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Biomedical subjects

C E Hayes

Publications and source records attributed to C E Hayes.

At least 55 records · Page 3Linked to original sources
PubMed1994

In vitamin A deficiency multiple mechanisms establish a regulatory T helper cell imbalance with excess Th1 and insufficient Th2 function.

In hypovitaminosis A, Ab-mediated immunity is severely impaired. We reported that Trichinella spiralis infection stimulates a strong Th2 cell response in control mice but in vitamin A-deficient mice it stimulates a strong Th1 cell response. Here we investigated the immunobiologic mechanisms underlying this shift from a Th2- to a Th1-dominated response. A kinetic analysis showed that the Th1 cells developed first and IFN-gamma secretion predominated in deficient mice, whereas the Th2 cells developed later and IL-5 and IL-10 secretion predominated in control mice. The IFN-gamma-secreting cell frequencies were the same but cells from deficient mice secreted IFN-gamma sixfold faster than cells from control mice, and retinoic acid addition in vitro decreased that rate 50%. In contrast, the IL-5-secretion rates were the same but the IL-5-secreting cell frequency was lower in deficient mice than in controls, and retinoic acid addition in vitro doubled this frequency independently of its inhibitory effect on IFN-gamma. The APC from deficient mice stimulated greater IFN-gamma release than control APC and retinoic acid addition in vitro decreased this activity 50%. Together these results identify at least three vitamin A activities that balance Th1 and Th2 functions, down-regulating Th1 cell IFN-gamma secretion directly, decreasing activated APC function, and promoting Th2 cell growth and/or differentiation. In this system and perhaps others, the imbalance between regulatory Th1 and Th2 cells is one mechanism underlying poor Ab-mediated immunity in hypovitaminosis A.

Animals↗
PubMed1994

The fornix in patients with seizures caused by unilateral hippocampal sclerosis: detection of unilateral volume loss on MR images.

OBJECTIVE: Because some of the axons of the fornix originate in the pyramidal cells of the hippocampus, we hypothesize that neuronal loss within the hippocampus may result in wallerian degeneration and subsequent atrophy of the ipsilateral fornix. Using high-resolution MR imaging, we evaluated the size of the fornix in patients who had lateralizing partial complex temporal lobe seizures after unilateral hippocampal sclerosis. The expectation is that unilateral forniceal atrophy will provide an additional, objective imaging criterion for determining the side of seizure involvement. MATERIALS AND METHODS: We retrospectively reviewed preoperative MR images of 13 patients with temporal lobe epilepsy who subsequently had unilateral hippocampal sclerosis proved surgically. The images were obtained with specially designed bilateral phased-array coils that permitted high-resolution (512 x 512, 16-cm field of view) T2-weighted fast spin-echo imaging of oblique coronal sections. The width of each rostral crus of the fornix was measured by three neuroradiologists who did not know the patients' history and surgical findings, and consensus measurements were obtained. The side with the smaller fornix was interpreted as abnormal. All 13 patients had lateralizing findings on EEG, unilateral anterior temporal lobectomy, and histologic findings of hippocampal sclerosis. RESULTS: The fornix was smaller on the side of hippocampal sclerosis in 12 (92%) of 13 patients. The percentage of asymmetry between the fornices (smallest/largest x 100) varied from 41% to 82% (mean, 68%). CONCLUSION: Our experience indicates that volume loss in the ipsilateral crus of the fornix can be seen on MR images in patients with unilateral hippocampal sclerosis. The size of the fornices should be analyzed in all patients being examined for temporal lobe epilepsy, as asymmetry in the size of the fornices may reveal the side of hippocampal sclerosis. Such knowledge can assist in the preoperative workup of patients with intractable temporal lobe epilepsy related to hippocampal sclerosis.

Atrophy↗
PubMed1993

Magnetic resonance neurography.

Radiological methods exist for generating tissue-specific images of bone, vessels, lymphatics, abdominal viscera, and the central nervous system, but there has been no reliable means to generate a clinical image of a nerve. We present the first "image neurogram" and report a method for producing such images by use of commercial magnetic resonance imaging systems. The image depicts a human nerve in situ in relation with a nerve graft, wherein the nerve is rendered in isolation much like a vessel appears in isolation in a subtraction angiogram.

Adult↗
PubMed1993

An adjustable RF coil loading device.

