57 research outputs found
Critical Evaluation of Organic Thin-Film Transistor Models
Thin-film transistors (TFTs) represent a wide-spread tool to determine the
charge-carrier mobility of materials. Mobilities and further transistor
parameters like contact resistances are commonly extracted from the electrical
characteristics. However, the trust in such extracted parameters is limited,
because their values depend on the extraction technique and on the underlying
transistor model. We propose a technique to establish whether a chosen model is
adequate to represent the transistor operation. This two-step technique
analyzes the electrical measurements of a series of TFTs with different channel
lengths. The first step extracts the parameters for each individual transistor
by fitting the full output and transfer characteristics to the transistor
model. The second step checks whether the channel-length dependence of the
extracted parameters is consistent with the model. We demonstrate the merit of
the technique for distinct sets of organic TFTs that differ in the
semiconductor, the contacts, and the geometry. Independent of the transistor
set, our technique consistently reveals that state-of-the-art transistor models
fail to reproduce the correct channel-length dependence. Our technique suggests
that contemporary transistor models require improvements in terms of
charge-carrier-density dependence of the mobility and/or the consideration of
uncompensated charges in the transistor channel.Comment: 20 pages, 10 figure
What can the activation energy tell about the energetics at grain boundaries in polycrystalline organic films?
Charge-carrier transport at the semiconductor-gate dielectric interface in
organic field-effect transistors is critically dependent on the degree of
disorder in the typically semi-crystalline semiconductor layer. Charge trapping
can occur at the interface as well as in the current-carrying semiconductor
layer itself. A detailed and systematic understanding of the role of grain
boundaries between crystallites and how to avoid their potentially detrimental
effects is still an important focus of research in the organic electronics
community. A typical macroscopic measurement technique to extract information
about the energetics of the grain boundaries is an activation energy
measurement. Here, we compare detailed experiments on the energetic properties
of monolayer thin films implemented in organic field-effect transistors, having
controlled numbers of grain boundaries within the channel region to kinetic
Monte-Carlo simulations of charge-carrier transport to elucidate the influence
of grain boundaries on the extracted activation energies. Two important
findings are: 1) whereas the energy at the grain boundary does not change with
the number of grain boundaries in a thin film, both the measured and simulated
activation energy increases with the number of grain boundaries. 2) In
simulations where both energy barriers and valleys are present at the grain
boundaries there is no systematic relation between the number of grain
boundaries and extracted activation energies. We conclude, that a macroscopic
measurement of the activation energy can serve as general quality indicator of
the thin film, but does not allow microscopic conclusions about the energy
landscape of the thin film
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Atomoxetine and citalopram alter brain network organization in Parkinson's disease.
Parkinson's disease has multiple detrimental effects on motor and cognitive systems in the brain. In contrast to motor deficits, cognitive impairments in Parkinson's disease are usually not ameliorated, and can even be worsened, by dopaminergic treatments. Recent evidence has shown potential benefits from restoring other neurotransmitter deficits, including noradrenergic and serotonergic transmission. Here, we study global and regional brain network organization using task-free imaging (also known as resting-state), which minimizes performance confounds and the bias towards predetermined networks. Thirty-three patients with idiopathic Parkinson's disease were studied three times in a double-blinded, placebo-controlled counter-balanced crossover design, following placebo, 40 mg oral atomoxetine (selective noradrenaline reuptake inhibitor) or 30 mg oral citalopram (selective serotonin reuptake inhibitor). Neuropsychological assessments were performed outside the scanner. Seventy-six controls were scanned without medication to provide normative data for comparison to the patient cohort. Graph theoretical analysis of task-free brain connectivity, with a random 500-node parcellation, was used to measure the effect of disease in placebo-treated state (versus unmedicated controls) and pharmacological intervention (drug versus placebo). Relative to controls, patients on placebo had executive impairments (reduced fluency and inhibitory control), which was reflected in dysfunctional network dynamics in terms of reduced clustering coefficient, hub degree and hub centrality. In patients, atomoxetine improved fluency in proportion to plasma concentration (P = 0.006, r 2 = 0.24), and improved response inhibition in proportion to increased hub Eigen centrality (P = 0.044, r 2 = 0.14). Citalopram did not improve fluency or inhibitory control, but its influence on network integration and efficiency depended on disease severity: clustering (P = 0.01, r 2 = 0.22), modularity (P = 0.043, r 2 = 0.14) and path length (P = 0.006, r 2 = 0.25) increased in patients with milder forms of Parkinson's disease, but decreased in patients with more advanced disease (Unified Parkinson's Disease Rating Scale motor subscale part III > 30). This study supports the use of task-free imaging of brain networks in translational pharmacology of neurodegenerative disorders. We propose that hub connectivity contributes to cognitive performance in Parkinson's disease, and that noradrenergic treatment strategies can partially restore the neural systems supporting executive function
18F-AV-1451 positron emission tomography in Alzheimer's disease and progressive supranuclear palsy.
