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Results for “Enhancer mapping”

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PubMed1990

A contribution of the core-promoter and its surrounding regions to the preferential transcription of the fibroin gene in posterior silk gland extracts.

Complementation of a posterior silk gland (psg) extract to a HeLa cell extract specifically enhances the transcription of the Bombyx mori fibroin gene. To map the regions responsible for this enhancement, the fibroin promoter was dissected and the transcriptional function of each region was analyzed. Besides the upstream promoter element 5' to the TATA box, two downstream elements were found to be important for the preferential transcription of the fibroin gene in the complementation system as well as in the psg extract. The minimal fibroin promoter from -37 to +10 (core-promoter) was preferentially transcribed in the psg extract, while the transcription efficiencies of other promoters like one of the Bombyx chorion genes and the adenovirus 2 major late promoter (Ad2MLP) were considerably lower. The transcription from the core-promoter was further enhanced when combined with either the intronic element from +156 to +454 or the upstream element. Both the upstream and intronic elements also stimulated the transcription from the Ad2MLP in an orientation independent manner. These results demonstrate that the transcription of the fibroin gene is mediated through an integration of multiple regulatory elements.

Animals↗

PubMed2002

Neurotrophins induce BDNF expression through the glutamate receptor pathway in neocortical neurons.

Neurotrophins jointly exert various functions in the nervous system, including neuronal differentiation, survival, and regulation of synaptic plasticity. However, the functional interactions of neurotrophins or mechanisms through which neurotrophins regulate each other are still not clear. In the present study, brain-derived neurotrophic factor (BDNF) mRNA expression is induced by neurotrophin-4/5 (NT-4/5) and by BDNF itself in neocortical neurons. K252a, a specific tyrosine kinase (Trk) inhibitor, completely suppresses BDNF- and NT-4/5-enhanced BDNF mRNA expression. NT-4/5 significantly augments BDNF protein production, which is also reversed by K252a. When neurons are incubated with neurotrophin-3 (NT-3) or nerve growth factor (NGF), there are no significant changes in BDNF mRNA or protein expression. Interestingly, the alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA) receptor blocker 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) or the N-methyl-D-aspartate (NMDA) receptor blocker AP-5 completely suppresses NT-4/5-enhanced BDNF protein production, while tetrodotoxin (TTX) only suppresses NT-4/5-enhanced BDNF production by 50%. Additionally, the mitogen activated protein (MAP) kinase inhibitor PD98059 enhances BDNF-induced glutamate receptor-1 (GluR1) protein expression, but a phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002 strongly reduces BDNF-induced GluR1 protein expression. Taken together, glutamate receptors are important for the regulation of BDNF expression by neurotrophins, and MAP and PI3K kinases differentially modulate AMPA receptor expression in the cortical neurons.

6-Cyano-7-nitroquinoxaline-2,3-dione↗

PubMedDate not supplied

Informatics in Radiology (infoRAD): Magnetic Resonance Imaging Workbench: analysis and visualization of dynamic contrast-enhanced MR imaging data.

Magnetic Resonance Imaging Workbench (MRIW) allows analysis of T1- and T2*-weighted dynamic contrast-enhanced magnetic resonance imaging data sets to extract tissue permeability and perfusion characteristics by using standard pharmacokinetic models. Parametric maps are calculated from individual pixel enhancement curves in regions of interest (ROIs) and displayed as color overlays on the anatomic images. User-defined ROIs can be saved to ensure consistency of later reanalysis. Individual parametric maps are visualized together with user-selected parameter time-series plots. The following selections are available: overall ROI enhancement curve and fit, histogram, and individual pixel enhancement curve and fit. Summary data (transfer constant, leakage space, rate constant, integrated area under the gadolinium curve after 60 seconds, relative blood volume, relative blood flow, and mean transit time) may be exported to permanent storage along with per-pixel results for statistical analysis. Numerical values for parameters are displayed below the plot for easy reference. The dynamic range of plots and parametric map overlays is interactively adjustable. Viewing individual enhancement curves and parametric maps allows radiologists to investigate the heterogeneity of contrast agent kinetics for lesion characterization and to scrutinize serial changes in response to therapy. MRIW is written in IDL, enabling it to be used on a variety of computer systems.

