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Genes regulating the remote wing margin enhancer in the Drosophila cut locus.

The mechanisms that allow enhancers to activate promoters from thousands of base pairs away are disrupted by the suppressor of Hairy-wing protein (SUHW) of Drosophila. SUHW binds a DNA sequence in the gypsy retrotransposon and prevents enhancers promoter-distal to a gypsy insertion in a gene from activating without affecting promoter-proximal enhancers. Several observations indicate that SUHW does not affect enhancer-binding activators. Instead, SUHW may interfere with factors that structurally facilitate interactions between an enhancer and promoter. To identify putative enhancer facilitators, a screen for mutations that reduce activity of the remote wing margin enhancer in the cut gene was performed. Mutations in scalloped, mastermind, and a previously unknown gene, Chip, were isolated. A TEA DNA-binding domain in the Scalloped protein binds the wing margin enhancer. Interactions between scalloped, mastermind and Chip mutations indicate that mastermind and Chip act synergistically with scalloped to regulate the wing margin enhancer. Chip is essential and also affects expression of a gypsy insertion in Ultrabithorax. Relative to mutations in scalloped or mastermind, a Chip mutation hypersensitizes the wing margin enhancer in cut to gypsy insertions. Therefore, Chip might encode a target of SUHW enhancer-blocking activity.

Animals↗

The importance of the 3'-enhancer region in immunoglobulin kappa gene expression.

The first enhancers to be identified in the immunoglobulin gene loci are located in the J-C intron. However, deletion of the immunoglobulin kappa intron-enhancer has little effect on the transcription of kappa transgenes. Here we ask whether the second kappa enhancer which we recently identified at the 3'-end of the locus plays a role in kappa gene expression. We show that its omission leads to 20-40 fold lower expression of kappa transgenes and to poor allelic exclusion. Transfection experiments show that activity of the 3'-enhancer, like that of the kappa-intron enhancer, can be induced in a pre-B cell line by incubation with bacterial lipopolysaccharide. Whereas induction of the kappa-intron enhancer is due to induction of NF-kappa B activity, deletion mapping of the 3'-enhancer localises its activity to a 50 nucleotide region that lacks an NF-kappa B site; indeed the 3'-enhancer allows kappa expression in a cell line which lacks NF-kappa B. Thus, both the 3'- and intron-enhancers can be induced at the same stage of differentiation but by distinct pathways. Furthermore, unlike the intron-enhancer, the 3'-enhancer plays a critical role in the transcription of rearranged immunoglobulin kappa genes.

Animals↗

Delineation of human papillomavirus type 18 enhancer binding proteins: the intracellular distribution of a novel octamer binding protein p92 is cell cycle regulated.

The enhancer of human papillomavirus type 18 consists of two functionally redundant domains, one is partially conserved between HPV18 and HPV16, both mediate strong transcriptional enhancement. In contrast, short fragments of the enhancer mediate low transcriptional enhancement, suggesting that there is functional cooperation between HPV enhancer binding factors. Previously interactions of the enhancer with NF-1, AP1 and steroid receptors were shown by EMSA. Here we show by binding site blotting, that four novel sequence specific proteins p110, p92, p42 and p40 bind to the enhancer. Nuclear proteins p110 and p92 bind at repeated sites in the enhancer, proteins p42 and p40 only at one site. Recognition sequences for p110 and p92 were identified in a TTGCTTGCATAA sequence motif and consist of an overlapping p110 and p92 recognition site. The specific interaction of p110 with G residues of this 12 nucleotide long sequence was demonstrated by a mutant recognition site. Single recognition sites for p42 and p40 were localized in the enhancer by the use of overlapping oligonucleotides. In addition, electrophoretic mobility shift analysis identified Oct-1 and AP2 interactions with the enhancer. The AP2 binding site was mapped to a AGGCACATATT motif. The p92 protein binds to enhancer oligonucleotides, containing at least one copy of Oct-1 like recognition sequences, these oligonucleotides also bind synthetic Oct-1 protein. During serum starvation or at high saturation density, p92 moves from the nucleus into the cytoplasm. Immunoblots of cytoplasmic extracts with anti-Oct-1 antisera showed, that p92 is a novel octamer binding factor, which is not immunologically related to the Oct-1 protein. The intracellular p92 distribution is regulated at the G0/G1 boundary of the cell cycle, by nucleo-cytoplasmic translocation.

