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PubMed1989

[Improved contrast enhancement with a positive pressure drip infusion method and 350 mg I/ml high concentration contrast media in routine contrast enhanced CT].

Sixty cases of routine contrast enhanced CT were analyzed about the utilities of positive pressure drip infusion method using high concentration contrast media 350 mgI/ml, 100 ml. They were divided into three groups and each twenty cases were received positive pressure drip infusion method using Iohexol 350 mg/ml, 100 ml (350PP), positive pressure drip infusion method using Iohexol 300 mgI/ml, 100 ml (300PP) or conventional drip infusion method using Iohexol 300 mgI/ml, 100 ml (300DI). Enhancement effects of the liver parenchyma, the aorta and the spleen at upper, middle and lower levels of the liver were evaluated with increased attenuation on pre- and postcontrast CT. And intrahepatic contrast was evaluated with attenuation difference between liver parenchyma and intrahepatic vessels on postcontrast CT. In result, 300PP kept better enhancement effects and obtained better intrahepatic contrast than 300DI at the each level of the liver, and 350PP was still better than 300PP. The analysis of relationship between intrahepatic contrast and body weight suggested that 300PP was the optimal choice for the cases with 40-50 kg body weight and 350PP was for the ones with 50-60 kg as the infusion method of routine contrast enhanced CT. And the dose of contrast media seemed to be more needed for the cases over 60 kg body weight. 350PP and 300PP were concluded as useful, safe and simple methods for routine contrast enhanced CT of the liver.

Body Weight↗

PubMed1981

Enhancement of N-hydroxy-2-aminofluorene bacterial mutagenicity by the soluble protein fraction from rat liver and partial purification of the enhancement activity.

Bacterial mutagenesis from 2-aminofluorene mediated by washed rat liver microsomes was elevated 2- to 3-fold by addition of the hepatic soluble protein fraction. Enhancement was observed at 2-aminofluorene concentrations between 1 and 20 micrograms/assay but not at 30 to 50 micrograms/assay. The soluble protein fraction (without added microsomes) did not activate 2-aminofluorene for bacterial mutagenesis. However, mutagenesis by N-hydroxy-2-aminofluorene or 2-nitrosofluorene was enhanced by the soluble protein fraction, but only when reduced nicotinamide adenine dinucleotide phosphate was also present. On the basis of chemical assay, reduced nicotinamide adenine dinucleotide phosphate reduced 2-nitrosofluorene to N-hydroxy-2-aminofluorene and protected the hydroxylamine from oxidation, thus indicating that it was the mutagenicity of N-hydroxy-2-aminofluorene (but not 2-nitrosofluorene) which was enhanced by the soluble protein fraction. Without the added soluble protein fraction, mutagenesis by N-hydroxy-2-aminofluorene or 2-nitrosofluorene was unaffected by reduced nicotinamide adenine dinucleotide phosphate. We succeeded in partially purifying a protein fraction with properties of the enhancement activity. The partially purified fraction, which represents a 14-fold increase in specific activity, was assigned a molecular weight of 33,500 by gel filtration through Sephadex G-100. This fraction was resolved into three components by polyacrylamide gel electrophoresis; the molecular weights of the three components were determined by sodium dodecyl sulfate-polyacrylamide gel (10%) electrophoresis to be 33,000, 27,000, and 16,250. The mechanism of mutagenesis enhancement remains unknown.

Animals↗

PubMed1997

Identification of a homolog of the C alpha 3'/hs3 enhancer and of an allelic variant of the 3'IgH/hs1,2 enhancer downstream of the human immunoglobulin alpha 1 gene.

