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PubMed2002

Myocardial enhancement on magnetic resonance imaging with gadolinium-diethylenetriamine pentaacetic acid and improvement of left ventricular function in patients with dilated cardiomyopathy.

OBJECTIVES: This study evaluated the significance of myocardial gadolinium-diethylenetriamine pentaacetic acid (Gd-DTPA) enhancement on magnetic resonance imaging for the improvement of left ventricular function in patients with dilated cardiomyopathy. METHODS: Twenty-seven patients with dilated cardiomyopathy (mean age 59 +/- 11 years) were studied. The magnitude of myocardial Gd-DTPA enhancement was quantitatively assessed using signal intensity ratio and compared to changes in left ventricular function and adverse cardiac events during a relatively long follow-up period. RESULTS: Regional high signal intensity ratio, defined as > or = mean + 2SD in seven normal subjects, was found in 14 patients: in three or more regions out of five myocardial regions analyzed in six patients (extensive enhancement) and in only one or two regions in eight patients (limited enhancement). The remaining 13 patients had no high signal ratio in any of the five regions analyzed (no enhancement). During the follow-up period of 3.9 +/- 1.9 years, four patients died of cardiac causes. The incidence of cardiac death was 33.3% in patients with extensive enhancement, 12.5% in those with limited enhancement and 7.7% in those without enhancement, but there was no statistical difference. Mild improvement in fractional shortening was observed in patients without enhancement during the follow-up (19 +/- 4%-->27 +/- 10%, p = 0.03). CONCLUSIONS: Evaluation of myocardial Gd-DTPA enhancement on magnetic resonance imaging may provide useful prognostic information for patients with dilated cardiomyopathy.

Adult↗

PubMed2003

Accuracy of contrast-enhanced MR angiography in predicting angiographic stenosis of the internal carotid artery: linear regression analysis.

BACKGROUND AND PURPOSE: We sought to assess whether contrast-enhanced MR angiography is able to predict the degree of angiographic stenosis of the internal carotid artery within a clinically acceptable margin of error, thereby decreasing the need for angiography. In addition, we sought to assess whether adding ultrasound peak systolic velocity (PSV) as an additional regressor improves the accuracy of prediction. METHODS: A retrospective review of our institution's records for a 4-year period was conducted to identify all patients who had undergone evaluation of their carotid arteries using digital subtraction angiography, contrast-enhanced MR angiography, and ultrasonography. All internal carotid artery stenoses ranging from 10% to 90% at carotid angiography were selected (n = 22). Measurements were then obtained based on the North American Symptomatic Carotid Endarterectomy Trial style by using the digital subtraction angiograms and contrast-enhanced MR angiograms in a blinded fashion. The correlation between digital subtraction angiography data and contrast-enhanced MR angiography data was assessed by conducting linear regression analysis. Multiple regression analysis was then conducted to determine whether the inclusion of ultrasound PSV as an additional regressor increased the accuracy of prediction. RESULTS: The correlation between the degree of stenosis measured by digital subtraction angiography and that measured by contrast-enhanced MR angiography was r = 0.967. The 95% confidence interval for the line of means showed low errors bounds, ranging as low as +/-2.8%. The 95% confidence interval for individual prediction of angiographic stenosis based on a given contrast-enhanced MR angiographic measurement, however, was significantly larger, being no less than +/-13.6%. With the inclusion of PSV, the adjusted correlation was r = 0.965. CONCLUSION: A clear linear relationship exists between digital subtraction angiographic and contrast-enhanced MR angiographic measurements of carotid stenosis. Increasing severity of stenosis as measured by contrast-enhanced MR angiography corresponds to increasing severity at angiography. Although the predictive value of contrast-enhanced MR angiography is excellent in the mean, it is less reliable for predicting the degree of angiographic stenosis in the individual patient, showing rather wide confidence intervals. Furthermore, the inclusion of PSV as an additional regressor does not improve the predictive accuracy beyond that of contrast-enhanced MR angiography alone.

Angiography, Digital Subtraction↗

PubMedDate not supplied

MR Gd-DTPA enhancement of radiation brain injury.