Base Sequence↗

Adjacent DNA sequences modulate Sox9 transcriptional activation at paired Sox sites in three chondrocyte-specific enhancer elements.

Expression of the type XI collagen gene Col11a2 is directed to cartilage by at least three chondrocyte-specific enhancer elements, two in the 5' region and one in the first intron of the gene. The three enhancers each contain two heptameric sites with homology to the Sox protein-binding consensus sequence. The two sites are separated by 3 or 4 bp and arranged in opposite orientation to each other. Targeted mutational analyses of these three enhancers showed that in the intronic enhancer, as in the other two enhancers, both Sox sites in a pair are essential for enhancer activity. The transcription factor Sox9 binds as a dimer at the paired sites, and the introduction of insertion mutations between the sites demonstrated that physical interactions between the adjacently bound proteins are essential for enhancer activity. Additional mutational analyses demonstrated that although Sox9 binding at the paired Sox sites is necessary for enhancer activity, it alone is not sufficient. Adjacent DNA sequences in each enhancer are also required, and mutation of those sequences can eliminate enhancer activity without preventing Sox9 binding. The data suggest a new model in which adjacently bound proteins affect the DNA bend angle produced by Sox9, which in turn determines whether an active transcriptional enhancer complex is assembled.

3T3 Cells↗

Prolonged skin allograft survival through enhancement effects on donor tissue.

A skin allograft retransplantation model was utilized to study the mechanism of immunological enhancement in a murine system. Enhancement was accomplished by treating allografted recipients with host antidonor serum (B6AF1 anti-B10.D2 alloantiserum). Grafts from enhanced or untreated hosts were retransplanted after seven days onto a second recipient. Enhanced retransplanted grafts had significantly prolonged survival as compared with unenhanced grafts. The survival of enhanced retransplanted grafts was as prolonged as that of primary skin grafts on antiserum-treated hosts. Splenocytes harvested from recipients of enhanced retransplanted allografts showed delayed and diminished development of T cell responses to graft alloantigens. Sensitization of the second recipient abrogated prolonged survival of enhanced retransplanted grafts. Also, enhancement prevented sensitization of allografted recipients. One interpretation of these studies suggests that a sensitization block is a sufficient mechanism of skin allograft enhancement. The site of action of antisera is within the graft itself. Decreased T cell responses in the host are indirect effects of diminished antigenicity of enhanced grafts. Further studies of immunological enhancement should be directed to the graft, not toward the graft recipient.

Animals↗

Neutralizing and enhancing activities of human respiratory syncytial virus-specific antibodies.

The neutralizing and enhancing activities of respiratory syncytial virus (RSV)-specific antibodies were examined. These two biological activities were measured for a panel of six monoclonal antibodies (MAbs) specific to the RSV surface F and G glycoproteins. Four MAbs specific for the F protein possessed both neutralizing and enhancing activities. One MAb (11-2-D2), specific to the G protein, enhanced RSV infection of U937 cells, a human macrophage cell line, but did not neutralize virus infectivity. One MAb (11-3-A3), specific to the F protein, efficiently neutralized virus infectivity but did not enhance RSV infection of U937 cells. MAb 11-3-A3 neutralized representative strains of the two antigenic subtypes of RSV. Assays performed with mixtures of MAbs showed that high concentrations of MAb 11-3-A3 masked the enhancing activity of MAb 11-2-D2. The assay of mixtures of two MAbs possessing only enhancing activities demonstrated that this response was synergistic. The role of neutralizing and enhancing antibodies in determining the outcome of RSV infection was examined for infants from whom cord blood serum samples were collected at birth. There was no significant difference in the magnitude of the serum-enhancing activities between infants who were hospitalized with RSV infections and a group of age- and sex-matched control infants with no reported respiratory illness requiring hospitalization. However, the results indicated a possible correlation between RSV infection of the infants and the occurrence of in vitro antibody-dependent enhancement of the cord blood sera at a serum dilution of 10(-2). A significant inverse correlation was found between the plaque-neutralizing and enhancing activities of the cord blood sera from infants, irrespective of subsequent RSV infection. These data are discussed in relation to the possible contribution of antibody-dependent enhancement to the normal course of RSV pathology in vivo.

