Biomedical subjects

W Li

Publications and source records attributed to W Li.

At least 1,135 records · Page 63Linked to original sources

PubMed1994

The influence of a stationary single line in darkness on the visual perception of eye level.

The angle of pitch of a visual field consisting of only a single vertical, 64 degrees-long, eccentrically-located line in otherwise total darkness influences the elevation of a target set to appear at eye level (VPEL). The influence changes linearly with the magnitude of pitch over the range from -30 degrees to +20 degrees. The average slope of the VPEL-vs-pitch function is +0.53. The influence on VPEL of a pitched visual field consisting of two parallel vertical lines is slightly greater (slope = +0.56), and the influence of the pitch of a complexly-structured well-illuminated pitched room is slightly greater yet (slope = +0.63). The pitch of a frontoparallel plane containing one horizontal line has a small influence on VPEL (slope = +0.08); the influence with two horizontal lines is slightly greater (slope = +0.18). The slope of the VPEL-vs-pitch function differs among individual subjects but is linear for each of the eight subjects. A great deal of consistency is manifested by individual subjects across all of the visual fields: an individual with a steep slope with one visual field tends to have a steep slope with all visual fields. The individual's characteristic response in total darkness is strongly correlated with the response to an erect well-illuminated visual field. The significant aspect of the pitched-from-vertical line stimulus is the change in orientation of its retinal image. An additional experiment with a small pupil (pilocarpine) indicates that cues related to other retinal gradients or to accommodation play no role in the influence of the visual field on VPEL. The experiments provide support for treating the visual influence on VPEL by means of the Great Circle Model.

Convergence, Ocular↗

PubMed1994

Spatial summation among coextensive and parallel line segments across wide separations (50 degrees): egocentric localization and the great circle model.

The elevation at which an observer sets a target to appear at eye level (VPEL) is systematically related to the angle of pitch of the visual field and is only a little less for a visual field consisting of a single line in darkness than for a complexly structured field [Matin and Li (1994a) Vision Research, 34, 311-330]. Three experiments are described which measure the quantitative characteristics of spatial summation among individual pitched-from-vertical line segments that control the visual influence on VPEL. As the length of a one-line stimulus increased from 0 degrees to 64 degrees the slope of the VPEL-vs-pitch function (S) increased from 0 to +0.56 along a negatively accelerated exponential with a 15.1 degree space constant. The combined influence on S of two simultaneously-presented, parallel, pitched-from-vertical lines, horizontally separated by 50 degrees, is slightly greater than the combined influence of two coextensive line segments with the same total length. S saturates at a locus that lies beyond any separate neural locus for the processing of the individual line. The results are effectively treated by the Great Circle Model (GCM) which converts stimulus "nonlocality" to neural "locality" by mapping the intersections of the images of parallel line sets in a spherical approximation of the eye on to a set of neural nodes. A neurophysiological realization of GCM is compatible with mediation by the long horizontal connections afferent to layer 6 of primary visual cortex (V1). The combination of visual influences with extraretinal information is compatible with the characteristics of posterior parietal cortex downstream from V1. The increase in the effectiveness of a line with increase in length is in accord with a more general division between the utilization of long lines for egocentric orientation and short lines for figural processes; end-inhibition from elongated layer 6 cells (which process long lines) onto layer 4 cells (which process short lines) in V1 may provide a means for separating the two streams of information.

Darkness↗

PubMed1994

Extensive integration field beyond the classical receptive field of cat's striate cortical neurons--classification and tuning properties.

Length- and width-summation curves of striate cortex cells revealed that there exist facilitatory, inhibitory or disinhibitory integration fields (IF) beyond the sides and ends of the classical receptive field (RF). The extent of the IFs is most frequently 2-5 times the size of the RFs. The tuning properties of IFs were studied using an annular surround grating patch while an optimal centre patch was placed at the excitatory RF to continuously activate the cell. The results show that, for most cells, the orientation, spatial frequency and speed tuning of the IFs were similar to, but broader than, the tuning of the RF, whereas the direction selectivity of the IF was not as pronounced as that of the RF. The possible functional significance of the IF is discussed.

