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Different studies have confirmed the association between cannabis use and psychosis and, also, the relationship between age at first cannabis use and age at onset of psychosis (Henquet et al 2005, Barnes et al 2006). In a young psychiatric sample, we aimed to investigate the correlation between cannabis use and the age at onset of psychotic and non-psychotic symptoms and whether this relationship is modulated by the genetic variability at COMT, CNR1 and CHRNA7genes.
The sample comprised 157 Caucasian patients (mean age: 17.01 (3.6)) diagnosed following DSM-IV-TR criteria: 80 patients with schizophrenia-spectrum disorders, 77 patients with affective or conduct disorders. Cannabis use was assessed with UNICA-A and DIGS scales (Nurnberger 1994) and 49% individuals were classified as consumers. SNPs were genotyped using Taqman 5′-exonuclease assays.
We observed a positive relationship between age at first cannabis use and age at onset in, both, schizophrenia-spectrum (β = 1.44 p < 0.001) and other psychiatric disorders (β = 0.56 p < 0.002). An interaction was observed between COMT Val158Met polymorphism and cannabis use specifically within schizophrenia-spectrum disorders’ group (β = −2.72 p = 0.04), with Val/Val genotype carriers showing an earlier age of onset than Val/Met carriers, and these, lower than the Met/Met carriers. No modulation effect of CNR1 or CHRNA7 polymorphisms was observed.
Our results seem to indicate the importance of maturation timing and brain development in which exposition to cannabis occurs. We provide new evidence about the COMT modulation effect on the association between cannabis use and age at onset of symptoms, specifically in individuals affected by schizophrenia-spectrum disorders.
The well-established relationship between childhood adversity and psychosis is likely to involve other factors such as genetic variants, which could help to understand why not everyone exposed to adverse events develops psychotic symptoms later in life (Van Winkel, et al. 2008; Simmons et al. 2009).
The present study investigated the influence of childhood abuse and neglect on positive and negative psychosis-like experiences in adulthood and the potential moderating effect of the BDNF-Val66Met polymorphism.
Psychosis-like experiences and childhood adversity were assessed in 533 individuals from the general population.
Childhood abuse showed a strong independent effect on the positive dimension of psychosis-like experiences (B = .16; SE = .05; p = .002). Furthermore, this association was moderated by the BDNF-Val66Met polymorphism (B = .17; SE = .09; p = .004).
Individuals exposed to childhood abuse are more likely to report positive psychosis-like experiences. Met carriers reported more positive psychosis-like experiences when exposed to childhood abuse than did individuals carrying the Val/Val genotype.
Therefore, the observed gene-environment interaction effect may be partially responsible for individual variation in response to childhood abuse.
The present study aimed to examine the prevalence of child abuse across the continuum of psychosis.
Patients and methods:
The sample consisted of 198 individuals divided in three groups: (1) 48 FEP patients, (2) 77 individuals scoring high in Community Assessment of Psychic Experiences (CAPE), classified as “High CAPE” group and (3) 73 individuals scoring low, classified as “Low CAPE” group. Childhood abuse was assessed using self-report instruments. Chi2 tests and logistic regression models controlling by sex, age and cannabis were used to perform three comparisons: (i) FEP vs. Low CAPE; (ii) FEP vs. High CAPE and (iii) High CAPE vs. Low CAPE.
The frequency of individuals exposed to childhood abuse for FEP, High CAPE and Low CAPE groups were 52.1%, 41.6% and 11%, respectively. FEP and High CAPE group presented significantly higher rates of childhood abuse compared to Low CAPE group, however, no significant differences were found between FEP and High CAPE groups regarding the frequency of childhood abuse.
There is an increasing frequency of childhood abuse from low subclinical psychosis to FEP patients. However, childhood abuse is equally common in FEP and at risk individuals.
To test whether firstly, different parental rearing components were associated with different dimensions of psychiatric symptoms in adulthood, secondly BDNF-Val66Met polymorphism moderated this association and thirdly, this association was due to genetic confounding.