Antibodies, Monoclonal↗

Lability of leukosis virus enhancer-binding proteins in avian hematopoeitic cells.

Bursal lymphomas induced by avian leukosis virus (ALV) are characterized by integration of long terminal repeat (LTR) enhancer sequences next to the myc proto-oncogene and by subsequent myc hyperexpression. Nuclear runoff transcription analyses have shown that protein synthesis inhibition specifically decreases transcription of LTR-enhanced genes in bursal lymphoma cell lines (M. Linial, N. Gunderson, and M. Groudine, Science 230:1126-1132, 1985). Here, we show that LTR-enhanced transcription is also labile in nontransformed bursa, bone marrow, and spleen but not in other ALV-infected tissues from lymphoma-susceptible chickens. The bursal cells demonstrated this lability of LTR-enhanced transcription only at an early stage of development, when chickens are susceptible to ALV-induced lymphomagenesis. Mature bursal cells show stable LTR transcription enhancement (unaffected by inhibition of protein synthesis) and are not susceptible to lymphomagenesis. In lymphoma-resistant chicken strains, LTR-enhanced transcription was stable in all tissues during development. These data suggest that lability of LTR transcription enhancement in hematopoietic cells is involved in susceptibility to lymphomagenesis, and we propose a model for the action of these labile enhancing factors. Gel shift analysis of nuclear proteins from lymphoma cells indicated that four or more binding proteins specifically interact with the three LTR enhancer regions. These proteins can be separated by their differential sensitivity to heat treatment or protein synthesis inhibition. The lability of a subset of these binding proteins correlates with lability of LTR-enhanced transcription in certain lymphoid cell types, suggesting that these proteins are essential for LTR transcription enhancement.

Animals↗

Activation of an endogenous retrovirus enhancer by insertion into a heterologous context.

An enhancer element is located in the U3 portion of exogenous avian retrovirus long terminal repeats (LTRs). A similar element has not been detected in the LTRs of ev-1 and ev-2, two avian endogenous viruses (evs) that normally are not expressed in vivo. Experiments were initiated to determine whether minor nucleotide differences in the U3 region of a previously untested ev that is ubiquitously expressed in vivo (ev-3) might confer enhancer function on the LTR of this provirus. This question was addressed by inserting U3 regions from ev-3 and from ev-1 and/or ev-2 both upstream of the herpesvirus thymidine kinase gene promoter and in place of the major enhancer domains of the Rous sarcoma virus LTR and determining their relative effects on transcription. U3 regions from all evs tested were unable to enhance transcription from the thymidine kinase gene promoter, indicating that nucleotide differences in the ev U3 regions do not affect their relative enhancer function and therefore are unlikely to play a role in their differential expression in vivo. Unexpectedly, however, all ev U3 regions were able to augment transcription in an orientation-independent manner in the ev-Rous sarcoma virus hybrid LTRs. Further experiments conducted to determine why this enhancer activity is not detectable in intact ev LTRs demonstrated that it was not due to removal of repressor sequences in the ev fragments used that might normally be present in intact ev LTRs. The lack of detectable enhancer activity in intact ev LTRs also was not explained by a defect in ev promoters that makes them unresponsive to enhancers in cis. These experiments therefore identify sequences that, although unable to function detectably as enhancers in their natural context, can function efficiently in a heterologous context. Data are discussed in terms of the modularity of enhancer elements and possible interactions between enhancers and promoter-specific sequences.

Avian Sarcoma Viruses↗

The -6.1-kilobase chicken lysozyme enhancer is a multifactorial complex containing several cell-type-specific elements.

