Body mass index dependent metabolic syndrome in severe mental illness patients

The aim of this study was to evaluate the body mass index dependent metabolic syndrome in severe mental illness patients in Gorgan. A total of 267 severe mental illness patients took part in this study. The prevalence of metabolic syndrome in severe mental illness patients in different body mass index were 6.67, 24.09 and 53.06. There were significant differences in the mean of waist circumference, HDL-cholesterol, triglyceride and fasting blood glucose in subjects with metabolic syndrome in different body mass index when compared with subjects without metabolic syndrome (p<0.05). The prevalence of high fasting glucose, low high density lipoprotein-cholesterol, high triglyceride levels, high waist circumference and high blood pressure were 14.23, 38.57, 41.57, 32.96 and 5.24, respectively. It shows that high triglyceride levels (41.57) and Low HDL-cholesterol levels (38.57) were the most frequent characteristics in comparison to other metabolic components. Our results show that, 26.96, 31.08, 21.35, 15.35 and 5.25 of subjects had zero, one, two, three and four criteria for metabolic syndrome, respectively. These results show that the prevalence of metabolic syndrome in severe mental illness patients in Gorgan is increased with elevated body mass index. The results of this study suggest that mental illness patients are at risk of metabolic syndrome, when the rate of body mass index increases. Risk factors such as high triglyceride level and low HDL-cholesterol may play an important role in the occurrence of metabolic syndrome in severe mental illness patients. © 2015, Asian Network for Scientific Information. All rights reserved

What Are The Cognitive Mechanisms That Underlie Our Theory Of Mind? Potential Insights From Information Theory

Theory of Mind (ToM) is the ability to infer mental states. The purpose of Study 1 was to reduce performance demands on a ToM test for forty (22 females) children (M age = 4.604; SD age = 1.128). Here, a low-uncertainty condition included a behaviour repetition manipulation, intended to increase success rate—but results did not confirm our hypothesis. Potential reasons for the results of Study 1 are discussed and tested in Study 2. The purpose of Study 2 was to determine the mechanism by which ToM operates in fifty-seven (26 females) adult participants (M age = 20.632; SD age = 3.368) by altering informational richness more directly. Results of Study 2 confirm that the mechanism by which ToM operates is via uncertainty reduction. These data motivate Study 3 in which child-appropriate vignettes will be used to address the limitations of Study 1 and implement the design of Study 2

Neural And Behavioural Responses To Rewards And Losses In Early Development: A Functional Magnetic Resonance Imaging Study

Functional magnetic resonance imaging (fMRI) was used to investigate the neural and behavioural correlates of learning from rewards and losses in children. Greater blood-oxygen-level dependent (BOLD) responses in the ventral striatum (VS) and the ventromedial prefrontal cortex (VMPFC) were found when participants received rewards compared to when they missed out on an opportunity to receive rewards. In contrast, greater BOLD responses in the anterior insula (AI) and the anterior cingulate cortex (ACC) were found when participants received losses compared to when they avoided losing. The BOLD response to rewards in the VS and VMPFC correlated positively with the tendency to select rewards. Greater incidence of early life adversity was associated with greater likelihood to select rewarding stimuli and a larger BOLD response in the VS and VMPFC to rewards. Findings suggest that the functional calibration of the mesocorticolimbic pathway is sensitive to the experience of early life adversity

Characterisation of novel matrix-binding interactions for latent transforming growth factor-β-binding protein-2 (LTBP-2), with emphasis on heparin and heparan sulphate proteoglycans.