Perceived parental rearing according to Parental Bonding Instrument (PBI), psychiatric symptoms evaluated with the Brief Symptom Inventory (BSI) and the BDNF-Val66Met polymorphism were analyzed in a sample of 232 adult twins from the general population.
In the whole sample, paternal care was negatively associated with depression. Maternal overprotection was positively associated with paranoid ideation, obsession-compulsion and somatization. Gene-environment interaction effects were detected between the BDNF-Val66Met polymorphism and maternal care on phobic anxiety, paternal care on hostility, maternal overprotection on somatization and paternal overprotection also in somatization. In the subsample of MZ twins, intrapair differences in maternal care were associated with anxiety, paranoid ideation and somatization.
Met carriers were, in general, more sensitive to the effects of parental rearing compared to Val/Val carriers in relation to anxiety and somatization. Contra-intuitively, our findings suggest that high rates of maternal care might be of risk for Met carriers regarding anxiety. Results from analyses controlling for genetic confounding were in line with this finding.
The interest in studying gene–gene interactions is increasing for psychiatric diseases such as schizophrenia-spectrum disorders (SSD), where multiple genes are involved. Dysbindin-1 (DTNBP1) and Neuritin-1 (NRN1) genes have been previously associated with SSD and both are involved in synaptic plasticity. We aimed to study whether these genes show an epistatic effect on the risk for SSD.
The sample comprised 388 SSD patients and 397 healthy subjects. Interaction was tested between: (i) three DTNBP1 SNPs (rs2619537, rs2743864, rs1047631) related to changes in gene expression; and (ii) an haplotype in NRN1 previously associated with the risk for SSD (rs645649-rs582262: HAP-risk C-C).
An interaction between DTNBP1 rs2743864 and NRN1 HAP-risk was detected by using the model based multifactor dimensionality reduction (MB-MDR) approach (P = 0.0049, after permutation procedure), meaning that the risk for SSD is significantly higher in those subjects carrying both the A allele of rs2743864 and the HAP-risk C-C. This interaction was confirmed by using a logistic regression model (P = 0.033, OR (95%CI) = 2.699 (1.08–6.71), R2 = 0.162).
Our results suggest that DTNBP1 and NRN1 genes show a joint effect on the risk for SSD. Although the precise mechanism underlying this effect is unclear, the fact that these genes have been involved in synaptic maturation, connectivity and glutamate signalling suggests that our findings could be of value as a link to the schizophrenia aetiology.
Torque measurements in Taylor–Couette flow, with large radius ratio and large aspect ratio, over a range of velocities up to a Reynolds number of 24 000 are presented. Following a specific procedure, nine states with distinct numbers of vortices along the axis were found and the aspect ratios of the vortices were measured. The relationship between the speed and the torque for a given number of vortices is reported. In the turbulent Taylor vortex flow regime, at relatively high Reynolds number, a change in behaviour is observed corresponding to intersections of the torque–speed curves for different states. Before each intersection, the torque for a state with a larger number of vortices is higher. After each intersection, the torque for a state with a larger number of vortices is lower. The exponent, from the scaling laws of the torque, always depends on the aspect ratio of the vortices. When the Reynolds number is rescaled using the mean aspect ratio of the vortices, only a partial collapse of the exponent data is found.
Understanding how linguistic cues map to the environment is crucial for early language comprehension and may provide a way for bootstrapping and learning words. Research has suggested that learning how plural syntax maps to the perceptual environment may show a trajectory in which children first learn surrounding cues (verbs, modifiers) before a full mastery of the noun morpheme alone. The Spanish plural system of simple codas, dominated by one allomorph -s, and with redundant agreement markers, may facilitate early understanding of how plural linguistic cues map to novel referents. Two-year-old Mexican children correctly identified multiple novel object referents when multiple verbal cues in a phrase indicated plurality as well as in instances when the noun morphology in novel nouns was the only indicator of plurality. These results demonstrate Spanish-speaking children's ability to use plural noun inflectional morphology to infer novel word referents which may have implications for their word learning.
