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Background and Objectives: Cocaine is a highly addictive substance, and with no approved medication for cocaine use disorder (CUD), leading to a heavy burden. Despite validated psychosocial treatments, relapse rates after detoxification are very high in CUD. Few consistent factors can predict abstinence after detoxification. Our study, therefore, aimed at identifying factors predicting abstinence among CUD patients after inpatient detoxification. Methods: Eighty‐one CUD inpatients were included during detoxification and characterized for clinical and sociodemographic data at baseline and at a follow‐up of 3 months after discharge, including a standard measure of their abstinence duration from cocaine. We performed Cox univariate analyzes to determine the factors associated with abstinence maintenance, followed by a multivariate Cox regression to identify independent predictors. Results: Abstinence maintenance was shorter in patients injecting cocaine (hazard ratio [HR] = 5.16, 95% confidence interval [CI]: 2.01–13.27, p <.001) and using cocaine heavily in the month before inclusion (HR = 1.03, 95% CI: 1.00–1.06, p =.046). Conversely, abstinence maintenance was longer in patients with longer inpatient detoxification stays (HR = 0.96, 95% CI: 0.94–0.99, p =.015) and prescribed with selective serotonin reuptake inhibitors (SSRIs) (HR = 0.30, 95% CI: 0.16–0.56, p <.001). Discussion and Conclusions: Patients with severe CUD may require longer inpatient stays to achieve abstinence. Regarding SSRI prescription, more specific studies are needed to provide stronger recommendations about their use in clinical practice. Scientific Significance: Our findings suggest several modifiable factors to improve inpatient treatment response in CUD. As there are no specific recommendations about the optimal duration of inpatient stay, our results could pave the way for evidence‐based guidelines. [ABSTRACT FROM AUTHOR]

General cognitive ability ("g") does not explain sex differences in academic test performance by the end of compulsory education. Instead, individual differences in specific reasoning abilities, after removing the effects of "g," may contribute to the observed gender gaps. Associations between general or specific cognitive abilities, sex, and educational attainments were analysed in a cross-sectional study of 11-year-olds (M = 133.5 months, SD = 3.5), at an age before substantive gender-related selection-bias occurred. The 178,599 pupils (89,545 girls and 89,054 boys) attending English state schools represented 93% of the UK's local education authorities. In 2004 each student completed the Cognitive Abilities Test-Third Edition (CAT3), assessing verbal, quantitative, and nonverbal reasoning abilities. These data were linked to each child's attainment scores on national Key Stage 2 tests in English, mathematics and science. A sex difference in "g," favoring girls, was statistically significant but of negligible effect size (Cohen's d = 0.01). Girls scored 26% of a "SD" higher than boys on a verbal residual factor, and boys scored 28% of a "SD" higher than girls on a quantitative residual factor, with negligible sex differences on a nonverbal residual factor (1% of a SD). In education, 10% more girls than boys achieved UK government targets in English. In mathematics and science, sex differences were less apparent at the government target grade (Level 4), although a 5% greater proportion of boys than girls performed at the highest level in mathematics (Level 5). General cognitive ability ("g") was strongly related to an educational factor score (r = 0.83) as expected, and did not explain sex differences in academic performance. In general linear models, a verbal residual factor explained up to 29% of girls' higher English attainment, and better quantitative skills among boys explained 50% of their higher attainment in mathematics. Besides the significant contributions of specific cognitive abilities to gender differences in English and mathematics, there remains substantive variance of the educational gender gap left to explain. (Contains 5 tables and 1 figure.)

Hunger is defined as a strong desire or need for food while satiety is the condition of being full or gratified. The maintenance of energy homeostasis requires a balance between energy intake and energy expenditure. The regulation of food intake is a complex behavior. It requires discrete nuclei within the central nervous system (CNS) to detect signals from the periphery regarding metabolic status, process and integrate this information in a coordinated manner and to provide appropriate responses to ensure that the individual does not enter a state of positive or negative energy balance. This review of hunger and satiety will examine the CNS circuitries involved in the control of energy homeostasis as well as signals from the periphery, both hormonal and neural, that convey pertinent information regarding short-term and long-term energy status of the individual.

This 5-year prospective longitudinal study of 70,000+ English children examined the association between psychometric intelligence at age 11 years and educational achievement in national examinations in 25 academic subjects at age 16. The correlation between a latent intelligence trait (Spearman's "g"from CAT2E) and a latent trait of educational achievement (GCSE scores) was 0.81. General intelligence contributed to success on all 25 subjects. Variance accounted for ranged from 58.6% in Mathematics and 48% in English to 18.1% in Art and Design. Girls showed no advantage in "g", but performed significantly better on all subjects except Physics. This was not due to their better verbal ability. At age 16, obtaining five or more GCSEs at grades A*-C is an important criterion. 61% of girls and 50% of boys achieved this. For those at the mean level of g at age 11, 58% achieved this; a standard deviation increase or decrease in g altered the values to 91% and 16%, respectively.