Although four regulatory elements are known downstream of the mouse IgH alpha gene, a single enhancer homologous to hs1,2 has been thus far described downstream of each human alpha gene (Chen, C. and Birshtein, B. K., J. Immunol. 1997. 159: 1310). We characterized a 10-kb region downstream of the human alpha 1 gene. Two B cell-specific regulatory elements homologous to the murine C alpha 3'/hs3 and hs1,2,3' enhancers were found, which are duplicated downstream of alpha 2. The hs1,2 element is in inverted orientation by comparison with a recently reported alpha 1 hs1,2 element: it appears as a common allelic variant carrying an internal tandem repeat insertion and its prevalence in the human population is 60%. As in the mouse, the human hs1,2 enhancer is flanked with long inverted repeats which may have promoted inversion events through homologous recombination. Although the palindromic organization of the region is maintained in human, sequence identity with rodents focuses on core enhancer elements rather than on flanking repeats. Concerted divergence of both sides of the dyad symmetry suggests that inverted repeats are not just evolutionary remnants but rather play an architectural role in the LCR function.

Alleles↗

PubMed1987

Two different factors bind to the alpha-domain of the polyoma virus enhancer, one of which also interacts with the SV40 and c-fos enhancers.

Two nuclear factors from mouse 3T6 cells bind to a 22-bp segment constituting the alpha-domain of the polyoma virus enhancer. Binding of each factor can be competed out selectively by the appropriate double-stranded oligonucleotide, indicating that this binding is not strictly cooperative. Sequence homology between the two binding sites and the similar size of the protected regions may indicate that both factors, PEA1 and PEA2, are closely related. The binding site of PEA1 is centered on a sequence showing strong homology to the SV40 enhancer, the binding site of PEA2 is located immediately adjacent to it and shows a strong homology to the c-fos enhancer. Surprisingly, both SV40 and c-fos enhancers interact with PEA1, probably due to the presence of an extra base pair relative to c-fos in the PEA2 site. Factor PEA1 is probably identical to the recently described activator protein 1 (AP1).

Animals↗

PubMed2005

Value of contrast-enhanced, balanced cine-MR sequences in the assessment of apparent infarct size after acute myocardial infarction: a prospective comparison with delayed-enhancement sequences.

PURPOSE: To evaluate the diagnostic value of contrast-enhanced (CE) delayed cine steady-state free precession (SSFP) sequences in the assessment of apparent infarct size after acute myocardial infarction (MI). MATERIALS AND METHODS: Contrast-enhanced (CE) balanced cine-SSFP sequences were compared with delayed-enhancement (DE) T1 sequences for their ability to detect segmental abnormal enhancement in 29 consecutive patients with recent successfully reperfused acute MI. RESULTS: The extent of myocardial involvement revealed by postcontrast cine-SSFP sequences and DE images was closely correlated (Spearman r = 0.86, P < 0.001). There was no significant difference between the two sequences in assessing subendocardial or transmural involvement. CONCLUSION: In addition to DE sequences, CE cine-SSFP sequences should play a role in assessing necrotic and jeopardized myocardium after acute MI.

Adult↗

PubMed2001

Dependence of venous enhancement on the field of view in 3D contrast-enhanced MRA using the elliptical centric view order.

The dependence of venous suppression on the acquisition field of view (FOV) in elliptical centric 3D contrast-enhanced magnetic resonance angiography (CE-MRA) is studied theoretically and experimentally. It is hypothesized that a reduced FOV in an arterial phase acquisition results in improved venous suppression. An expression is derived linking the k-space representation of a vein to venous return time and acquisition parameters. For a y x z FOV reduction from 24 cm x 7.2 cm to 18 cm x 3.6 cm, equivalent voxel size, and venous return times ranging from 0-7 s, the mean improvement in venous suppression ranged from 7.0% for the 19-mm-diameter vein to 32.1% in the 6-mm-diameter vein, assuming a step function-shaped venous enhancement profile. Decreased venous enhancement with reduced FOV is also observed for scans with equivalent acquisition times, although the degree of suppression is dependent on the shape of the venous enhancement curve.