Computer Graphics↗

PubMed2002

Experimental cerebral fat embolism: embolic effects of triolein and oleic acid depicted by MR imaging and electron microscopy.

BACKGROUND AND PURPOSE: In fat embolism, free fatty acid is more toxic than neutral fat in terms of tissue damage. We evaluated the hyperacute embolic effects of triolein and oleic acid in cat brains by using MR imaging and electron microscopy. METHODS: T2-weighted imaging, diffusion-weighted imaging, and contrast-enhanced T1-weighted imaging were performed in cat brains after the injection of triolein (group 1, n = 8) or oleic acid (group 2, n = 10) into the internal carotid artery. MR images were quantitatively assessed by comparing the signal intensity ratios of the lesions with their counterparts on T2-weighted images, apparent diffusion coefficient (ADC) maps, and contrast-enhanced T1-weighted images. Electron microscopic findings in group 1 were compared with those in group 2. RESULTS: Qualitatively, MR images revealed two types of lesions. Type 1 lesions were hyperintense on diffusion-weighted images and hypointense on ADC maps. Type 2 lesions were isointense or mildly hyperintense on diffusion-weighted images and isointense on ADC maps. Quantitatively, the signal intensity ratios of type 1 lesions in group 2 specimens were significantly higher on T2-weighted images (P =.013)/(P =.027) and lower on ADC maps compared with those of group 1. Electron microscopy of type 1 lesions in both groups revealed more prominent widening of the perivascular space and swelling of the neural cells in group 2, in contrast to notable endothelial defects in group 1. CONCLUSION: MR and electron microscopic data on cerebral fat embolism induced by either triolein or oleic acid revealed characteristics suggestive of both vasogenic and cytotoxic edema in the hyperacute stage. Tissue damage appeared more severe in the oleic acid group than in the triolein group.

Animals↗

PubMed1999

RHO-associated protein kinase alpha potentiates insulin-induced MAP kinase activation in Xenopus oocytes.

We recently identified Xenopus Rho-associated protein kinase alpha (xROKalpha) as a Xenopus insulin receptor substrate-1 binding protein and demonstrated that the non-catalytic carboxyl terminus of xROKalpha binds Xenopus insulin receptor substrate-1 and blocks insulin-induced MAP kinase activation and germinal vesicle breakdown in Xenopus oocytes. In the current study we further examined the role of xROKalpha in insulin signal transduction in Xenopus oocytes. We demonstrate that injection of mRNA encoding the xROKalpha kinase domain or full length xROKalpha enhanced insulin-induced MAP kinase activation and germinal vesicle breakdown. In contrast, injection of a kinase-dead mutant of xROKalpha or pre-incubation of oocytes with an xROKalpha inhibitor significantly reduced insulin-induced MAP kinase activation. To further dissect the mechanism by which xROKalpha may participate in insulin signalling, we explored a potential function of xROKalpha in regulating cellular Ras function, since insulin-induced MAP kinase activation and germinal vesicle breakdown is known to be a Ras-dependent process. We demonstrate that whereas injection of mRNA encoding c-H-Ras alone induced xMAP kinase activation and GVBD in a very low percentage (about 10%) of injected oocytes, co-injection of mRNA encoding xROKalpha and c-H-Ras induced xMAP kinase activation and germinal vesicle breakdown in a significantly higher percentage (50-60%) of injected oocytes. These results suggest a novel function for xROKalpha in insulin signal transduction upstream of cellular Ras function.

Animals↗

PubMed1991

Central administration of a specific angiotensin II receptor antagonist on baroreflex function in spontaneously hypertensive rats.

