Electronic edge-state and space-charge phenomena in long GaN nanowires and nanoribbons.

We studied space-charge-distribution phenomena in planar GaN nanowires and nanoribbons (NRs). The results obtained at low voltages demonstrate that the electron concentration changes not only at the edges of the NR, but also in the middle part of the NR. The effect is stronger with decreasing NR width. Moreover, the spatial separation of the positive and negative charges results in electric-field patterns outside the NR. This remarkable feature of electrostatic fields outside the NR may be even stronger in 2D material structures. For larger voltages the space-charge-limited current (SCLC) effect determines the main mechanism of transport in the NR samples. The onset of the SCLC effect clearly correlates with the NR width. The results are confirmed by noise spectroscopy studies of the NR transport. We found that the noise increases with decreasing NR width and the shape of the spectra changes with voltage increase with a tendency toward slope (3/2), reflecting diffusion processes due to the SCLC effect. At higher voltages noise decreases as a result of changes in the scattering mechanisms. We suggest that the features of the electric current and noise found in the NRs are of general character and will have an impact on the development of NR-based devices.

Giant magnetoconductance oscillations in hybrid superconductor-semiconductor core/shell nanowire devices.

The magnetotransport of GaAs/InAs core/shell nanowires contacted by two superconducting Nb electrodes is investigated, where the InAs shell forms a tube-like conductive channel around the highly resistive GaAs core. By applying a magnetic field along the nanowire axis, regular magnetoconductance oscillations with an amplitude in the order of e(2)/h are observed. The oscillation amplitude is found to be larger by 2 orders of magnitude compared to the measurements of a reference sample with normal metal contacts. For the Nb-contacted core/shell nanowire the oscillation period corresponds to half a flux quantum Φ0/2 = h/2e in contrast to the period of Φ0 of the reference sample. The strongly enhanced magnetoconductance oscillations are explained by phase-coherent resonant Andreev reflections at the Nb-core/shell nanowire interface.

Gate-induced transition between metal-type and thermally activated transport in self-catalyzed MBE-grown InAs nanowires.

Electronic transport properties of InAs nanowires are studied systematically. The nanowires are grown by molecular beam epitaxy on a SiOx-covered GaAs wafer, without using foreign catalyst particles. Room-temperature measurements revealed relatively high resistivity and low carrier concentration values, which correlate with the low background doping obtained by our growth method. Transport parameters, such as resistivity, mobility, and carrier concentration, show a relatively large spread that is attributed to variations in surface conditions. For some nanowires the conductivity has a metal-type dependence on temperature, i.e. decreasing with decreasing temperature, while other nanowires show the opposite temperature behavior, i.e. temperature-activated characteristics. An applied gate voltage in a field-effect transistor configuration can switch between the two types of behavior. The effect is explained by the presence of barriers formed by potential fluctuations.

Realization of nanoscaled tubular conductors by means of GaAs/InAs core/shell nanowires.

We investigated the transport properties of GaAs/InAs core/shell nanowires grown by molecular beam epitaxy. Owing to the band alignment between GaAs and InAs, electrons are accumulated in the InAs shell as long as the shell thickness exceeds 12 nm. By performing simulations using a Schrödinger-Poisson solver, it is confirmed that confined states are present in the InAs shell, which are depleted if the shell thickness is below a threshold value. The existence of a tubular-shaped conductor is proved by performing magnetoconductance measurements at low temperatures. Here, flux periodic conductance oscillations are observed which can be attributed to transport in one-dimensional channels based on angular momentum states.

Nanoimprint and selective-area MOVPE for growth of GaAs/InAs core/shell nanowires.

We report on the technology and growth optimization of GaAs/InAs core/shell nanowires. The GaAs nanowire cores were grown selectively by metal organic vapor phase epitaxy (SA-MOVPE) on SiO(2) masked GaAs (111)B templates. These were structured by a complete thermal nanoimprint lithography process, which is presented in detail. The influence of the subsequent InAs shell growth temperature on the shell morphology and crystal structure was investigated by scanning and transmission electron microscopy in order to obtain the desired homogeneous and uniform InAs overgrowth. At the optimal growth temperature, the InAs shell adopted the morphology and crystal structure of the underlying GaAs core and was perfectly uniform.

Electronic transport with dielectric confinement in degenerate InN nanowires.