Animals↗

PubMed1994

Bovine NK and LAK susceptibility is independent of class I expression on B lymphoblastoid variants.

Numerous tumors express low or no class I molecules, resulting in their avoidance of recognition and destruction by different effector cells of the immune system. Using a parent and two MHC class I mutant cell lines, we have tested the role of MHC class I molecules in natural killer (NK) cells, lymphokine activated killer (LAK) cells and cytotoxic T lymphocytes (CTLs). Both class I expressing parent cells and class I loss mutants were insensitive to NK cell lysis as assayed, regardless of the amount of class I molecules on the target cell surface. However, LAK cells demonstrated higher cytolysis on these target cells than NK cells, suggesting different mechanisms of target cell recognition or different levels of lytic activity by these two effector cell populations. Up-regulation of class I expression on the target surface by gamma interferon (gamma-IFN) had little influence on NK and LAK susceptibility, indicating there was no correlation between class I expression and bovine NK or LAK cytolysis. However, allogeneic CTLs mediated a lytic pattern distinct from NK and LAK cells, in which target sensitivity to allogeneic CTLs correlated with the amount of class I molecules expressed on the cell surface. Additionally, effector-target cell conjugation studies demonstrated that target class I expression was not involved in NK and LAK cells binding to targets. These results demonstrate that NK and LAK cytolysis of these two class I mutant cell lines is independent of the amount of class I molecules expressed on the target cell surface.

Animals↗

PubMed1994

Reduction of class I expression in a bovine B-lymphoblastoid cell line is locus specific.

A bovine B-lymphoblastoid cell line, BL3.1.2, defective in MHC class I expression was isolated following gamma irradiation and immunoselection of a previously mutated cell, BL3.1. Flow microfluorimetry demonstrated that BL3.1.2 cells expresed reduced amount of class I molecules on the cell surface when compared with the parent cells. 2D gel electrophoresis showed that two less class I gene products were synthesized by BL3.1.2 cells than the parent cells. However, no detectable RFLP difference was revealed between this mutant and the parent cell lines as analyzed by Southern blots using bovine class I cDNA and locus-specific oligonucleotide probes, suggesting no major deletions, insertions, or translocations within class I genes. Northern blot analysis, using class I cDNA probes, revealed a marked reduction of class I mRNA in BL3.1.2 cells. RNA unblots, probed with loci-specific oligonucleotides, and slot blot analysis demonstrated that absence of class I gene transcription was locus specific. This finding indicates there is separate regulation of each class I locus in bovine cells. Furthermore, recombinant IFN-gamma upregulated class I gene expression on the BL3.1.2 cells, as indicated by flow cytometry and slot blot analysis. These findings indicate that the locus-specific MHC class I gene was functionally downregulated in its expression. The silent class I gene could be activated by cytokines known to activate the cis-interferon-responsive element for subsequent transcription and translation of the newly synthesized class I RNA.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

Temporal averaging for quantification of lumen dimensions in intravascular ultrasound images.

Quantitative analysis of arterial dimensions from high frequency intravascular ultrasound images (30 MHz) may be hampered by strong blood scattering. Replacement of blood by saline is one method to provide a clear view of the arterial lumen; another method is that of temporal averaging of successive ultrasound images. The accuracy of this latter method was tested by comparing the lumen area measurements on the temporal-averaged image, with the data of the same cross-section obtained from the single-frame and saline-filled images. The mean lumen area measured on the temporal-averaged images was similar to that measured on the single-frame images (mean difference: -0.02 +2- 1.16 mm2; p = ns). The mean lumen area of the saline-filled images was 8% larger than the values obtained from the temporal-averaged and single-frame images (mean difference: -1.14 +/- 0.85 mm2, p < 0.05), probably due to the difference in sound velocity between saline and blood. Intraobserver variation in the averaging method were 2.4 times smaller than the measurements of the single-frame images and close to the data obtained by saline injection (variation coefficient: single-frame: 8.8%; temporal-averaged: 3.6%; saline-filled: 2.9%). It is concluded that analysis from temporal-averaged images is more efficient, enabling accurate and reproducible measurement of the luminal dimensions from images containing blood scattering echoes. This technique is suitable to replace the laborious saline injection method and facilitates off-line quantitative analysis.

