Maternal affective disorder and children’s representation of their families

Children’s perceptions of family relationship are related to their later emotional and social adjustment. This is of particular relevance in the context of family stressors such as maternal affective disorder. This study investigated the effects of maternal postnatal depression and anxiety on children’s family representations. In our sample of postnatally depressed mothers we also explored marital conflict as mediator between maternal psychopathology and children’s representations. Family drawings of 235 4–5 year-old children (93 control, 53 depressed and 89 anxious) were examined. When compared to controls, children of depressed, but not of anxious mothers, were more likely to draw themselves as less prominent than other family members and to represent a dysfunctional family, less likely to represent themselves with a happy face and showed a greater tendency of drawing bizarre pictures. Marital conflict mediated the association between maternal depression and dysfunctionality in drawings.

History of eating disorder in mothers of children with early onset eating disorder or disturbance

The literature suggests that there is significant familial aggregation of eating disorders. A specific association has also been reported between childhood feeding problems and maternal eating disorder. This study investigates whether subgroups of children with early onset eating disturbance are distinguished by maternal eating disorder history. The mothers of 66 children with either anorexia nervosa (AN), food avoidance emotional disorder (FAED) or selective eating (SE) were interviewed to ascertain eating disorder history. Seventeen per cent of mothers reported a history of eating disorder, compared with 3%–5% reported for community samples. A history of eating disorder was reported by 5.9% of mothers of children with SE, 12.9% of mothers of children with AN and 33.3% of mothers of children with FAED. The findings, based on this small sample, suggest that children with FAED are especially likely to have grown up in a dysfunctional food environment.

Behavioural expressions, imagery and perfectionism

Background: High levels of multidimensional perfectionism may be dysfunctional in their own right and can also impact on the maintenance and treatment of Axis I psychiatric disorders. Aims: This paper sought to describe the behavioural expressions and imagery associated with perfectionism in a non-clinical sample. Method: Participants (n=59) completed a newly developed questionnaire to assess behavioural expressions of perfectionism, and an adapted interview to assess perfectionism-related intrusive mental images. Results: The study found that those high in perfectionism took longer to complete tasks, experienced more checking and safety behaviour whilst carrying out tasks, and had greater trouble actually completing tasks compared to those low in perfectionism. In addition, those with higher levels of perfectionism experienced intrusive mental imagery, which was more distressing, harder to dismiss, and had more impact on behaviour than those with lower levels of perfectionism. Conclusions: This research provides an initial exploration of the specific behaviours and intrusive mental imagery associated with perfectionism. The new behavioural measure of perfectionism could prove useful clinically in the assessment of change; however, these findings are preliminary and warrant replication in a clinical sample in order to examine their treatment implications.

TRIM32 regulates skeletal muscle stem cell differentiation and is necessary for normal adult muscle regeneration

Limb girdle muscular dystrophy type 2H (LGMD2H) is an inherited autosomal recessive disease of skeletal muscle caused by a mutation in the TRIM32 gene. Currently its pathogenesis is entirely unclear. Typically the regeneration process of adult skeletal muscle during growth or following injury is controlled by a tissue specific stem cell population termed satellite cells. Given that TRIM32 regulates the fate of mammalian neural progenitor cells through controlling their differentiation, we asked whether TRIM32 could also be essential for the regulation of myogenic stem cells. Here we demonstrate for the first time that TRIM32 is expressed in the skeletal muscle stem cell lineage of adult mice, and that in the absence of TRIM32, myogenic differentiation is disrupted. Moreover, we show that the ubiquitin ligase TRIM32 controls this process through the regulation of c-Myc, a similar mechanism to that previously observed in neural progenitors. Importantly we show that loss of TRIM32 function induces a LGMD2H-like phenotype and strongly affects muscle regeneration in vivo. Our studies implicate that the loss of TRIM32 results in dysfunctional muscle stem cells which could contribute to the development of LGMD2H.