The aim of this research is to present a Spanish Word Association Norms (WAN) database of concrete nouns. The database includes 234 stimulus words (SWs) and 67,622 response words (RWs) provided by 478 young Mexican adults. Eight different measures were calculated to quantitatively analyze word-word relationships: 1) Associative strength of the first associate, 2) Associative strength of the second associate, 3) Sum of associative strength of first two associates, 4) Difference in associative strength between first two associates, 5) Number of different associates, 6) Blank responses, 7) Idiosyncratic responses, and 8) Cue validity of the first associate. The resulting database is an important contribution given that there are no published word association norms for Mexican Spanish. The results of this study are an important resource for future research regarding lexical networks, priming effects, semantic memory, among others.
A potential role for epigenetic mechanisms in the regulation of mammary function in the dairy cow is emerging. Epigenetics is the study of heritable changes in genome function that occur because of chemical changes rather than DNA sequence changes. DNA methylation is an epigenetic event that results in the silencing of gene expression and may be passed on to the next generation. However, recent studies investigating different physiological states and changes in milk protein gene expression suggest that DNA methylation may also play an acute, regulatory, role in gene transcription. This overview will highlight the role of DNA methylation in the silencing of milk protein gene expression during mastitis and mammary involution. Moreover, environmental factors such as nutrition may induce epigenetic modifications of gene expression. The current research investigating the possibility of in utero, hence cross-generational, epigenetic modifications in dairy cows will also be discussed. Understanding how the mammary gland responds to environmental cues provides a potential to enhance milk production not only of the dairy cow but also of her daughter.
Twin and sibling studies have identified specific cognitive phenotypes that may mediate the association between genes and the clinical symptoms of attention deficit hyperactivity disorder (ADHD). ADHD is also associated with lower IQ scores. We aimed to investigate whether the familial association between measures of cognitive performance and the clinical diagnosis of ADHD is mediated through shared familial influences with IQ.
Multivariate familial models were run on data from 1265 individuals aged 6–18 years, comprising 920 participants from ADHD sibling pairs and 345 control participants. Cognitive assessments included a four-choice reaction time (RT) task, a go/no-go task, a choice–delay task and an IQ assessment. The analyses focused on the cognitive variables of mean RT (MRT), RT variability (RTV), commission errors (CE), omission errors (OE) and choice impulsivity (CI).
Significant familial association (rF) was confirmed between cognitive performance and both ADHD (rF=0.41–0.71) and IQ (rF=−0.25 to −0.49). The association between ADHD and cognitive performance was largely independent (80–87%) of any contribution from etiological factors shared with IQ. The exception was for CI, where 49% of the overlap could be accounted for by the familial variance underlying IQ.
The aetiological factors underlying lower IQ in ADHD seem to be distinct from those between ADHD and RT/error measures. This suggests that lower IQ does not account for the key cognitive impairments observed in ADHD. The results have implications for molecular genetic studies designed to identify genes involved in ADHD.
Adverse childhood experiences have been described as one of the major environmental risk factors for depressive disorder. Similarly, the deleterious impact of early traumatic experiences on depression seems to be moderated by individual genetic variability. Serotonin transporter (5-HTT) and brain-derived neurotrophic factor (BDNF) modulate the effect of childhood adversity on adult depression, although inconsistencies across studies have been found. Moreover, the gene×environment (G×E) interaction concerning the different types of childhood adversity remains poorly understood. The aim of this study was to analyse the putative interaction between the 5-HTT gene (5-HTTLPR polymorphism), the BDNF gene (Val66Met polymorphism) and childhood adversity in accounting for adult depressive symptoms.
A sample of 534 healthy individuals filled in self-report questionnaires of depressive symptomatology [the Symptom Check List 90 Revised (SCL-90-R)] and different types of childhood adversities [the Childhood Trauma Questionnaire (CTQ)]. The 5-HTTLPR polymorphism (5-HTT gene) and the Val66Met polymorphism (BDNF gene) were genotyped in the whole sample.