Background and aims: There is uncertainty about the extent or even existence of sex differences in the mean and variability of reasoning test scores ( Jensen, 1998; Lynn, 1994, ; Mackintosh, 1996). This paper analyses the Cognitive Abilities Test (CAT) scores of a large and representative sample of UK pupils to determine the extent of any sex differences. Sample: A nationally representative UK sample of over 320,000 school pupils aged 11-12 years was assessed on the CAT (third edition) between September 2001 and August 2003. The CAT includes separate nationally standardized tests for verbal, quantitative, and non-verbal reasoning. The size and recency of the sample is unprecedented in research on this issue. Methods: The sheer size of the sample ensures that any sex difference will achieve statistical significance. Therefore, effect sizes (d) and variance ratios (VR) are employed to evaluate the magnitude of sex differences in mean scores and in score variability, respectively. Results: The mean verbal reasoning score for girls was 2.2 standard score points higher than the mean for boys, but only 0.3 standard points in favour of girls for non-verbal reasoning (NVR), and 0.7 points in favour of boys for quantitative reasoning (QR). However, for all three tests there were substantial sex differences in the standard deviation of scores, with greater variance among boys. Boys were over represented relative to girls at both the top and the bottom extremes for all tests, with the exception of the top 10% in verbal reasoning. Conclusions: Given the small differences in means, explanations for sex differences in wider domains such examination attainment at age 16 need to look beyond conceptions of "ability". Boys tend to be both the lowest and the highest performers in terms of their reasoning abilities, which warns against the danger of stereotyping boys as low achievers.

To maintain homeostasis autonomic control centers in the hypothalamus and medulla must respond appropriately to both external and internal stimuli. Although protected behind the blood-brain barrier, neurons in these autonomic control centers are known to be influenced by changing levels of important signaling molecules in the systemic circulation (e.g., osmolarity, glucose concentrations, and regulatory peptides). The subfornical organ belongs to a group of specialized central nervous system structures, the circumventricular organs, which are characterized by the lack of the normal blood-brain barrier, such that circulating lipophobic substances may act on neurons within this region and via well-documented efferent neural projections to hypothalamic autonomic control centers, influence autonomic function. This review focuses on the role of the subfornical organ in sensing peripheral signals and transmitting this information to autonomic control centers in the hypothalamus. autonomic; cardiovascular; satiety signals; immune regulation; blood-brain barrier doi: 10.1152/ajpregu.00103.2010.

Baraboi ED, Smith P, Ferguson AV, Richard D. Lesions of area postrema and subfomical organ alter exendin-4-induced brain activation without preventing the hypophagic effect of the GLP-1 receptor agonist. Am J Physiol Regul Integr Comp Physiol 298: R1098-R1110, 2010. First published January 27, 2010; doi:10.1152/ajpregu.003226.2009.--The mechanism and route whereby glucagon-like peptide 1 (GLP-I) receptor agonists, such as GLP-I and exendin-4 (Ex-4), access the central nervous system (CNS) to exert their metabolic effects have yet to be clarified. The primary objective of the present study was to investigate the potential role of two circumventficular organs (CVOs), the area postrema (AP) and the subfornical organ (SFO), in mediating the metabolic and CNS-stimulating effects of Ex-4. We demonstrated that electrolytic ablation of the AP, SFO, or AP + SFO does not acutely prevent the anorectic effects of Ex-4. AP + SFO lesion chronically decreased food intake and body weight and also modulated the effect of Ex-4 on the neuronal activation of brain structures involved in the hypothalamic-pituitary-adrenal axis and glucose metabolism. The results of the study also showed that CVO lesions blunted Ex-4-induced expression of c-fos mRNA (a widely used neuronal activity marker) in 1) limbic structures (bed nucleus of the stria terminalis and central amygdala), 2) hypothalamus (paraventricular hypothalamic nucleus, supraoptic nucleus, and arcuate nucleus), and 3) hindbrain (lateral and lateral-external parabrachial nucleus, medial nucleus of the solitary tract, and ventrolateral medulla). In conclusion, although the present results do not support a role for the CVOs in the anorectic effect induced by a single injection of Ex-4, they suggest that the CVOs play important roles in mediating the actions of Ex-4 in the activation of CNS structures involved in homeostatic control. food intake; energy expenditure; hypothalamic-pituitary-adrenal axis; glucose metabolism; c-fos doi: 10.1152/ajpregu.00326.2009.