In this Letter, we present the size effects on charge conduction in InN nanowires by comprehensive transport studies supported by theoretical analysis. A consistent model for highly degenerate narrow gap semiconductor nanowires is developed. In contrast to common knowledge of InN, there is no evidence of an enhanced surface conduction, however, high intrinsic doping exists. Furthermore, the room-temperature resistivity exhibits a strong increase when the lateral size becomes smaller than 80 nm and the temperature dependence changes from metallic to semiconductor-like. This effect is modeled by donor deactivation due to dielectric confinement, yielding a shift of the donor band to higher ionization energies as the size shrinks.

Electronic phase coherence in InAs nanowires.

Magnetotransport measurements at low temperatures have been performed on InAs nanowires grown by In-assisted molecular beam epitaxy. Information on the electron phase coherence is obtained from universal conductance fluctuations measured in a perpendicular magnetic field. By analysis of the universal conductance fluctuations pattern of a series of nanowires of different length, the phase-coherence length could be determined quantitatively. Furthermore, indications of a pronounced flux cancelation effect were found, which is attributed to the topology of the nanowire. Additionally, we present measurements in a parallel configuration between wire and magnetic field. In contrast to previous results on InN and InAs nanowires, we do not find periodic oscillations of the magnetoconductance in this configuration. An explanation of this behavior is suggested in terms of the high density of stacking faults present in our InAs wires.

Gate-controlled quantum collimation in nanocolumn resonant tunneling transistors.

Nanoscaled resonant tunneling transistors (RTT) based on MBE-grown GaAs/AlAs double-barrier quantum well (DBQW) structures have been fabricated by a top-down approach using electron-beam lithographic definition of the vertical nanocolumns. In the preparation process, a reproducible mask alignment accuracy of below 10 nm has been achieved and the all-around metal gate at the level of the DBQW structure has been positioned at a distance of about 20 nm relative to the semiconductor nanocolumn. Due to the specific doping profile n++/i/n++ along the transistor nanocolumn, a particular confining potential is established for devices with diameters smaller than 70 nm, which causes a collimation effect of the propagating electrons. Under these conditions, room temperature optimum performance of the nano-RTTs is achieved with peak-to-valley current ratios above 2 and a peak current swing factor of about 6 for gate voltages between -6 and +6 V. These values indicate that our nano-RTTs can be successfully used in low power fast nanoelectronic circuits.

Electrical transport properties of single undoped and n-type doped InN nanowires.

Electrical transport properties of undoped and n-type doped InN nanowires grown by molecular beam epitaxy were studied by current-voltage and back-gate field-effect transistor measurements. The current-voltage characteristics show ohmic behavior in the temperature range between 4 and 300 K. Down to about 120 K a linear decrease in resistance with temperature is observed. The investigation of a large number of nanowires revealed for undoped as well as doped wires an approximately linear relation between the normalized conductance and diameter for wires with a diameter below 100 nm. This shows that the main conduction takes place in the tubular surface accumulation layer of the wires. In contrast, for doped wires with a diameter larger than 100 nm a quadratic dependence of conduction on the diameter was found, which is attributed to bulk conductance as the main contribution. The successful doping of the wires is confirmed by an enhanced conduction and by the results of the back-gate field-effect transistor measurements.

[Psychiatric disorders and childhood trauma in prisoners with antisocial personality disorder]. / Psychische Störungen und Kindheitstraumata bei Strafgefangenen mit antisozialer Persönlichkeitsstörung.

Previous studies indicate high prevalence rates of mental disorders and trauma among prisoners. Based on a sample of 102 male German prisoners, the comorbidity and childhood trauma experiences in 72 criminals with antisocial personality disorder were investigated. Furthermore, associations of antisocial personality disorder and early traumatic experiences with the age at first conviction and the lifetime months of imprisonment were examined. Subjects had high rates of comorbid lifetime and current disorders as well as childhood trauma experiences. Physical abuse in childhood and adolescence was identified as a predictor for lifetime months of imprisonment, antisocial personality disorder was found to be a predictor for the age at first conviction. Our findings confirm the hypothesis of prisoners with antisocial personality disorder being a severely traumatized population with serious mental disorders. Traumatic childhood experiences and antisocial personality disorder are associated with criminality variables. This has important implications on preventive treatments as well as on how prison services are addressing these problems.

Raman scattering study of GaN nanostructures obtained by bottom-up and top-down approaches.