Aged↗

PubMed1994

Biological function of PDGF-induced PI-3 kinase activity: its role in alpha PDGF receptor-mediated mitogenic signaling.

The tyrosine phosphorylation sites in the human alpha PDGF receptor (alpha PDGFR) required for association with PI-3 kinase have been identified as tyrosines 731 and 742. Mutation of either tyrosine substantially reduced PDGF-induced PI-3 kinase activity but did not impair the receptor-mediated mitogenic response. We sought to determine whether PDGF-induced PI-3 kinase activity could be further ablated so as to exclude a low threshold requirement for PDGFR signal transduction. Thus, we mutated both tyrosine 731 and 742 and expressed the double mutant (Y731F/Y742F) in 32D hematopoietic cells. In such transfectants, PDGF induced no detectable receptor-associated or anti-P-Tyr recoverable PI-3 kinase activity. Under the same conditions, neither mobility shift of raf-1 nor tyrosine phosphorylation of either PLC gamma or MAP kinase was impaired. 32D transfectants expressing the double mutant showed wild-type alpha PDGFR levels of mitogenic and chemotactic responses to PDGF. To examine the effect of the double mutation in cells that normally respond to PDGF, we generated chimeras in which the cytoplasmic domains of wild-type alpha PDGFR, Y731F, and Y731F/Y742F were linked to the extracellular domain of colony-stimulating factor-1 (CSF-1) receptor (fms). After introduction of the chimeric receptors into mouse NIH/3T3 fibroblasts, the ability of CSF-1 to stimulate growth of these transfectants was examined. Our data show that all these chimeric receptors exhibited similar abilities to mediate CSF-1-stimulated cell growth. These findings lead us to conclude that PDGF-induced PI-3 kinase activity is not required for PDGF-stimulated mitogenic pathway in both NIH/3T3 fibroblasts and 32D hematopoietic cells.

3T3 Cells↗

PubMed1994

The human cytomegalovirus UL100 gene encodes the gC-II glycoproteins recognized by group 2 monoclonal antibodies.

In human cytomegalovirus (HCMV) the envelope glycoprotein complexes designated gC-II contain two immunologically and biochemically distinct glycoproteins. Monoclonal antibodies (MAbs) recognizing the gC-II glycoproteins have been divided into two groups based on the M(r) of the glycoproteins they recognize. We have now identified the HCMV UL100 gene as the gene encoding the gC-II glycoprotein recognized by the Group 2 MAbs. To do this, gC-II complexes were immunoaffinity purified and cleaved with cyanogen bromide (CNBr). CNBr peptides were separated by reverse phase high performance liquid chromatography (RPHPLC). Amino acid sequences which matched sequences found in the protein encoded by the HCMV UL100 gene were obtained from three purified peptides. To confirm the assignment we made synthetic peptides using amino acid sequence from the carboxyl terminus of the protein encoded by the UL100 gene. These peptides were used to make murine antibodies. The anti-UL100 antibodies immunoprecipitated gC-II complexes and were reactive with gC-II glycoproteins recognized by Group 2 MAbs in Western blotting. Several overlapping UL100 fusion proteins were expressed in E. coli. Only one of these fusion proteins was recognized by gC-II Group 2 MAbs. None of these UL100 fusion proteins were recognized by gC-II Group 1 MAbs. These data showed that the UL100 gene encoded the gC-II glycoprotein recognized by the Group 2 MAbs and that the epitope recognized by these antibodies was located between amino acids 315 to 372 at the carboxyl terminus.

Amino Acid Sequence↗

PubMed1994

Cyclic AMP stimulates K+ channel activity in mesophyll cells of Vicia faba L.