The President above parties: a founding illusion of the Fifth Republic

De Gaulle, founder of the Fifth French Republic, cherished the notion that the president of the Republic could somehow stand above party politics. In many ways this belief shaped the early institutional configuration of the new Republic. Party politics, however, rapidly reached the presidency, especially with the move, under the constitutional reform of 1962, to direct election of the president. This article charts the development of France's 'political constitution' and the relationship between president and parties over the first decade of the Fifth Republic. It finds that although the presidency became the prime goal of party political competition, the (often dysfunctional) illusion of a head of state above politics continues to shape the behaviour and perceptions of French presidents.

A microchannel neuroprosthesis for bladder control after spinal cord injury in rat

A severe complication of spinal cord injury is loss of bladder function (neurogenic bladder), which is characterized by loss of bladder sensation and voluntary control of micturition (urination), and spontaneous hyperreflexive voiding against a closed sphincter (detrusor-sphincter dyssynergia). A sacral anterior root stimulator at low frequency can drive volitional bladder voiding, but surgical rhizotomy of the lumbosacral dorsal roots is needed to prevent spontaneous voiding and dyssynergia. However, rhizotomy is irreversible and eliminates sexual function, and the stimulator gives no information on bladder fullness. We designed a closed-loop neuroprosthetic interface that measures bladder fullness and prevents spontaneous voiding episodes without the need for dorsal rhizotomy in a rat model. To obtain bladder sensory information, we implanted teased dorsal roots (rootlets) within the rat vertebral column into microchannel electrodes, which provided signal amplification and noise suppression. As long as they were attached to the spinal cord, these rootlets survived for up to 3 months and contained axons and blood vessels. Electrophysiological recordings showed that half of the rootlets propagated action potentials, with firing frequency correlated to bladder fullness. When the bladder became full enough to initiate spontaneous voiding, high-frequency/amplitude sensory activity was detected. Voiding was abolished using a high-frequency depolarizing block to the ventral roots. A ventral root stimulator initiated bladder emptying at low frequency and prevented unwanted contraction at high frequency. These data suggest that sensory information from the dorsal root together with a ventral root stimulator could form the basis for a closed-loop bladder neuroprosthetic. Copyright © 2013, American Association for the Advancement of Science

Endocannabinoids, FOXO and the metabolic syndrome: redox, function and tipping point--the view from two systems

The endocannabinoid system (ECS) was only 'discovered' in the 1990s. Since then, many new ligands have been identified, as well as many new intracellular targets--ranging from the PPARs, to mitochondria, to lipid rafts. It was thought that blocking the CB-1 receptor might reverse obesity and the metabolic syndrome. This was based on the idea that the ECS was dysfunctional in these conditions. This has met with limited success. The reason may be that the ECS is a homeostatic system, which integrates energy seeking and storage behaviour with resistance to oxidative stress. It could be viewed as having thrifty actions. Thriftiness is an innate property of life, which is programmed to a set point by both environment and genetics, resulting in an epigenotype perfectly adapted to its environment. This thrifty set point can be modulated by hormetic stimuli, such as exercise, cold and plant micronutrients. We have proposed that the physiological and protective insulin resistance that underlies thriftiness encapsulates something called 'redox thriftiness', whereby insulin resistance is determined by the ability to resist oxidative stress. Modern man has removed most hormetic stimuli and replaced them with a calorific sedentary lifestyle, leading to increased risk of metabolic inflexibility. We suggest that there is a tipping point where lipotoxicity in adipose and hepatic cells induces mild inflammation, which switches thrifty insulin resistance to inflammation-driven insulin resistance. To understand this, we propose that the metabolic syndrome could be seen from the viewpoint of the ECS, the mitochondrion and the FOXO group of transcription factors. FOXO has many thrifty actions, including increasing insulin resistance and appetite, suppressing oxidative stress and shifting the organism towards using fatty acids. In concert with factors such as PGC-1, they also modify mitochondrial function and biogenesis. Hence, the ECS and FOXO may interact at many points; one of which may be via intracellular redox signalling. As cannabinoids have been shown to modulate reactive oxygen species production, it is possible that they can upregulate anti-oxidant defences. This suggests they may have an 'endohormetic' signalling function. The tipping point into the metabolic syndrome may be the result of a chronic lack of hormetic stimuli (in particular, physical activity), and thus, stimulus for PGC-1, with a resultant reduction in mitochondrial function and a reduced lipid capacitance. This, in the context of a positive calorie environment, will result in increased visceral adipose tissue volume, abnormal ectopic fat content and systemic inflammation. This would worsen the inflammatory-driven pathological insulin resistance and inability to deal with lipids. The resultant oxidative stress may therefore drive a compensatory anti-oxidative response epitomised by the ECS and FOXO. Thus, although blocking the ECS (e.g. via rimonabant) may induce temporary weight loss, it may compromise long-term stress resistance. Clues about how to modulate the system more safely are emerging from observations that some polyphenols, such as resveratrol and possibly, some phytocannabinoids, can modulate mitochondrial function and might improve resistance to a modern lifestyle.