Carotid Artery, Common↗

PubMed1996

Cloning of Rous sarcoma virus enhancer factor genes. II. RSV-EF-II, abundantly expressed in fibroblasts and muscle tissue, binds to an octamer sequence, 5'-GTACCACC-3', in the noncoding strand of RSV enhancer.

Rous sarcoma virus (RSV) mainly replicates in avian fibroblasts, and the U3 enhancer region of the long terminal repeats of RSV contains the determinants for its tissue-tropic expression. We describe the cloning and characterization of an avian gene that encodes a protein capable of binding to the enhancer region of Rous sarcoma virus. A PCR-derived probe corresponding to the U3 region of RSV was used to isolate a cDNA clone by screening a chicken cDNA expression library. The cDNA is predicted to encode a polypeptide of 298 amino acids that is homologous to the Y-box (inverted CCAAT) family of DNA-binding transcription factors. This factor, which we refer to as Rous sarcoma virus enhancer factor-II (RSV-EF-II), shows 99% aa identity over a 105-amino-acid stretch that is highly conserved in all Y-box proteins, and is commonly referred to as the cold shock domain. RSV-EF-II selectively binds to single-stranded DNA, and the binding site, as determined by electrophoretic mobility shift assays, consists of the sequence 5' GTACCACC 3' located between nucleotides -112 to -119 in the noncoding strand of the RSV enhancer. Although RSV-EF-II shares considerable homology with the Y-box family of proteins, it does not bind to the inverted CCAAT boxes at positions -65 to -69 and -129 to -133 in the RSV LTR. Northern analysis indicates that RSV-EF-II-specific transcripts are expressed predominantly in avian fibroblasts and muscle tissue. The results of these binding and mRNA expression expriments suggest that RSV-EF-II may play an important role in tissue- and host-specific expression of RSV LTR-driven gene expression. Further, we show that RSV-EF-II acts as a repressor of transcription.

3T3 Cells↗

PubMed2006

Comparison of contrast-enhanced ultrasonography versus baseline ultrasound and contrast-enhanced computed tomography in metastatic disease of the liver: diagnostic performance and confidence.

AIM: The aim of this study was to compare contrast-enhanced ultrasonography (CEUS) to baseline US and contrast-enhanced computed tomography (CT) in metastatic disease of the liver diagnosed or suspected by US during presurgical staging or postsurgical follow-up for primary malignancies. MATERIALS AND METHODS: Two hundred-fifty-three patients considered suitable for US due to the complete explorability of the liver and with one to five proven or suspected liver metastases at baseline US were included. All patients underwent US before and after microbubble injection, and multiphase contrast-enhanced CT. Independent panels of readers reviewed US and CT scans and recorded liver metastases according to a 5-grade scale of diagnostic confidence. Sensitivity, specificity (diagnostic performance) and area under the receiver operating characteristics (ROC) curve (diagnostic confidence) were calculated. RESULTS: Reference standards revealed no metastases in 57/253, more than five in 59/253, and one to five in 137/253 patients. In patients with one to five metastases, CEUS versus baseline US revealed more metastases in 64/137 and the same number in 73/137 patients while CEUS versus CT revealed more metastases in 10/137, the same number in 99/137, and lower number in 28/137. Sensitivity, specificity, and area under ROC curve of CEUS (83%, 84%, 0.929, respectively) differed from baseline US (40%, 63%, 0.579, respectively; P<0.01) while did not differ from CT (89%, 89%, 0.945, respectively; P>0.05). CONCLUSION: CEUS improved liver metastases diagnosis in comparison with baseline US while it revealed similar diagnostic performance and confidence to contrast-enhanced CT in patients considered suitable for US and with proven or suspected liver metastases at baseline US.

Aged↗

PubMed1991

Prokaryotic transcriptional enhancers and enhancer-binding proteins.