Whole-cell patch-clamp recordings from Vicia faba mesophyll protoplasts reveal that outward K+ current is increased in a dose-dependent fashion by intracellular application of cAMP. The enhancement of the outward current by cAMP is specific and it cannot be mimicked by a series of nucleotides that includes AMP, cGMP, and GMP. The enhancement is evoked by micromolar concentrations of cAMP in the presence of the phosphodiesterase inhibitor 3-isobutyl-1-methyl-xanthine. PKI or Walsh inhibitor, a specific peptide inhibitor of cAMP-dependent protein kinase (PKA), inhibits the outward K+ current. Adenosine 3',5'-phosphothioate, a competitive inhibitor of PKA, has a similar effect. Conversely, the catalytic subunit of PKA (cAMP independent) from bovine brain enhances the magnitude of the outward K+ current in the absence of added cAMP. Our results indicate that cAMP modulates K+ channel activity in mesophyll cells and suggest that this modulation occurs through a cAMP-regulated protein kinase.

1-Methyl-3-isobutylxanthine↗

PubMed1994

Evidence for protein phosphatase 1 and 2A regulation of K+ channels in two types of leaf cells.

Ion channels control ion fluxes across membranes, membrane potential, and signal transduction between and within cells. Protein kinases and phosphatases are important regulators involved in stimulus-response coupling in eukaryotic organisms. We have identified in extracts of Vicia faba leaf cells protein phosphatase activities inhibited by okadaic acid (OA) and calyculin A (CA), two inhibitors of protein phosphatases 1 and 2A. Using whole-cell patch-clamp techniques, we have demonstrated that inward K+ currents in guard cells are inhibited by nanomolar concentrations of OA or CA, whereas outward K+ currents are not affected. However, the same inhibitors enhance the magnitude of outward K+ currents in mesophyll cells. A phosphatase antagonist, adenosine-5'-O-(3-thiotriphosphate), has an effect similar to OA and CA on outward K+ currents in mesophyll cells. Our findings suggest that protein phosphatases 1 and/or 2A play different physiological roles in modulating the activity of K+ channels in mesophyll cells and guard cells.

Adenosine Triphosphate↗

PubMed1994

A Saccharomyces cerevisiae mutant with echinocandin-resistant 1,3-beta-D-glucan synthase.

A novel, potent, semisynthetic pneumocandin, L-733,560, was used to isolate a resistant mutant in Saccharomyces cerevisiae. This compound, like other pneumocandins and echinocandins, inhibits 1,3-beta-D-glucan synthase from Candida albicans (F.A. Bouffard, R.A. Zambias, J. F. Dropinski, J.M. Balkovec, M.L. Hammond, G.K. Abruzzo, K.F. Bartizal, J.A. Marrinan, M. B. Kurtz, D.C. McFadden, K.H. Nollstadt, M.A. Powles, and D.M. Schmatz, J. Med. Chem. 37:222-225, 1994). Glucan synthesis catalyzed by a crude membrane fraction prepared from the S. cerevisiae mutant R560-1C was resistant to inhibition by L-733,560. The nearly 50-fold increase in the 50% inhibitory concentration against glucan synthase was commensurate with the increase in whole-cell resistance. R560-1C was cross-resistant to other inhibitors of C. albicans 1,3-beta-D-glucan synthase (aculeacin A, dihydropapulacandin, and others) but not to compounds with different modes of action. Genetic analysis revealed that enzyme and whole-cell pneumocandin resistance was due to a single mutant gene, designated etg1-1 (echinocandin target gene 1), which was semidominant in heterozygous diploids. The etg1-1 mutation did not confer enhanced ability to metabolize L-733,560 and had no effect on the membrane-bound enzymes chitin synthase I and squalene synthase. Alkali-soluble beta-glucan synthesized by crude microsomes from R560-1C was indistinguishable from the wild-type product. 1,3-beta-D-Glucan synthase activity from R560-1C was fractionated with NaCl and Tergitol NP-40; reconstitution with fractions from wild-type membranes revealed that drug resistance is associated with the insoluble membrane fraction. We propose that the etg1-1 mutant gene encodes a subunit of the 1,3-beta-D-glucan synthase complex.