In the chromatin domain of the chicken lysozyme gene of myeloid and oviduct cells, which both have the potential to activate the gene, a developmentally stable DNase I-hypersensitive site is formed around 6.1 kb upstream of the gene. This implies that this DNA region, which has previously been demonstrated to function as a transcriptional enhancer element in myeloid cells, is intimately involved in the cell-type-specific activation of the lysozyme gene locus. Deletion analysis identifies a 157-bp minimal fragment that confers the same promacrophage-specific enhancer activity as the originally described 562-bp -6.1-kb enhancer fragment. By introducing specific point mutations, we demonstrate in transient gene transfer experiments that the minimal fragment consists of at least six adjacent elements, each substantially contributing to enhancer function. The compact multifactorial enhancer complex includes a nuclear factor I (NF-I)/TGGCA binding site, homologies to AP1, and octanucleotide or enhancer core consensus motifs. Point mutation of the NF-I binding site results in the loss of NF-I binding in vitro and enhancer activity in vivo after gene transfer. Surprisingly, four overlapping oligonucleotides, each consisting of at least two elements of the -6.1-kb enhancer, confer myeloid-cell-specific enhancer activity. We found several myeloid-cell-specific DNA-binding proteins interacting with the -6.1-kb enhancer, a result consistent with that described above. Therefore, we suggest that more than a single trans-acting factor mediates the cell type specificity of the -6.1-kb enhancer.

Animals↗

Activation of the adenovirus and BK virus late promoters: effects of the BK virus enhancer and trans-acting viral early proteins.

We have examined the activation of the adenovirus major late promoter (MLP) by the cis-acting enhancer element of the human polyomavirus BK and by the trans-acting simian virus 40 (SV40) T antigen and adenovirus E1A proteins. By using chloramphenicol acetyltransferase expression vectors, we found that the MLP (pLP-CAT) was trans-activated in human and monkey kidney cells expressing the SV40 T antigen. In addition, the MLP could be cis-activated by the BK virus enhancer in both human and monkey kidney cells; approximately 20 times more chloramphenicol acetyltransferase was produced from expression vectors containing a hybrid promoter (BL), in which the BK enhancer was upstream of the MLP, than from expression vectors containing the MLP alone. This same level of enhancement of the MLP by the BK enhancer was observed in cells expressing the T antigen of SV40. However, in the 293 cell line, greater enhancement of MLP activity (70-fold) was observed with the BK enhancer sequence. In contrast, MLP activity in the 293 cell line was unchanged by the SV40 enhancer. In cotransfection experiments, MLP activity, augmented by the BK enhancer, could be further stimulated with a plasmid coding for the E1A gene products. By creating deletion mutants, we determined that the high-level activation of the hybrid BL transcriptional unit by the E1A proteins requires both MLP sequences and an intact BK virus enhancer. On the other hand, activation of the BL transcriptional unit by the T antigen did not require an intact enhancer sequence. Our results suggest that the SV40 T antigen and E1A proteins trans-activate the BL promoter by different mechanisms. We also demonstrate in cotransfection experiments that the BK late promoter is activated 45-fold by the SV40 T antigen.

Adenovirus Early Proteins↗

Multiple subelements within the polyomavirus enhancer function synergistically to activate DNA replication.

The polyomavirus origin for DNA replication comprises at least two essential, but functionally distinct, cis-acting components. One of these, the origin core, is required only for DNA replication. It includes binding sites for large T antigen and the origin of bidirectional DNA replication. The other component is required for both transcription and DNA replication and is represented by two functionally redundant regions, alpha and beta, which are elements of the polyomavirus enhancer. Whereas either enhancer element will activate DNA replication, both enhancer elements are required to constitute a functional enhancer of transcription. To identify the sequences that make up each enhancer element, we have subjected them separately to in vitro mutagenesis and measured their capacity to activate replication in cis of the origin core in MOP-8 cells, which provide all trans-acting replicative functions including large T antigen. The results reveal that the beta enhancer element is composed of three subelements, two auxiliary subelements, and a core subelement. The core subelement independently activated DNA replication, albeit poorly. The auxiliary subelements, which were inactive on their own, acted synergistically with the core subelement to increase its activity. Interestingly, dimers of the beta core subelement functioned as well as the combination of a beta auxiliary subelement and a core subelement, suggesting that the subelements are functionally equivalent. The alpha enhancer element is organized similarly; it too comprises an auxiliary subelement and a core subelement. These results lead us to suggest that the polyomavirus enhancer comprises two levels of organization; two or more enhancer elements form an enhancer, and two or more subelements make up an enhancer element. The subelements share few sequences and serve as binding sites for distinct cellular factors. It appears, therefore, that a number of different cellular proteins function cooperatively to activate polyomavirus DNA replication by a common mechanism.