MR examinations of 104 patients who had undergone radiotherapy to the brain were reviewed. Thirty-six patients received Gd-DTPA enhanced study during the course of MR evaluation and six of the patients showed enhancing radiation necrosis. Histopathological confirmations were obtained in three patients. Gd-DTPA enhancing radiation lesions were multiple and patchy in three patients, multiple and patchy with cyst formation in two and ring shaped in one. In terms of their distribution, enhancing lesions in four patients were seen only in the white matter within the irradiated field and these patients had undergone radiotherapy within five years. The interval after radiotherapy was more than eight years in two patients and their enhanced lesions were observed in both the white and gray matter. Histopathological findings of Gd-DTPA enhancing radiation necrosis were gliosis and coalescing vacuoles of the neural tissue. None of these enhanced radiation lesions showed significant mass effects. Patterns of the enhancement were not specific. It was considered to be difficult to differentiate tumor recurrence from radiation necrosis with conventional Gd-DTPA enhanced MR examinations. In one patient, delayed MR images after Gd-DTPA administration showed increases in the size and number of radiation enhanced lesions. Dynamic and delayed MR study might add more information to conventional imaging after Gd-DTPA. Further studies are necessary to differentiate radiation lesions from tumor recurrences.

Adult↗

PubMed1992

[Evaluation of non-contrast-enhanced CT in blunt abdominal trauma].

We compared the findings of noncontrast-enhanced CT with those of contrast-enhanced CT in 126 patients with blunt abdominal trauma to evaluate the usefulness of noncontrast-enhanced CT. In 112 of the patients, visceral injuries were confirmed by surgery or clinical follow-up including CT. Although noncontrast-enhanced CT diagnosed all patients with 12 intestinal injuries requiring immediate surgery, contrast-enhanced CT missed two of these patients because high density hematomas on noncontrast-enhanced CT became isodense after IV administration of contrast material. However, contrast-enhanced CT was superior to noncontrast-enhanced CT in the diagnosis of hepatic and renal injuries. A case of renal artery occlusion was only visualized on contrast-enhanced CT. We conclude that both noncontrast- and contrast-enhanced CT should be performed for the CT evaluation of blunt abdominal trauma.

Abdominal Injuries↗

PubMed2005

Transthyretin-related familial amyloid polyneuropathy: evaluation of CSF enhancement on serial T1-weighted and fluid-attenuated inversion recovery images following intravenous contrast administration.

BACKGROUND AND PURPOSE: CSF enhancement on MR images after intravenous administration of gadolinium chelate, which mimics subarachnoid hemorrhage, has been reported. The purpose of this study was to determine whether CSF enhancement can be seen on serial MR images following administration of contrast material in patients with transthyretin-related familial amyloid polyneuropathy (FAP) and to assess other ancillary MR findings. METHODS: We serially studied T1-weighted and fluid-attenuated inversion recovery (FLAIR) images of the brain before, immediately after, and 3, 6, and 24 hours after contrast administration in 6 patients with genetically confirmed transthyretin-related FAP. By consensus, 2 radiologists assessed the presence, degree, and extent of enhancement of the CSF, leptomeninges, brain parenchyma, and other structures. Statistical analysis was performed to define the difference of the enhancement between the 2 MR imagings. RESULTS: In 3/6 patients with cysteine-for-tyrosine substitutions at position 114 (Tyr114Cys mutations), marked CSF enhancement was observed on the FLAIR images at 3 and 6 hours and on T1-weighted images at 3 hours after contrast administration. Although there was no significant difference between the 2 MR imagings, leptomeningeal enhancement for these 3 patients was evident only on FLAIR images. The labyrinth and vitreous body was also enhanced on postcontrast delayed MR images of these 3 patients. These enhancements were not observed in the other 3 patients with Val30Met mutation. In none of the 6 patients did images demonstrate parenchymal enhancement of the brain. CONCLUSION: In FAP patients with Tyr114Cys mutations, contrast material can leak into the CSF. This finding may depend on the subtype of FAP and be more evident with FLAIR images. The enhancement of the leptomeninges, labyrinth, and vitreous body was also seen in the patients.

Adult↗

PubMed2006

[Effects of absorption enhancers on intestinal absorption of lumbrokinase].