Anti-Bacterial Agents↗

PubMed1994

The bovine papillomavirus type 1 E5 transforming protein specifically binds and activates the beta-type receptor for the platelet-derived growth factor but not other related tyrosine kinase-containing receptors to induce cellular transformation.

The 44-amino-acid E5 protein of bovine papillomavirus type 1 is a highly hydrophobic protein which appears to transform cells through the activation of growth factor receptors. To investigate the specificity of E5-growth factor receptor interactions required for mitogenic signaling, we utilized a nontumorigenic, murine myeloid cell line (32D) which is strictly dependent on interleukin-3 (IL-3) for sustained proliferation in culture. This IL-3 dependence can be functionally substituted by the expression of a variety of surrogate growth factor receptors and the addition of the corresponding ligand. Several receptor cDNAs for the alpha- and beta-type platelet-derived growth factor receptors [alpha PDGFR and beta PDGFR], the epidermal growth factor receptor, and the colony-stimulating factor 1 receptor) were transfected into 32D cells constitutively expressing the E5 protein to test for IL-3-independent growth. Only beta PDGFR was capable of abrogating the IL-3 dependence of 32D cells. The proliferative signal induced by the coexpression of beta PDGFR and E5 was accompanied by stable complex formation between these proteins, constitutive tyrosine phosphorylation of the receptor, and tumorigenicity in nude mice. The lack of cooperative interaction between E5 and the epidermal growth factor receptor, the colony-stimulating factor 1 receptor, and the highly related alpha PDGFR was paralleled by the inability of E5 to bind to these receptors and failure to increase receptor tyrosine phosphorylation. Thus, these data indicate that the ability of E5 to induce sustained proliferation and transformation of 32D cells is a direct consequence of specific interaction between the E5 protein and the beta PDGFR signaling complex and the subsequent stimulation of receptor tyrosine phosphorylation.

Animals↗

PubMed1994

A new function for a phosphotyrosine phosphatase: linking GRB2-Sos to a receptor tyrosine kinase.

Autophosphorylated growth factor receptors provide binding sites for the src homology 2 domains of intracellular signaling molecules. In response to epidermal growth factor (EGF), the activated EGF receptor binds to a complex containing the signaling protein GRB2 and the Ras guanine nucleotide-releasing factor Sos, leading to activation of the Ras signaling pathway. We have investigated whether the platelet-derived growth factor (PDGF) receptor binds GRB2-Sos. In contrast with the EGF receptor, the GRB2 does not bind to the PDGF receptor directly. Instead, PDGF stimulation induces the formation of a complex containing GRB2; 70-, 80-, and 110-kDa tyrosine-phosphorylated proteins; and the PDGF receptor. Moreover, GRB2 binds directly to the 70-kDa protein but not to the PDGF receptor. Using a panel of PDGF beta-receptor mutants with altered tyrosine phosphorylation sites, we identified Tyr-1009 in the PDGF receptor as required for GRB2 binding. Binding is inhibited by a phosphopeptide containing a YXNX motif. The protein tyrosine phosphatase Syp/PTP1D/SHPTP2/PTP2C is approximately 70 kDa, binds to the PDGF receptor via Tyr-1009, and contains several YXNX sequences. We found that the 70-kDa protein that binds to the PDGF receptor and to GRB2 comigrates with Syp and is recognized by anti-Syp antibodies. Furthermore, both GRB2 and Sos coimmunoprecipitate with Syp from lysates of PDGF-stimulated cells, and GRB2 binds directly to tyrosine-phosphorylated Syp in vitro. These results indicate that GRB2 interacts with different growth factor receptors by different mechanisms and the cytoplasmic phosphotyrosine phosphatase Syp acts as an adapter between the PDGF receptor and the GRB2-Sos complex.

3T3 Cells↗

PubMed1994

Stimulation of the platelet-derived growth factor beta receptor signaling pathway activates protein kinase C-delta.