The transaction cost economics theory of the family firm: family-based human asset specificity and the bifurcation bias

We develop a transaction cost economics theory of the family firm, building upon the concepts of family-based asset specificity, bounded rationality, and bounded reliability. We argue that the prosperity and survival of family firms depend on the absence of a dysfunctional bifurcation bias. The bifurcation bias is an expression of bounded reliability, reflected in the de facto asymmetric treatment of family vs. nonfamily assets (especially human assets). We propose that absence of bifurcation bias is critical to fostering reliability in family business functioning. Our study ends the unproductive divide between the agency and stewardship perspectives of the family firm, which offer conflicting accounts of this firm type's functioning. We show that the predictions of the agency and stewardship perspectives can be usefully reconciled when focusing on how family firms address the bifurcation bias or fail to do so.

The effects of acute fluoxetine administration on temporal discounting in youth with ADHD

Background Serotonin is under-researched in attention deficit hyperactivity disorder (ADHD), despite accumulating evidence for its involvement in impulsiveness and the disorder. Serotonin further modulates temporal discounting (TD), which is typically abnormal in ADHD relative to healthy subjects, underpinned by reduced fronto-striato-limbic activation. This study tested whether a single acute dose of the selective serotonin reuptake inhibitor (SSRI) fluoxetine up-regulates and normalizes reduced fronto-striato-limbic neurofunctional activation in ADHD during TD. Method Twelve boys with ADHD were scanned twice in a placebo-controlled randomized design under either fluoxetine (between 8 and 15 mg, titrated to weight) or placebo while performing an individually adjusted functional magnetic resonance imaging TD task. Twenty healthy controls were scanned once. Brain activation was compared in patients under either drug condition and compared to controls to test for normalization effects. Results Repeated-measures whole-brain analysis in patients revealed significant up-regulation with fluoxetine in a large cluster comprising right inferior frontal cortex, insula, premotor cortex and basal ganglia, which further correlated trend-wise with TD performance, which was impaired relative to controls under placebo, but normalized under fluoxetine. Fluoxetine further down-regulated default mode areas of posterior cingulate and precuneus. Comparisons between controls and patients under either drug condition revealed normalization with fluoxetine in right premotor-insular-parietal activation, which was reduced in patients under placebo. Conclusions The findings show that a serotonin agonist up-regulates activation in typical ADHD dysfunctional areas in right inferior frontal cortex, insula and striatum as well as down-regulating default mode network regions in the context of impulsivity and TD.

Prolonged exposure to palmitate impairs fatty acid oxidation despite activation of AMP-activated protein kinase in skeletal muscle cells

