Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033036 (APC)
 10,214 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sixty-six consecutive patients without left ventricular volume overload, significant arrhythmia or significant pericardial effusion were examined by M-mode echocardiography immediately before diagnostic left- and right-heart catheterization. Using various echocardiographic measurements, left ventricular stroke volume (SV) was calculated according to eight different echocardiographic formulas (SVE) that have been proposed previously. At catheterization SV was also determined by thermodilution (SVT) and by single-plane left ventricular cineangiography in the right anterior oblique projection (SVA). When comparing SVE with SVT, the four formulas developed to calculate mitral or aortic flow failed (r = 0.10 to 0.54). As expected, poor correlations (r = 0.22 to 0.47) were also found when formulas used to calculate ventricular volumes from the ventricular diameter or SV from the change in diameter (left ventricular formulas) were used in coronary patients with grossly asymmetrical ventricular contraction patterns. When the use of the left ventricular formulas was confined to patients with symmetrical or almost symmetrical contraction, two formulas yielded favorable correlations of r = 0.84, SEE = 12.7 ml and r = 0.86, SEE = 12.2 ml, respectively. These correlations were comparable to the correlation between our two invasive reference techniques (r = 0.81; SEE = 12.2 ml). The comparison between SVE and SVA confirmed the results of the thermodilution study, though the correlations were generally weaker. We conclude that the formula of Teichholz et al., which was the best of all tested formulas, may be used to obtain a clinically useful estimate of SV in patients in whom symmetrical or almost symmetrical left ventricular contraction can be anticipated.
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PMID:Comparative value of eight M-mode echocardiographic formulas for determining left ventricular stroke volume. A correlative study with thermodilution and left ventricular single-plane cineangiography. 49 56

Stroke volume (SV) and systolic time intervals (STI) were measured automatically using impedance cardiography signals (ICG) and compared with those obtained by pulsed-wave Doppler echocardiography using the apex approach. The comparison was made in 9 healthy male subjects, mean age 24.9 +/- 12.2 years, using recordings of 10 heart cycles simultaneously obtained by the two methods. During measurements the subjects rested in the supine position. There were no differences between mean values of SV determined by the two methods as well as between mean values of ejection time (ET) (p > 0.8 and p > 0.9, respectively). The pre-ejection period (PEP) estimated by ICG was 22 ms longer than that determined by echocardiography (p < 0.001). The relationship between SV values measured by impedance cardiography (SVA) vs those calculated by echocardiography (SVE) was found to be close to the line of identity in the range of measurements. The regression equation for SV was: SVA = 0.784.SVE + 15 (r = 0.69, p < 0.001, SEE = 10.7 ml). We conclude that automatic determination of SV and ET from ICG signals provides results comparable in absolute values with those obtained by the pulsed wave Doppler ultrasonocardiography using the apex approach for subjects remaining in the supine position.
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PMID:A comparison between the automatized impedance cardiography and pulsed-wave Doppler echocardiography methods for measurements of stroke volume (SV) and systolic time intervals (STI). 824 26

Bacterial superantigens can bind TCR in the absence of MHC class II molecules and activate T lymphocytes when cocultured with certain class II-deficient accessory cells. It has not been determined, however, whether these accessory cells provide direct costimulation to the T cell or serve to present superantigens via a nonconventional ligand. We have identified a human adenocarcinoma cell line, SW480, that assists in the activation of human T cells by the staphylococcal enterotoxins B (SEB), C1 (SEC1), and D (SED), but not SEA, SEC2, SEC3, or SEE. SW480 cells did not express class II molecules, and anti-class II mAbs did not inhibit T cell proliferation, supporting the hypothesis that class II is not absolutely required for enterotoxin-mediated T cell activation. The TCR Vbeta profile of T cells stimulated by SEB plus SW480 cells was similar to that of T cells stimulated by SEB plus class II+ APC, indicating that TCR-SEB interactions were preserved in the absence of class II molecules. Binding studies failed to detect specific association of SEB with SW480 cells, suggesting that SW480 cells do not express receptors for enterotoxin. SEB coupled to beads, however, stimulated T cell proliferation, but only in the presence of SW480 cells. SW480 cells express both ICAM-1 and LFA-3 molecules, and the addition of Abs to these receptors inhibited T cell proliferation. These findings support a model in which certain enterotoxins engage the TCR independent of MHC class II or other specific presenting molecules and induce T cell proliferation with signals provided by nonconventional accessory cells.
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PMID:Intercellular adhesion molecule-1 and leukocyte function-associated antigen-3 provide costimulation for superantigen-induced T lymphocyte proliferation in the absence of a specific presenting molecule. 955 95