We have employed microarray technology using Affymetrix 230 2.0 genome chips to initially catalog the transcriptome of the subfornical organ (SFO) under control conditions and to also evaluate the changes (common and differential) in gene expression induced by the challenges of fluid and food deprivation. We have identified a total of 17,293 genes tagged as present in one of our three experimental conditions, transcripts, which were then used as the basis for further filtering and statistical analysis. In total, the expression of 46 genes was changed in the SFO following dehydration compared with control animals (22 upregulated and 24 downregulated), with the largest change being the greater than fivefold increase in brain-derived neurotrophic factor (BDNF) expression, while significant changes in the expression of the calcium-sensing (upregulated) and apelin (downregulated) receptors were also reported. In contrast, food deprivation caused greater than twofold changes in a total of 687 transcripts (222 upregulated and 465 downregulated), including significant reductions in vasopressin, oxytocin, promelanin concentrating hormone, cocaine amphetamine-related transcript (CART), and the endothelin type B receptor, as well as increases in the expression of the [GABA.sub.B] receptor. Of these regulated transcripts, we identified 37 that are commonly regulated by fasting and dehydration, nine that were uniquely regulated by dehydration, and 650 that are uniquely regulated by fasting. We also found five transcripts that were differentially regulated by fasting and dehydration including BDNF and CART. In these studies we have for the first time described the transcriptome of the rat SFO and have in addition identified genes, the expression of which is significantly modified by either water or food deprivation. dehydration; circumventricular organ; receptors

Transepithelial [[sup.14]C]urea fluxes were measured across cultured Madin-Darby canine kidney (MDCK) cells permanently transfected to express the urea transport protein UT-A1. The urea fluxes were typically increased from a basal rate of 2 to 10 and 25 nmol x [cm.sup.-2] x [min.sup.-1] in the presence of vasopressin and forskolin, respectively. Flux activation consisted of a rapid-onset component of small amplitude that leveled off within ~ 10 min and at times even decreased again, followed by a delayed, strong increase over the next 30-40 min. Forskolin activated urea transport through activation of adenylyl cyclase; dideoxyforskolin was inactive. Vasopressin activated urea transport only from the basolateral side and was blocked by OPC-31260, indicating that its action was mediated by basolateral [V.sub.2] receptors. In the presence of the phosphodiesterase inhibitor IBMX, vasopressin activated as strongly as forskolin. By itself, IBMX caused a slow increase over 50 min to ~5 nmol x [cm.sup.-2] x [min.sup.-1] x 8-Bromoadenosine 3',5'-cyclic monophosphate (8-BrcAMP; 300 [micro]M) activated urea flux only when added basolaterally. IBMX augmented the activation by basolateral 8-BrcAMP. Urea flux activation by vasopressin and forskolin were only partially blocked by the protein kinase A inhibitor H-89. Even at concentrations >10 [micro]M, urea flux after 60 min of stimulation was reduced by urea transporter: Madin-Darby canine kidney cells

Urea transport in MDCK cells that are stably transfected with UT-A1. Am J Physiol Cell Physiol 286: C1264-C1270, 2004. First published February 4, 2004; 10.1152/ ajpcelh00499.2003.--Progress in understanding the cell biology of urea transporter proteins has been hampered by the lack of an appropriate cell culture system. The goal of this study was to create a polarized epithelial cell line that stably expresses the largest of the rat renal urea transporter UT-A isoforms, UT-A1. The gene for UT-A1 was cloned into pcDNA5/FRT and transfected into Madin-Darby canine kidney (MDCK) cells with an integrated Flp recombination target site. The cells from a single clone were grown to confluence on collagen-coated membranes until the resistance was > 1,500 [ohm].[cm.sup.2]. Transepithelial [[.sub.14]C]urea fluxes were measured at 37[degrees]C in a HC[O.sup.-.sub.3]/ C[O.sub.2] buffer, pH 7.4, with 5 mM urea. The baseline fluxes were not different between unstimulated UT-Al-transfected MDCK cells and nontransfected or sham-transfected MDCK cells. However, only in the UT-Al-transfected cells was UT-Al protein expressed (as measured by Western blot analysis) and urea transport stimulated by forskolin or arginine vasopressin. Forskolin and arginine vasopressin also increased the phosphorylation of UT-Al. Thionicotinamide, dimethylurea, and phloretin inhibited the forskolin-stimulated [[.sup.14]C]-urea fluxes in the UT-A1-transfected MDCK cells. These characteristics mimic those seen in rat terminal inner medullary collecting ducts. This new polarized epithelial ceil line stably expresses UT-Al and reproduces several of the physiological responses observed in rat terminal inner medullary collecting ducts. urea transporter-A1; arginine vasopressin; collecting duct; Madin-Darby canine kidney cells

Grammaire (1572). By PIERRE DE LA RAMEE. Ed. by COLETTE DEMAIZIERE. (Textes de la Renaissance, 3: Langue francaise, 40) Paris: Champion. 2001. 165 pp. 240 F. Specialists in the history [...]