GaN nanocolumnar structures were grown by plasma-assisted molecular beam epitaxy (PAMBE) and also fabricated by electron cyclotron resonance reactive ion etching (ECR-RIE) of a compact GaN film parallel to the [111] direction of the Si(111) substrates. Scanning electron microscopy shows that the nanocolumns fabricated by PAMBE have a length of about 300-500 nm with diameters ranging from 20 to 150 nm while nanowhiskers formed by RIE have diameters of 40-80 nm and a height between 1.4 and 1.7 µm. A comparative study of the vibrational spectrum (including optical and interface phonons) of the nanostructures using conventional macro-Raman and micro-Raman scattering as well as surface-enhanced Raman scattering is presented.

Crosslinking of alpha-synuclein by advanced glycation endproducts--an early pathophysiological step in Lewy body formation?

An excess of reactive carbonyl compounds (carbonyl stress) and their reaction products, advanced glycation endproducts (AGEs), are thought to play a decisive role in the pathogenesis of neurodegenerative disorders and Parkinson's disease (PD) in particular. Accumulation of AGEs in various intracellular pathological hallmarks of PD, such as Lewy bodies, densely crosslinked intracellular protein deposits formed from neurofilament components and alpha-synuclein, have already been described in patients in advanced stages of the disease. There is, however, no indication of the involvement of AGE-induced crosslinking of alpha-synuclein in very early stages of the disease. In this study, we observed that AGEs and alpha-synuclein are similarly distributed in very early Lewy bodies in the human brain in cases with incidental Lewy body disease. These cases might be viewed as pre-Parkinson patients, i.e. patients who came for autopsy before the possible development of clinical signs of PD. AGEs are both markers of transition metal induced oxidative stress as well as, inducers of protein crosslinking and free radical formation by chemical and cellular processes. Thus, it is likely that AGE promoted formation of Lewy bodies reflects very early causative changes rather than late epiphenomenons of PD.

Activated mitogenic signaling induces a process of dedifferentiation in Alzheimer's disease that eventually results in cell death.

Neurodegeneration in Alzheimer's disease (AD) is associated with the appearance of dystrophic neuronal growth profiles that most likely reflect an impairment of neuronal reorganization. This process of morphodysregulation, which eventually goes awry and becomes a disease itself, might be triggered either by a variety of life events that place an additional burden on the plastic capability of the brain or by genetic pertubations that shift the threshold for decompensation. This paper summarizes recent evidence that impairment of the p21ras intracellular signal transduction, which is is mediated by a hierarchy of phosphorylation signals and eventually results in loss of differentiation control and an attempt of neurons to re-enter the cell-cycle, is critically involved in this process. Neurodegeneration might thus be viewed as an alternative effector pathway of those events that in the dividing cell would lead to cellular transformation. This hypothesis might be of heuristic value for the development of a therapeutic strategy.

Co-expression of APP with cNOS but not iNOS after cortical injury in rat.

Alterations in the expression of both the beta-amyloid precursor protein (APP) and nitric oxide synthase (NOS) might be involved in neurodegenerative conditions and/or in the neuronal response to injury. We have investigated the relationship between the increased expression of beta-amyloid precursor protein (APP) and the reactive changes in the expression of isoforms of nitric oxide synthase (NOS) in neurons and glial cells after small electrolytic lesions placed to the cerebral cortex. An increase in the expression of APP in both neurons and glial cells was detected 4 days post-operation. The inducible NOS (iNOS) was observed in macrophages or glial cells surrounding the lesion site. No major changes in constitutive NOS (cNOS) were found. APP immunoreactivity was not co-localized with either iNOS or cNOS at this survival time. At longer survival times (8 and 12 days post-lesion), a reactive increase in the expression of cNOS in cortical pyramidal neurons was seen in addition to the elevated expression of iNOS in astrocytes. The reactive expression of cNOS was confined to a subset of neurons also showing a high expression of APP. The present results suggest a relationship between reactive changes in the expression of APP and cNOS during the neuronal response to injury.

Insect-based BioFETs with improved signal characteristics.

Insect-based BioFETs (biologically sensitive field-effect transistors) with improved signal characteristics have been developed. These BioFETs require a specifically adapted signal interfacing between a FET as signal transducer and an intact insect antenna as biocomponent. Therefore, different field-effect transistors have been fabricated in order to study the signal transfer at the bioelectronic interface. As relevant features of the BioFET, its current-voltage characteristics, the transconductance and the signal-to-noise ratio have been investigated as affected by the choice of gate insulator materials and gate dimensions (width-to-length ratio, thickness of the dielectric layers). The performance of the improved FET arrangement in the isolated-antenna BioFET was validated by employing dilution series of the plant odour component Z-3-hexen-1-ol.