The murine myeloid progenitor cell line 32D was recently shown to undergo monocytic differentiation when protein kinase C-delta (PKC-delta) was overexpressed and activated by 12-O-tetradecanoylphorbol-13-acetate (TPA) (H. Mischak, J.H. Pierce, J. Goodnight, M.G. Kazanietz, P.M. Blumberg, and J.F. Mushinski, J. Biol. Chem. 268:20110-20115, 1993). Tyrosine phosphorylation of PKC-delta occurred when PKC-delta-transfected 32D cells were stimulated by TPA (W. Li, H. Mischak, J.-C. Yu, L.-M. Wang, J.F. Mushinski, M.A. Heidaran, and J.H. Pierce, J. Biol. Chem. 269:2349-2352, 1994). In order to elucidate the role played by PKC-delta in response to activation of a receptor tyrosine kinase, we transfected platelet-derived growth factor beta receptor (PDGF-beta R) alone (32D/PDGF-beta R) or together with PKC-delta (32D/PDGF-beta R/PKC-delta) into 32D cells. NIH 3T3 cells which endogenously express both PDGF-alpha R and PDGF-beta R were also transfected with PKC-delta (NIH 3T3/PKC-delta). Like TPA treatment, PDGF-BB stimulation caused striking phosphorylation of PKC-delta in vivo and translocation of some PKC-delta from the cytosol fraction to the membrane fraction in both cell systems. Some of the phosphorylation induced by PDGF-BB treatment was found to be on a tyrosine residue(s). Tyrosine-phosphorylated PKC-delta was observed only for the membrane fraction after stimulation with PDGF-BB or TPA. The enzymatic activity of PKC-delta in the membrane fraction also increased after stimulation with TPA or PDGF, providing a positive correlation between PKC-delta tyrosine phosphorylation and its activation. Overnight treatment of 32D/PDGF-beta R/PKC-delta cells with PDGF-BB induced monocytic differentiation as judged by an increase in expression of cell surface macrophage differentiation markers. PDGF-BB had much weaker effects on 32D/PDGF-beta R cell differentiation, suggesting that increased PKC-delta expression enhanced monocytic differentiation. These results indicate that PKC-delta is a downstream molecule in the PDGFR signaling pathway and may play a pivotal role in PDGF-beta R-mediated cell differentiation.

Animals↗

PubMed1994

Interferons block protein kinase C-dependent but not-independent activation of Raf-1 and mitogen-activated protein kinases and mitogenesis in NIH 3T3 cells.

Interferons (IFNs) exert antiproliferative effects on many types of cells. The underlying molecular mechanism, however, is unclear. One possibility is that IFNs block growth factor-induced mitogenic signaling, which involves activation of Ras/Raf-1/MEK/mitogen-activated protein kinase. We have tested this hypothesis by using HER14 cells (NIH 3T3 cell expressing both platelet-derived growth factor [PDGF] and epidermal growth factor [EGF] receptors) as a model system. Our studies showed that IFNs (alpha/beta and gamma) blocked PDGF-and phorbol ester- but not EGF-stimulated DNA synthesis and cell proliferation. While the ligand-stimulated receptor tyrosine phosphorylation and interaction with downstream signaling molecules, such as GRB2, were not affected, IFNs specifically blocked PDGF- and phorbol ester- but not EGF-stimulated activation of Raf-1, mitogen-activated protein kinases, and tyrosine phosphorylation of an unidentified 34-kDa protein. This inhibition could be detected as early as 5 min after IFN treatments and was insensitive to cycloheximide, indicating that de novo protein synthesis is not required. The IFN-induced inhibition acted upstream of Raf-1 kinase and downstream of diacyl glycerol/phorbol ester, suggesting that protein kinase C (PKC) is the potential primary target. Consistently, downregulation of PKC by chronic phorbol myristate acetate treatment or inhibition of PKC by H7 and staurosporine blocked PDGF- and phorbol myristate acetate- but not EGF-induced signaling and DNA synthesis. Moreover, incubating cells with antisense oligodeoxyribonucleotides of PKC delta eliminated production of PKC delta protein and specifically blocked PDGF- but not EGF-stimulated mitogenesis in these cells. Thus, these studies have elucidated a major difference in the early events of EGF-and PDGF-stimulated signal transduction and, more importantly, revealed a novel mechanism by which IFNs may execute their antiproliferative function.

