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Results for “Enhancer mapping”

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At least 559 records · Page 31Linked to original sources

PubMed1996

[Usefulness of change ratio map in 99mTc-HMPAO SPECT with acetazolamide enhancement].

Although a sequential 99mTc-HMPAO SPECT technique with Diamox test (seq-SPECT) is a simple and time-saving procedure to assess brain perfusion reserve, the influence of the first dose of the tracer on the second one is not negligible. Therefore, a subtraction of the rest-SPECT from the 2nd SPECT is widely-used. However, subtracted SPECT images not only need to be corrected for the injected dose and the radiochemical purity due to inherent instability of HMPAO but also are usually degraded in quality. This study was undertaken to resolve these problems utilizing a change ratio (CR) map. The CR map was obtained by dividing 2nd SPECT by rest-SPECT. Prior to subtraction, the 2nd SPECT was normalized with the ratio of the mean whole brain counts between both SPECTs. To validate CR map, 7 patients were studied with both seq-SPECT and 133Xe inhalation CBF measurement (Xe-CBF). The right to left count ratio obtained from the ROIs placed on MCA territory of CR map correlated well with that from Xe-CBF (r = 0.89, p < 0.01). Fifty-three patients with stroke underwent the seq-SPECT which was compared with the cerebral angiography (CAG) and classified into 4 groups according to the CR map. In 25 patients, all of the rest-, the subtracted-SPECT and the CR map did not show any difference between the affected side and the contralateral normal side. Seven patients with normal rest-SPECT showed decreased subtracted-SPECT counts and CR on the affected side. Three of them showed more than 75% stenosis on CAG. Four patients with the decreased counts both at the rest- and the subtracted-SPECT revealed no difference on the CR map suggesting the matched decrease of both blood flow and metabolism in the affected side. In conclusion, the CR map was a simple and useful method to evaluate the brain perfusion reserve with the seq-SPECT.

Acetazolamide↗

PubMed2004

Variation in recombination rate may bias human genetic disease mapping studies.

The availability of the human genome sequence and variability information (as from the International HapMap project) will enhance our ability to map genetic disorders and choose targets for therapeutic intervention. However, several factors, such as regional variation in recombination rate, can bias conclusions from genetic mapping studies. Here, we examine the impact of regional variation in recombination rate across the human genome. Through computer simulations and literature surveys, we conclude that genetic disorders have been mapped to regions of low recombination more often than expected if such diseases were randomly distributed across the genome. This concentration in low recombination regions may be an artifact, and disorders appearing to be caused by a few genes of large effect may be polygenic. Future genetic mapping studies should be conscious of this potential complication by noting the regional recombination rate of regions implicated in diseases.

Bias↗

PubMed1999

Specific activation of the p38 mitogen-activated protein kinase signaling pathway and induction of neurite outgrowth in PC12 cells by bone morphogenetic protein-2.

Bone morphogenetic protein (BMP)-2 has the capacity to induce the neuronal differentiation of PC12 cells. Unlike nerve growth factor, however, BMP-2 failed to induce the activation of the 41-/43-kDa mitogen-activated protein (MAP) kinase pathway in these cells. In contrast, BMP-2 characteristically induced the sustained activation of the p38 MAP kinase pathway. Pretreatment of PC12 cells with SB203580 inhibited the BMP-2-induced neurite outgrowth formation in a dose-dependent manner; this inhibition coincided well with the ability of SB203580 to inihibit the BMP-2-induced activation of the p38 MAP kinase pathway. Overexpression in PC12 cells of wild-type MAP kinase kinase (MKK)-6 enhanced the BMP-2-induced activation of p38 MAP kinase, whose activation correlated well with the ability of these cells to induce neurite outgrowth in response to BMP-2. Transient expression of kinase-negative forms of MKK3/6 inhibited the formation of neurite outgrowth in response to BMP-2. Furthermore, expression of constitutively active forms of MKK3/6 induced neurite outgrowth without BMP-2 stimulation, and SB203580 inhibited this induction. These results clearly indicate that activation of the p38 MAP kinase pathway is necessary for BMP-2-induced neuronal differentiation of PC12 cells. Our results also suggest that activation of the p38 MAP kinase pathway alone can induce the neuronal differentiation of PC12 cells.

Amino Acid Sequence↗

PubMed2005

Magnetic resonance temperature imaging.