AIM: To explore the intestinal absorption characteristics of lumbrokinase (YJM-I) in the absence or presence of various absorption enhancers and to find the optimum intestinal site for YJM-I absorption. METHODS: The absorption kinetics and absorption intestinal sites for YJM-I absorption were investigated with the method of diffusion cell in vitro, duodenum bolus injection, recirculating perfusion and in situ duodenum perfusion in vivo. RESULTS: YJM-I could be transported into blood and kept its biological activity across intestinal endothelial membrane after administration via duodenum site, whereas with lower bioavailability. Some of the absorption enhancers were shown good enhancement effects on intestinal absorption of YJM-I in vitro and in situ experiments. The order of enhanced efficiencies of various enhancers on duodenum, ileum and jejunum in vitro permeation experiments were shown as follows: 1% chitosan > 1% SDCh > 1% Na2EDTA > 1% SDS > 1% sodium caprylate > 1% poloxamer > 1% HP-beta-CD. The order of enhanced efficiencies of various enhancers on duodenum absorption of YJM-I in vivo were as follows: 2.5% SDCh > 2.5% Na2EDTA > 2.0% chitosan > 2.5% SDS > 2.5% sodium caprylate > 2.5% Poloxamer > 2.5% HP-beta-CD. CONCLUSION: The results indicated that the absorption of YJM-I could be enhanced by various enhancers, and duodenum was the optimum absorption site of YJM-I. Furthermore, bio-adhesive chitosan might be a potential enhancer of intestinal YJM-I absorption.

Administration, Oral↗

PubMedDate not supplied

Optimizing brain MR imaging protocols with gadopentetate dimeglumine: enhancement of intracranial lesions on spin-density- and T2-weighted images.

To determine whether long TR MR imaging is best performed before or after IV administration of gadopentetate dimeglumine, we obtained spin-density- and T2-weighted images before and after contrast administration in 21 patients with known intracranial enhancing lesions. Of 25 lesions demonstrating enhancement on T1-weighted sequences, 21 showed mild or moderate enhancement on spin-density-weighted sequences and 20 showed mild enhancement on T2-weighted sequences. Importantly, no spin-density or T2 information was obscured by the administration of gadopentetate dimeglumine, and no T2 shortening effects were visible. Two new foci of enhancement were visible on postcontrast spin-density- and T2-weighted images that were missed on postcontrast T1-weighted images and on precontrast spin-density- and T2-weighted studies. Visualization of new areas of enhancement is the main advantage provided by the long TR images obtained after IV injection of gadopentetate dimeglumine. The most likely reason for the appearance of these newly visualized lesions is thought to be delayed enhancement. This imaging protocol also allows the display of adjacent edema or gliosis and enhancing lesions on a single image. Additionally, in three cases, posterior fossa phase-shift artifacts raised the suspicion of an enhancing lesion on postcontrast T1-weighted images, but the cerebellum was shown to be normal on the postcontrast spin-density- and T2-weighted studies. On the basis of our results, we recommend obtaining long TR images after rather than before the administration of gadopentetate dimeglumine in patients with intracranial enhancing lesions.

Astrocytoma↗

PubMed1991

Disodium cromoglycate enhances ongoing immunoglobulin production in vitro in human B cells.

The effect of disodium cromoglycate (DSCG) upon human immunoglobulin (Ig) isotypes and IgG subclasses production by purified B cells was studied. DSCG enhanced IgM, IgG1, IgG2, IgG3, IgG4 and IgA production in a dose-dependent fashion, while DSCG failed to induce IgE production at any concentrations tested by purified B cells. When B cells were separated into small resting and large activated B cells, DSCG failed to induce Ig production from small resting B cells in the presence or absence of Staphylococcus aureus Cowan strain I (SAC). In contrast, in large activated B cells DSCG significantly enhanced all types of Ig production (two-to threefold), especially IgG4 production (seven-to 11-fold), except IgE, which large B cells did not produce. The enhancement of IgG subclass production was not subclass switching, since DSCG failed to enhance IgG1 production in B cells depleted of surface IgG1+ cells (sIgG1+ cells). Similarly, DSCG did not enhance IgG2, IgG3 or IgG4 production from sIgG2-, sIgG3- or sIgG4- B cells, respectively, Interleukin-4 (IL-4) or interleukin-6 (IL-6) also enhanced Ig production except IgG4 from large activated B cells. The enhancing effect of DSCG was not mediated by IL-4 or IL-6 since anti-IL-4 or anti-IL-6 antibody failed to block the DSCG-induced enhancement. DSCG also enhanced IgG2 and IgM production from human B-cell lines GM-1500 and CBL, respectively. These results suggest that DSCG directly and preferentially stimulates activated B cells which are producing Ig and, in addition, enhances their Ig production.