Total childhood adversity (β=0.27, p<0.001), childhood sexual abuse (CSA; β=0.17, p<0.001), childhood emotional abuse (β=0.27, p<0.001) and childhood emotional neglect (β=0.22, p<0.001) had an impact on adult depressive symptoms. CSA had a greater impact on depressive symptoms in Met allele carriers of the BDNF gene than in the Val/Val group (F=5.87, p<0.0001), and in S carriers of the 5-HTTLPR polymorphism (5-HTT gene) (F=5.80, p<0.0001).
Childhood adversity per se predicted higher levels of adult depressive symptoms. In addition, BDNF Val66Met and 5-HTTLPR polymorphisms seemed to moderate the effect of CSA on adult depressive symptoms.
Silver sulfide (Ag2S) and cadmium sulfide (CdS) nanoparticles of adjustable sizes are synthesized using a water-in-hexane microemulsion method and stabilized by dodecanethiol. The stabilized metal sulfide nanoparticles can be deposited homogenously on flat substrates forming ordered 2D arrays in supercritical fluid carbon dioxide (Sc-CO2). The use of Sc-CO2 leaves the particles unaffected by de-wetting effects and surface tension caused by traditional solvents and produces uniform arrays. The Sc-CO2 deposition technique can effectively fill the metal sulfide nanoparticles into nanoscale features, which is difficult to achieve by conventional solvent evaporation methods.
Low-voltage organic transistors are sought for implementation in high volume low-power portable electronics of the future. Here we assess the suitability of three phosphonic acid based self-assembling molecules for use as ultra-thin gate dielectrics in low-voltage solution processable organic field-effect transistors. In particular, monolayers of phosphonohexadecanoic acid in metal-monolayer-metal type sandwich devices are shown to exhibit low leakage currents and high geometrical capacitance comparable to previously demonstrated self-assembled monolayer (SAM) type dielectrics but with a higher surface energy. The improved surface energy characteristics enable processing of a wider range of organic semiconductors from solution. Transistors based on a number of solution-processed organic semiconductors with operating voltages below 2 V are also demonstrated.
In this work, blends of dispersed short (∼500 nm) single-walled carbon nanotubes (SWCNTs) with poly(3,4-ethylene dioxythiophene):polystyrene sulfonic acid (PEDOT:PSS) were investigated as hole injection layers in OLEDs consisting of N,N′-di(naphthalene-1-yl)-N,N′-diphenylbenzidine (NPB) as a hole transporting and tris-(8-hydroxyquinoline) aluminum (Alq3) as electron transporting and emitting layer. The devices were characterized by electroluminescence and current-voltage measurements. By comparing the performance of devices fabricated using different surfactants (polyethyleneimine (PEI) and Gum Arabic (GA)) in dispersing SWCNTs and those prepared without surfactants, it was found that the use of appropriate surfactants can improve the OLEDs performance. Improved efficiency was obtained for optimized SWCNTs concentration compared to the devices with pure PEDOT:PSS, although maximum luminance is lower. The PEDOT:PSS:SWCNT nanocomposite layers are characterized and the reasons for the improved OLED performance are discussed.
Photoactive organic field-effect transistors, photOFETs, based on a conjugated polymer/fullerene blend, MDMO-PPV: PCBM (1:4), and polymeric dielectrics as polyvinylalcohol (PVA) or divinyltetramethyldisiloxane-bis(benzocyclobutene) (BCB) with top source and drain electrodes were fabricated and characterized in dark and under AM1.5 illumination. With LiF/Al as top source and drain contacts the devices feature n-type transistor behavior in dark with electron mobility of 10-2 cm2/Vs. Under illumination, a large free carrier concentration from photo-induced charge transfer at the polymer/fullerene bulk heterojunction (photodoping) is created. The device performance was studied with different illumination intensities and showed to be strongly influenced by the nature of the organic dielectric/organic semiconductor interface resulting in phototransistor behavior in BCB-based photOFETs and in phototransistor or photoresistor behavior for PVA-based photOFETs.