This paper describes an adjustable loading device that can substitute for the tissue losses of various sized patients in a whole-body MR imager. It resembles a lowpass birdcage resonator but with resistors replacing the capacitors on the cylindrical surface. Power dissipated is a monotonic function of the total surface conductance of the loader. The loader can be used in conjunction with a low loss water filled phantom to measure signal-to-noise ratios (SNR). The impact on measured SNR due to screening by the loader and changing the phantom size or composition are also briefly discussed.

Artifacts↗
PubMed1993

Temporal lobes: surface MR coil phased-array imaging.

The authors describe a four-coil surface phased-array coil for magnetic resonance (MR) imaging of the temporal lobes. On the basis of measurements in a phantom, the signal-to-noise ratio of the array is 1.67 times or more better than that obtained with a standard quadrature head coil in the region of the hippocampi. The higher sensitivity of this phased array permits use of imaging pulse sequences for which the head coil is inadequate.

Epilepsy↗
PubMed1992

Influence of resistant and susceptible genotype, IL-1, and lymphoid organ on Trichinella spiralis-induced cytokine secretion.

The relative importance of cell-mediated inflammatory responses and antibody-mediated responses in controlling parasitic helminth infection is debated. To study the relationship between these responses and resistance or susceptibility to primary Trichinella spiralis infection, we infected resistant AKR mice and susceptible B10.BR mice and analyzed the lymphokines IL-2, IFN-gamma, and IL-5 produced by their T cells as a function of time and lymphoid organ. IL-2-secretors occurred maximally between days 3 and 6 postinfection, whereas IL-5-secretors peaked between days 6 and 9. Previously, we found that IFN-gamma producers peaked before day 6, whereas IL-4 producers peaked between days 6 and 9. Most cytokine secretors were CD4+. The simultaneous development of IL-2- and IFN-gamma-secreting cells, and IL-4- and IL-5-secreting cells, suggests that the infection may be stimulating T cells to differentiate into cells capable of secreting specific cytokine sets, analogous to the postulated Th1 and Th2 subsets. In the spleen and mesenteric lymph nodes, cells from B10.BR mice secreted more IL-5 than cells from AKR mice, as we found previously for IL-4. For both strains, mesenteric lymph node cells produced more IL-5 than splenocytes. The AKR mesenteric lymph node cells produced more IL-2 than the B10.BR cells, but the reverse occurred in splenocytes. The AKR peripheral lymph node cells also secreted more IFN-gamma than the B10.BR cells, but the strains were equivalent for peritoneal exudate cell IFN-gamma production. Thus, the lymphoid organ microenvironment plays an important role in regulating cytokine-secreting cell development in this system. We also tested the possible regulatory role of IL-1. Exogenous rIL-1 alpha increased IFN-gamma secretion early but not late in mesenteric lymph node cells from both strains; this reflected an increased IFN-gamma-secreting cell frequency, not a change in IFN-gamma mRNA transcript level. Exogenous rIL-1 alpha did not consistently affect IL-2, IL-4, or IL-5 secretion. These data suggest that IL-1 alpha availability in vivo may regulate IFN-gamma-secreting cell development. In sum, early activation of IFN-gamma-secreting T cells in lymph nodes, with little subsequent activation of IL-4- and IL-5-secreting cells, distinguished the resistant from susceptible strain responses to T. spiralis infection, and IL-1 alpha and lymphoid organ environment influence IFN-gamma-secreting cell activation.

Animals↗
PubMed1992

Immunity to Trichinella spiralis infection in vitamin A-deficient mice.