B-Lymphocytes↗

PubMed1989

2,3,7,8-Tetrachlorodibenzo-p-dioxin enhancement of N-methyl-N'-nitro-N-nitrosoguanidine-induced transformation of rat tracheal epithelial cells in culture.

The abilities of various dioxins to induce toxicity or transformation of rat tracheal epithelial cells in culture were examined. 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) was not cytotoxic and did not induce transformation as measured by the induction of growth-altered, preneoplastic cells (termed enhanced growth variants). However, TCDD enhanced the transformation of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)-initiated rat tracheal epithelial cells. Other dioxin congeners with 0 to 3 chloro substitutions were inactive in enhancing MNNG transformation. TCDD was most effective at a concentration of 0.3 nM and when treatment was administered immediately after MNNG exposure. The dose-response curves for enhancement of MNNG-induced transformation and induction of aryl hydrocarbon hydroxylase activity by TCDD were similar. These results are consistent with the hypothesis that the enhancement of cell transformation by TCDD is mediated through the TCDD receptor. TCDD also enhanced transformation when the cells were treated before MNNG treatment. The ability of 12-O-tetradecanoylphorbol-13-acetate (TPA) to enhance MNNG-induced rat tracheal epithelial transformation was also examined. In contrast to the findings with TCDD, the number of transformed colonies was increased only by pretreatment with TPA followed by MNNG. TPA-pretreatment enhanced equally the number of normal cells forming colonies and the total number of transformed colonies after selection; therefore, the transformation frequency (transformants per total surviving colonies) was unchanged by TPA. In contrast, TCDD treatment enhanced the transformation frequency in MNNG-exposed cultures since the number of transformed colonies increased while the number of total colonies remained constant. Thus, TCDD appears to act by a different mechanism than TPA. TCDD enhancement of MNNG-induced transformation may be attributed to a promotional effect, a comutagenic action, or a modulation of cell proliferation and/or differentiation mediated through the TCDD receptor.

Animals↗

PubMed1986

Effect of hyperthermia on the antiproliferative activities of murine alpha-, beta-, and gamma-interferon: differential enhancement of murine gamma-interferon.

Fever is frequently an important side effect of interferon (IFN) therapy. Studies have shown that culturing interferon-treated cells at elevated temperature heightens the antiproliferative activity of IFN-alpha and IFN-beta. Since IFN-gamma has also been shown to be a potent antiproliferative agent, the effect of elevated temperature on IFN-gamma activity was compared to its effect on IFN-alpha and IFN-beta. Mouse B-16 melanoma cells were simultaneously cultured under cloning conditions at a range of temperatures (37.3, 38.1, 38.6, and 39.4 degrees C) in the presence of MuIFN-alpha, MuIFN-beta, and MuIFN-gamma. The antiproliferative activities of all three interferons were enhanced by incubation at the elevated temperatures. However, the elevated temperatures had a more dramatic enhancing effect on the antiproliferative activity of MuIFN-gamma (10-fold enhancement) than of either MuIFN-alpha or MuIFN-beta (2.9- and 3.4-fold enhancement, respectively). Next, the enhancing effect of elevated temperature (39.4 degrees C) was examined for a range of interferon concentrations. The degree of the enhancing effect increased with increasing concentrations of MuIFN-gamma but not with increasing concentrations of MuIFN-alpha or MuIFN-beta. Enhancing effects of temperature as high as 14-fold were observed for 100 units of MuIFN-gamma/ml. This dramatic enhancement was observed for both natural and recombinant MuIFN-gamma and was neither a function of greater relative perception of MuIFN-gamma titer at elevated temperature nor a function of greater relative stability of MuIFN-gamma at the elevated temperature. The differential enhancement of MuIFN-gamma activity by elevated temperature appeared to be specific for the antiproliferative activity, since the antiviral activity of MuIFN-gamma was not relatively more enhanced at 39.4 degrees C than were the antiviral activities of MuIFN-alpha and MuIFN-beta. These results suggest that fever may be an important factor in maximizing the antitumor effects of MuIFN-gamma and perhaps of human IFN-gamma. They also raise the possibility that a combination treatment regimen of hyperthermia and interferon therapy, particularly IFN-gamma therapy, may provide a significant antitumor effect.

