This is a copy of the slides presented at the meeting but not formally written up for the volume.

Description: Semiconductor physics contains a rich body of theory and working designs. However, their material properties seem to be reaching their limits. Perovskite oxides on the other hand have abundant physical properties, but are still under active investigation. The advent of RHEED-monitoring of pulsed laser deposition allows for the fabrication of structures with single unit cell (4 Å) thick layers. In this way we may be able to fabricate quantum well structures for both applications and fundamental investigations. Superlattices of the Mott insulator LaTiO3 (LTO) and the band gap insulator SrTiO3 (STO) form such a structure. The superlattices are metallic, both as-grown and post-annealed [1]. This has been attributed to the existence of metallic states at the interfaces between LTO and STO [2]. At these interfaces the electron density is found to extend about 10 Å into the STO. However, theoretically, the required length scale for quantum confinement is of the order of 4 Å. A possible way to increase this confinement is to use a buffer material with a larger band gap than that of LTO (similar to semiconductor band gap engineering) and/or with a lower dielectric constant [2]. LaAlO3 (LAO) is such a material (ΔELAO = 5.6 eV vs. ΔESTO = 3.2 eV, εLAO = 24 vs. εSTO = 300). Here we report on the growth of LTO/LAO superlattices on STO substrates. As-grown superlattices of LTO/LAO are metallic, while post-annealing turns them insulating. This may be explained from a disorder-order transition in a 2D Mott-Hubbard model [3]. XPS and EELS measurements of the titanium valence show interesting differences for LTO layers close to and far away from the sample surface. The former, for thin LAO capping layers, show the presence of Ti4+ while the latter only have Ti3+. Hard XPS of samples with varying capping layer thickness shows an exponential dependence of the Ti3+ contents on a length scale of about 5 unit cells. [1] A. Ohtomo et al., Nature 419, 378-380 (2002). [2] S. Okamoto & A.J. Millis, Phys. Rev. B 70, 075101 (2004). [3] D. Heidarian & N. Trivedi, Phys. Rev. Lett. 93, 126401 (2004).

The enhanced error monitoring in patients with obsessive–compulsive disorder (OCD), typically measured with the error-related negativity (ERN), has been found to be temporally stable and independent of symptom expression. Here, we examined whether the error monitoring in patients with OCD could be experimentally modulated by individually tailored symptom provocation.

Twenty patients with OCD and 20 healthy controls performed a flanker task in which OCD-relevant or neutral pictures were presented prior to a flanker stimulus. An individualized stimulus set consisting of the most provoking images in terms of OCD symptoms was selected for each patient with OCD. Response-locked event-related potentials were recorded and used to examine the error-related brain activity.

Patients with OCD showed larger ERN amplitudes than did control subjects in both the OCD-symptom provocation and neutral conditions. Additionally, while patients with OCD exhibited a significant increase in the ERN under the OCD-symptom provocation condition when compared with the neutral condition, control subjects showed no variation in the ERN between the conditions.

Our results strengthen earlier findings of hyperactive error monitoring in OCD, as indexed by higher ERN amplitudes in patients with OCD than in controls. Importantly, we showed that the patients’ overactive error-signals were experimentally enhanced by individually tailored OCD-symptom triggers, thus suggesting convincing evidence between OCD-symptoms and ERN. Such findings imply that therapeutic interventions should target affective regulation in order to alleviate the perceived threatening value of OCD triggers.

Obsessive–compulsive disorder (OCD) has been associated with abnormal cognitive and emotional functions and these dysfunctions may be dependent on the disruption of dynamic interactions within neuronal circuits associated with emotion regulation. Although several studies have shown the aberrant cognitive–affective processing in OCD patients, little is known about how to characterize effective connectivity of the disrupted neural interactions. In the present study, we applied effective connectivity analysis using dynamic causal modeling to explore the disturbed neural interactions in OCD patients.

A total of 20 patients and 21 matched healthy controls performed a delayed-response working memory task under emotional or non-emotional distraction while undergoing functional magnetic resonance imaging.

During the delay interval under negative emotional distraction, both groups showed similar patterns of activations in the amygdala. However, under negative emotional distraction, the dorsolateral prefrontal cortex (DLPFC) and the orbitofrontal cortex (OFC) exhibited significant differences between groups. Bayesian model averaging indicated that the connection from the DLPFC to the OFC was negatively modulated by negative emotional distraction in patients, when compared with healthy controls (p < 0.05, Bonferroni-corrected).

Exaggerated recruitment of the DLPFC may induce the reduction of top-down prefrontal control input over the OFC, leading to abnormal cortico-cortical interaction. This disrupted cortico-cortical interaction under negative emotional distraction may be responsible for dysfunctions of cognitive and emotional processing in OCD patients and may be a component of the pathophysiology associated with OCD.

Obsessive-compulsive disorder (OCD) is a chronic, relapsing mental illness. Selective serotonin reuptake inhibitors block serotonin transporters (SERTs) and are the mainstay of treatment for OCD. SERT abnormalities are reported in drug-free patients with OCD, but it is not known what happens to SERT levels during treatment. This is important as alterations in SERT levels in patients under treatment could underlie poor response, or relapse during or after treatment. The aim of the present study was first to validate a novel approach to measuring SERT levels in people taking treatment and then to investigate SERT binding potential (BP) using [11C]DASB PET in patients with OCD currently treated with escitalopram in comparison with healthy controls.

Twelve patients and age- and sex-matched healthy controls were enrolled. The patients and healthy controls underwent serial PET scans after administration of escitalopram and blood samples for drug concentrations were collected simultaneously with the scans. Drug-free BPs were obtained by using an inhibitory E max model we developed previously.

