Costs that would be incurred in establishing "difficult airway register" could be better spent.
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Biomedical subjects
Publications and source records attributed to E Morris.
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BACKGROUND: Three-dimensional echocardiography can allow us to address uniquely three-dimensional scientific questions, for example, the hypothesis that the impact of a stenotic valve depends not only on its limiting orifice area but also on its three-dimensional geometry proximal to the orifice. This can affect the coefficient of orifice contraction (Cc = effective/anatomic area), which is important because for a given flow rate and anatomic area, a lower Cc gives a higher velocity and pressure gradient, and Cc, routinely assumed constant in the Gorlin equation, may vary with valve shape (60% for a flat plate, 100% for a tube). To date, it has not been possible to study this with actual valve shapes in patients. METHODS AND RESULTS: Three-dimensional echocardiography reconstructed valve geometries typical of the spectrum in patients with mitral stenosis: mobile doming, intermediate conical, and relatively flat immobile valves. Each geometry was constructed with orifice areas of 0.5, 1.0 and 1.5 cm2 by stereolithography (computerized laser polymerization) (total, nine valves) and studied at physiological flow rates. Cc varied prominently with shape and was larger for the longer, tapered dome (more gradual flow convergence proximal and distal to the limiting orifice): for an anatomic orifice of 1.5 cm2, Cc increased from 0.73 (flat) to 0.87 (dome), and for an area of 0.5 cm2, from 0.62 to 0.75. For each shape, Cc increased with increasing orifice size relative to the proximal funnel (more tubelike). These variations translated into important differences of up to 40% in pressure gradient for the same anatomic area and flow rate (greatest for the flattest valves), with a corresponding variation in calculated Gorlin area (an effective area) relative to anatomic values. CONCLUSIONS: The coefficient of contraction and the related net pressure loss are importantly affected by the variations in leaflet geometry seen in patients with mitral stenosis. Three-dimensional echocardiography and stereolithography, with the use of actual information from patients, can address such uniquely three-dimensional questions to provide insight into the relations between cardiac structure, pressure, and flows.
Performance on an attentional task was assessed in posttraumatic stress disorder patients with substance abuse histories (PTSD-SA). Positron emission tomography (PET) was used to measure concurrent regional cerebral blood flow (rCBF). Eight male PTSD-SA patients and eight normal subjects each received three serial PET scans with 15O-labeled water under the following conditions: (1) resting, (2) auditory continuous performance task (ACPT1), and (3) repeat auditory task (ACPT2). PTSD-SA patients made more errors of commission on the ACPT than normal subjects. Examination of right frontal and parietal cortex ACPT task substrates revealed decreased parietal blood flow in PTSD-SA, which may represent a pathophysiology for poor attentional task performance in PTSD-SA. Attentional problems may underlie other symptomatology in PTSD.
OBJECTIVES: The purpose of this study was to determine, in a large referral population, the rate of echocardiographic change in mitral valve area (MVA) without interim intervention, to determine which factors influence progression of narrowing and to examine associated changes in the right side of the heart. BACKGROUND: Little information is currently available on the echocardiographic progression of mitral stenosis, particularly on progressive changes in the right side of the heart and the ability of a previously proposed algorithm to predict progression. METHODS: We studied 103 patients (mean age 61 years; 74% female) with serial two-dimensional and Doppler echocardiography. The average interval between entry and most recent follow-up study was 3.3 +/- 2 years (range 1 to 11). RESULTS: During the follow-up period, MVA decreased at a mean rate of 0.09 cm2/year. In 28 patients there was no decrease, in 40 there was only relatively little change (< 0.1 cm2/year) and in 35 the rate of progression of mitral valve narrowing was more rapid (> or = 0.1 cm2/year). The rate of progression was significantly greater among patients with a larger initial MVA and milder mitral stenosis (0.12 vs. 0.06 vs. 0.03 cm2/year for mild, moderate and severe stenosis, p < 0.01). Although the rate of mitral valve narrowing was a weak function of initial MVA and echocardiographic score by multivariate analysis, no set of individual values or cutoff points of these variables or pressure gradients could predict this rate in individual patients. There was a significant increase in right ventricular diastolic area (17 to 18.7 cm2) and tricuspid regurgitation grade (2 + to 3 +; p < 0.0001 between entry and follow-up studies). Progression in right heart disease occurred even in patients with minimal or no change in MVA. Patients with associated aortic regurgitation had a higher rate of decrease in MVA than did those with trace or no aortic regurgitation (0.19 vs. 0.086 cm2/year, p < 0.05). CONCLUSIONS: The rate of mitral valve narrowing in individual patients is variable and cannot be predicted by initial MVA, mitral valve score or transmitral gradient, alone or in combination. Right heart disease can progress independent of mitral valve narrowing.