Continuous, real-time, 3D temperature mapping during a hyperthermic procedure may provide (i) enhanced safety by visualizing temperature maps in and around the treated region, (ii) improved efficiency by adapting local energy deposition with feedback coupling algorithms and (iii) therapy end-points based on the accumulated thermal dose. Non-invasive mapping of temperature changes can be achieved with MRI and may be based on temperature dependent MRI parameters. The excellent linearity of the temperature dependency of the proton resonance frequency (PRF) and its near-independence with respect to tissue type make the PRF-based methods the preferred choice for many applications, in particular at mid- to-high field strength (> or =0.5 T). The PRF methods employ RF-spoiled gradient echo imaging methods and incorporate fat suppression techniques for most organs. A standard deviation of less than 1 degrees C, for a temporal resolution below 1 s and a spatial resolution of approximately 2 mm is feasible for immobile tissues. Special attention is paid to methods for reducing artifacts in MR temperature mapping caused by intra-scan and inter-scan motion and motion and temperature-induced susceptibility effects in mobile tissues. Real-time image processing and visualization techniques, together with accelerated MRI acquisition techniques, are described because of their potential for therapy guidance.

Humans↗

PubMed1996

Stereoscopically guided characterization of three-dimensional dynamic MR images of the breast.

A workstation was used to postprocess volume-rendered three-dimensional (3D) dynamic contrast material-enhanced magnetic resonance (MR) images of a breast carcinoma and a breast adenoma. Use of a 3D cursor allowed stereoscopic interactive probing of specific voxels to quantify contrast enhancement over time, which was mapped to a gray scale that effectively displayed enhancement as a fourth dimension. This technique is generally applicable to any time-dependent 3D imaging modality.

Breast↗

PubMed2005

Quantitative chemical mapping of sodium acrylate- and N-vinylpyrrolidone-enhanced alginate microcapsules.

Alginate microcapsules enclosing recombinant cells secreting therapeutic products have been used successfully to treat several murine models of human diseases. The mechanical and chemical properties of these alginate capsules can be improved by the addition and in situ photo-polymerization of sodium acrylate and N-vinylpyrrolidone in the alginate capsule. The purpose of this modification was to form additional covalent cross-links. In this work we have used scanning transmission X-ray microscopy (STXM) to probe the nature and location of the chemical modifications in the modified capsules by comparison with unmodified capsules. Analysis of X-ray image sequences and selected area spectra has been used to map the calcium gradient in capsules, to identify the presence of polyacrylate throughout the capsules and the localization of poly-N-vinylpyrrolidone in the outer regions of the alginate capsules. The differences in the spatial distributions of these species have led to better understanding of the chemical modifications that provide a mechanically more stable capsule structure.

Acrylates↗

PubMed2005

Role of cytosolic phospholipase A2 in the enhancement of alpha2-adrenoceptor-mediated vasoconstriction by the thromboxane-mimetic U46619 in the porcine isolated ear artery: comparison with vasopressin-enhanced responses.

Pre-contraction with the thromboxane-mimetic U46619 enhances the subsequent alpha(2)-adrenoceptor-mediated vasoconstriction in the porcine ear artery through an enhanced activation of ERK-MAP kinase. In this study we determined the role of cPLA(2) in this enhanced response, and determined whether vasopressin is also able to enhance alpha(2)-adrenoceptor-mediated vasoconstriction through the same pathway. The cPLA(2) inhibitors AACOCF3 (50 microM) and MAFP (50 microM) both inhibited the U46619-enhanced alpha(2)-adrenoceptor response, but had no effect on the direct alpha(2)-adrenoceptor response. AACOCF3 also inhibited the enhanced ERK activation associated with the enhanced alpha(2)-adrenoceptor-mediated vasoconstriction. Pre-contraction with arachidonic acid mimicked the effect of U46619 by enhancing the contractile response to the alpha(2)-adrenoceptor agonist UK14304 (1 microM) and enhancing the alpha(2)-adrenoceptor-mediated ERK activation. Pre-contraction with vasopressin also enhanced the contractile response to UK14304, but neither PD98059 (50 microM) nor AACOCF3 (50 microM) had any effect this vasopressin-enhanced response, indicating that neither the ERK pathway, nor cPLA(2) are involved in vasopressin-enhanced responses. The alpha(2)-adrenceptor-stimulated activation of ERK was also unaffected by pre-contraction with vasopressin. On the other hand, inhibition of PKCzeta inhibited the enhanced alpha(2)-adrenoceptor contraction after pre-contraction with both U46619 and vasopressin. This study demonstrates that alpha(2)-adrenoceptor-mediated vasoconstriction can be enhanced through two different pathways-one dependent upon the enhanced activation of ERK-MAP kinase through activation of cPLA(2), and the other through a different, ERK/cPLA(2)-independent pathway.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

PubMedDate not supplied

Towards an understanding of microtubule function and cell organization: an overview.