Elastic fibres are important components of the extracellular matrices, being composed of an elastin core and fibrillin-microfibrils around the periphery. Elastic fibre formation is a complex developmentally regulated process whereby fibrillin-microfibrils act as templates for the deposition of elastin. Additional matrix macromolecules, including fibulin-4, fibulin-5 and as yet unidentified heparan sulphate proteoglycans (HSPGs), have also been identified as playing important roles in this process. Fibrillins-1, -2, -3 and latent transforming growth factor-β binding protein (LTBP)-1, -2, -3, -4, associated components of fibrillin-microfibrils, make up a superfamily of extracellular matrix proteins. Fibrillins and LTBPs share a high degree of structural similarity since they both have rod-like structures of tandem EGF-like 6-cysteine repeats interspersed with unique 8-cysteine motifs. LTBP-1, -3 and -4 covalently bind TGF-β and target and store the latent growth factor in the matrix. Unlike the other LTBPs, LTBP-2 does not bind latent TGF-β and its function is poorly understood. LTBP-2 has been shown to bind fibulin-5, an elastin-binding protein and through this interaction it may target tropoelastin-fibulin-5 complexes on to fibrillin-1-microfibrils during elastic fibre assembly. In order to understand more about the role of LTBP-2 in the assembly of elastic fibres and to identify other novel functions, this study involved screening for potential molecular interactions of LTBP-2 with other matrix components, particularly heparin/HSPGs. In elastic tissues HSPGs are found on cell surfaces as syndecans and glypicans and in basement membranes as perlecan. Full length human recombinant LTBP-2 (rLTBP-2) was expressed in 293 EBNA cells using a modified pCEP-4 vector and purified by nickel affinity chromatography. Upon validation of the purified protein using western blots, solid phase binding assays were used to screen for interaction between rLTBP-2 and heparin. Heparin serves as a useful model for heparan sulphate; due to the lack of adherence of heparin to microtitre plates heparin-BSA conjugate was synthesised and purified for the binding assays. Recombinant LTBP-2 was found to interact with heparin-BSA conjugates using an established solid phase binding assay. The binding was blocked by the addition of heparin (but not chondroitin sulphate) to the liquid phase, confirming the specificity of the interaction. Furthermore, the binding was blocked by the addition of 5mM EDTA and 5mM EGTA, showing that the interaction was cation (calcium) dependent. An apparent Kd of 14.5±3.7nM was calculated from non-linear regression analysis of the LTBP-2-heparin binding curve, indicating a strong affinity. To identify the location of the heparin binding site(s) on LTBP-2, expression constructs were produced encoding three fragments of LTBP-2, i.e. rLTBP-2NT(H), rLTBP-2C(H) and rLTBP-2CT(H), corresponding to the N-terminal, central and C-terminal regions of the molecule. Good yields of rLTBP-2C(H) were obtained using the pCEP4-293-EBNA system, and rLTBP-2CT(H) was previously expressed and purified by members of the Gibson laboratory. However, difficulties were encountered with the rLTBP-2NT(H) expression construct and no LTBP-2NT(H) was available during the candidature. The central fragment LTBP-2C(H), (but not the C-terminal fragment LTBP-2CT(H)), was found to bind heparin. However, the apparent Kd of 52.2±6.9nM was significantly higher than that for full length LTBP-2, indicating that LTBP-2C(H) had relatively lower heparin-binding affinity. This result suggested that an additional heparin binding site(s) is present in the N-terminal region of the molecule. It was considered that the true tissue ligand(s) for LTBP-2 would be a HSPG rather than heparin. Therefore, LTBP-2 was screened for interaction with HSPGs, recombinant syndecans-2 and -4, and endothelial cell-derived perlecan. Interestingly, LTBP-2 bound strongly to r-syndecan-4 but not r-syndecan-2 even though both molecules were produced in the same mammalian cell system and had been screened for binding to HS-binding growth factor, fibroblast growth factor-2. This finding indicates that LTBP-2 does not interact with all HS and must recognise specific microstructures within the heparan sulphate chains. It appears that syndecan-4 is now a strong candidate as mediator of LTBP-2-cell signalling. LTBP-2 was also found to specifically interact with perlecan in a cation-dependent, heparininhibitable manner. Confocal immunohistochemical studies using foetal human aorta showed that LTBP-2 and perlecan generally had distinct distribution patterns within the medial layer, located on fibrillin-microfibrils and basement membranes respectively. However, there were small but widespread regions of LTBP-2-perlecan colocalisation which showed a similar pattern to the fibrillin-1-perlecan colocalisation. Thus it would appear that LTBP-2 is present at microfibril-basement membrane interfaces and may be involved in stabilising the interaction between these two structural elements of the matrix. This concept needs to be confirmed at the ultrastructural level. The interaction of LTBP-2 with perlecan during embryonic development is also worthy of investigation. In parallel studies, a proteomic approach was used to identify other matrix binding proteins for LTBP-2. This was carried out in parallel with another matrix protein of poorly defined function, transforming growth factor-beta-inducible gene-h3 (βig-h3). Recombinant LTBP-2 and βig-h3 coupled to sepharose were used as bait proteins to screen complex mixtures of matrix proteins from the elastic tissue nuchal ligament and basement membrane preparation Matrigel. Initial studies showed that non-specific background binding to these proteins was a major problem. In efforts to overcome this difficulty, binding conditions were varied with limited success. A two-dimensional gel approach was used to fractionate and compare proteins binding to LTBP-2 with those binding to βig-h3. The differentially displayed protein spots were to be identified by mass spectrometry. However, complications in comparing the patterns on two separate gels made identification of candidate spots challenging. Finally, CyDye DIGE fluor dyes were used to fractionate proteins binding to LTBP-2 and βig-h3 on the same gel, but unfortunately this work could not be completed in the time frame of the candidature.Thesis (Ph.D.) -- University of Adelaide, School of Medical Sciences School, 201