To determine whether the increase in baroreflex sensitivity previously reported in lifetime captopril-treated spontaneously hypertensive rats (SHR) was due to an inhibition of brain angiotensin II mechanisms, we tested the effect of intracerebroventricular administration of an angiotensin II receptor antagonist on baroreflex control of heart rate in lifetime captopril-treated and untreated male and female SHR. Baroreceptor reflex control of heart rate was assessed by the slope of the relationship between changes in mean arterial pressure (delta MAP, mmHg) and changes in pulse interval (delta PI, ms). MAP was raised and lowered with infusions of phenylephrine and nitroprusside, respectively. Following basal assessment of baroreflex control of heart rate, rats received an intracerebroventricular injection (100 pmol) of Sar1Thr8 angiotensin II (sarthran) and reflex control of heart rate was reassessed. Adequacy of blockade was tested with central and peripheral administration of angiotensin II. Captopril-treated male (130 +/- 7 mmHg) and female (123 +/- 4 mmHg) rats had significantly lower MAP than untreated rats (174 +/- 4 and 173 +/- 8 mmHg, respectively) and enhanced bradycardia in response to increases in MAP. Intracerebroventricular administration of sarthran had no effect on basal blood pressure or heart rate but enhanced the bradycardia in response to increases in MAP in both untreated and captopril-treated rats. The increase in the slope of the line relating delta MAP to delta PT was greater for untreated than captopril-treated SHR (male untreated 2.7-fold versus captopril-treated 1.5-fold; female untreated 1.6-fold versus captopril-treated 1.5-fold).(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗

PubMed2002

A new contrast parameter for visualization of the cross-link density in rubber based on the dipolar-correlation effect.

A new parameter for NMR mapping is suggested on the basis of the mean squared dipolar fluctuation (MSDF). The MSDF characterizes the relaxation mechanism due to ultra-slow dipolar fluctuations in liquids subject to local anisotropy of molecular motions. These fluctuations can be monitored on the time scale exceeding a few microseconds. In rubber materials, the MSDF is a function of the density of chemical cross-links strongly affecting (anisotropic) mesh chain fluctuations. Experimentally, the MSDF is determined from the attenuation curves of the quotient of the amplitudes of the stimulated and the primary echoes produced by the three 90 degrees radio-frequency pulse sequence. In order to evaluate the MSDF maps, the latter sequence was combined with the standard scheme of the magnetic field gradients providing a spatial resolution. The pixel values of the MSDF are "visualized" using grey shades related to the equidistant intervals covering the whole range of the measured values. The MSDF maps are demonstrated for the two composite samples. The first sample consists of a water filled tube in the middle part surrounded by high molecular mass polyisoprene (PI) in the outer part. The relaxation weighted spin density image of this sample is dominated by a water signal with PI producing a much weaker intensity. The MSDF map, on the contrary, enhances the relative intensity of the outer, PI, part while scaling the middle, water, part down to the level of noise. The second sample consists of the four rubber pieces with different cross-link density. This sample thus models an inhomogeneous rubber object. The MSDF map produces clear contrast for the relevant regions. The advantages of employing this kind of NMR mapping for a characterization of materials are discussed.

Journal Article↗

PubMed1999

Tyrosine phosphatase SHP-2 dephosphorylates the platelet-derived growth factor receptor but enhances its downstream signalling.

SHP-2 is a widely distributed Src homology 2 (SH2) domain-containing tyrosine phosphatase that is recruited to growth factor receptors on stimulation. We have transiently co-expressed several catalytically active and inactive forms of the enzyme with the platelet-derived growth factor (PDGF) receptor in human embryonic kidney 293 cells. The catalytically active forms of SHP-2 decreased the tyrosine phosphorylation of the receptor, whereas the catalytically inactive forms increased the phosphorylation. However, PDGF-induced activation of the mitogen-activated protein (MAP) kinase pathway was enhanced by the active forms of SHP-2 but decreased by the inactive forms. The results suggest that the PDGF receptor is a physiological substrate of SHP-2 and that SHP-2 has a positive role in the PDGF-stimulated activation of MAP kinase. The dissociation of the receptor phosphorylation from the activation of MAP kinase suggests that signalling through growth factor receptors does not depend merely on their tyrosine phosphorylation.