Animals↗

PubMed1987

Cross-infection enhancement among African flaviviruses by immune mouse ascitic fluids.

Cross-infection enhancement of seven African flaviviruses by subneutralising concentrations of antibody in immune ascitic fluids was investigated in P388D1 cell culture. Infection by all the seven flaviviruses tested was enhanced by homologous and at least one of six heterologous immune mouse ascitic fluids (IMAF) tested. Enhancement ratios and enhancing antibody titres were higher in homologous than in heterologous enhancement. Zika, Wesselsbron, Uganda S and West Nile viruses were enhanced in culture by all the IMAF tested. Enhancement of Dakar bat and Yellow fever viruses was produced by five heterologous IMAF, but Potiskum virus was enhanced by one heterologous flavivirus antibody. The antibody to Potiskum virus was the most potent mediator of heterologous infection enhancement; all six heterologous flaviviruses were markedly enhanced by this antibody.

Animals↗

PubMed1993

Enhancement of daunorubicin accumulation, retention, and cytotoxicity by verapamil or cyclosporin A in blast cells from patients with previously untreated acute myeloid leukemia.

This work was designed to discern the frequency of expression of classical multidrug resistance (MDR) in acute myeloid leukemia (AML) at the time of diagnosis, using Western blotting for P-glycoprotein (Pgp) and functional assays for an MDR phenotype (enhancement of daunorubicin [DNR] accumulation/retention and cytotoxicity by the known MDR modulators verapamil, cyclosporin A, and progesterone). Blast cells were studied from 49 newly diagnosed AML patients who were subsequently treated with the "3 and 7" combination of cytosine arabinoside (ara-C) and DNR. DNR accumulation (1 microgram/mL, 3 hours) and retention (16 hours) were determined by flow cytometry. Cyclosporin A (CsA, 5 mumol/L) or verapamil (6.6 mumol/L) each caused significant enhancement of DNR accumulation and retention in these blast cell samples (P < .001, Wilcoxon's test). Verapamil or CsA caused greater than 20% enhancement of DNR accumulation or retention in over 25% or 50% of these patients, respectively; however, there was no correlation with the presence or degree of enhancement and response to treatment. Progesterone (10 mumol/L) caused no significant enhancement of DNR accumulation or retention. The effects of the MDR modulators on the cytotoxicity of DNR was also determined in blast cells from 40 of the patients, using a flow cytometric assay. CsA alone was cytotoxic (caused an approximate 20% decrease in cell survival compared with control, P < .001); CsA or verapamil caused enhancement of 1 mumol/L DNR cytotoxicity (P < .001). Greater than 40% enhancement of cell kill by CsA or verapamil was observed in over 75% of patients studied. There was no difference in the degree of enhancement of cytotoxicity between patients clinically sensitive or resistant to treatment. Progesterone caused no enhancement in DNR cytotoxicity. In contrast to the functional assays, highly sensitive immunoblots using the C219 antibody to Pgp showed evidence of low level expression of Pgp in blast cells from only 3 of these patients: 1 was chemotherapy resistant, 2 were sensitive. Thus, although the functional assays suggest a high frequency of expression of a classic MDR phenotype in AML patients at the time of diagnosis, with enhancement by CsA obtained at a clinically relevant concentration (5 mumol/L), the frequency of Pgp expression detectable by C219 Western blots was low in these patients. This could be interpreted either that the method used was not sufficiently sensitive to detect Pgp in all of the blast cell specimens that actually overexpressed mdr1, or that the accumulation/efflux-based MDR phenotype observed is not always mediated by Pgp in these previously untreated patients.

ATP Binding Cassette Transporter, Subfamily B, Mem↗

PubMed1993

Spacing ensures autonomous expression of different stripe enhancers in the even-skipped promoter.