The aim of this study was to investigate the chronic effects of palmitate on fatty acid (FA) oxidation, AMPK/ACC phosphorylation/activation, intracellular lipid accumulation, and the molecular Mechanisms involved in these processes in skeletal muscle cells. Exposure of L6 myotubes for 8 h to 200, 400, 600, and 800 mu M of palmitate did rot affect cel viability but significantly reduced FA oxidation by similar to 26.5%, similar to 43.5%, similar to 50%, and similar to 47%, respectively. Interestingly, this occurred despite significant increases in AMPK (similar to 2.5-fold) and ACC (similar to 3-fold) phosphorylation and in malonyl-CoA decarboxylase activity (similar to 38-60%). Low concentrations of palmitate (50-100 mu M) caused an increase (similar to 30%) in CPT-I activity. However, as the concentration of palmitate increased, CPT-I activity decreased by similar to 32% after exposure for 8 h to 800 mu M of palmitate. Although FA uptake was reduced (similar to 35%) in cells exposed to increasing, palmitate concentrations, intracellular lipid accumulation increased in a dose-dependent manner, reaching values similar to 2.3-, similar to 3-, and 4-fold higher than control in muscle cells exposed to 400, 600, and 800 mu M palmitate, respectively. Interestingly, myotubes exposed to 400 mu M of palmitate for 1h increased basal glucose uptake and glycogen synthesis by similar to 40%. However, as time of incubation in the presence of palmitate progressed from 1 to 8h, these increases were abolished and a time-dependent inhibition of insulin-stimulated glucose uptake (similar to 65%) and glycogen synthesis (30%) was observed in myotubes. These findings may help explain the dysfunctional adaptations that occur in glucose and FA Metabolism in skeletal muscle under conditions of chronically elevated circulating levels of non-esterified FAs. Such as in obesity and Type 2 Diabetes.

The role of proliferator-activated receptor gamma coactivator-1 alpha in the fatty-acid -dependent transcriptional control of interleukin-10 in hepatic cells of rodents

Interleukin-10 (IL-10) is an endogenous factor that restrains hepatic insulin resistance in diet-induced steatosis Reducing IL-10 expression increases proinflammatory activity in the steatotic liver and worsens insulin resistance As the transcriptional coactivator proliferator-activated receptor gamma coactivator-1 alpha (PGC-1 alpha) plays a central role in dysfunctional hepatocytic activity in diet-induced steatosis, we hypothesized that at least part of the action of PGC-1 alpha could be mediated by reducing the transcription of the IL-10 gene Here, we used immunoblotting, real-time polymerase chain reaction, immunocytochemistry, and chromatin immunoprecipitation assay to investigate the role of PGC-1 alpha in the control of IL-10 expression in hepatic cells First, we show that, in the intact steatotic liver, the expressions of IL-10 and PGC-1 alpha are increased Inhibiting PGC-1 alpha expression by antisense oligonucleotide increases IL-10 expression and reduces the steatotic phenotype. In cultured hepatocytes, the treatment with saturated and unsaturated fatty acids increased IL-10 expression. This was accompanied by increased association of PGC-1 alpha with c-Maf and p50-nuclear factor (NF) kappa B, 2 transcription factors known to modulate IL-10 expression In addition, after fatty acid treatment. PGC-1 alpha, c-Maf, and p50-NF kappa B migrate from the cytosol to the nuclei of hepatocytes and bind to the IL-10 promoter region Inhibiting NF kappa B activation with salicylate reduces IL-10 expression and the association of PGC-1 alpha with p50-NF kappa B Thus, PGC-1 alpha emerges as a potential transcriptional regulator of the inflammatory phenomenon taking place in the steatotic liver (C) 2010 Elsevier Inc All rights reserved

Inflammation of the Hypothalamus Leads to Defective Pancreatic Islet Function

Type 2 diabetes mellitus results from the complex association of insulin resistance and pancreatic beta-cell failure. Obesity is the main risk factor for type 2 diabetes mellitus, and recent studies have shown that, in diet-induced obesity, the hypothalamus becomes inflamed and dysfunctional, resulting in the loss of the perfect coupling between caloric intake and energy expenditure. Because pancreatic beta-cell function is, in part, under the control of the autonomic nervous system, we evaluated the role of hypothalamic inflammation in pancreatic islet function. In diet-induced obesity, the earliest markers of hypothalamic inflammation are present at 8 weeks after the beginning of the high fat diet; similarly, the loss of the first phase of insulin secretion is detected at the same time point and is restored following sympathectomy. Intracerebroventricular injection of a low dose of tumor necrosis factor a leads to a dysfunctional increase in insulin secretion and activates the expression of a number of markers of apoptosis in pancreatic islets. In addition, the injection of stearic acid intracerebroventricularly, which leads to hypothalamic inflammation through the activation of tau-like receptor-4 and endoplasmic reticulum stress, produces an impairment of insulin secretion, accompanied by increased expression of markers of apoptosis. The defective insulin secretion, in this case, is partially dependent on sympathetic signal-induced peroxisome proliferator receptor-gamma coactivator Delta a and uncoupling protein-2 expression and is restored after sympathectomy or following PGC1 alpha expression inhibition by an antisense oligonucleotide. Thus, the autonomic signals generated in concert with hypothalamic inflammation can impair pancreatic islet function, a phenomenon that may explain the early link between obesity and defective insulin secretion.