Calcium-Calmodulin-Dependent Protein Kinases↗

PubMed2001

Regulation of the levels of small heat-shock proteins during differentiation of C2C12 cells.

Levels of the small heat-shock proteins (sHSPs) HSP27 and alphaB-crystallin during differentiation of mouse C2C12 cells were determined using specific immunoassays. Increases of these proteins were about 3-fold and 10-fold, respectively. Under the same conditions, however, the level of HSP70 in C2C12 cells barely increased, indicating selective accumulation of HSP27 and alphaB-crystallin with differentiation. While expression of mRNA for alphaB-crystallin was also markedly increased and that for HSP27 was but to a lesser extent, mRNA for HSP70 could barely be detected during differentiation. Activation of the heat-shock factor was not observed, in contrast to the case with heat-stressed undifferentiated cells. Various inhibitors of protein kinases affected the differentiation and the associated increase of sHSPs. Rapamycin, an inhibitor of p70 S6 kinase, completely inhibited the differentiation and suppressed the accumulation of HSP27 and alphaB-crystallin. SB203580, an inhibitor of p38 MAP kinase, also inhibited differentiation, but the accumulation of alphaB-crystallin was rather enhanced. PD98059, an inhibitor of MAP kinase kinase, significantly increased expression of a differentiation marker for muscle cells, creatine kinase M isozyme, as well as accumulation of alphaB-crystallin. These results suggest that accumulation of sHSPs during differentiation of C2C12 cells is regulated in a complex manner.

Animals↗

PubMed1994

Effects of subacute administration of methamphetamine and nicotine on locomotor activity in transgenic mice expressing the human tyrosine hydroxylase gene.

We produced transgenic (Tg) mice carrying the human tyrosine hydroxylase (TH) gene. To investigate differences in the dopaminergic (DAergic) neuronal activity between the Tg and nTg mice, we examined changes in the locomotor activity induced by methamphetamine (MAP) and nicotine (NIC), which enhances DA release and induces TH enzyme activation, respectively. Surprisingly, however, the intensity of MAP (2.5 mg/kg, once a day for 14 days)-induced hyperlocomotion in the nTg mice was greater than that in the Tg mice, and, furthermore, the Tg mice were less sensitive to subacute administration of NIC (0.5 mg/kg, once a day for 14 days) than the nTg mice. These results suggest that DAergic neuronal function is suppressed in Tg mice to compensate for the overexpression of TH.

Animals↗

PubMed2001

The 5' boundary of the human apolipoprotein B chromatin domain in intestinal cells.

The 5' boundary of the chromosomal domain of the human apolipoprotein B (apoB) gene in intestinal cells has been localized and characterized. It is composed of two kinds of boundary elements; the first, functional boundary is an insulator activity exhibited by a 1.8 kb DNA fragment located between -58 and -56 kb upstream of the human apoB promoter. In this region, an enhancer-blocking activity has been mapped to a CTCF binding site that is located upstream of two apoB intestinal enhancers (IEs), the 315 IE and the 485 IE. The CTCF site represents a boundary between two types of chromatin structure: an open, DNaseI-sensitive region 3' of the CTCF site containing the intestinal regulatory elements and a closed, DNaseI-resistant region 5' of the CTCF site. The 1.8 kb fragment harboring the CTCF site also insulated mini-white transgenes against position effects in Drosophila melanogaster. The second, structural boundary is represented by a nuclear matrix attachment region (MAR), situated about 3 kb 5' of the CTCF site. This MAR may represent the 5' anchorage site for a chromosomal loop that functions to bring the intestinal regulatory elements closer to the apoB promoter.