A number of prokaryotic enhancer-binding proteins activate transcription by specialized forms of RNA polymerase. The enhancer-binding proteins catalyse isomerization of the initial complex formed between RNA polymerase and a promoter from the closed to the open state. To do so, one class of enhancer-binding proteins contacts its cognate polymerase by DNA loop formation but the other, which is represented by a single member, does not. Despite this difference, both classes of enhancer-binding proteins must hydrolyse ATP to catalyse open complex formation.

Amino Acid Sequence↗

PubMed2006

Comparison of the performance of tracer kinetic model-driven registration for dynamic contrast enhanced MRI using different models of contrast enhancement.

RATIONALE AND OBJECTIVES: The quantitative analysis of dynamic contrast-enhanced (DCE) magnetic resonance imaging (MRI) data is subject to model fitting errors caused by motion during the time-series data acquisition. However, the time-varying features that occur as a result of contrast enhancement can confound motion correction techniques based on conventional registration similarity measures. We have therefore developed a heuristic, locally controlled tracer kinetic model-driven registration procedure, in which the model accounts for contrast enhancement, and applied it to the registration of abdominal DCE-MRI data at high temporal resolution. MATERIALS AND METHODS: Using severely motion-corrupted data sets that had been excluded from analysis in a clinical trial of an antiangiogenic agent, we compared the results obtained when using different models to drive the tracer kinetic model-driven registration with those obtained when using a conventional registration against the time series mean image volume. RESULTS: Using tracer kinetic model-driven registration, it was possible to improve model fitting by reducing the sum of squared errors but the improvement was only realized when using a model that adequately described the features of the time series data. The registration against the time series mean significantly distorted the time series data, as did tracer kinetic model-driven registration using a simpler model of contrast enhancement. CONCLUSION: When an appropriate model is used, tracer kinetic model-driven registration influences motion-corrupted model fit parameter estimates and provides significant improvements in localization in three-dimensional parameter maps. This has positive implications for the use of quantitative DCE-MRI for example in clinical trials of antiangiogenic or antivascular agents.

Abdominal Neoplasms↗

PubMed2006

Biased dA/dT somatic hypermutation as regulated by the heavy chain intronic iEmu enhancer and 3'Ealpha enhancers in human lymphoblastoid B cells.

Somatic hypermutation (SHM) in immunoglobulin gene (Ig) variable (V) regions is critical for the maturation of the antibody response. It is dependent on the expression of activation-induced cytidine deaminase (AID) and translesion DNA polymerases in germinal center B cells as well as Ig V transcription, as regulated by the Ig heavy chain (H) intronic enhancer (iEmu) and the 3' enhancer (3'Ealpha) region. We analyzed the role of these cis elements in SHM by stably transfecting Ramos human lymphoblastoid B cells with a rearranged human IgH chain VD (diversity) J (joining) DNA construct containing a V(H) promoter at the 5' end and C(H)1 and C(H)2 exons of Cgamma1 at the 3' end. In this construct, mutations preferentially targeted dA/dT basepairs in the RGYW/WRCY hotspot. Most of the dA/dT mutations and accompanying dC/dG mutations were transitions. Deletion of iEmu resulted in decreased SHM which could be partially restored by insertion of the IgH hs1,2 enhancer. Other two 3'Ealpha enhancers, hs3-hs4, did not significantly increase the mutation frequency, but further strengthened the dA/dT bias. The frequency and spectrum of the mutations were independent of the genomic integration of the transgene or V gene transcription level. Thus, we have established a novel in vitro system to analyze SHM and identify the role of multiple cis-regulatory elements in regulating dA/dT biased SHM. This model system will be useful to further address the role of other cis-regulating elements and recruited trans-acting factors in expressing the modalities of SHM.

B-Lymphocytes↗

PubMedDate not supplied

Differential diagnosis of hepatic tumors with delayed enhancement at gadolinium-enhanced MRI: a pictorial essay.