Microtubules exhibit dynamic instability, converting abruptly between assembly and disassembly with continued growth dependent on the presence of a tubulin-GTP cap at the plus end of the organelle. Tubulin, the main structural protein of microtubules, is a heterodimer composed of related polypeptides termed alpha-tubulin and beta-tubulin. Most eukaryotic cells possess several isoforms of the alpha- and beta-tubulins, as well as gamma-tubulin, an isoform restricted to the centrosome. The isoforms of tubulin arise either as the products of different genes or by posttranslational processes and their synthesis is subject to regulation. Tubulin isoforms coassemble with one another and isoform composition does not appear to determine whether a microtubule is able to carry out one particular activity or another. However, the posttranslational modification of polymerized tubulin may provide chemical signals which designate microtubules for a certain function. Microtubules interact with proteins called microtubule-associated proteins (MAPs) and they can be divided into two groups. The structural MAPs stimulate tubulin assembly, enhance microtubule stability, and influence the spatial distribution of microtubules within cells. The dynamic MAPs take advantage of microtubule polarity and organization to vectorially translocate cellular components. The interactions between microtubules and MAPs contribute to the structural-functional integration that characterizes eukaryotic cells.

Animals↗

PubMed1986

Topographic cerebral blood flow mapping in children with ischemic cerebrovascular diseases using xenon-enhanced computed tomography.

A non-invasive technique using xenon-enhanced computed tomography (Xe-CT) for obtaining topographic regional cerebral blood flow (rCBF) maps has been developed. During the past 3 years, the Xe-CT has been performed in 22 children with ischemic cerebrovascular diseases, including 17 cases with moyamoya disease. In moyamoya disease, rCBF maps revealed low flow in the bilateral frontal and temporal cortices, and high flow in the thalamus and putamen on both sides. Other diseases showed low perfused areas. Xe-CT can be easily performed even in infants and children and it gives valuable information that may be of clinical use.

Brain Ischemia↗

PubMed1987

Enhancement of the apparent cleavage specificities of restriction endonucleases: applications to megabase mapping of chromosomes.

We have described how DNA methylases may be used to enhance the apparent specificities of restriction endonucleases [9-11, 17, 18] to generate DNA fragments averaging 6000 to 270,000,000 base pairs on random DNA. Taking into account the non-random arrangement of natural DNA, we have predicted the rarity of certain recognition sequences in the genomes of several species.

Base Sequence↗

PubMed2003

Drinking attenuates the noradrenaline release in the lateral hypothalamic area induced by angiotensin II activation of the subfornical organ in rats.

Experiments were conducted to investigate the role of noradrenergic systems in the lateral hypothalamus area (LHA) in the water intake caused by injection of angiotensin II (ANG II) into the subfornical organ (SFO) in rats. Intracerebral microdialysis techniques were utilized to quantify the extracellular content of noradrenaline (NA) in the LHA. Microinjection of ANG II into the SFO significantly increased NA release in the LHA when water was not available for drinking. The increase in the release of NA in the LHA was significantly attenuated by water intake. In urethane-anesthetized rats, injections of ANG II into the SFO significantly enhanced the release of NA in the LHA that accompanied an elevation in mean arterial pressure (MAP). Intravenous administration of the alpha-agonist metaraminol, on the other hand, significantly decreased the NA release in the LHA that accompanied an increase in MAP, suggesting that the enhanced NA release in the LHA caused by ANG II into the SFO may be not mediated by increasing in arterial pressure. These results show the involvement of the noradrenergic systems in the LHA in the dipsogenic response induced by angiotensinergic activation of the SFO.

Adrenergic alpha-Agonists↗

PubMed1988

Functional mapping of the human papillomavirus type 11 transcriptional enhancer and its interaction with the trans-acting E2 proteins.