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Transfection with a plasmid encoding the 3' untranslated region (3' UTR) of skeletal muscle tropomyosin induces chicken embryonic fibroblasts to express skeletal tropomyosin. Such cells become spindle shaped, fuse, and express titin, a marker of striated muscle differentiation. Skeletal muscle tropomyosin and titin organize in sarcomeric arrays. When the tropomyosin 3' UTR is expressed in osteoblasts, less skeletal muscle tropomyosin is expressed, and titin expression is delayed. Some transfected osteoblasts become spindle shaped but do not fuse nor organize these proteins into sarcomeres. Transfected cells expressing muscle tropomyosin organize muscle and nonmuscle isoforms into the same structures. Thus, the skeletal muscle tropomyosin 3' UTR induces transdifferentiation into a striated muscle phenotype in a cell-type-specific context.
Popliteal artery entrapment is difficult to diagnose even at surgery. Early diagnosis is important as the prognosis is better if detected before the onset of complications. There is no sensitive method for the evaluation of this condition. We describe three cases detected by a new technique using 99mTc methoxy isobutyl isonitrile (MIBI) with single photon emission tomography. The scintigraphic features of entrapment and the advantage of MIBI leg scintigraphy over other methods are discussed.
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The structure of F-actin was investigated by fitting the crystallographically determined actin monomer structure to F-actin electron microscopy data sets obtained by a variety of methods. A reciprocal-space global search procedure was applied to non-equatorial reciprocal-space amplitudes and phases of the microscopy data to locate minima. Fits were performed over a range of cross-sectional radii-of-gyration encompassing values obtained from X-ray solution scattering measurements. Five data sets from four laboratories were investigated: one from frozen-hydrated single filaments, three from negatively stained single filaments, and one from negatively stained single-layer paracrystals. In this last case the paracrystal data were straightened to improve resolution. The best fits nearly unanimously favored a monomer orientation having long-pitch connectivity that was close to that obtained by fitting X-ray fiber diffraction patterns. In certain cases where the resolving power was low, competitive fits were obtained with a quite different orientation, one having only protomer connectivity along the genetic helix. Using a running 10-residue deletion from the monomer in the Holmes-type orientation, subtle differences between the monomer structure and the protomer structure in F-actin could be detected. In particular, differences in the "DNase loop" (residues 41 to 50) and the "hydrophobic loop" (residues 264 to 273) were seen in single-filament data. In addition, a perturbation of the structure was seen in a region near residues 81 to 90. A rearrangement within the protomer structure reported in the literature did not produce fits as good as those obtained when using the undistorted monomer crystallographic structure without 10-residue deletions. These results, taken as a whole, provide strong support for a structure of Mg(2+)-ADP F-actin similar to that originally suggested by Holmes et al. but with alterations of the hydrophobic loop, the DNase loop and in the region near residues 81 to 90. These latter two regions have been proposed as secondary binding sites for myosin heads. The available evidence from electron microscopy and from other sources suggests that residues 40 to 49 are disordered in Mg(2+)-ADP F-actin.
The convergence of structures, all determined by independent global searches and subsequent refinement on different electron microscopy data sets, with the X-ray fiber diffraction results strongly suggests that we now have the approximately correct structure for F-actin. This consensus structure will now provide a reliable, well-defined platform upon which to study the structure and function of proteins bound to actin. Among these are capping proteins, such as severin and gelsolin, contractile proteins, such as myosin and its subfragments, and proteins involved in regulation, such as troponin and tropomyosin.
