bluuebunny/crossref_metadata_2025_split huggingface dataset:
Superluminal interactions in near‐field optics
Authors: Broe J. , Keller O. 
Published: March 2003

The fact that photons emitted from an electric‐dipole active atom cannot be spatially localized better than to the near‐field zone of the atom is seen as the origin of genuine superluminality. By means of a simple model dipole current density the general theory is used to demonstrate numerically how superluminality enters the near‐field dynamics, and how from a measurement one could be tempted to believe that superluminal propagation effects occur. Furthermore, it is shown how for source‐detector distances larger than a pulse length one should be able to divide the pulse into two separate parts: one purely superluminal part arising solely in the non‐local generation process of the field, and another part seemingly propagating with superluminal speed. We comment on different velocity analyses, and we argue that the only fundamental velocity entering the problem is the vacuum velocity of light, which in a measurement would appear as the velocity of the trailing edge of the pulse.
Artificially induced unusual shape of erythrocytes: an atomic force microscopy study
Authors: Girasole M. , Cricenti A. , Generosi R. , Congiu‐Castellano A. , Boumis G. , Amiconi G. 
Published: March 2003

We used air operating atomic force microscopy (AFM) to study several morphological modifications of human erythrocytes, artificially produced by addition of exogenous agents including phospholipids, low ionic strength media and drugs. Most experiments were performed on unfixed samples to avoid treating red blood cells (RBCs) with chemical agents that can, in principle, induce morphological alteration.After detailed quantitative AFM characterization, the artificially produced abnormally shaped RBCs were compared with cells that occur with high incidence in blood pathologies. This morphological approach suggests a new strategy to describe and understand the biochemical and/or mechanical modifications responsible for the underlying pathologically induced changes and prove AFM to be a suitable tool to study erythrocyte deformation.
Extracting twins from orientation imaging microscopy scan data
Authors: Wright S. I. , Larsen R. J. 
Published: March 2003

SummaryAutomated electron backscatter diffraction or orientation imaging microscopy (OIM) provides spatially specific measurements of crystallographic orientation. These measurements are typically collected on regular grids. By inspecting the misorientation between neighbouring measurements on the grid, potential twin boundaries can be identified. If the misorientation is within some given tolerance of a specified twin misorientation, the boundary separating the two measurements may be identified as a potential twin boundary. In addition, for a coherent twin, the twinning planes must be coincident with the grain boundary plane. As OIM scans are inherently two‐dimensional, the scan data provide only limited information on the boundary plane. Thus, it is not possible to ascertain definitively whether the twinning planes are coincident with the boundary plane. Nonetheless, the alignment of the surface traces of the twinning planes with the trace of the boundary provides a partial indication of coincidence. An automated approach has been developed that allows data concerning both twin criterion to be extracted from OIM scans. Application of the methodology to deformed zirconium suggests that the twinning planes remain coherent during deformation. The methodology was also used to improve grain size distributions measured by OIM. These results more closely match those obtained by conventional metallography.
Application of electron backscatter diffraction (EBSD) to fracture studies of ferritic steels
Authors: Davies P. A. , Novovic M. , Randle V. , Bowen P. 
Published: March 2003

SummaryThe application of electron backscatter diffraction (EBSD) to fracture studies has provided a new method for investigating the crystallography of fracture surfaces. The crystallographic indices of cleavage planes can be measured both directly from the fracture surface and indirectly from metallographic sections perpendicular to the plane of the adjoining fracture surfaces. The results of direct individual cleavage facet plane orientation measurements are presented for carbon–manganese (C–Mn) and low‐alloy Mn–Mo–Ni (similar to ASTM A553 type‐B). Pressure vessel steel weld metals, obtained from fracture surfaces of Charpy impact test specimens fractured at various test temperatures and for an ultra‐low carbon steel (Fe–0.002C–0.058P) fractured at –196 °C by impact. In addition to the direct measurement from the fracture surface, cleavage facet orientation measurements for the ultra‐low carbon steel were complemented by the results obtained from the metallographic sections. Fractographic observations revealed that cleavage fracture is accommodated by a microvoid coalescence fracture micromechanism, which was induced by decohesion of second phase particles (inclusions). The correlation between the direct and indirect methodologies shows that the cleavage facet planes are dominated by the {001} plane orientations, and indicated that even when information concerning the full five degrees of freedom is inaccessible, the cleavage facet plane could still be determined. Finally, the advantages and disadvantages of direct orientation measurements from the fracture surface and indirectly by a destructive sectioning technique are discussed.
The smooth fractionator
Authors: Gundersen H. J. G. 
Published: March 2003