Base Sequence↗

Contrast-enhanced digital mammography: initial clinical experience.

PURPOSE: To investigate the potential of using intravenous contrast material with full-field digital mammography to facilitate the detection and characterization of lesions in the breast. MATERIALS AND METHODS: Twenty-two women scheduled for biopsy because they were suspected of having abnormalities at breast imaging underwent imaging with contrast material-enhanced digital mammography. Six sequential images of the affected breast were obtained, with a contrast agent injected intravenously between the time the first and second images were obtained. Image processing included registration and logarithmic subtraction. Lesions were evaluated for the presence, morphology, and kinetics of enhancement. Lesion type, size, and pathologic findings were correlated with the findings at contrast-enhanced digital mammography. RESULTS: At contrast-enhanced digital mammography, enhancement was observed in eight of 10 patients with biopsy-proved cancers. In one case of ductal carcinoma in situ and one case of invasive ductal carcinoma, enhancement was not observed. No enhancement was seen in seven of 12 cases in which lesions were suspected of being malignant at initial imaging but were benign. Morphology generally correlated with the pathologic diagnosis. The kinetics of lesion enhancement showed similarity to that seen with gadolinium-enhanced magnetic resonance imaging but was not consistent. CONCLUSION: The results of this preliminary study suggest that contrast-enhanced digital mammography potentially may be useful in identification of lesions in the mammographically dense breast. Further investigation of contrast-enhanced digital mammography as a diagnostic tool for breast cancer is warranted.

Adult↗

Multiphasic injection method for uniform prolonged vascular enhancement at CT angiography: pharmacokinetic analysis and experimental porcine model.

PURPOSE: To determine if multiphasic injection provides uniform, prolonged vascular contrast medium enhancement at computed tomographic (CT) angiography. MATERIALS AND METHODS: With a computer-based, compartmental model of the cardiovascular system, theoretic analysis was performed to estimate an injection algorithm for uniform, prolonged vascular enhancement. For algorithm validation, four pigs were scanned after intravenous injection of 50 or 70 mL of contrast medium (282 mg of iodine per milliliter). Uni-, bi-, and multiphasic injection schemes were tested. In most cases, the initial injection rate was 2 mL/sec. In each CT study, 27 dynamic images were acquired every 2 seconds at a fixed mid-abdominal aortic level. Time-enhancement curves were calculated. Injection duration, peak aortic enhancement, and enhancement uniformity (duration of enhancement achieved within 90% of the peak [90% DCE]) were evaluated. RESULTS: Theoretic and experimental results agreed well. Compared with uniphasic injection, biphasic injection resulted in more prolonged enhancement but generated two enhancement peaks with a valley between, and multiphasic injection yielded more uniform and prolonged enhancement. With 50- and 70-mL multiphasic injections, respectively, injection duration increased by 32% and 51%, peak enhancement decreased by 19% and 18%, and 90% DCE increased by 81% and 94%. CONCLUSION: Uniform, prolonged vascular enhancement, which is desirable for CT angiography and essential for steady-state quantification of blood volume in organs, can be achieved with multiphasic injection.

Angiography↗

Comparison of standard and task-specific enhancement of Digora storage phosphor images for approximal caries diagnosis.