Sex Differences in Self-Regulation: An Evolutionary Perspective

Bjorklund and Kipp (1996) provide an evolutionary framework predicting that there is a female advantage in inhibition and self-regulation due to differing selection pressures placed on males and females. The majority of the present review will summarize sex differences in self-regulation at the behavioral level. The neural and hormonal underpinnings of this potential sexual dimorphism will also be investigated and the results of the experiments summarized will be related to the hypothesis advanced by Bjorklund and Kipp (1996). Paradoxically, sex differences in self-regulation are more consistently reported in children prior to the onset of puberty. In adult cohorts, the results of studies examining sex differences in self-regulation are mixed. A few recent experiments suggesting that females are less impulsive than males only during fertile stages of the menstrual cycle will be reviewed. A brief discussion of an evolutionary framework proposing that it is adaptive for females to employ a self-regulatory behavioral strategy when fertile will follow

The differential calibration of the HPA axis as a function of trauma versus adversity: A systematic review and p-curve meta-analyses

Although there is an abundance of evidence linking the function of the hypothalamic-pituitary-adrenal (HPA) axis to adverse early-life experiences, the precise nature of the association remains unclear. Some evidence suggests early-life adversity leads to cortisol hyper-reactivity, while other evidence suggests adversity leads to cortisol hypo-reactivity. Here, we distinguish between trauma and adversity, and use p-curves to interrogate the conflicting literature. In Study 1, trauma was operationalized according to DSM-5 criteria; the p-curve analysis included 68 articles and revealed that the literature reporting associations between trauma and blunted cortisol reactivity contains evidential value. Study 2 examined the relationship between adversity and cortisol reactivity. Thirty articles were included in the analysis, and p-curve demonstrated that adversity is related to heightened cortisol reactivity. These results support an inverted U-shaped function relating severity of adversity and cortisol reactivity, and underscore the importance of distinguishing between “trauma” and “adversity”

The role of attachments to mother, father, and peer in depression among male and female middle adolescents

While both parent and peer attachment security have been found to be related to adolescent's well-being, the relative importance of each on the adolescent's adjustment is in question. Further, insecure attachment appears to be a more important factor in depression for adolescent girls than boys (Kobak, Sudler, & Gamble, 1991). The present study investigates the role of parental and peer attachments in depression among adolescent boys and girls, and whether secure attachment to peers protects adolescents insecurely attached to parents, particularly girls, against depression. Adolescents (n = 176) completed self-reports measuring their depressed feelings and their attachment to mother, father, and best friend, and a computer task consisting of hypothetical situations in which they were asked how they would feel. The results suggested that attachment security to a close peer only protected girls insecurely attached to their father against depression. Attachment security to both parents appeared to protect adolescents against depression. These findings substantiate the importance of attachment security to parents in adolescence and the need to examine gender differences and the separate effects of both mother and father when studying the importance of security to parents and to peers on the adolescent's mental health