3T3 Cells↗

PubMed1994

Auxotonic loading and airway smooth muscle shortening.

Isometric and isotonic contractions represent two extremes in loading regimens that can be imposed on a contracting smooth muscle preparation in vitro. Under physiological conditions, however, it is likely that smooth muscle in hollow organs contracts against auxotonic loads, the magnitude of which is a function of muscle shortening. Therefore, attempts to determine physiologically significant contractile properties of smooth muscle should be made under auxotonic loading conditions. An electronic loader was built to provide four auxotonic loading modes: linear, logarithmic, sigmoidal, and exponential. These shortening-dependent auxotonic loads were imposed on an actively shortening canine tracheal smooth muscle. Results confirmed that (i) active force generated by the muscle is load dependent but that (ii) at the same load borne by the muscle in its steady state, i.e., at the same maximum force generated by the muscle, the maximum shortenings under different loading modes were significantly altered. The shortening was maximal under the exponential loading mode, which provided the smallest load in the early phase of contraction, while it was the least under the logarithmic loading mode, which provided the greatest load in that phase. We concluded that the shortening achieved by an airway smooth muscle was a function not only of the magnitude of the final load imposed on the muscle but, more importantly, of the time course of loading.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

Contrast-enhanced echo-planar MR imaging of myocardial perfusion: preliminary study in humans.

PURPOSE: To evaluate the usefulness of T1- and T2*-weighted echo-planar magnetic resonance (MR) imaging in the assessment of cardiac perfusion. MATERIALS AND METHODS: Sixteen subjects underwent MR imaging. Fifteen subjects were healthy volunteers and one had coronary artery disease. T2*-weighted echo-planar imaging with free induction decay was performed in 11 subjects and T1-weighted inversion-recovery spin-echo echo-planar imaging was performed in five. Images were obtained before and after administration of gadopentetate dimeglumine. RESULTS: The contrast-to-noise ratio for pre- and postcontrast T2*-weighted images obtained with an echo time of 16 msec (n = 8) was -9.9 +/- 3.4, and the contrast enhancement ratio was -0.37 +/- 0.07. The values for T2*-weighted images obtained with an echo time of 30 msec (n = 3) were -9.5 +/- 6.8 and 0.44 +/- 0.02, respectively. For T1-weighted echo-planar imaging, the values were 26.7 +/- 8.0 and 4.6 +/- 2.8, respectively. CONCLUSION: Inversion-recovery spin-echo echo-planar imaging provides excellent temporal resolution, myocardial detail, and myocardium-blood pool contrast, with minimal artifact. It is presently the technique of choice for the MR imaging evaluation of myocardial perfusion.

Adult↗

PubMed1994

Hepatic hemangiomas: a multi-institutional study of appearance on T2-weighted and serial gadolinium-enhanced gradient-echo MR images.

PURPOSE: To define the appearance of hepatic hemangiomas on T2-weighted and serial gadolinium-enhanced gradient-echo magnetic resonance (MR) images. MATERIALS AND METHODS: In four university hospitals, with 1.0- or 1.5-T MR imaging, T2-weighted and T1-weighted gradient-echo images were obtained in 66 adult patients before and at 1, 45, and 90 seconds and 10 minutes after injection of a gadolinium chelate. Hemangiomas were categorized as small (< 1.5-cm-diameter), medium (1.5-5.0-cm), and large (> 5.0-cm) tumors. RESULTS: In all, 154 hemangiomas were depicted (81 small, 56 medium, and 17 large tumors). All 154 lesions were hyperintense on T2-weighted images. Three patterns of contrast enhancement were observed: (a) uniform enhancement at 1 second (35 of 81 small lesions and no medium or large lesions), (b) peripheral nodular enhancement progressing centripetally to uniform enhancement (75 of all 154 lesions), and (c) peripheral nodular enhancement with persistent hypointensity centrally (44 of all 154 lesions, including 16 of 17 large lesions). CONCLUSION: Three patterns of enhancement of hemangiomas were observed. High signal intensity on T2-weighted images provided complementary information.

Adult↗