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Notes: A simple method for producing a Au:p-n-CdTe Schottky barrier is described. The shallow p-n junction is formed by photoelectrochemical surface oxidization of n-CdTe. X-ray photoelectron spectroscopy, Auger electron spectroscopy depth profiling, and electron-beam-induced-current measurements provide important insight into the underlying causes of the formation of the p-type layer. Current-voltage and capacitance-voltage measurements show that the thin p-layer enhances the effective barrier height relative to that of a traditional Au:n-CdTe junction. These results account for the Au:p-n-CdTe cells exhibiting higher open-circuit photovoltages and higher photoconversion efficiencies than do Au:n-CdTe Schottky-barrier cells. From temperature dependence studies of the current-voltage characteristics, detailed information on the charge-transport mechanism of the junction was obtained. Photocurrent spectra of Au:p-n-CdTe as a function of temperature reveal that exciton excitation in CdTe contributes to the photocurrent.

Notes: Plane mirror interferometers are widely used in the measurement of x–y motions. Although large range planar motion can be measured, it suffers from very tight angular tolerance. In this article an interferometer system having improved angular range and linear resolution is developed. In the system, a tilted laser beam is incident to a plane mirror attached to a moving stage and an additional retroreflector and a plane mirror are placed off the stage to help return the measuring beam. In such a design both the resolution and angular tolerance are improved. Meanwhile, large travel ranges along both the x and y directions remain. The optical principle pertinent to the proposed optical configuration is explained and an optical path analysis is performed to establish the relation between the optical path change and the motion to be measured. Based on the established relation, design of system parameters and workspace analysis are also discussed. Experimental results including resolution test and scaling procedure are then demonstrated. Using the developed interferometer an x–y theta measurement scheme is introduced. In the proposed scheme, using three interferometers the rotation angle of an x–y theta stage can be obtained first and it can then be used to compensate errors of the measured linear motion. © 2000 American Institute of Physics.

Notes: Prostaglandin E2, a product of the cyclooxygenation of arachidonic acid released from membrane phospholipids, plays major roles in regulating brain injury and inflammation. Although prostaglandin E2 has frequently been considered as a possible inducer of brain damage and degeneration, it may exert beneficial effects in the CNS. Indeed, in spite of its classic role as a pro-inflammatory molecule, several recent in vitro observations indicate that prostaglandin E2 can inhibit microglial activation. This study investigated the effect of central prostaglandin E2 injection on circulating lipopolysaccharide-induced gene expression of different pro-inflammatory molecules in both vascular and parenchymal elements of the brain. Localized, but strong, expression of tumor necrosis factor-α and interleukin-1β mRNA was found at the edge of the intracerebroventricular tract, which was largely prevented by the central prostaglandin E2 injection. Systemic lipopolysaccharide injection caused a profound transcriptional activation of cyclooxygenase-2 and the inhibitory factor κBα (IκBα, index of NF-κB activity) in the cerebral endothelium and tumor necrosis factor-α in microglial cells across the brain parenchyma. Although exogenous prostaglandin E2 increased lipopolysaccharide-induced NF-κB activity and cyclooxygenase-2 transcription in vascular-associated elements, it significantly reduced microglial activation and tumor necrosis factor-α expression in the brain parenchyma. These results indicate that prostaglandin E2 may play an important role in modulating the immune response occurring at the injured site and the pro-inflammatory signaling events taking place in both vascular- and microglial-associated elements of the CNS.