Aberrant expression of nNOS in pyramidal neurons in Alzheimer's disease is highly co-localized with p21ras and p16INK4a.

Aberrancies of growth and proliferation-regulating mechanisms might be critically involved in the processes of neurodegeneration in Alzheimer's disease (AD). Expression of p21ras and further downstream signalling elements involved in regulation of proliferation and differentiation as, for example, MEK, ERK1/2, cyclins, cyclin-dependent kinases and their inhibitors such as those of the p16INK4a family, are elevated early during the course of neurodegeneration. Activation of p21ras can also directly be triggered by nitric oxide (NO), synthesized in the brain by various isoforms of nitric oxide synthase (NOS) that might be differentially involved into the pathomechanism of AD. To study the potential link of NO and critical regulators of cellular proliferation and differentiation in the process of neurofibrillary degeneration, we analyzed the expression pattern of NOS-isoforms, p21ras and p16INK4a compared to neurofibrillary degeneration in AD. Additionally to its expression in a subtype of cortical interneurons that contain the nNOS-isoform also in normal brain, nNOS was detected in pyramidal neurons containing neurofibrillary tangles or were even unaffected by neurofibrillary degeneration. Expression of nNOS in these neurons was highly co-localized with p21ras and p16INK4a. Because endogenous NO can activate p21ras in the same cell which in turn leads to cellular activation and stimulation of NOS expression [H.M. Lander, J.S. Ogiste, S.F.A. Pearce, R. Levi, A. Novogrodsky, Nitric oxide-stimulated guanine nucleotide exchange on p21 ras, J. Biol. Chem. 270 (1995) 7017-7020], the high level of co-expression of NOS and p21ras in neurons vulnerable to neurofibrillary degeneration early in the course of AD thus provides the basis for an autocrine feedback mechanism that might exacerbate the progression of neurodegeneration in a self-propagating manner.

Expression of endothelial and inducible NOS-isoforms is increased in Alzheimer's disease, in APP23 transgenic mice and after experimental brain lesion in rat: evidence for an induction by amyloid pathology.

The nitric oxide-synthesizing enzyme nitric oxide synthase (NOS) is present in the mammalian brain in three different isoforms, two constitutive enzymes (i.e., neuronal, nNOS, and endothelial eNOS) and one inducible enzyme (iNOS). All three isoforms are aberrantly expressed in Alzheimer's disease giving rise to elevated levels of nitric oxide apparently involved in the pathogenesis of this disease by various different mechanisms including oxidative stress and activation of intracellular signalling mechanisms. It still is a matter of debate, however, whether the abnormal expression of NOS isoforms has some primary importance in the pathogenetic chain and might thus be a potential therapeutic target or only reflects a secondary effect that occurs at more advanced stages of the disease process. To tackle this question, we analysed the expression of both eNOS and iNOS in patients with sporadic AD, in transgenic mice expressing human amyloid precursor protein (APP) with the Swedish double mutation under control of the Thy1 promotor (APP23 mice), and after electrolytic cortical lesion in rat, an experimental paradigm associated with elevated expression of APP. In all three conditions, an astrocytosis was induced accompanied by a strong increase of both iNOS and eNOS. Both NOS isoforms were frequently though not always colocalized. Thus, based on the expression pattern of NOS isoforms three types of astrocytes, expressing only one of the two isoforms or both together could be distinguished. In both AD and transgenic mice eNOS-expressing astrocytes exceeded iNOS-expressing astrocytes in number. Astrocytes with elevated levels of iNOS or eNOS were constantly seen in direct association with Abeta-deposits in AD and transgenic mice and were found in the vicinity of the lesion site in the rat cortex. The results of the present study show that expression of both iNOS and eNOS is increased in activated astrocytes under experimental conditions associated with elevated expression of APP (electrolytic brain lesion) or Abeta-deposition (APP23 transgenic mice). Therefore, it is suggested that altered expression of these NOS isoforms being part of AD pathology is secondary to the amyloid pathology and might not be primarily involved in the pathogenetic chain though it might contribute to the maintenance, self-perpetuation and progression of the neurodegenerative process.

Advanced glycation endproducts co-localize with inducible nitric oxide synthase in Alzheimer's disease.