5' Untranslated Regions↗

PubMed1990

The repressing and enhancing functions of the herpes simplex virus regulatory protein ICP27 map to C-terminal regions and are required to modulate viral gene expression very early in infection.

The phenotypic properties of ICP27 temperature-sensitive and deletion mutants and the results of transient expression assays have demonstrated that ICP27 has a modulatory effect on viral gene expression induced by ICPs 0 and 4. In order to identify the regions of the ICP27 molecule that are responsible for its enhancing and repressing activities, 10 nonsense and 3 in-frame deletion mutations were introduced into the coding sequence of the cloned ICP27 gene. These mutant genes were tested in transient expression assays for their ability to complement an ICP27 null mutant and to enhance and repress expression from a spectrum of herpes simplex virus type 1 promoters in reporter CAT genes when expression was induced by ICP0 or ICP4. The results of assays with cloned mutant genes demonstrate that the ICP27 polypeptide contains two regions, located between amino acid residues 327 and 407 and residues 465 and 511, that contribute to its repressing activity. The amino acid region located between the two repressing regions (residues 407 to 465) is able to interfere with ICP27 repressing activity. None of the mutant genes exhibited efficient enhancing activity for any of the herpes simplex type 1 promoters tested, demonstrating that amino acids comprising the carboxy-terminal half of the ICP27 molecule, including the terminal phenylalanine residue, are required for wild-type enhancement as well as for efficient complementation of an ICP27 null mutant. Phenotypic characterization of an in-frame deletion mutant, vd3, and a previously isolated null mutant, 5dl 1.2 (A. M. McCarthy, L. and P. A. Schaffer, J. Virol. 63:18-27, 1989), demonstrated that ICP27 is required to induce the expression of all classes of viral genes very early in infection and confirmed the requirement for ICP27 later in infection (i) to repress early gene expression, (ii) to induce wild-type levels of delayed-early or gamma 1 gene expression, and (iii) to induce true late or gamma 2 gene expression. The vd3 mutant, which specifies an ICP27 peptide lacking the repressing region between residues 327 and 407, is able to (i) repress early gene expression, consistent with the repressing ability of the d3 mutation in transient expression assays, (ii) induce the synthesis of significant but reduced levels of delayed-early (gamma 1) proteins and no gamma 2 proteins (thus vd3 exhibits a late protein phenotype intermediate between that of the wild-type virus and 5dl 1.2), and (iii) confer altered electrophoretic mobility on ICP4, demonstrating a role for ICP27 in the posttranslational modification of this essential regulatory protein.(ABSTRACT TRUNCATED AT 250 WORDS)

Base Sequence↗

PubMed2002

Glutathione redox regulates lipopolysaccharide-induced IL-12 production through p38 mitogen-activated protein kinase activation in human monocytes: role of glutathione redox in IFN-gamma priming of IL-12 production.

We examined whether changes in intracellular reduced (GSH) or oxidized (GSSG) glutathione of human monocytes regulate lipopolysaccharide (LPS)-induced IL-12 production and defined the molecular mechanism that underlies glutathione redox regulation. Monocytes exposed to glutathione reduced form ethyl ester (GSH-OEt) or maleic acid diethyl ester (DEM) increased or decreased the intracellular GSH/GSSG ratio, respectively. LPS-induced IL-12 production and p38 mitogen-activated protein (MAP) kinase activation were enhanced by GSH-OEt but suppressed by DEM. Selective p38 inhibitors showed that p38 promoted GSH-OEt-enhanced IL-12 production. Furthermore, IFN-gamma priming increased the GSH/GSSG ratio and enhanced IL-12 production through p38, and DEM negated the priming effect of IFN-gamma on p38 activation and IL-12 production as well as on the GSH/GSSG ratio. These findings reveal that glutathione redox regulates LPS-induced IL-12 production from monocytes through p38 MAP kinase activation and that the priming effect of IFN-gamma on IL-12 production is partly a result of the glutathione redox balance.