Vitamin A-deficient (A-) mice make strikingly poor IgG responses when they are immunized with purified protein antigens. Previously, we showed that A- T cells overproduce interferon gamma (IFN-gamma), which then could inhibit interleukin 4 (IL-4)-stimulated B cell IgG responses. To determine if the altered IFN-gamma regulation pattern and its immunological consequences would extend to a natural infection, we studied mice infected with the parasitic helminth Trichinella spiralis. The course of the infection was similar in A- and A-sufficient (A+) mice. These mice did not differ with respect to newborn larvae/female/hour produced in the intestine, or muscle larvae burden 5 wk postinfection. They also did not differ in the intestinal worm expulsion rate until day 15, when A- mice still harbored parasites, whereas A+ mice had cleared intestinal worms. Vitamin A deficiency reduced both the frequency of B lymphocytes secreting IgG1 antibodies to parasite antigens, and the bone marrow eosinophilia associated with helminth infection. The cytokine secretion patterns in infected mice were consistent with these observations and with previous studies. Mesenteric lymph node cells from infected A- mice secreted significantly more IFN-gamma, and significantly less IL-2, IL-4, and IL-5 than infected A+ controls. A- splenocytes secreted significantly more IFN-gamma, and equivalent amounts of IL-2, IL-4, and IL-5 compared with A+ controls. Interestingly, CD4-CD8- cells secreted the majority of the IL-4 produced in the spleen. The IL-2, IL-4, and IL-5 steady-state transcript levels correlated with secreted protein levels, but IFN-gamma transcripts did not. Although they secreted more protein, A- cells contained fewer IFN-gamma transcripts than A+ cells. These results suggest two vitamin A-mediated regulation steps in IFN-gamma gene expression: positive regulation of IFN-gamma transcript levels, and negative regulation posttranscriptionally. The essentially unaltered outcome of T. spiralis infection in vitamin A-deficient mice probably reflects a balance between cellular and humoral responses. The IFN-gamma overproduction might have a positive effect on the gut inflammatory response, but the decrease eosinophilia, cytokine production in mesenteric lymph node, and IgG1-secreting cell frequency might have a negative effect on T. spiralis immunity.

Animals↗
PubMed1992

A single autosomal gene defect severely limits IgG but not IgM responses in B lymphocyte-deficient A/WySnJ mice.

Antigen-stimulated B lymphocytes either differentiate into IgM-secreting plasma cells or into memory B cells that secrete other immunoglobulin isotypes upon antigen restimulation. The mechanisms that generate and maintain memory B cells are poorly understood. Previously, we described a severe B lymphocyte deficiency in adult strain A/WySnJ mice compared to subline A/J. Here we show that the single, autosomal co-dominant locus responsible for the deficiency also diminishes IgG-secreting B cell formation without interfering with IgM-secreting plasma cell differentiation. A/WySnJ secondary IgG1 responses to the protein antigens hemocyanin, bovine gamma-globulin, ovalbumin, lysozyme and beta-galactosidase were 6- to 50-fold lower than A/J responses. The defect also decreased secondary IgG2a and IgG3 responses, and primary IgG1 and IgG2a responses. The reduced A/WySnJ secondary IgG1 response was not due to differential response kinetics or dose responsiveness, and could not be augmented to A/J levels by repeated immunizations. Serum IgG1, IgG2a and IgG3 levels from nonimmune A/WySnJ mice were similarly reduced. The secondary IgG1 response and splenic B cell percentage showed significant positive correlation (r = 0.72) in F2 mice, suggesting that a single locus controlled both traits. In contrast, A/WySnJ mice made good primary IgM responses to hemocyanin, beta-galactosidase, and the thymus-independent antigen trinitrophenyl-Ficoll. The A/WySnJ splenic adherent cells were competent in antigen-presenting function, and A/WySnJ immune T cells proliferated in response to antigen and provided the requisite B cell stimulatory signals for an IgG1 response. Together, our results suggest that A/WySnJ mice have a genetic lesion that causes a selective IgG immune response dysfunction. The absence of IgG-secreting cell precursors or a defect in precursor activation or differentiation are two possible mechanisms which could precipitate a selective IgG response dysfunction. We propose that the defective A/WySnJ and normal A/J strain pair offer the opportunity to use a natural genetic variation as a tool to investigate B lymphocyte development and function.

Animals↗
PubMed1992

Reduction of RF penetration effects in high field imaging.

A method of correcting for the RF inhomogeneity in the body by dielectric loading of the coil-to-shield space in an RF resonator (coil and shield assembly) is described. The presence of the RF coil and RF shield have significant effects on RF homogeneity. Based on theoretical calculations, a method for adjusting the RF homogeneity by manipulating the axial propagation constant, kappa z, is proposed. This is accomplished by loading the coil-to-shield space with dielectric material of suitable relative permittivity so as to increase kappa z and decrease the radial propagation constant, kappa rho. In this manner, the radial wavelength (lambda rho = 2 pi/kappa rho) can be increased relative to the body dimensions, and the field amplitude variations in the axial plane minimized. Theoretical calculations indicate that a value of between 30 and 40 for the relative permittivity of the dielectric material in the coil-to-shield space would reduce the RF field inhomogeneity from +/- 15% to about +/- 3% over a central 30-cm-diameter region of a homogeneous 40-cm-diameter body at both 64 and 170 MHz. The theoretical model was verified in laboratory measurements of the [formula; see text] field generated in a test coil at 170 MHz which was scaled to correspond to a body at 64 MHz. However, the improved RF field homogeneity would be accompanied by increased RF power requirements and reduced coil sensitivity.

