Visible light emission from silicon: a quantum effect in highlyporous materials

The authors discuss progress in the control of the luminescent properties of porous silicon and in the understanding of the basic mechanisms which govern the light emission. The main features of porous silicon formation and properties are briefly recalled. The photoluminescence characteristics are reported. It is shown that anodic oxidation of porous silicon is a technique which provides photoluminescent layers with good mechanical properties and enhanced emission efficiency. A model accounting for the quite long measured carrier lifetimes is outlined. The electroluminescence which appears during the anodic oxidation of porous silicon in pure water was studied     

Imaging streptavidin 2D crystals on biotinylated lipid monolayers at high resolution with the atomic force microscope

Streptavidin crystals were grown on biotinylated lipid monolayers at an air/water interface and transferred onto highly oriented pyrolytic graphite (HOPG). These arrays could be imaged to a resolution below 1 nm using the atomic force microscope. The surface topographs obtained were compared with negative-stain electron microscopy images and the atomic model as determined by X-ray crystallography. The streptavidin tetramer (60 kDa) exposes two free biotin-binding sites to the buffer solution, while two are occupied by linkage to the lipid monolayer. Therefore, the streptavidin 2D crystals can be used as nanoscale matrices for binding biotinylated compounds. Furthermore, this HOPG-based preparation method provides a general novel approach to study the structure of protein arrays assembled on lipid monolayers with the AFM.     

Changes in goal selection induced by cue conflicts are in register with predictions from changes in place cell field locations.

In the cognitive mapping theory of hippocampal function, currently active place cells represent a rat's spatial location (J. O'Keefe & L. Nadel, 1978). A systematic shift of firing field locations should therefore produce a similar shift in a rat's judgment of its location. A. A. Fenton, G. Csizmadia, and R. U. Muller (2000a) recorded place cells in cylinders with 2 cue cards separated by 135°. When the separation was changed, firing fields moved systematically, as described by a vector-field equation (A. A. Fenton, G. Csizmadia, & R. U. Muller, 2000b). Given this cohesive movement of firing fields, the mapping theory predicts that a rat's decisions about the location of an unmarked goal should move after card separation changes, as described by the vector-field equation. The authors tested this reasoning with a task in which the rat earned a food reward by pausing in a small, unmarked goal zone. When cues were shifted in the absence of reward, goal choice shifts were accurately predicted by the vector-field equation, providing strong support for the notion that a rat's judgment of its spatial location is intimately related to the across-cell discharge pattern of simultaneously active place cells. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Role of tissue factor in adhesion of mononuclear phagocytes to and trafficking through endothelium in vitro

An in vitro model consisting of endothelium grown on collagen was used to investigate how mononuclear phagocytes traverse endothelium in the basal-to-apical direction (reverse transmigration), a process that mimics their migration across vascular and/or lymphatic endothelium during atherosclerosis and resolution of inflammation, respectively. Monoclonal antibody (MoAb) VIC7 against tissue factor (TF) inhibited reverse transmigration by 77%. Recombinant tissue factor fragments containing at least six amino acids C-terminal to residue 202 also strongly inhibited reverse transmigration. TF was absent on resting monocytes but was induced on these cells after initial apical-to-basal transendothelial migration. Two additional observations suggest that TF is involved in adhesion between mononuclear phagocytes and endothelium: (1) when monocytes were incubated with lipopolysaccharide (LPS) to stimulate expression of TF before they were added to endothelium, VIC7 or soluble TF modestly inhibited their adhesion to the apical endothelial surface, each by about 35%; and (2) endothelial cells specifically bound to surfaces coated with TF fragments containing amino acids 202-219. This binding was blocked by anti-TF MoAb, suggesting that endothelial cells bear a receptor for TF. These data suggest that mononuclear phagocytes use TF, perhaps as an adhesive protein, to exit sites of inflammation.     

Are circulating neutrophils intravascularly activated in patients with anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitides?

Vascular injury in vasculitis may be due to activation of circulating neutrophils resulting in their increased adhesiveness to locally activated endothelium (Shwartzman phenomenon). Previously, we demonstrated up-regulation of endothelial intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in biopsies from patients with ANCA-associated vasculitis. In the present study, we investigated the expression of adhesion molecules (CD11b, ICAM-1, VLA-4, L-selectin) and activation markers (CD66b, CD64, CD63) on circulating neutrophils from patients with ANCA-associated vasculitis in comparison with their expression on cells from healthy volunteers and patients with sepsis. We related these findings to parameters of disease activity. Surface marker expression was determined by using a non-activating whole blood flow cytometric assay. The expression of activation markers, but not the expression of adhesion molecules, was increased on neutrophils from patients with active vasculitis. The expression of CD63 and CD66b on neutrophils correlated with disease activity as determined by the Birmingham Vasculitis Activity Score (BVAS). In contrast to patients with active vasculitis, patients with sepsis showed up-regulation of all markers, including adhesion molecules, suggesting that circulating neutrophils are fully activated in sepsis. We conclude that in ANCA-associated vasculitis, circulating neutrophils are not fully activated, since they do not express increased levels of adhesion molecules as sepsis or in the Shwartzman reaction. These findings are compatible with the concept that in vivo vascular damage in ANCA-associated vasculitides does not occur due to a Shwarzman-like reaction but only after ANCA-induced neutrophil activation at the endothelial cell surface.     