The even-skipped (eve) promoter contains a series of enhancers that control the expression of different segmentation stripes in the Drosophila embryo. The stripe 3 enhancer is located 1.7 kb upstream of the stripe 2 enhancer. Here we demonstrate that these enhancers must be physically separated by a minimum distance for proper stripe expression. When they are directly coupled in either orientation, the enhancers generate abnormal patterns of expression in the early embryo. For example, the levels of stripe 2 expression are augmented and there is a posterior expansion of the pattern when the stripe 3 enhancer is positioned immediately upstream of the stripe 2 enhancer. Despite this spacing requirement, the order of the enhancers within the eve promoter can be reversed without affecting the normal expression pattern. These results suggest that spacing maintains the autonomous activities of the stripe enhancers and that interactions between enhancers can generate novel patterns of gene expression.

Animals↗

PubMed1994

Idiopathic, herpetic, and HIV-associated facial nerve palsies: abnormal MR enhancement patterns.

PURPOSE: To determine specific criteria that can be used to define normal versus abnormal MR contrast enhancement of the facial nerve. METHODS: Twenty-three patients with acute unilateral inflammatory peripheral facial nerve palsy were examined on a 1.5-T MR using multiplanar T1-weighted spin-echo sequences before and after injection of gadopentetate dimeglumine. These MR patterns were compared with those of healthy control subjects. RESULTS: The normal facial nerve usually showed a mild to moderate enhancement of the geniculate ganglion and the tympanic-mastoid segment. The intracanalicular-labyrinthine segment did not enhance. All patients showed abnormal enhancement of the distal intracanalicular and the labyrinthine segment. An intense enhancement could be observed in the geniculate ganglion and the proximal tympanic segment, especially in herpetic palsy. Associated enhancement of the vestibulocochlear nerve was seen in herpetic and idiopathic palsy. Enhancement of the inner ear structures was detected only in herpetic palsy. CONCLUSIONS: Abnormal contrast enhancement of the distal intracanalicular and the labyrinthine facial nerve segment is observed in all patients and is the only diagnostically reliable MR feature proving an inflammatory facial nerve lesion. The intense enhancement of the geniculate ganglion and the proximal tympanic segment is possibly correlated with the reactivation of the latent infection in the sensory ganglion. The abnormal enhancement results from breakdown of the blood-peripheral nerve barrier and/or from venous congestion in the venous plexuses of the epi- and perineurium.

Acquired Immunodeficiency Syndrome↗

PubMed1993

Direct evidence that interferon-beta mediates enhanced HLA-class I expression in measles virus-infected cells.

Viral infection results in enhancement of HLA-class I expression in a number of cell types, including glial cells, which normally do not express these molecules. This enhancement may occur through a direct interaction between a viral component and the HLA-class I gene or indirectly through virus-induced soluble factors produced by infected cells. These include cytokines such as IFN-gamma, IFN-alpha/beta, and TNF-alpha, known to enhance class I expression. Measles virus (MV) infection of a human glioma cell line (U-105 MG) and of primary human umbilical vein endothelial cells enhances the expression of HLA-class I molecules on these cells. The enhancement of HLA-class I is dependent on infectious virus, as antibody-neutralized MV has no effect on class I expression. In this study, we demonstrate the presence of an HLA-class I-enhancing factor in supernatants from MV-infected cells. The supernatant class I-enhancing factor is not IFN-gamma, IFN-alpha, or TNF-alpha because MV-infected cells did not produce measurable levels of these cytokines as detected by immunoassay or polymerase chain reaction. In contrast, IFN-beta is produced by the infected cells and the supernatant class I-enhancing factor could be entirely neutralized by antibodies to IFN-beta, but not antibodies to IFN-alpha, TNF-alpha, or non-immune sera. Furthermore, preincubation of cells with neutralizing antibodies to IFN-beta prior to infection blocked MV enhancement of HLA-class I completely in the U-105 MG cells and by as much as 74% in the umbilical vein endothelial cells. The results of these experiments provide direct evidence that enhanced HLA-class I expression in MV-infected cells is mediated primarily by IFN-beta.

Cells, Cultured↗

PubMedDate not supplied

Spinal nerve enhancement with Gd-DTPA: MR correlation with the postoperative lumbosacral spine.