The transcriptional enhancer sequences of the papillomaviruses are regulated by trans-acting factors encoded by the viral E2 open reading frame. We have performed detailed functional and physical analyses of the enhancer of the human papillomavirus type 11 (HPV-11). Using the chloramphenicol acetyltransferase (CAT) assay in transiently transfected monkey CV-1 cells, the enhancer region has been localized to a 270-bp tract immediately preceding the E6 open reading frame, and it consists of two functional components. The first is a constitutive enhancer containing sequences homologous to the GT-, Sph-, and P-motifs found in the SV40 and polyomavirus enhancers; others resemble the recognition sequence for CTF (NF-1), a factor which stimulates transcription of certain eukaryotic genes and replication of adenovirus DNA. The second component is an inducible enhancer with a consensus sequence ACCN6GGT responsive to the E2 protein encoded by papillomaviruses. Tandem copies of portions of the constitutive enhancer function as an E2-independent enhancer, whereas multiple copies of HPV-11 DNA restriction fragments or synthetic oligonucleotides containing the E2-responsive sequence (E2-RS) act as an enhancer in the presence of the E2 protein encoded by HPV-1, HPV-11, or bovine papillomavirus type 1 (BPV-1). The inducible activity is lost when mutations are introduced into the E2-RS or when a mutant palindromic sequence is substituted. We have also expressed the E2 proteins of HPV-1, HPV-11, and BPV-1 in Escherichia coli and studied their physical interactions with the E2-responsive sequence in vitro. Filter-binding analyses with crude Escherichia coli lysates show that the E2 proteins bind to the E2-RS, but not to mutated motifs, with an affinity proportional to the copy number. These E2 proteins have been purified to near-homogeneity by sequence-specific DNA affinity chromatography using the synthetic E2-RS as a ligand. The purified proteins protect a DNA segment containing the E2-RS and several flanking nucleotides in pancreatic DNase I footprinting analyses. Based on these results, we conclude that E2 proteins activate the enhancer by binding directly to the E2-RS and interacting with other transcriptional factors and that the sequence ACCN6GGT is both necessary and sufficient for the E2 protein binding in vitro and for activation of RNA transcription in vivo.

Chromosome Deletion↗

PubMed2001

Shotgun optical maps of the whole Escherichia coli O157:H7 genome.

We have constructed NheI and XhoI optical maps of Escherichia coli O157:H7 solely from genomic DNA molecules to provide a uniquely valuable scaffold for contig closure and sequence validation. E. coli O157:H7 is a common pathogen found in contaminated food and water. Our approach obviated the need for the analysis of clones, PCR products, and hybridizations, because maps were constructed from ensembles of single DNA molecules. Shotgun sequencing of bacterial genomes remains labor-intensive, despite advances in sequencing technology. This is partly due to manual intervention required during the last stages of finishing. The applicability of optical mapping to this problem was enhanced by advances in machine vision techniques that improved mapping throughput and created a path to full automation of mapping. Comparisons were made between maps and sequence data that characterized sequence gaps and guided nascent assemblies.

Contig Mapping↗

PubMed1999

Hyperoxia induces the neuronal differentiated phenotype of PC12 cells via a sustained activity of mitogen-activated protein kinase induced by Bcl-2.

We previously reported that rat pheochromocytoma PC12 cells express the neuronal differentiated phenotype under hyperoxia through the production of reactive oxygen species (ROS). In the present study, we found that in this phenotype, Bcl-2, an apoptosis inhibitor, affects mitogen-activated protein (MAP)-kinase activity, which is known as a key enzyme of the signal-transduction cascade for differentiation. When PC12 cells were cultured under hyperoxia, a rapid increase in MAP-kinase activity, including that of both p42 and p44, was observed. Although the activity level then decreased quickly, activity higher than the control level was observed for 48 h. PD98059, an inhibitor of MAP kinase, suppressed the hyperoxia-induced neurite extensions, suggesting the involvement of MAP-kinase activity in the mechanism of differentiation induced by ROS. An elevation of Bcl-2 expression was observed after culturing PC12 cells for 24 h under hyperoxia. This Bcl-2 elevation was not affected by treatment with PD98059, suggesting that it did not directly induce neurite extension under hyperoxia. However, the blockade of the Bcl-2 elevation by an antisense oligonucleotide inhibited the sustained MAP-kinase activity and neurite extensions under hyperoxia. Further, in PC12 cells highly expressing Bcl-2, the sustained MAP-kinase activity and neurite extensions under hyperoxia were enhanced. These results suggested that MAP kinase is activated through the production of ROS, and the subsequent elevation of Bcl-2 expression sustains the MAP-kinase activity, resulting in the induction of the neuronal-differentiation phenotype of PC12 cells under hyperoxia.

Animals↗

PubMed1993

Role of the carboxy terminal region of beta tubulin on microtubule dynamics through its interaction with the GTP phosphate binding region.