Quantitation of valvular regurgitation remains an important goal in clinical cardiology. It has been described previously that with the use of color Doppler flow mapping, simple measurements of apparent jet size do not correlate closely with quantitative regurgitant indices. Recently the proximal flow convergence method has been proposed to quantify valvular regurgitation by analysis of the converging flow field proximal to a regurgitant lesion. Assuming hemispherical convergence, flow rate Q can be calculated as Q = 2 pi r2va, where va is the aliasing velocity at a distance r from the orifice. For maximal accuracy, previously validated correction factors must be used to account for the flattening effect of the isovelocity contours close to the orifice and for the actual sector angle subtended by the valve leaflets (alpha), to yield a flow rate formula Q = 2 pi r2va.(vp/vp - va).(alpha/180), where vp is the orifice velocity obtained by continuous wave Doppler. In 45 patients (35 in sinus rhythm, 10 with atrial fibrillation) with tricuspid regurgitation, regurgitant stroke volume, regurgitant flow rate, and regurgitant fraction were calculated using the proximal flow convergence method and were compared with values obtained by the Doppler two-dimensional echocardiographic method. Regurgitant stroke volumes (SV) calculated by the proximal flow convergence method correlated very closely with values obtained by the Doppler two-dimensional method with r = 0.95 (y = 0.94x + 0.99) and delta SV = -0.3 +/- 5.2 cm3. Regurgitant flow rates (Q) calculated by both methods showed a similar correlation: r = 0.96 (y = 0.97x + 45) and delta Q = 1.6 +/- 429 cm3/min.(ABSTRACT TRUNCATED AT 250 WORDS)
Analysis of the flow-convergence zone proximal to a regurgitant orifice permits the noninvasive, quantitative measurement of clinically useful parameters of valvular insufficiency. However, many indexes such as flow rate reflect not only the size of the regurgitant lesion but are also highly dependent on the hemodynamic loading conditions. The effective regurgitant orifice area (ROA) in contrast is a more fundamental parameter, less dependent on hemodynamics and more reflective of real changes in the geometry of the valve, making it a promising index for serial assessment of patients. In this study, the measurement of regurgitant orifice area by the flow-convergence method was tested in tricuspid regurgitation and then used to monitor patients noninvasively over time. The effective ROA was calculated in 45 patients with tricuspid regurgitation by means of the flow-convergence method and compared with the ROA obtained with pulsed Doppler echocardiographic methods. An excellent correlation was obtained between the two assessments of ROA (r = 0.96, delta ROA = -0.09 +/- 6.5 mm2). ROA also showed an excellent correlation with other indexes of valvular insufficiency such as regurgitant stroke volume (r = 0.89) and regurgitant fraction (r = 0.88). In a subgroup of 22 patients thought to be clinically stable, ROA was calculated serially over a mean follow-up period of 2 months and its variability compared with that of other flow-based parameters obtainable from proximal acceleration. The variation between the two studies in regurgitant stroke volume and regurgitant flow rate was 5% +/- 20.6% and 5.2% +/- 35.7%, respectively. The effective ROA showed significantly less variability at 1.8% +/- 15%.(ABSTRACT TRUNCATED AT 250 WORDS)
BACKGROUND: Quantitation of valvular regurgitation remains an important goal in cardiology. It has been described previously that using color Doppler flow mapping, measurements of apparent jet size do not correlate always closely with quantitative regurgitant indexes. Recently the proximal flow convergence method has been proposed to quantify valvular regurgitation by analysis of the converging flow field proximal to a regurgitant lesion. Assuming hemispherical convergence, peak flow rate Qp can be calculated as Qp = 2 pi r2Va, where Va is the aliasing velocity at a distance r from the orifice. For maximal accuracy, previously validated correction factors must be used to account for the flattening effect of the isovelocity contours close to the orifice and for the actual sector angle subtended by the valve leaflets (alpha) to yield a flow rate formula Qp = 2 pi r2Va (Vp/Vp-Va) (alpha/180), where Vp is the orifice velocity obtained by continuous wave Doppler. METHODS: In 45 patients (35 in sinus rhythm, 10 with atrial fibrillation) with tricuspid regurgitation, regurgitant stroke volume, regurgitant flow rate were calculated using the proximal flow convergence method and compared with values obtained by the Doppler two-dimensional echocardiographic method. RESULTS: Regurgitant stroke volumes (SV) calculated by the proximal flow convergence method correlated very closely with values obtained by the Doppler two-dimensional method with r = 0.95 (y = 0.94x + 0.99) and delta SV = -0.3 +/- 5.2 cm3. Regurgitant flow rates (Q) calculated by both methods showed a similar correlation: r = 0.96 (y = 0.97x + 45) and delta Q = 1.6 +/- 4.29 cm3/min. All correlations were slightly better for the group of patients in sinus rhythm. CONCLUSION: This study demonstrates that the proximal flow convergence method is an accurate and reproducible technique for quantifying tricuspid regurgitation. While improvements of this method are to be expected, flow calculations based on the proximal flow field show excellent results and appear appropriate for clinical use.
