente ainsi une cible thérapeutique potentielle du diabète. L'objectif de cette thèse a été de comprendre le mécanisme conduisant à l'activité de JNK dans les adipocytes et cellules β, dans l'obésité et le diabète de type 2. Nous montrons que les variations de JNK sont la conséquence de taux anormaux de JIP-1/EB1, une protéine qui a été impliquée dans certaines formes génétiques de diabète de type 2. En outre nous décrivons le mécanisme responsable des anomalies de JIP1/IB1 dans les adipocytes et cellules β. La restauration des taux de JIP-1/EB1 dans les deux types cellulaires pourrait être un objectif des thérapeutiques antidiabétiques actuelles et futures. - Le nombre d'individus touchés par le diabète de type 2 atteint aujourd'hui des proportions épidémiques à l'échelle mondiale. L'augmentation de la prévalence de l'obésité est la cause principale du développement de la maladie, qui, en général, survient suite à une perte de la sensibilité à l'insuline des tissus périphériques. Dans un grand nombre des cas, l'insulino-résistance est compensée par une augmentation de la sécrétion de l'insuline par les cellules β pancréatiques. Le diabète apparaît lorsque l'insuline n'est plus produite en quantité suffisante pour contrecarrer la résistance à l'insuline des tissus. Le défaut de production de l'insuline résulte du dysfonctionnement et de la réduction massive des cellules β. Les acides gras libres non estérifiés, en particulier le palmitate, provenant d'une alimentation riche en lipides et libérés par les adipocytes insulino-résistants contribuent au déclin de la cellule β en activant la voie de signalisation «cJun N-terminal kinase» (JNK). L'activation de JNK contribue aussi à la résistance à l'insuline des adipocytes dans l'obésité, soulignant ainsi l'importance de cette voie de signalisation dans la pathophysiologie du diabète. L'objectif de cette thèse a été de comprendre les mécanismes qui régulent JNK dans les cellules β et les adipocytes. Nous montrons que l'activation de JNK dans ces deux types cellulaires est la conséquence de la variation des taux de «JNK interacting protein 1» appelé aussi «islet brain 1» (JEP-1/ΓΒΙ), une protéine qui attache les kinases de la signalisation de JNK et dont des variations génétiques ont été associées avec le diabète de type 2. Dans les cellules β cultivées avec du palmitate, ainsi que dans les adipocytes dans l'obésité, l'expression de JEP-l/BBl est modifiée. Les modulations de l'expression de JEP-1/ΓΒΙ sont réalisées par le facteur de transcription «inducible cAMP early repressor» (ICER). L'expression d'ICER dans les adipocytes est diminuée dans l'obésité, et corrèle avec l'augmentation des niveaux de JEP-1/IB1. A l'inverse, le niveau d'expression d'ICER est augmenté dans les cellules β cultivées avec du palmitate, et cette augmentation perturbe le bon fonctionnement des cellules en réduisant les niveaux de JEP-l/IBl. Comme le palmitate, les particules pro-athérogéniques LDL-cholesterol oxydés, sont élevées chez les personnes obèses et diabétiques et sont délétères aux cellules β. Ces particules modifiées activent JNK dans les cellules β en diminuant l'expression de JIP-1/IB1 via ICER. Tous ces résultats montrent que le dérèglement de l'expression de JIP-l/EBl par ICER joue un rôle central dans l'activation de JNK dans les adipocytes et cellules β en souffrance dans l'obésité et le diabète de type 2. La restauration appropriée des niveaux de JEPl/IBl et d'ICER pourrait être considérée comme un objectif pour mesurer l'efficacité des traitements antidiabétiques actuels et futurs. - Type 2 diabetes has reached epidemic proportions worldwide, and poses a major socio-economic burden on developed and developing societies. The disease is often accompanied by obesity, and arises when β-cells produce insufficient insulin to meet the increased hormone demand, caused by insulin resistance. In obesity, enlargement of adipocytes contribute to their dysfunction, which is characterized by the abnormal release of some bioactive products such as non-esterified free fatty acids (NEF As). Chronic plasma elevation of NEF As elicits β-cell dysfunction and death, thereby, representing a key feature for development of diabetes in obesity (diabesity). Palmitate is the most abundant circulating NEF As in obesity, which triggers adipocytes and β-cell dysfunction. The effects of palmitate rely on the induction of the cJun N-terminal kinase (JNK) pathway. Activation of JNK promotes both β-cells dysfunction and insulin resistance in adipocytes. This thesis was undertaken to investigate the mechanisms accounting for the induction of the JNK pathway caused by palmitate. JNK is regulated by the scaffold protein JNK interacting protein-1, also called islet brain 1 (JIP-1/IB1). The levels of JDM/IB1 are critical for glucose homeostasis, as genetic variations within the gene were associated with diabetes. We found that activation of JNK in both, β-cells exposed to palmitate, and in adipocytes of obese mice, results from variations in the expression of JIP-l/EBl. Modifications in the JIP-1/IB1 levels were the consequence of abnormal expression of the inducible cAMP early repressor (ICER) in the two cell types. In addition, our data show that this repressor plays a key role in abnormal production of adipocyte hormones and β-cell dysfunction evoked by the pro-atherogenic oxidized LDL. Taken together, this study proposes that fine-tuning of appropriate levels of JIP-l/EBl, and ICER could circumvent β-cell failure, adipocyte dysfunction, and thereby, development of diabesity.

Anàlisis antropològica de les restes neolítiques de la Caserna de Sant Pau (Biometria, Dentició, ADN i Microestriació Dentària).

Les restes esquelètiques analitzades corresponen tant al nivell neolític (n=26) com a l"època del bronze (n=2), encara que aquí es presenten tan sols els resultats de la població neolítica (taula 1). En tots els casos les sepultures són individuals, amb l"única excepció de la sepultura 20, on s"han recuperat les restes corresponents a un individu femení adult (CSP201) i un fetus (CSP202) (taula 1). Per tal de caracteritzar biomètricament la població s"ha emprat la metodologia proposada per Martin i Saller (1959), Brothwell (1981) i Bass (1971). La determinació del sexe s"ha realitzat a través dels caràcters sexuals secundaris del crani i de la pelvis, i se"n pot trobar una descripció més detallada a Estebaranz et alii (2007). En el cas específic de les paleopatologies es van seguir les recomanacions de Campillo (Campillo, 1977).