Malignant pyodermas revisited

The concept of malignant pyoderma (MP) has created controversy since its origin. The distinction of this disease from pyoderma gangrenosum was based on clinical criteria and response to treatment. Herein we discuss our current ideas on this entity and its possible relationship to Wegener's granulomatosis (WG). Follow-up data from the three original cases of MP are reported, as well as additional clinical and laboratory data from cases subsequently thought to represent MP. Many of these cases have similar clinical features such as facial and periauricular ulceration and occasionally signs or symptoms of WG, including positive titers of antineutrophil cytoplasmic antibodies (with a diffuse cytoplasmic staining pattern) (cANCA). MP represents a distinctive clinical disorder and may be a dermal manifestation of WG. Some cases of MP may represent pyoderma gangrenosum or other undefined systemic illnesses. Such cases of WG can be distinguished on the basis of clinical, histopathologic, and laboratory evidence including cANCA titers. MP should no longer be used as a final clinical diagnosis.     

AT2-antagonist sensitive potentiation of angiotensin II-induced vasoconstrictions by blockade of nitric oxide synthesis in rat renal vasculature

1. Although the actions of angiotensin II (Ang II) on renal haemodynamics appear to be mediated by activation of the AT1 receptor subtype, AT2 binding sites have also been evidenced in the adult kidney vasculature. As NO is known to mask part of the renal effects of vasoconstrictor drugs, we queried whether the Ang II-induced vasoconstrictions could occur via multiple receptor subtypes during inhibition of NO synthesis. We explored the effect of AT1 and AT2 receptor (AT-R) antagonists on Ang II-induced pressure increases during NO synthase or soluble guanylyl cyclase inhibition in rat isolated kidneys perfused in the presence of indomethacin at constant flow in a single-pass circuit. 2. In the absence of NO blockade, the AT1-R antagonist L-158809 (500 nM) antagonized the Ang II-induced vasoconstrictions, while the AT2-R antagonist PD-123319 (500 nM) had no effect. 3. Perfusing kidneys in the presence of either NO synthase inhibitors, L-NAME (100 microM) or L-NOARG (1 mM), or soluble guanylyl cyclase inhibitor, LY-83583 (10 microM), significantly increased both molar pD2 (from 9.40+/-0.25 to 10.36+/-0.11) and Emax values (from 24.9+/-3.1 to 79.9+/-4.9 mmHg) of the concentration-response curve for Ang II-induced vasoconstriction. 4. In the presence of L-NAME, 500 nM L158809 abolished the Ang II-induced vasoconstrictions whatever the concentration tested. On the other hand, 500 nM PD-123319 reversed the left shift of the concentration-response curve for Ang II (molar pD2 value 9.72+/-0.13) leaving Emax value unaffected (91.3+/-7.6 mmHg). 5. In the presence of L-NAME, the potentiated vasoconstriction induced by 0.1 nM and the augmented vasoconstriction induced by 10 nM Ang II were fully inhibited in a concentration-dependent manner by L-158809 (0.05-500 nM). By contrast, PD-123319 (0.5-500 nM) did not affect the 10 nM Ang II-induced vasoconstriction and concentration-dependently decreased the 0.1 nM Ang II-induced vasoconstriction plateauing at 65% inhibition above 5 nM antagonist. 6. Similar to PD-123319, during NO blockade the AT2-R antagonist CGP-42112A at 5 nM decreased by 50% the 0.1 nM Ang II-induced vasoconstriction and at 500 nM had no effect on 10 nM Ang II-induced vasoconstriction. 7. In conclusion, the renal Ang II-induced vasoconstriction, which is antagonized only by AT1-R antagonist in the presence of endogenous NO, becomes sensitive to both AT1- and AT2-R antagonists during NO synthesis inhibition. While AT1-R antagonist inhibited both L-NAME-potentiated and -augmented components of Ang II-induced vasoconstriction, AT2-R antagonists inhibited only the L-NAME-potentiated component.     

Maternally modulated infant separation responses are regulated by D2-family dopamine receptors.

Although dopamine is necessary for mammalian adult pair-bond formation and maternal behavior, its function in infant social behavior and attachment has been less thoroughly explored. The vocalization rate of an isolated rat pup is influenced by recent social contact. Interactions with the dam potentiate vocalization rate. Interactions with littermates or adult males do not. Systemic administration of the D2-family agonist quinpirole specifically blocked maternal potentiation at doses that did not alter vocalization rate in an isolation prior to dam contact. This result was not explained by quinpirole's effects on body temperature or locomotion. The results are consistent with a role for dopamine in infant social behavior. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Impairment in long-term retention but not short-term performance on a water maze reversal task following hippocampal or mediodorsal striatal n-methyl-d-aspartate receptor blockade.

Male Long-Evans rats were injected with 32 ng/μl of the N-methyl-D-aspartate (NMDA) receptor antagonist 3-(2-carboxypiperazin-4-yl) propyl-1-phosphonic acid (CPP) or vehicle and trained to locate a hidden platform in a different location (reversal training) than used on the initial 4 days of training. Rats treated with vehicle or CPP into the dorsal hippocampus, basolateral amygdala, or mediodorsal striatum had similar latencies to locate the platform on the reversal day. Rats infused with CPP into the dorsal hippocampus or mediodorsal striatum failed to search preferentially in the novel location during a 24-hr, drug-free retention test, whereas all other groups searched preferentially in this location. Therefore, blocking dorsal hippocampal or mediodorsal striatal NMDA receptors selectively blocked long-term spatial retention without producing short-term performance deficits. (PsycINFO Database Record (c) 2010 APA, all rights reserved)