SummaryA modification of the general fractionator sampling technique called the smooth fractionator is presented. It may be used in almost every situation in which sampling is performed from distinct items that are uniquely defined, often they are physically separated items or clusters like pieces, blocks, slabs, sections, etc. To each item is associated a ‘guesstimate’ or an associated variable with a more‐or‐less close – and possibly biased − relationship to the content of the item. The smooth fractionator is systematic sampling among the items arranged according to the guesstimates in a unique, symmetric sequence with one peak and minimal jumps. The smooth fractionator is both very simple to implement and so efficient that it should probably always be used unless the natural sequence of the sampling items is equally smooth.So far, there is no theory for the prediction of the efficiency of smooth fractionator designs in general, and their properties are therefore illustrated with a range of real and simulated examples. At the cost of a slightly more elaborate sampling scheme, it is, however, always possible to obtain an unbiased estimate of the real precision and of some of the variance components.The only real practical problem for always obtaining a high precision with the smooth fractionator is specimen inhomogeneity, but that is detectable at almost no extra cost.With careful designs and for sample sizes of about 10, the sampling variation for the primary, smooth fractionator sampling step may in practice often be small enough to be ignored.
Neuropeptide Y Counteracts the Anorectic and Weight Reducing Effects of Ciliary Neurotropic Factor
Authors: Pu S. , Dhillon H. , Moldawer L. L. , Kalra P. S. , Kalra S. P. 
Published: March 2003

AbstractCiliary neurotrophic factor (CNTF), a cytokine of the interleukin‐6 superfamily, has been shown to induce hypophagia and weight loss. Neuropeptide Y (NPY) and orexin are potent orexigenic signals in the hypothalamus. Anorexia, normally seen in response to infection, injury and inflammation, may result from diminished hypothalamic orexigenic signalling caused by persistently elevated cytokines, including CNTF. To test this hypothesis, we first examined the effects of chronic intracerebroventricular (i.c.v.) infusion of CNTF for 6–7 days on food intake and body weight as well as hypothalamic NPY and orexin gene expression in male rats. Subsequently, the effectiveness of NPY replacement to counteract the effects of CNTF by coinfusion of NPY and CNTF was evaluated. Chronic i.c.v. infusion of CNTF (2.5 µg/day) reduced body weight (14.3% vs control) at the end of 7 days. Food intake remained suppressed for 5 days postinfusion and subsequently gradually returned to the control range by day 7. Serum leptin concentrations in these rats were in the same range seen in control rats. Chronic i.c.v. infusion of higher doses of CNTF (5.0 µg/day) produced sustained anorexia and body weight loss (29% vs controls) through the entire duration of the experiment. This severe anorexia was accompanied by markedly suppressed serum leptin concentrations. Furthermore, CNTF infusion alone significantly reduced hypothalamic NPY gene expression (P < 0.05) without affecting orexin gene expression. As expected, in fusion of NPY alone (18 µg/day) augmented food intake (191.6% over the initial control, P < 0.05) and produced a 25.1% weight gain in conjunction with a 10‐fold increase in serum leptin concentrations at the end of the 7‐day period. Interestingly, coinfusion of this regimen of NPY with the highly effective anorectic and body reducing effects of CNTF (5.0 µg/day) not only prevented the CNTF‐induced anorexia and weight loss, but also normalized serum leptin concentrations and hypothalamic NPY gene expression. These results demonstrate that chronic central infusion to produce a persistent elevation of the cytokine at pathophysiological levels (a situation that may normally manifest during infection, injury and inflammation) produced severe anorexia and weight loss in conjunction with reduction in both serum leptin concentrations and hypothalamic NPY gene expression. Reinstatement of hypothalamic NPY signalling by coinfusion of NPY counteracted these CNTF‐induced responses.
Selective Blockade of the Mineralocorticoid Receptor Impairs Hypothalamic‐Pituitary‐Adrenal Axis Expression of Habituation
Authors: Cole M. A. , Kalman B. A. , Pace T. W. W. , Topczewski F. , Lowrey M. J. , Spencer R. L. 
Published: March 2003