Cells, Cultured↗

PubMedDate not supplied

Localized echo-volume imaging methods for functional MRI.

To perform true three-dimensional activation experiments in the human brain, dedicated localized echo-volume imaging (L-EVI) methods were developed. Three-dimensional acquisition allows generation of activation maps with minimal vascular enhancement related to inflow effects. The rapid acquisition of the L-EVI (approximately 100 msec) reduces signal instabilities caused by motion, facilitating the detection of the small intensity changes expected with brain activation. Single-shot L-EVI was performed on normal volunteers at 1.5 T, imaging a three-dimensional predefined volume (240 x 45 x 45 mm3) in the superior portion of the brain with a spatial resolution of 3.75 x 5 x 5 mm3. Increased brain coverage was achieved with a multi-volume imaging (three-shot) version, which simultaneously achieved effective suppression of signals from cerebrospinal fluid. In addition, both asymmetric spin-echo (ASE) and spin-echo (SE) versions of the technique were used to detect blood oxygenation level dependent (BOLD) signal changes in the motor cortex with a finger-tapping paradigm. Images obtained by the L-EVI sequence were qualitatively comparable to standard multislice two-dimensional echo-planar images. Both ASE and SE functional MRI (fMRI) experiments showed consistent activation in the contralateral primary sensorimotor cortex. Furthermore, significant differences in location and magnitude of activation was observed between the two methods, confirming theoretical predictions.

Brain Mapping↗

PubMed1998

Hydrogen peroxide enhances signal-responsive arachidonic acid release from neurons: role of mitogen-activated protein kinase.

Hydrogen peroxide (H2O2) is a potent stimulator of signal-responsive phospholipase A2 (PLA2) in vascular smooth muscle and cultured endothelial cells. We investigated whether H2O2 plays a similar regulatory role in neurons. H2O2 did not stimulate a release of arachidonic acid from cultured neurons when applied alone but strongly enhanced the liberation of arachidonic acid evoked by maximally effective concentrations of either glutamate, the glutamate receptor agonist N-methyl-D-aspartate (NMDA), the muscarinic receptor agonist carbachol, the Na+-channel opener veratridine, or the Ca2+-ionophore ionomycin. The potentiating effects of H2O2 were strongly inhibited in the presence of the PLA2 inhibitor mepacrine, suggesting that the site of action was within the signal responsive arachidonic acid cascade. The enhancing effect of H2O2 was not reversed by protein kinase C inhibitors (chelerythrine chloride or GF 109203X) nor was it mimicked by phorbol ester treatment. H2O2 alone strongly enhanced the levels of immunodetectable activated mitogen-activated protein kinase (activated MAP kinases ERK1 and ERK2) in a Ca2+-dependent manner and this effect was additive with increases in the levels of activated MAP kinase evoked by glutamate. The enhanced release of arachidonic acid, however, was not clearly reversed by the MAP kinase kinase (MEK) inhibitor PD 98059, although this treatment effectively abolished H2O2 activation of MAP kinase. Thus, MAP kinase activation and Ca2+-dependent arachidonic acid release are regulated by oxidative stress in cultured striatal neurons.

Animals↗

PubMed1987

Modifiers of position-effect variegation in the region from 86C to 88B of the Drosophila melanogaster third chromosome.

Four dominant suppressor and one enhancer of variegation loci were mapped in the polytene chromosome region extending from section 86C to section 88B of the Drosophila melanogaster third chromosome using a set of deficiencies. The suppressor locus Su-var(3)14 maps in 86CD, Su-var(3)13 in 86F4-7, Su-var(3)6 in 87B4-7 and Su-var(3)7 in 87E4-5. The enhancer locus E-var(3)3 maps in 87E12-F11. Su-var(3)13, Su-var(3)6 and Su-var(3)7 are also defined by point mutant alleles originally identified by other criteria (Reuter et al. 1986). Duplications covering the suppressor loci Su-var(3)14, Su-var(3)13, Su-var(3)6 and Su-var(3)7 were found to reduce considerably the haplo-abnormal effect of heterozygous point mutants of the corresponding loci. One suppressor locus, Su-var(3)7, maps within a region which has previously been cloned. The positions of deficiency breakpoints delimiting the suppressor locus indicate that all the necessary sequences for its function are located within 10 kb of cloned DNA.