Notes: Abstract: Proinflammatory cytokines released by cells of myeloid lineage have the ability to stimulate different populations of neurons through intermediate molecules released by cells of the blood-brain barrier. The aim of the present study was to verify the hypothesis that prostaglandins (PGs) play a site-specific role in activating selective groups of neurons via a privileged interaction between PG of the E2 type and its EP4 receptor. In a first set of experiments, animals were treated with the inhibitor of PG synthesis ketorolac to determine the endogenous contribution of PG in mediating the neuronal activation and EP4 expression in response to circulating interleukin-1β (IL-1β). The subsequent experiment consisted of evaluating the role of PGE2 in activating EP4-expressing neurons in the rat brain. Ketorolac completely abolished the endogenous release of PGE2 in the liver and prevented the induction of immediate-early genes and up-regulation of EP4 mRNA in specific groups of neurons, such as the parvocellular paraventricular nucleus and the A1 catecholaminergic population of cells. This effect was, however, not generalized throughout the brain as PGE2 inhibition failed to abolish IL-1β-induced c-fos transcription in the nucleus of the solitary tract, parabrachial nucleus, bed nucleus of the stria terminalis, and the circumventricular organs. Of interest are the data that central PGE2 injection activated EP4 gene transcription in neurons that no longer responded to the intravenous IL-1β bolus when the animals were pretreated with ketorolac. Site-specific interaction between the ligand and its receptor was further supported by the induction of c-fos-immunoreactive nuclei within EP4-expressing neurons in response to intracerebroventricular PGE2 infusion. Both intracerebroventricular PGE2 and intravenous IL-1β injection provoked a sharp and rapid increase in plasma corticosterone levels, an effect that was completely prevented in inhibiting PG production in IL-1β-challenged rats. These data provide the evidence that EP4 is expressed in numerous nuclei involved in autonomic and neuroendocrine control, although a privileged interaction seems to take place in specific nuclei and areas, including the endocrine hypothalamus and the A1 cell group of the ventrolateral medulla. It is quite possible that EP4 acts as the functional receptor for PGE2 to activate the neuronal circuit involved in the activation of the glucocorticoid axis, as an essential neuroendocrine response for the appropriate control of systemic inflammation.

Notes: Abstract: Somatostatin (SRIF) receptor subtypes (sst) were characterized in hypothalamic neurons and astrocytes by quantitative reverse transcription-polymerase chain reaction and radioreceptor assays using [125I-Tyr0,d-Trp8]SRIF-14 as a ligand in ionic conditions discriminating between SRIF-1 (sst2, -3, and -5 receptors) and SRIF-2 (sst1 and -4 receptors) binding sites. In neurons, sst1 mRNA levels were twofold higher than those of sst2, and sst3–5 expression was only minor. Astrocytes expressed 10-fold less sst mRNAs than neurons, which corresponded mostly (80%) to sst2. SRIF-1 binding site radioautography indicated that 10% of hypothalamic neurons were labelled on both cell bodies and neuritic processes, as were 35% of astrocytes. On neuronal and glial membranes, SRIF-14 and octreotide, an sst2/sst3/sst5-selective analogue, completely displaced SRIF-1 binding, whereas des-AA1,2,5[d-Trp8,IAmp9]SRIF (CH-275), an sst1-selective analogue, was ineffective. Using SRIF-2 conditions, only SRIF-14 and CH-275 displaced the binding on neurons. No SRIF-2 binding was observed on glia. SRIF-14 and octreotide inhibited forskolin-stimulated adenylyl cyclase activity in neurons and glia, whereas CH-275 was effective in neurons only. In patch-clamp experiments, SRIF-14 modulated the glutamate sensitivity of hypothalamic neurons with either synergistic or antagonistic effects; CH-275 was only stimulatory and octreotide inhibitory. It is concluded that hypothalamic neurons express primarily sst1 and sst2, sst2 predominates in astrocytes, and both receptors induce distinct biological effects.

Notes: The electrochromic mechanism in amorphous tungsten oxide films is studied using Raman scattering measurements. The Raman spectra of as-deposited films show two strong peaks at 770 and 950 cm−1 due to vibrations of the W6+–O and W6+(Double Bond)O bonds, respectively, and a weaker peak at 220 cm−1 that we attribute to the W4+–O bonds. When lithium or hydrogen ions and electrons are inserted, extra Raman peaks due to W5+–O and W5+(Double Bond)O bonds appear at 330 and 450 cm−1, respectively. Comparison of the Raman spectra of sputtered isotopic a-W16O3−y and a-W18O3−y films confirms these assignments. We conclude that the as-deposited films contain mainly the W4+ and W6+ states, and the W5+ states are generated as a result of reduction of the W6+ states when lithium or hydrogen ions and electrons are inserted. We propose that the optical absorption in the colored films is caused by transitions between the W6+ and W5+, and W5+ and W4+ states. © 1999 American Institute of Physics.