Humans↗
PubMed1992

Retinoid repletion of vitamin A-deficient mice restores IgG responses.

Vitamin A-deficient (A-) mice produce poor IgG antibody responses due to a helper T cell dysfunction. We performed retinoid repletion studies to determine the minimum dietary retinyl acetate dose and the most active retinoid for supporting immune function. Dietary retinyl acetate repletion at 2 (R2 group) or 4 (R4 group) microgram/g diet restored serum retinol in A- mice to vitamin A-sufficient (A+) control levels within 24 h. However, in R4 mice, liver retinyl palmitate was restored about twofold faster than in R2 mice; liver retinyl palmitate reached A+ control levels by d 30 in R4 mice but not in R2 mice. We challenged the mice with antigen 24 h post repletion; the R4 mice gave an IgG1 response equal to that of A+ controls, but the R2 mice were comparable with the A- controls. We also compared four retinoids for IgG1 response restoration in vitro; 1 nmol/L retinoic acid fully repleted A- cell IgG1 responses and helper T cell frequencies to the unsupplemented A+ control levels. Retinoic acid was at least 10-fold more active than retinyl acetate or retinaldehyde, and 100-fold more active than retinol. Collectively, our results suggest that retinoic acid is probably the physiologically important metabolite for sustaining IgG immune responses in vivo. We discuss the possible relationship between liver retinyl palmitate levels and availability of retinoic acid to support immune function.

Animals↗
PubMed1992

High-resolution MR imaging of the wrist and eye with short TR, short TE, and partial-echo acquisition.

High-resolution spin-echo and two- and three-dimensional gradient-recalled acquisition in the steady state (GRASS) and spoiled GRASS images of the wrist and eye were obtained with a whole-body magnetic resonance imager by using trapezoidal phase-encoding gradient waveforms and by lowering receiver bandwidth to +/- 8 kHz, which results in a minimum field of view (FOV) of 4 cm and pixel resolution of 156 microns for a 256 x 256 matrix. Short echo times were achieved by using partial-echo acquisition. Poor signal-to-noise ratio resulting from smaller voxel sizes was overcome by using prototype receive-only eye and wrist coils. Images were obtained in reduced time and were superior to those obtained in studies performed with an 8-12-cm FOV and commercially available coils.

Adult↗
PubMed1992

Pulmonary vasculature: single breath-hold MR imaging with phased-array coils.

The authors obtained magnetic resonance images of the pulmonary vasculature with reduced artifacts caused by cardiac and respiratory motion by acquiring a series of moderately thin sections in a single breath-hold with an ultrafast gradient-echo pulse sequence. The series of two-dimensional images was postprocessed with a maximum-intensity projection algorithm. Time-of-flight inflow enhancement increased the signal intensity of arteries and veins while radiofrequency phase spoiling produced limited stationary spin suppression of the chest wall. Moderately thin (8-mm) section thicknesses were used to attain the resolution necessary to visualize smaller pulmonary vascular segments up to the chest wall while the number of acquired sections was minimized. Because the body coil did not provide an adequate signal-to-noise ratio (S/N) for a single excitation and thin-section acquisitions, phased-array coils covering either the right or left lung were used to single breath-holds prevented the misregistration and blurring that occurred in examinations performed with multiple breath-holds.

Humans↗
PubMed1991

Abnormal regulation of IFN-gamma secretion in vitamin A deficiency.

T lymphocytes from vitamin A-deficient (A-) mice show a decreased ability to stimulate B lymphocytes for Ag-specific secondary IgG1 responses in vivo and in vitro. Experiments reported here traced the molecular basis for this functional defect to an overproduction of IFN-gamma by A- CD4+ T cells compared with cells from A-sufficient (A+) mice. Secretion of IL-2 and IL-4 by cells from A- and A+ mice was equivalent. Retinoic acid supplementation in vitro decreased IFN-gamma secretion from A- T cells, indicating that IFN-gamma production is retinoid-responsive. Adding IFN-gamma neutralizing antibodies to cultures established with cells from immune A- mice substantially increased IgG1 production, whereas IL-4 addition moderately increased IgG1 production. Adding retinoic acid to the cultures either at initiation, or 48 h later, fully restored IgG1 production by A- cultures to the level of A+ control cultures. These results are consistent with a role for vitamin A in negatively regulating IFN-gamma secretion.