The ability to assess the distribution and extent of tau pathology in Alzheimer's disease and progressive supranuclear palsy in vivo would help to develop biomarkers for these tauopathies and clinical trials of disease-modifying therapies. New radioligands for positron emission tomography have generated considerable interest, and controversy, in their potential as tau biomarkers. We assessed the radiotracer 18F-AV-1451 with positron emission tomography imaging to compare the distribution and intensity of tau pathology in 15 patients with Alzheimer's pathology (including amyloid-positive mild cognitive impairment), 19 patients with progressive supranuclear palsy, and 13 age- and sex-matched controls. Regional analysis of variance and a support vector machine were used to compare and discriminate the clinical groups, respectively. We also examined the 18F-AV-1451 autoradiographic binding in post-mortem tissue from patients with Alzheimer's disease, progressive supranuclear palsy, and a control case to assess the 18F-AV-1451 binding specificity to Alzheimer's and non-Alzheimer's tau pathology. There was increased 18F-AV-1451 binding in multiple regions in living patients with Alzheimer's disease and progressive supranuclear palsy relative to controls [main effect of group, F(2,41) = 17.5, P 2.2, P's 2.7, P's < 0.02). The support vector machine assigned patients' diagnoses with 94% accuracy. The post-mortem autoradiographic data showed that 18F-AV-1451 strongly bound to Alzheimer-related tau pathology, but less specifically in progressive supranuclear palsy. 18F-AV-1451 binding to the basal ganglia was strong in all groups in vivo. Postmortem histochemical staining showed absence of neuromelanin-containing cells in the basal ganglia, indicating that off-target binding to neuromelanin is an insufficient explanation of 18F-AV-1451 positron emission tomography data in vivo, at least in the basal ganglia. Overall, we confirm the potential of 18F-AV-1451 as a heuristic biomarker, but caution is indicated in the neuropathological interpretation of its binding. Off-target binding may contribute to disease profiles of 18F-AV-1451 positron emission tomography, especially in primary tauopathies such as progressive supranuclear palsy. We suggest that 18F-AV-1451 positron emission tomography is a useful biomarker to assess tau pathology in Alzheimer's disease and to distinguish it from other tauopathies with distinct clinical and pathological characteristics such as progressive supranuclear palsy.This study was funded by the National Institute for Health Research (NIHR, RG64473) Cambridge Biomedical Research Centre and Biomedical Research Unit in Dementia, PSP Association, the Wellcome Trust (JBR 103838), the Medical Research Council of Cognition and Brain Sciences Unit, Cambridge (MC-A060-5PQ30), and partially by a Medical Research Council grant (MR/K02308X/1) held by J.T.O., J.B.R., and F.I.A. The Human Research Tissue Bank is supported by the NIHR Cambridge Biomedical Research Centre
Atomoxetine Enhances Connectivity of Prefrontal Networks in Parkinson's Disease.
Cognitive impairment is common in Parkinson's disease (PD), but often not improved by dopaminergic treatment. New treatment strategies targeting other neurotransmitter deficits are therefore of growing interest. Imaging the brain at rest ('task-free') provides the opportunity to examine the impact of a candidate drug on many of the brain networks that underpin cognition, while minimizing task-related performance confounds. We test this approach using atomoxetine, a selective noradrenaline reuptake inhibitor that modulates the prefrontal cortical activity and can facilitate some executive functions and response inhibition. Thirty-three patients with idiopathic PD underwent task-free fMRI. Patients were scanned twice in a double-blind, placebo-controlled crossover design, following either placebo or 40-mg oral atomoxetine. Seventy-six controls were scanned once without medication to provide normative data. Seed-based correlation analyses were used to measure changes in functional connectivity, with the right inferior frontal gyrus (IFG) a critical region for executive function. Patients on placebo had reduced connectivity relative to controls from right IFG to dorsal anterior cingulate cortex and to left IFG and dorsolateral prefrontal cortex. Atomoxetine increased connectivity from the right IFG to the dorsal anterior cingulate. In addition, the atomoxetine-induced change in connectivity from right IFG to dorsolateral prefrontal cortex was proportional to the change in verbal fluency, a simple index of executive function. The results support the hypothesis that atomoxetine may restore prefrontal networks related to executive functions. We suggest that task-free imaging can support translational pharmacological studies of new drug therapies and provide evidence for engagement of the relevant neurocognitive systems.This work was funded by the Wellcome trust (103838), Parkinson’s UK, National Institute for Health Research’s Cambridge Biomedical Research Centre and the Medical Research Council (MC_US_A060_0016 and RG62761) and the James F McDonnell Foundation (21st century science initiative on Understanding Human Cognition). The BCNI is supported by a joint award from the Wellcome Trust and Medical Research Council.This is the final version of the article. It first appeared from Nature Publishing Group via http://dx.doi.org/10.1038/npp.2016.1
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