OBJECTIVES: To compare approximal caries detection on Digora storage phosphor images pre-enhanced with the automatic "caries-specific Oslo enhancement procedure" ("Oslo-enhanced" method) and storage phosphor images individually enhanced by observers particularly experienced in digital imaging using standard brightness and contrast functions of the Digora system ("Digora-enhanced" method). METHODS: Seven staff members from four oral radiology departments rated 240 approximal surfaces for caries with regard to lesion depth in the inner and outer half of the enamel and dentine, using a 5-point confidence scale. The observations were validated histologically. A receiver operating characteristic (ROC) analysis and an analysis of variance with three dependent variables (observer confidence, observer signed error and observer absolute error) were performed. RESULTS: The most evident difference between the methods as elucidated by the ROC analysis was the highly significant smaller interobserver and intraobserver variance with the Oslo-enhanced method for all but one observer. The methods were not different with regard to average diagnostic accuracy (A(z) values) as tested with paired t-tests, and there was no correlation between A(z) across methods. The method and lesion main effects, as well as the lesion by method interaction effect, were multivariately significant (P<0.001) in favour of the Oslo-enhanced method. On a univariate level, the method main effect was not significant for the absolute observer error (P=0.330). All other univariate effects were significant (P<0.001). CONCLUSIONS: The accuracy of approximal caries detection with Digora storage phosphor images pre-enhanced and images individually enhanced was similar, but interobserver and intraobserver variability improved with the Oslo-enhanced method. Since image manipulation is not performed with the Oslo-enhanced method, the increased speed of the diagnostic procedure combined with the improved observer variability would probably be even more pronounced for the general dental practitioner.

Analysis of Variance↗

MR imaging of the cranial meninges with emphasis on contrast enhancement and meningeal carcinomatosis.

MR imaging was used to investigate normal and abnormal meningeal enhancement, with an emphasis on meningeal carcinomatosis. Three groups of patients were studied on a 1.5-T system. In group 1, the normal meninges were examined in 20 patients and were found to show fine linear enhancement in short segments, especially in a parasagittal distribution. In group 2, all gadolinium-enhanced head scans were reviewed retrospectively. Abnormal meningeal enhancement was detected in 52 patients. In some of these, the enhancement was associated with pathologic conditions of the meninges, including leptomeningeal tumor and meningeal infections and other inflammatory conditions; in others the enhancement was adjacent to subdural hematomas, subacute infarcts, and skull lesions, such as metastases or postoperative defects. In group 3, 30 cases of meningeal carcinomatosis were studied prospectively. Enhancement was seen in approximately two-thirds of cases and usually was quite diffuse and applied to the inner table of the skull. Frank nodules were seen less often. Contrast-enhanced CT was equal to MR in the detection of nodules but was nearly always unable to show diffuse meningeal enhancement against the inner table of the skull. Contrast-enhanced MR was more sensitive than contrast-enhanced CT in the examination of normal and abnormal meninges. Abnormal findings, such as meningeal carcinomatosis, were demonstrated more often by MR than by CT.

Adolescent↗

Gadolinium-enhanced MR imaging of temporomandibular disorders: improved lesion detection of the posterior disk attachment on T1-weighted images obtained with fat suppression.

OBJECTIVE: The purpose of this study was to assess the potential for improved lesion detection in the posterior disk attachment and its surrounding tissue in temporomandibular disorders when gadolinium-enhanced MR imaging performed with fat suppression is used. MATERIALS AND METHODS: Forty-five patients underwent MR imaging with conventional T1- and T2-weighted, gadolinium-enhanced T1-weighted, and gadolinium-enhanced fat-suppressed spin-echo imaging sequences. Qualitative and quantitative assessments of the contrast enhancement of each type of imaging were also performed. RESULTS: The contrast-enhanced fat-suppressed T1-weighted imaging sequence had several advantages over the other imaging techniques in detecting abnormalities of the posterior disk attachment and in detecting bone marrow lesions in the mandibular condyle. The most significant advantage was better enhancement of lesion conspicuity. The diagnostic accuracy of contrast-enhanced fat-suppressed imaging was 77% versus 70% for conventional contrast-enhanced imaging. The kappa value for interobserver agreement was .95 for contrast-enhanced fat-suppressed imaging and .72 for conventional contrast-enhanced imaging. CONCLUSION: Contrast-enhanced fat-suppressed T1-weighted spin-echo MR imaging is a valuable technique for visualizing the extent and degree of lesions in the posterior disk attachment and bone marrow lesions in the mandibular condyle.