Animals↗
PubMed1991

Phenotypic and genetic characterization of a unique B lymphocyte deficiency in strain A/WySnJ mice.

The elucidation of B lymphocyte development has been partially achieved through genetic models such as the X-linked immunodeficiency (xid) mutation. We discovered a unique B lymphocyte developmental defect in strain A/WySnJ mice. We used single- and two-color flow cytometry to analyze lymphocytes from A/J and A/WySnJ mice. Adult A/WySnJ mice had a severe B cell deficiency, which was apparent in the spleen, lymph nodes, peritoneum and peripheral blood, compared to adult A/J mice. An ontogeny study revealed that a developmental defect, inhibiting B lymphocyte maturation or differentiation but not B lymphopoiesis, was responsible for the deficiency. This maturational defect blocked the production of B220hi/Iahi/surface IgMlo B cells, and was manifested in the adult bone marrow and neonatal spleen, but not the adult spleen. Neither Ly-1 B cells nor peripheral T cells were apparently affected by the A/WySnJ defect. The B cell immunodeficiency segregated as an autosomal co-dominant trait in F1 and F2 mice. We propose that A/WySnJ mice have a novel genetic defect arresting B cell differentiation in adult bone marrow and neonatal spleen.

Animals↗
PubMed1991

Volume imaging with MR phased arrays.

A volume MR phased array was constructed with two coils placed anteriorly and two coils posteriorly. Data acquired simultaneously from the four coils on a phantom were combined into a single image having a signal-to-noise ratio 80% better than that from the body coil. Additional comparisons of the four-coil phased array with a two-coil phased array and a Helmholtz pair having the same overall dimensions show how variations of signal amplitude and phase in the individual coils affect the composite SNR. Images of the male and female pelvis demonstrate how the improved SNR can be used to reduce the number of excitations, decrease the field of view, increase the echo time, or reduce the slice thickness.

Algorithms↗
PubMed1991

An analytical model for the design of RF resonators for MR body imaging.

A closed form, analytical solution describing the RF fields generated by an RF body coil resonator for MR imaging at 1.5 and 4.0 T is presented. This solution extends the results of earlier studies of RF penetration in the body by explicitly including the RF coil, the RF shield, and the field variation along the z axis for high-pass bird cage coils. A salient feature of this treatment is the calculation of the axial propagation constant, kz, which determines the z dependence of the RF field. We have determined the relative power deposition in the body, the B1 field homogeneity, and coil losses, which are functions of the coil-to-shield separation and body size. The relative power deposition in the body has been calculated to vary as the 1.58 power of the body radius. The calculations have also predicted that the field homogeneity in the z direction exhibits greater degradation at higher frequencies in a high-pass coil than in a low-pass coil. The model predicts an increase in coil losses by a factor of 2.8 as the coil-to-shield separation is reduced from 5 to 2 cm in a standard body resonator. Although the results for only a homogeneous cylindrical object or body are presented, the theory can be extended to a multilayered heterogeneous object of varying permittivity and conductivity.

Body Constitution↗
PubMed1991

Trichinella spiralis: influence of an immunodominant, carbohydrate-associated determinant on the host antibody response repertoire.

Host antibody responses to the G2.1 epitope, a carbohydrate-associated determinant shared by several Trichinella spiralis glycoproteins, were examined by competitive inhibition enzyme-linked immunosorbent assay (ELISA). The G2.1 epitope dominated the AKR/J mouse antibody response whether the antigens were injected or introduced through infection, as determined by the serum blocking ability of a G2.1 epitope-specific monoclonal antibody (mAb). Serum T. spiralis-binding activity from several other infected mouse strains was blocked 22 to 86% by the G2.1 epitope-specific mAb. In addition to mice, the G2.1 epitope evoked powerful antibody responses in four other species. The binding activity of Trichinella-reactive antibodies from infected rats and pigs was inhibited 56 and 34%, respectively, by the mAb. Greater than 48% of the T. spiralis serum-binding activity from 4/5 infected humans was G2.1-specific. Most of the rabbit antibody response induced by injection of a previously characterized 43-kDa antigen was also directed to the G2.1 determinant. The specificities of 10 T. spiralis-reactive mAb were examined, and 7 reacted with the immunodominant epitope. Finally, of nine helminth species examined, only T. spiralis and T. pseudospiralis extracts efficiently blocked G2.1-specific antibody binding to solid-phase antigens. These results suggest that the responses to G2.1 epitope may play an important role during infection.

Animals↗