AbstractThe present study investigated the role of mineralocorticoid receptors (MR) and glucocorticoid receptors (GR) in the expression of habituation of the hypothalamic‐pituitary‐adrenal (HPA) axis response to stress. Male rats were restrained for 1 h per day for six consecutive days. On day 6, 1 h prior to restraint stress, both restraint‐naive and repeatedly restrained rats were injected s.c. with either vehicle (propylene glycol) or one of three corticosteroid receptor antagonist treatments: selective MR antagonist (RU28318 or spironolactone), selective GR antagonist (RU40555), or both MR and GR antagonists combined (RU28318 + RU40555). Blood samples were collected for corticosterone measurement at the beginning of stress, during stress, and 1 h after stress termination. Repeated restraint stress produced significant habituation of corticosterone responses. Acute treatment with the combined MR and GR antagonists prevented the expression of habituation. When tested alone, the MR antagonist also blocked the expression of corticosterone‐response habituation, whereas the GR antagonist had no effect. Neither the MR, nor the GR antagonists alone, significantly altered the corticosterone response to restraint in rats exposed to restraint for the first time. The final experiment examined the corticosterone response to a corticotropin releasing hormone (CRH, 3 µg/kg i.p.) challenge. Neither previous exposure to restraint or acute pretreatment with the combined MR and GR antagonists (RU28318 + RU40555) altered the corticosterone response to CRH challenge. This result indicates that the expression of habituation and its blockade by corticosteroid receptor antagonists is not a result of altered pituitary‐adrenal response to CRH. Overall, this study suggests that MR plays an important role in constraining the HPA axis response to restraint stress in restraint‐habituated rats. The dependence of the HPA axis on MR‐mediated corticosteroid negative feedback during acute stress may be an important mechanism that helps maximize the expression of stress habituation and thereby minimize exposure of target tissues to corticosteroids in the context of repeated stress.
Analysis of Adrenocortical Secretory Responses During Acute and Prolonged Immune Stimulation in Inflammation‐Susceptible and‐Resistant Rat Strains
Authors: Andersson I. M. , Lorentzen J. C. , Ericsson‐Dahlstrand A. 
Published: March 2003

AbstractEndogenous corticosterone secreted during immune challenge restricts the inflammatory process and genetic variations in this neuroendocrine–immune dialogue have been suggested to influence an individuals sensitivity to develop chronic inflammatory disorders. We have tested inflammation‐susceptible Dark Agouti (DA) rats and resistant, MHC‐identical, PVG.1AV1 rats for their abilities to secrete corticosterone in response to acute challenge with bacterial lipopolysaccharide (LPS) or a prolonged activation of the nonspecific immune system with arthritogenic yeast β‐glucan. Intravenous injection of LPS triggered equipotent secretion of corticosterone in both rat strains. Interestingly, peak concentrations of corticosterone did not differ significantly between the strains. Intradermal injection of β‐glucan caused severe, monophasic, polyarthritis in DA rats while PVG.1AV1 responded with significantly milder joint inflammation. Importantly, serial sampling of plasma from glucan‐injected DA and PVG.1AV1 rats did not reveal elevated concentrations of plasma corticosterone at any time from days 1–30 postinjection compared to preinjection values, in spite of the ongoing inflammatory process. Interestingly, adrenalectomized, β‐glucan‐challenged DA rats responded with an aggravated arthritic process, indicating an anti‐inflammatory role for the basal levels of corticosterone that were detected in intact DA rats challenged with β‐glucan. Moreover, substitution with subcutaneous corticosterone‐secreting pellets, yielding moderate stress‐levels, significantly attenuated the arthritic response. In contrast, adrenalectomized and glucan‐challenged PVG.1AV1 rats did not respond with an elevated arthritic response, suggesting that these rats contain the arthritic process via corticosterone‐independent mechanisms. In conclusion, the hypothalamic‐pituitary‐adrenal axis in both rat strains exhibited strong activation after challenge with LPS. This contrasted to the basal corticosterone levels observed strains during a prolonged arthritic process. No correlation between ability to secrete corticosterone and susceptibility to inflammation could be demonstrated. Basal levels of endogenous corticosterone appeared to restrain inflammation in β‐glucan‐challenged DA rats whereas resistance to inflammation in PVG.1AV1 rats may be mediated via corticosterone‐independent mechanisms.
Priming with Interleukin‐1β Suppresses Experimental Allergic Encephalomyelitis in the Lewis Rat
Authors: Huitinga I. , Schmidt E. D. , Van Der Cammen M. J. F. , Binnekade R. , Tilders F. J. H. 
Published: March 2003