Adolescent↗

Assessment of vascularity in hepatic tumors: comparison of power Doppler sonography and intraarterial CO(2)-enhanced sonography.

OBJECTIVE: The purpose of the study was to compare power Doppler sonography with intraarterial CO(2)-enhanced sonography for revealing vascularity in treated and untreated hepatic tumors. SUBJECTS AND METHODS: Fifty-five patients with 93 liver tumors were prospectively examined with power Doppler sonography and CO(2)-enhanced sonography. These tumors included 29 hepatocellular carcinomas in patients with no previous treatment, 26 treated hepatocellular carcinomas, and 38 hemangiomas. The vascular depiction of power Doppler sonography was compared with that obtained in the early phase of CO(2)-enhanced sonography. The results of angiography were also recorded for comparison. RESULTS: In the hepatocellular carcinomas, power Doppler sonography was the same as CO(2)-enhanced sonography in 18 (62%) of 29 tumors, was inferior to CO(2)-enhanced sonography in nine (31%) of 29 tumors, and was superior to CO(2)-enhanced sonography in two (7%) of 29 tumors. In the treated hepatocellular carcinomas, power Doppler sonography was the same as CO(2)-enhanced sonography in 15 (58%) of 26 tumors and was inferior in 11 (42%) of 26 tumors. In hemangiomas, the same vascularity was found in both studies in 15 (39%) of 38 tumors, CO(2)-enhanced sonography was superior in 22 (58%) of 38 tumors, and power Doppler sonography was superior in one (3%) of 38 tumors. As a whole, 45% of the 93 tumors showed better vascular depiction on CO(2)-enhanced sonography. However, 19.4% of tumors were hypovascular using power Doppler sonography but hypervascular using CO(2)-enhanced sonography. CONCLUSION: Power Doppler sonography is a useful technique for screening hepatic tumor vascularity. CO(2)-enhanced sonography is superior to power Doppler sonography in depicting tumor vascularity in treated hepatocellular carcinomas and in hemangiomas, especially small hemangiomas.

Adult↗

Evolution of MR contrast enhancement patterns during the first week after acute ischemic stroke.

BACKGROUND AND PURPOSE: Intravascular and parenchymal enhancement have been detected with contrast-enhanced T1-weighted MR imaging in patients with ischemic stroke. Diffusion-weighted MR imaging depicts infarct within minutes after the onset of symptoms. The aims of this study were to study the different MR enhancement findings during the first week after stroke and to ascertain whether the presence of intravascular enhancement over a larger area than the infarct on diffusion-weighted images on day 1 is able to predict substantial infarct growth during the first week. METHODS: Forty-eight patients were imaged on the first and second days and again 1 week after the onset of ischemic stroke. T1-weighted spin-echo imaging was performed before and after a 0.2 mmol/kg bolus of gadolinium chelate. Diffusion-weighted imaging was performed at the same slice positions. Enhancement findings were categorized as intravascular and parenchymal, with further categorization of parenchymal enhancement as cortical, subcortical, and deep; these findings were then compared with diffusion-weighted imaging findings. RESULTS: Intravascular enhancement in the infarcted area was detected on day 1 in 78% of the cases, on day 2 in 78% of the cases, and at 1 week in 30% of the cases. Parenchymal enhancement was detected in 26%, 56%, and 100% of the cases, respectively. Intravascular enhancement over a larger area than the infarct on diffusion-weighted images on day 1 was not associated with the extent of infarct growth. CONCLUSION: Detection of different patterns of contrast enhancement can help in determining the age of infarct. Parenchymal enhancement may be intense and can cause diagnostic uncertainty in cases in which the clinical history is obscure.

Aged↗