Advanced glycation endproducts (AGEs), protein-bound oxidation products of sugars, have been shown to be involved in the pathophysiological processes of Alzheimer's disease (AD). AGEs induce the expression of various pro-inflammatory cytokines and the inducible nitric oxide synthase (iNOS) leading to a state of oxidative stress. AGE modification and resulting crosslinking of protein deposits such as amyloid plaques may contribute to the oxidative stress occurring in AD. The aim of this study was to immunohistochemically compare the localization of AGEs and beta-amyloid (Abeta) with iNOS in the temporal cortex (Area 22) of normal and AD brains. In aged normal individuals as well as early stage AD brains (i.e. no pathological findings in isocortical areas), a few astrocytes showed co-localization of AGE and iNOS in the upper neuronal layers, compared with no astrocytes detected in young controls. In late AD brains, there was a much denser accumulation of astrocytes co-localized with AGE and iNOS in the deeper and particularly upper neuronal layers. Also, numerous neurons with diffuse AGE but not iNOS reactivity and some AGE and iNOS-positive microglia were demonstrated, compared with only a few AGE-reactive neurons and no microglia in controls. Finally, astrocytes co-localized with AGE and iNOS as well as AGE and were found surrounding mature but not diffuse amyloid plaques in the AD brain. Our results show that AGE-positive astrocytes and microglia in the AD brain express iNOS and support the evidence of an AGE-induced oxidative stress occurring in the vicinity of the characteristic lesions of AD. Hence activation of microglia and astrocytes by AGEs with subsequent oxidative stress and cytokine release may be an important progression factor in AD.

The localization of AChE in the dorsal lateral geniculate nucleus of different mammals--a light and electron microscopical study.

AchE has been histochemically demonstrated in the dLGN of different mammals. In the rat dLGN the enzyme is light microscopically localized in fibres only. This reaction is somewhat higher in the superficial than in the innermost region of the dLGN. The same distribution has been observed in other rodents like hamster, mouse, and guinea pig. Reaction products have been found electron microscopically in afferent fibres of the rat's dLGN with characteristic vesicle types and synaptic contacts to dendrites. We concluded that these fibres originate from the formatio reticularis of the brain stem. Nerve cells show a very weak reaction in the nuclear envelope and in the endoplasmatic reticulum. In the rabbit dLGN cell bodies with strong AchE-reaction are demonstrable. The AchE-activity in the laminae of the dLGN of tree shrew, cat and monkey is compared with the morphologically characterized cell types. It is discussed that X-cells in the mammalian dLGN are more influenced by AchE-containing afferent axons than other types of geniculo-cortical relay cells. Light microscopic results of AchE-localization in the visual cortex of rodents, tree shrew, and cats are described.

[Localization and behaviour of hydrolases and transmitter enzymes in the dorsal Corpus geniculatum laterale of the rat after unilateral enucleation (author's transl)]. / Lokalisation und Verhalten von Hydrolasen und Transmitterenzymen im dorsalen Corpus geniculatum laterale der Ratte nach unilateraler Enucleation

In the Corpus geniculatum laterale [pars dorsalis] (Cgl d) of the rat the distribution of the following enzymes is described on the light microscopical level: acid phosphatase, nonspecific esterases, Thiaminepyrophosphatase (TPPase), cholinesterases (AchE and ChE), GABA-alpha-ketoglutarat-transaminase (GABA-T), monoaminooxidase (MAO) and leucin-aminopeptidase. The acid phosphatase and TPPase are localized in the pericarya of different cell types of the Cgl d. The nonspecific esterases are present intracellularly and in the neuropil. With the GABA-T-reaction single cells of Cgl d are stained. The leucine aminopeptidase could not be demonstrated in the Cgl. The nonspecific cholinesterase is localized in the vessel walls. AChE and MAO are present in different fiber structures in the Cgl. Electron microscopical investigations of AChE showed a localization of the enzym in the extracellular room, intraaxonal and in the synaptic cleft. Separation of ChE in polyacrylamid gel resulted in 2 bands for the AChE and 1 band for the nonspecific ChE. After left side enucleation the reaction of the enzymes acid phosphatase, nonspecific esterases cholinesterases and TPPase was proofed topochemically at the section and biochemically at the homogenate. A decrease of enzyme activity in the enzymes acid phosphatase, nonspecific esterases and AchE is shown. The alterations are discussed in connection with the transneuronal degeneration.