AbstractLewis rats exhibit multiple defects in their hypothalamus‐pituitary‐adrenal (HPA) system that are considered to play a causal role in the susceptibility of this strain to autoimmune diseases, i.e. experimental allergic encephalomyelitis (EAE). In the present study, we aimed to modulate the HPA response of the Lewis rat and establish its consequences for the susceptibility to EAE. Because in Wistar rats, single administration of interleukin (IL)‐β (priming) is known to induce long‐lasting (weeks) sensitization of HPA responses to stressors and immune stimuli, Lewis rats were given a single dose of hIL‐1β or vehicle 1 week prior to induction of EAE by immunization with myelin basic protein (MBP). Subsequently, neurological deficits were monitored once daily. The results show that IL‐1 priming markedly suppresses the neurological symptoms of EAE, without affecting the onset or duration of the disease. Measurement of vasopressin and corticotropin releasing hormone (CRH) in the external zone of the median eminence revealed that, as compared to Wistar rats, Lewis rats exhibit low vasopressin but identical CRH, and that IL‐1 priming increases (0.001) vasopressin without affecting CRH stores, which is consistent with a shift to vasopressin‐dominated control of adrenocorticotropic hormone (ACTH) secretion as described in Wistar rats under conditions of HPA hyper(re)activity. However, IL‐1 priming did not affect a.m. corticosterone levels following immunization with MBP or during the clinical phase of EAE. IL‐1 priming of Lewis rats attenuated the ACTH responses to an IL‐1 challenge 11 days later, which may relate to an increase in resting corticosterone levels. Thus, the mechanisms underlying IL‐1 induced suppression of EAE are not related to enhanced HPA responses. In addition, we did not find IL‐1 priming‐induced alterations in MBP‐specific immunoglobulin (Ig)M, IgG1, IgGa and IgGb plasma titres, or gross alterations in T cell activation as reflected in spontaneous or concanavalin‐induced T cell proliferation. We therefore speculate that IL‐1‐induced elevation of resting corticosterone levels may influence the development of EAE.
Localization of the Melatonin‐Related Receptor in the Rodent Brain and Peripheral Tissues
Authors: Drew J. E. , Barrett P. , Mercer J. G. , Moar K. M. , Canet E. , Delagrange P. , Morgan P. J. 
Published: March 2003

AbstractPrevious studies have provided a limited examination of the expression of the orphan melatonin‐related receptor in the pituitary and hypothalamus of human and sheep and retinal tissue in the sheep. The present study reports evidence of conservation of expression in regions of the hypothalamus (dorsal medial hypothalamus, lateral hypothalamus, arcuate nucleus), the epithelial layer lining the third ventricle and the paraventricular thalamic nucleus of the mouse, rat and hamster. An extensive and detailed analysis of melatonin‐related receptor mRNA expression in the mouse central nervous system and peripheral tissues is presented. Mapping the distribution throughout the entire mouse brain has revealed new sites of expression in a number of brain nuclei, including preoptic areas, parabrachial nuclei and widespread distribution in the olfactory bulb. Reverse transcriptase‐polymerase chain reaction was performed with RNA isolated from peripheral tissues revealing expression of the melatonin‐related receptor mRNA in the mouse kidney, adrenal gland, intestine, stomach, heart, lung, skin, testis and ovary. These results suggest a conserved function in neuroendocrine regulation and a potential role in coordinating physiological responses in the central nervous system and peripheral tissues.
Corticosterone Exerts Site‐Specific and State‐Dependent Effects in Prefrontal Cortex and Amygdala on Regulation of Adrenocorticotropic Hormone, Insulin and Fat Depots
Authors: Akana S. F. , Chu A. , Soriano L. , Dallman M. F. 
Published: March 2003