Kön, kroppsbild och dysfunktionella tankar : en sambandsstudie

Body esteem is the affective aspect of body image, which is shaped by social experience. Compared with men, women have a more negative body image, which is more frequently correlated with depression and dysfunctional thoughts, especially in the case of eating disorders. The purpose of the present study was to examine gender differences in body esteem and its subcategories, and to find out whether there exists a stronger link between negative body esteem and higher levels of dysfunctional thoughts in women. The relationship between body esteem, dysfunctional thoughts and mental illness was examined. Participants were 73 college students doing social sciences and sports training educations. Body esteem questionnaire and dysfunctional thoughts questionnaire as well as a self made questionnaire on mental illness were used. Results showed that women had a more negative body esteem compared to men, especially considering weight. In women, there was a medium-strong negative relation between body esteem and dysfunctional thoughts. The results indicate that the norms for female body ideal that abound in the Western society have a negative affect on women's thinking and body image.Key words: Gender, body esteem, dysfunctional thoughts, mental illness.

Characterization of residential chimney conditions for flue gas flow measurements

A literature survey and a theoretical study were performed to characterize residential chimney conditions for flue gas flow measurements. The focus is on Pitot-static probes to give sufficient basis for the development and calibration of a velocity pressure averaging probe suitable for the continuous dynamic (i.e. non steady state) measurement of the low flow velocities present in residential chimneys. The flow conditions do not meet the requirements set in ISO 10780 and ISO 3966 for Pitot-static probe measurements, and the methods and their uncertainties are not valid. The flow velocities in residential chimneys from a heating boiler under normal operating condi-tions are shown to be so low that they in some conditions result in voiding the assumptions of non-viscous fluid justifying the use of the quadratic Bernoulli equation. A non-linear Reynolds number dependent calibration coefficient that is correcting for the viscous effects is needed to avoid significant measurement errors. The wide range of flow velocity during normal boiler operation also results in the flow type changing from laminar, across the laminar to turbulent transition region, to fully turbulent flow, resulting in significant changes of the velocity profile during dynamic measurements. In addition, the short duct lengths (and changes of flow direction and duct shape) used in practice are shown to result in that the measurements are done in the hydrodynamic entrance region where the flow velocity profiles most likely are neither symmetrical nor fully developed. A measurement method insensitive to velocity profile changes is thus needed, if the flow velocity profile cannot otherwise be determined or predicted with reasonable accuracy for the whole measurement range. Because of particulate matter and condensing fluids in the flue gas it is beneficial if the probe can be constructed so that it can easily be taken out for cleaning, and equipped with a locking mechanism to always ensure the same alignment in the duct without affecting the calibration. The literature implies that there may be a significant time lag in the measurements of low flow rates due to viscous effects in the internal impact pressure passages of Pitot probes, and the significance in the discussed application should be studied experimentally. The measured differential pressures from Pitot-static probes in residential chimney flows are so low that the calibration and given uncertainties of commercially available pressure transducers are not adequate. The pressure transducers should be calibrated specifically for the application, preferably in combination with the probe, and the significance of all different error sources should be investigated carefully. Care should be taken also with the temperature measurement, e.g. with averaging of several sensors, as significant temperature gradients may be present in flue gas ducts.

Den skickligt inkompetente chefen

The skilled incompetent manager Based on a critical interpretation of a leadership seminar we illustrate how the performance of the managers involved skilled incompetence. It expresses itself through a non-critical attitude, easily-made solutions and pseudo-communication, which together fuel a kind of knowledge flexibility. This uncritical, somewhat shallow and pragmatic attitude towards knowledge (e.g. management concepts), ought not to be understood as just dysfunctional, but also as a more or less unaware but adjusted competence, that in some situations works as a social lubricant in bureaucratic organizations.