BACKGROUND: It has been shown previously that using color Doppler flow mapping, simple measurements of apparent jet size do not correlate closely with regurgitant flow rate and regurgitant fraction. Recently the proximal flow convergence method has been proposed to quantify valvular regurgitation by analysis of the converging flow field proximal to a regurgitant lesion. Flow rate Q can be calculated as Q = 2 pi r2va where va is the aliasing velocity at a distance r from the orifice. PATIENTS AND METHODS: In 54 patients (43 in sinus rhythm, 11 with atrial fibrillation) with at least mild mitral regurgitation by semi-quantitative assessment, regurgitant stroke volume, regurgitant flow rate, and regurgitant fraction were calculated using the proximal flow convergence method and compared with values obtained by the Doppler/two-dimensional echocardiographic method. RESULTS: Regurgitant stroke volumes (VL) calculated by the proximal flow convergence method correlated very closely with values obtained by the Doppler-2D method with r = 0.93 (y = 0.95x + 0.55) and delta VL = -0.3 +/- 4.0 cm3. Regurgitant flow rates (Q) calculated by both methods showed a similar correlation: r = 0.93 (y = 0.95x + 54) and delta Q = -34 +/- 284 cm3/min. The correlation for regurgitant fraction (RF) calculated by both techniques showed r = 0.89 (y = 0.98x + 0.006) and delta RF = -0.005 +/- 0.06. All correlations were slightly better for the group of patients in sinus rhythm compared with the study group in atrial fibrillation. CONCLUSION: This study demonstrates that the proximal flow convergence method is an accurate and reproducible technique to quantify mitral regurgitation. This approach is easy and less time-consuming than the Doppler-echocardiographic method. While future improvements of this method are to be expected, flow calculations based on the assumption of simple hemispheric symmetry of the proximal flow field appear suitable for clinical application at the present time.
The visual assessment of jet area has become the most common method used in daily clinic practice to evaluate valvular regurgitation. Despite the high prevalence of tricuspid regurgitation, however, few studies have systematically compared TR jet areas with a quantitative standard. To evaluate this, 40 patients in sinus rhythm with tricuspid regurgitation were analyzed: 16 with centrally directed free jets and 24 with impinging wall jets. The size of the maximal planimetered color jet area (cm2) was compared with parameters derived using the pulsed Doppler 2-dimensional echocardiographic method: regurgitant fraction and the flow convergence method (peak flow rate, effective regurgitant orifice area and momentum). Mean tricuspid regurgitant fraction averaged 33 +/- 15%, peak flow rate 76 +/- 54 cm3/s, effective regurgitant orifice area 27 +/- 21 mm2 and momentum 21,717 +/- 15,014 cm4/s2. An average of 4-chamber, and long- and short-axis areas in free jets correlated well with regurgitant fraction (r = 0.81, p < 0.001), better with peak flow rate (r = 0.94, p < 0.001), effective regurgitant orifice (r = 0.92, p < 0.001) and momentum (r = 0.94, p < 0.001). The correlation was worse, but still significant, in wall jets. For the same peak flow rate, wall jets were 75% of the size of a corresponding free jet. Jet area measurement is a good semiquantitative tool to measure tricuspid regurgitation in free jets, which correlates well with regurgitant fraction and better with new parameters available from analysis of the proximal acceleration field. In patients with eccentrically directed wall jets the correlation with planimetered jet area was worse, but still significant.