AbstractChronic stress stimulates corticosterone secretion and recruits brain pathways that regulate energy balance (caloric acquisition and deposition) and facilitate hypothalamic‐pituitary‐adrenal responsiveness to new stressors. We implanted corticosterone or cholesterol bilaterally either near the central nucleus of the amygdala (CeA) or in the prefrontal cortex to determine whether high concentrations of the steroid act at either site, with or without chronic stress. Rats were adrenalectomized and treated systemically with low doses of corticosterone. Half were maintained at room temperature and the other half were exposed to 5 °C cold for 5 days before all rats were restrained. There was limited diffusion of corticosterone from brain implants. Corticosterone in prefrontal cortex, but not CeA, decreased plasma insulin and adrenocorticotropic hormone (ACTH) responses to acute restraint in both control and chronically cold stressed rats. Corticosterone implants near CeA decreased the weight of fat depots only in cold; corticosterone implants in prefrontal cortex were ineffective. We conclude that (i) corticosterone inhibits insulin and ACTH secretion by an action in prefrontal cortex but not CeA; (ii) high concentrations of corticosterone secreted during chronic stress alter metabolism through (autonomic) outputs of the CeA and prefrontal cortex in site‐ and variable‐specific fashion; and (iii) the amygdala is a component of a stress‐recruited, state‐dependent pathway.
Nitric Oxide Directly Activates GABAA Receptor Function Through a cGMP/Protein Kinase‐Independent Pathway in Frog Pituitary Melanotrophs
Authors: Castel H. , Vaudry H. 
Published: March 2003

AbstractThe direct effects of nitric oxide (NO) donors and sulfhydryl‐modifying agents on the GABAA receptor function were examined by perforated patch, whole‐cell and single channel recordings in cultured frog melanotrophs. In amphotericin B‐perforated cells incubated with the soluble guanylyl cyclase inhibitors LY 83583 and ODQ (10−4 M each), the NO donor sodium nitroprusside (SNP) (10−3 M) reversibly increased the current evoked by GABA (5 × 10−6 M). In the whole‐cell configuration, internal application of the oxidizing agent H2O2 (0.05%) potentiated the GABA‐evoked current while the reducing agent 2‐mercaptoethanol (5 × 10−3 M) slightly decreased the current amplitude. In inside‐out patches, GABA (2 × 10−7 M) triggered single channel bursts of openings. Incubation with the NO donors SNP or DEA/NO (10−4 M each) enhanced the open probability of the GABAA receptor channel but did not modify the chloride reversal potential and did not affect the conductance states. The oxidizing agents H2O2 (0.05%) or DTNB (10−4 M) mimicked the stimulatory effect of the NO donors on the open probability while the reducing compounds 2‐mercaptoethanol (5 × 10−3 M) or DTT (10−4 M) markedly attenuated the channel activity. Potentiation of the GABA‐induced single channel activity by SNP or H2O2 was blocked by 2‐mercaptoethanol. Similarly, the potentiating effect produced by DEA/NO or DTNB on the open probability was reversed by DTT. In outside‐out patches, incubation with SNP also significantly enhanced the open probability of single channels activated by GABA (10−6 M). These data indicate that, in frog pituitary melanotrophs, NO potentiates the GABA‐evoked current independently of the cGMP/protein kinase pathway. The effect of NO can be accounted for by S‐nitrosylation/oxidation of thiol groups either directly on the GABAA receptor subunits or on a regulatory protein tightly associated with the GABAA receptor.