Hepatic lesions with delayed enhancement are sometimes encountered on gadolinium-enhanced MRI of the liver. This study illustrates the varied appearances of several pathologic entities with delayed enhancement, including hepatic hemangioma, hepatic metastases, intrahepatic cholangiocarcinoma, focal nodular hyperplasia, hepatic abscess, hepatocellular carcinoma, and hepatocellular carcinoma after transcatheter arterial chemoembolization, and presents the utility of arterial-phase dynamic MRI in the differential diagnosis of these lesions. Possible causes of these delayed enhancements are also discussed.

Bile Duct Neoplasms↗

PubMed1999

A developmental switch from TCR delta enhancer to TCR alpha enhancer function during thymocyte maturation.

V(D)J recombination and transcription within the TCR alpha/delta locus are regulated by three characterized cis-acting elements: the TCR delta enhancer (Edelta), TCR alpha enhancer (Ealpha), and T early alpha (TEA) promoter. Analysis of enhancer and promoter occupancy and function in developing thymocytes in vivo indicates Edelta and Ealpha to be developmental-stage-specific enhancers, with Edelta "on" and Ealpha "off" in double-negative III thymocytes and Edelta "off" and Ealpha "on" in double-positive thymocytes. Edelta downregulation reflects a loss of occupancy. Surprisingly, Ealpha and TEA are extensively occupied even prior to activation. TCR delta downregulation in double-positive thymocytes depends on two events, Edelta inactivation and removal of TCR delta from the influence of Ealpha by chromosomal excision.

Animals↗

PubMed2002

Essential roles of the kappa light chain intronic enhancer and 3' enhancer in kappa rearrangement and demethylation.

The kappa intronic (MiE(kappa)) and 3' (3'E(kappa)) enhancers are both quantitatively important to, but not essential for, immunoglobulin kappa rearrangement. To determine the functional redundancy between these two enhancers, B cells derived from mutant embryonic stem cells--in which both MiE(kappa) and 3'E(kappa) were deleted on both kappa alleles--were analyzed for kappa rearrangement. Our findings indicate that these double-mutant B cells have essentially no kappa rearrangement but do rearrange and express lambda. Therefore, these two kappa enhancers share essential roles in activating V(kappa)J(kappa) rearrangement. Our findings also indicate that the two kappa enhancers play overlapping and distinct roles in the demethylation of kappa in B cells.

3' Flanking Region↗

PubMed1992

Structural and functional analysis of a replication enhancer: separation of the enhancer activity from origin function by mutational dissection of the replication origin gamma of plasmid R6K.

The plasmid R6K possesses three distinct origins of replication: alpha, beta, and gamma. The replication origin gamma of plasmid R6K performs a dual function: (i) as an origin itself and (ii) as an enhancer element required in cis for the activation at a distance of the other two replication origins alpha and beta. We have dissected the gamma origin/enhancer by site-directed mutagenesis and have reached the following conclusions. The origin function can be specifically inactivated without impairing the enhancer function by insertion and/or deletion mutations near the opposite ends of the origin gamma sequence. One such mutation deleted sequences that included the left DnaA site I. The second mutation involved insertion of linker sequences that resulted in a spatial alteration between the right DnaA site II and the VIIth pi binding iteron (tandemly repeated binding sites). Other mutations that either partly or completely deleted the A+T-rich sequence adjacent to, but not including, the pi binding iterons also abrogated enhancer and origin function and suggested that pi binding sites were necessary but not sufficient for enhancer activity. Finally, the functional analysis of a set of mutants of the gamma origin/enhancer suggested that a continuous stretch of 300 base pairs is necessary for origin gamma function and that the sequences that included the binding sites for pi, DnaA, and integration host factor proteins are required in the correct stereochemical alignment to impart origin activity.

Bacterial Proteins↗

PubMed1995

Involvement of a protein distinct from transcription enhancer factor-1 (TEF-1) in mediating human chorionic somatomammotropin gene enhancer function through the GT-IIC enhanson in choriocarcinoma and COS cells.