PURPOSE: To search for a probable source of the recurrent signs and symptoms associated with lumbosacral postsurgical syndrome on intravenous gadolinium-enhanced MR. METHODS: A retrospective study of 120 patients with recurrent symptomatology following lumbar disk surgery was carried out with spin-echo MR pre- and postenhancement with gadopentetate dimeglumine (0.1 mmol/kg). In addition, 10 asymptomatic subjects were evaluated at least 6 months postoperatively using the same imaging protocol. RESULTS: 21.6% of the symptomatic subjects (N = 26) had enhancement of one or more spinal nerve root. This enhancement was focal or multisegmental, and involved single or multiple nerve roots. The abnormal neural enhancement was associated with otherwise isolated epidural fibrosis in 88.5%, and with herniated nucleus pulposus in the remaining 11.5%. The overall clinical correlation of single root enhancement with a monoradiculopathy and multiroot enhancement with a polyradiculopathy was 95.7%. However, 21.7% of these same cases also showed additional nerve root enhancement that did not have an overt clinical correlation. All of these latter patients were imaged relatively early in the postoperative period (5 days to 8 months). The 10 patients in the asymptomatic group all manifested degrees of postoperative epidural scarring on MR, but no abnormal radicular enhancement or other associated pathology. CONCLUSION: In the chronic postoperative phase (more than 6 to 8 months), the presence of radicular enhancement on MR imaging in symptomatic individuals, and its absence in asymptomatic subjects, suggests that neural enhancement serves as a marker for active neural pathology that may in certain individuals be related temporally to the signs and symptoms associated with the lumbosacral postsurgical syndrome.

Adult↗

PubMedDate not supplied

Enhanced and unenhanced MR with magnetization transfer in multiple sclerosis.

PURPOSE: To evaluate the use of magnetization transfer and the apparent enhancement of lesions on contrast-enhanced MR images in patients with multiple sclerosis. METHODS: Contrast-enhanced T1-weighted spin-echo MR images obtained in 20 patients with relapsing-remitting multiple sclerosis, with and without magnetization transfer, were evaluated to determine the number of enhancing plaques. Comparison was made with unenhanced T1-weighted magnetization transfer images. Contrast-to-noise ratios were obtained for these lesions on both the enhanced and unenhanced magnetization transfer T1-weighted spin-echo MR images. RESULTS: Ten plaques were considered enhancing only when the enhanced magnetization transfer T1-weighted images (11% or more) were used; however, they were all hyperintense on unenhanced T1-weighted magnetization transfer images. The contrast-to-noise ratios of these lesions were 16.52 for the enhanced images and 15.65 for the unenhanced images. The two values were not statistically different. CONCLUSIONS: In patients with multiple sclerosis, examination with contrast-enhanced magnetization transfer MR images alone may overestimate the number of enhancing plaques.

Brain↗

PubMed2005

Characterization of the proximal enhancer element and transcriptional regulatory factors for murine recombination activating gene-2.

Recombination-activating gene (RAG)-1 and RAG-2 are essential for V(D)J recombination and are expressed specifically in lymphoid cells. We previously identified two putative enhancer elements, the proximal and distal enhancers, located at -2.6 and -8 kb, respectively, 5' upstream of mouse RAG-2, and characterized the distal enhancer element in detail. In this study, to characterize the proximal enhancer in vitro as well as in vivo, we first defined a 170-bp core enhancer element within the proximal enhancer (Ep) and determined its activity in various cells. Ep conferred enhancer activity only in B-lymphoid cell lines, but not in T- or non-lymphoid cell lines. Analysis of the transgenic mice carrying an EGFP reporter gene linked with Ep revealed that Ep activated the transcription of the reporter gene in bone marrow and spleen, but not in thymus or non-lymphoid tissues. Ep was active in both B220+IgM- and B220+IgM+ subpopulations in the bone marrow and in the B220+ subpopulation in the spleen. Using electrophoretic mobility shift assays and mutational assays, we found that Ikaros and CCAAT/enhancer binding protein cooperatively bind Ep and function as the transcription factors responsible for B cell-specific enhancer activity. These results demonstrate the role of Ep as a cis-regulatory enhancer element for RAG-2-specific expression in B-lymphoid lineages.

Animals↗