Animals↗

PubMed1997

Further argument for the existence of a pacemaker in the human information processing system.

To support the idea that temporal information processing may depend on an internal clock, Treisman et al. proposed a pacemaker model (Treisman, M., Faulkner, A., Naish, P.L.N., Brogan, D., 1990. The internal clock: Evidence for a temporal oscillator underlying time perception with some estimates of its characteristics frequency. Perception 19, 705-743.) and a technique for interfering with it by introducing an external periodic phenomenon. Experimental results obtained by these authors on time estimation and production tasks support this model. In another study, Treisman et al. established that the pacemaker also affects reaction times (RT) (Treisman, M., Faulkner, A., Naish, P.L.N., 1992. On the relation between time perception and the timing of motor action: Evidence for a temporal oscillator controlling the timing of movement. Quarterly Journal of Experimental Psychology 45A, 235-263.). In the present study, we addressed the question as to which information processing stage (Sanders, A.F., 1980. Stage analysis of reaction process, In: Stelmach, G.E., Requin, J. (Eds.). Tutorials in motor behavior. North-Holland, Amsterdam, pp. 331-354.) is affected by this internal clock. For this purpose, we used the Additive Factors Method (Sternberg, S., 1969. The discovery of processing stages: Extension of Donder's method. In: Koster, W.G. (Ed.). Attention and Performance II. Acta Psychologica 30, 276-315.). To vary sensorial processing time, we used two visual stimulus intensities. Stimulus-response mapping was manipulated to enhance central processing time. To modify the duration of the motor stages, the two responses could be given by two fingers on the same hand (right ring vs. middle finger) or by two fingers of the different hands (right ring vs. left middle finger). Intensity of the stimulus, stimulus-response mapping, and repertoire of responses were found to be additive. We obtained RT modulations similar to those obtained by Treisman et al. in 1992. No first order interactions were observed between the periodical phenomenon and the other manipulated factors but only a third order one. Two possible interpretations of these results are proposed.

Adult↗

PubMed2003

Near-infrared fluorescence contrast-enhanced imaging with intensified charge-coupled device homodyne detection: measurement precision and accuracy.

Fluorescence frequency-domain photon migration (FDPM) through tissue refers to the propagation of intensity-modulated fluorescent light that originates from tissue-laden fluorophores following illumination with an intensity-modulated excitation light source. FDPM measurements of modulation amplitude and phase are ultimately employed in an inversion algorithm for tomographic reconstruction of interior optical and fluorescent property maps that delineate disease enhanced with fluorescent contrast agent. Because the inverse problem is underdetermined, measurement precision and accuracy crucially impact its solution. Reported here are the precision and accuracy of FDPM measurements acquired using an intensified CCD homodyne detection system. By introducing 32 phase delays between the oscillators used to modulate the intensifier gain and light source intensity at 100 MHz, mean precision is maximized at +/-0.46% and +/-0.26 deg for measurements of modulation amplitude and phase, respectively. Measurement precision improves when the number of phase delays increases. Measurements of fluorescence modulation amplitude and phase, acquired from the surface of a tissue phantom at distances ranging between 0.71 and 3.6 cm from an incident excitation point source, exhibit a mean accuracy of 17% and 1.9 deg, respectively. Measurement accuracy deteriorates with increasing distance from the point source, but for distances up to 1.0 cm from the point source, measurements of fluorescence modulation amplitude and phase exhibit a mean accuracy of 5.4% and 0.30 deg, respectively.

Breast Neoplasms↗