Previous studies suggested that transcription enhancer factor-1 (TEF-1) was involved in mediating the human chorionic somatomammotropin (hCS) gene enhancer (CSEn) function (Jiang, S.-W., and Eberhardt, N. L. (1994) J. Biol. Chem. 269, 10384-10392). We now show that an unrelated protein (CSEF-1) found in BeWo and COS-1 cells binds to the GT-IIC enhanson in CSEn and is correlated with CSEn activity in these cells. TEF-1 and CSEF-1 were distinguished by differential migration as GT-IIC complexes, thermal stability, molecular mass, and cross-reactivity with chicken TEF-1 antibodies. TEF-1 and CSEF-1 bound to the GT-IIC and Sph-I/Sph-II enhansons with identical binding properties, and in vitro generated TEF-1 competed with CSEF-1 binding to the GT-IIC motif, suggesting that their actions might be mutually exclusive. Up- and down-regulation of TEF-1 levels by expression systems and antisense oligonucleotides demonstrated that TEF-1 inhibited the hCS promoter in a manner independent of the enhancer or a known TEF-1 DNA binding site. The data suggest that TEF-1 may provide a counter-regulatory stimulus to the actions of CSEF-1, which may be involved in mediating enhancer stimulatory activity.

Base Sequence↗

PubMed2006

A method for pharmacokinetic modelling of dynamic contrast enhanced MRI studies of rapidly enhancing lesions acquired in a clinical setting.

Abnormal microcirculation is a feature of many neoplastic and non-neoplastic diseases. Physiological variables that characterize tissue microcirculation (capillary permeability and the volume of the extravascular extracellular fluid) are altered in pathological states. Pharmacokinetic analysis of dynamic contrast enhanced MRI (DCE-MRI) has found a widespread use in the assessment of abnormal microcirculation due to the direct link between the contrast agent kinetics and underlying microcirculatory properties. A representation of temporal variation of contrast agent concentration in blood plasma (C(p)(t)) is central to this analysis. In clinical applications of DCE-MRI, signal intensity curves derived from rapidly enhancing lesions often display a sigmoid shape during the initial phase of contrast uptake and rapid arrival at the equilibrium phase. In this work, the features of two principal methods for pharmacokinetic analysis of DCE-MRI which allow for theoretical representation of C(p)(t) are examined and combined to improve analysis of this particular class of DCE-MRI curves. The proposed method allows the representation of the initial sigmoid part of the enhancement profiles whilst retaining a realistic representation of C(p)(t) based on previously published measurements obtained in healthy volunteers. The results of the computer simulations indicate that in rapidly enhancing lesions, with the transfer constant K(trans) greater than 0.1 min(-1), the DCE-MRI acquisition can be restricted to 5 min post-injection and a mono-exponential representation of C(p)(t) decay is sufficient. Furthermore, non-ideal bolus delivery can be represented as a short constant rate infusion when the tissue under investigation exhibits a sigmoid pattern of contrast uptake.

Animals↗

PubMed1987

The enhancer sequence of human hepatitis B virus can enhance the activity of its surface gene promoter.

The transcriptional enhancer sequence has recently been demonstrated in the hepatitis B viral genome. This enhancer sequence has also been shown to increase the activity of HBcAg gene promoter. Using the chloramphenicol acetyltransferase gene expression system, we demonstrated that the intrinsic promoter activity of HBsAg gene promoter was stronger than that of HBcAg gene promoter in both human hepatoma cell lines, Hep3B and HuH-7. Furthermore, we showed that the HBV enhancer sequence not only stimulated the HBcAg gene promoter activity, but also stimulated the HBsAg gene promoter activity in both Hep3B and HuH-7 cells. The enhancer sequence increased the HBsAg gene promoter activity 20-fold in both Hep3B and HuH-7 cell lines, while the increase of the HBcAg gene promoter was 2- and 8-fold in Hep3B and HuH-7 cells, respectively.

Acetyltransferases↗