The inhibitory E max model was able to accurately predict drug-free SERT BP in people taking drug treatment. The drug-free BP in patients with OCD currently treated with escitalopram was significantly different from those in healthy volunteers [Cohen's d = 0.03 (caudate), 1.16 (putamen), 1.46 (thalamus), −5.67 (dorsal raphe nucleus)].

This result extends previous findings showing SERT abnormalities in drug-free patients with OCD by indicating that altered SERT availability is seen in OCD despite treatment. This could account for poor response and the high risk of relapse in OCD.

Depression is common after acute coronary syndrome (ACS) with adverse effects on prognosis. There is little evidence on whether depression treatment improves quality of life (QoL) in ACS patients. The aim of this study was to investigate the effects of co-morbid depression and its treatment on QoL in ACS.

In total, 1152 patients were recruited at baseline, 2–14 weeks after a confirmed ACS episode, and 828 were followed 1 year thereafter. Of 446 baseline participants with co-morbid depressive disorders, 300 were randomized to a 24-week double blind trial of escitalopram or placebo, while the remaining 146 received medical treatment only (MTO). QoL was measured by the World Health Organization Quality of Life –Abbreviated form (WHOQOL-BREF).

At baseline, QoL was significantly lower in patients with co-morbid depressive disorder than those without. QoL improvement was significantly greater in those receiving escitalopram than those receiving placebo over the 24-week treatment period. In the 1-year follow-up, the better outcomes associated with escitalopram remained evident against both placebo and MTO.

Depression was significantly associated with worse QoL even in patients with recently developed ACS. Depression treatment was associated with QoL improvement in ACS patients in the 24-week treatment period, the effects of which extended to 1 year.

Additional high-quality evidence for predictors of peritonsillar abscess recurrence could lead to better-informed treatment decisions regarding tonsillectomy.

In this study, 172 patients, who had been diagnosed and treated for peritonsillar abscess, were evaluated at follow up. A retrospective review of medical records and a telephone survey were performed. The clinical characteristics analysed included underlying disease, laboratory findings and computed tomography findings. Cox proportional hazard models were used to identify risk factors for peritonsillar abscess recurrence.

The recurrence rate of peritonsillar abscess was 13.9 per cent. Univariate analysis indicated that extraperitonsillar spread of the abscess (beyond the peritonsillar area) on computed tomography and a history of recurrent tonsillitis were associated with recurrence. Multivariate analysis also indicated that extraperitonsillar spread (p = 0.007; hazard ratio = 3.399) and recurrent tonsillitis history (p < 0.001; hazard ratio = 11.953) were significant risk factors for recurrence.

Our results suggest that tonsillectomy may be indicated as a treatment for peritonsillar abscess in patients with a history of recurrent tonsillitis or extraperitonsillar spread on computed tomography.

Previous studies have implicated the relationship between environmental phthalate exposure and attention deficit hyperactivity disorder (ADHD) symptoms of childhood, but no studies have been conducted in children who have a confirmed diagnosis of ADHD obtained through meticulous diagnostic testing. We aimed to determine whether phthalate metabolites in urine would be higher in children with ADHD than in those without ADHD and would correlate with symptom severity and cortical thickness in ADHD children.

A cross-sectional examination of urine phthalate metabolite concentrations was performed; scores for ADHD symptoms, externalizing problems, and continuous performance tests were obtained from 180 children with ADHD, and brain-imaging data were obtained from 115 participants. For the control group, children without ADHD (N = 438) were recruited. Correlations between phthalate metabolite concentrations and clinical measures and brain cortical thickness were investigated.

Concentrations of phthalate metabolites, particularly the di(2-ethylhexyl) phthalate (DEHP) metabolite, were significantly higher in boys with ADHD than in boys without ADHD. Concentrations of the di-n-butyl phthalate (DBP) metabolite were significantly higher in the combined or hyperactive-impulsive subtypes compared to the inattentive subtype, and the metabolite was positively correlated with the severity of externalizing symptoms. Concentrations of the DEHP metabolite were negatively correlated with cortical thickness in the right middle and superior temporal gyri.

The results of this study suggest an association between phthalate concentrations and both the diagnosis and symptom severity of ADHD. Imaging findings suggest a negative impact of phthalates on regional cortical maturation in children with ADHD.

We examined the cross-sectional relationship between environmental tobacco smoke exposure, continuous performance test (CPT) measures, and attention deficit hyperactivity disorder (ADHD) or learning disability symptoms in school-aged children.

In total, 989 children (526 boys, mean age 9.1 ± 0.7 years), recruited from five South Korean cities participated in this study. We used urine cotinine as a biomarker for environmental tobacco smoke exposure, and obtained the children's scores on a CPT. Parents completed the Korean versions of the ADHD Rating Scale – IV (ADHD-RS) and Learning Disability Evaluation Scale (LDES). Using generalized linear mixed model (GLMM), we assessed the associations between urine cotinine concentrations, neuropsychological variables, and symptoms of ADHD and learning disabilities. Additionally, we conducted structural equation models to explore the effects' pathways.

After adjusting for a range of relevant covariates, GLMM showed urinary cotinine levels were significantly and positively associated with CPT scores on omission errors, commission errors, response time, and response time variability, and with parent- and teacher-rated ADHD-RS scores. In addition, urine cotinine levels were negatively associated with LDES scores on spelling and mathematical calculations. The structural equation model revealed that CPT variables mediated the association between urine cotinine levels and parental reports of symptoms of ADHD and learning disabilities.

Our data indicate that environmental exposure to tobacco smoke is associated with ADHD and learning disabilities in children, and that impairments in attention and inhibitory control probably mediate the effect.