The dynamic instability of microtubules depends on the GTP binding to tubulin, the rate of hydrolysis of GTP bound to tubulin molecules, at the microtubule caps, and on the affinity and exchange rate of tubulin for GTP versus GDP. It has been demonstrated that the binding of microtubule-associated proteins (MAPs) such as Tau or MAP2 notably enhances microtubule stability in vivo. These MAPs bind to the tubulin carboxy terminal domain. Consequently, an attractive hypothesis to explain the modulation of microtubule dynamics by MAPs is that the carboxy terminal domain of tubulin interacts with a region close to the GTP binding site, preventing the binding of GTP or exchange of GDP for GTP. By carrying out a combined analysis of crosslinking and limited proteolysis, an intramolecular interaction between the carboxy terminus and the tubulin region containing the GTP binding site in beta tubulin has been observed. It is proposed that this interaction modifies the binding of GTP to the tubulin beta-subunit and, therefore, affects tubulin assembly dynamics. This suggests a molecular explanation for the effect of MAPs in facilitating tubulin polymerization through the regulation of the interaction of GTP.

Amino Acid Sequence↗

PubMed2006

Believe it or not, QTLs are accurate!

It is generally believed that mapping quantitative trait loci (QTLs) does not accurately position genes underlying polygenic traits on the genome, which limits the application of QTL analysis in marker-assisted selection and gene discovery. However, now that a few plant QTLs have been cloned or accurately tagged, it appears that they might be accurate to within 2cM or less. This means that there will be circumstances when map-based cloning using only original mapping data would be a realistic option that avoids time-consuming and expensive fine mapping. Acceptance of this view would enhance the value of past and future mapping experiments, particularly those revealing small and environmentally sensitive QTLs that are often considered intractable at the molecular level.

Chromosome Mapping↗

PubMed2004

User-defined vascular input function curves: influence on mean perfusion parameter values and signal-to-noise ratio.

The authors reviewed 40 computed tomographic (CT) perfusion studies to determine the effect of arterial and venous input function properties on perfusion parameter values and tissue signal-to-noise ratio (SNR). A 10-subject subset was analyzed to evaluate the effect of varying venous region of interest (ROI) locations. Venous peak enhancement correlated significantly with mean tissue cerebral blood flow (CBF) and cerebral blood volume (CBV); venous and arterial peak enhancement correlated significantly with SNR of perfusion maps. Different ROI locations within the same vein resulted in significantly different CBV and CBF values. Perfusion map parameters are related to peak enhancement within user-selected ROIs. Optimal ROI selection should limit variability and increase quality of CT perfusion images.

Adult↗

PubMed2000

Mechanisms of induction of human tissue inhibitor of metalloproteinases-1 (TIMP-1) gene expression by all-trans retinoic acid in combination with basic fibroblast growth factor.

The addition of all-trans retinoic acid (ATRA) in combination with basic fibroblast growth factor (bFGF) to human fibroblasts results in a synergistic induction of tissue inhibitor of metalloproteinases-1 (TIMP-1) protein production. The synergistic stimulation of TIMP-1 protein by ATRA and bFGF increased across 72 h. An incubation of 10 min to 12 h with bFGF alone followed by ATRA gave a similar synergistic induction of TIMP-1 protein to that seen with both agents together. Treatment of cells with ATRA first followed by bFGF was ineffective. Expression of RARbeta mRNA was induced by ATRA alone, but not further induced by ATRA and bFGF; expression of RARgamma mRNA was induced by both ATRA or bFGF alone, and further induced by both reagents together; expression of RXRgamma was repressed by ATRA alone, but not by ATRA in combination with bFGF. Steady-state levels of TIMP-1 mRNA were induced 14 to 40-fold above control by ATRA and bFGF. Treatment with ATRA and bFGF did not alter the stability of TIMP-1 mRNA. The induction of TIMP-1 mRNA by ATRA and bFGF was greatly diminished by cycloheximide and therefore required new protein synthesis. The tyrosine kinase inhibitor genistein caused a dose-dependent inhibition of TIMP-1 protein induction by ATRA and bFGF. A MEK1 inhibitor (PD98059) inhibited both basal and induced levels of TIMP-1. At high concentrations, p38 MAP kinase inhibitors further enhanced the synergistic stimulation of TIMP-1 protein by ATRA and bFGF, but at these concentrations, p42/44 MAP kinase was strongly activated. These data begin to elucidate the mechanisms by which TIMP-1 gene expression can be upregulated.

Cells, Cultured↗