Identification of human myocardial infarction in vitro based on the frequency dependence of ultrasonic backscatter.

It has been reported previously that acute and mature myocardial infarction in dogs can be differentiated in vitro and in vivo by ultrasonic tissue characterization based on measurement of the frequency dependence of ultrasonic backscatter. To characterize human infarction with an index of the frequency dependence of backscatter that could be obtained in patients, cylindrical biopsy specimens from 7 normal regions and 12 regions of infarction of 6 fixed, explanted human hearts in 2-deg steps around their entire circumference with a 5-MHz broadband transducer were insonified. One to six consecutive transmural levels were studied for each specimen. The dependence of apparent (uncompensated for attenuation or beam width) backscatter, /B(f)/2, on frequency (f) was computed from spectral analyses of radio-frequency data as /B(f)/2 = afn, where from theoretical considerations the magnitude of n decreases as scatterer size increases. Apparent integrated backscatter was computed as the average of /B(f)/2 from 3 to 7 MHz. The average value for n for normal tissue (0.9 +/- 0.1) exceeded that for tissue from regions of infarction (0.6 +/- 0.1; p less than 0.05). Infarct manifested a significant decrease of n from epicardial to endocardial levels (epi----mid----endo: 0.9----0.7----0.2; p less than 0.05) whereas normal tissue manifested similar values for n at each transmural level (0.8----1.1----0.9; p = NS). Average integrated backscatter across all transmural levels for infarct was significantly greater than for normal tissue (-48.3 +/- 0.5 vs -53.4 +/- 0.4 dB, infarct versus normal; p less than 0.05). The presence of fibrosis was associated with smaller values of n and greater integrated backscatter.(ABSTRACT TRUNCATED AT 250 WORDS)     

Classical dynamical theory of heavy ion fusion and scattering

A classical dynamical model which includes dissipative forces is suggested for heavy ion reactions high above the Coulomb barrier. Internal degrees of freedom corresponding to rotation of the ions are included. The reactions divide into three parts: (1) quasi-elastic scattering, with relatively small energy loss, associated with higher angular momenta, (2) deep inelastic scattering, with larger energy loss and considerable transfer of mass, associated with intermediate angular momenta, and (3) complete fusion where a highly excited compound state is formed, generally associated with the lowest angular momenta. One can predict a fusion cross section for two values of the friction coefficient, “weak” and “strong” friction cases. Reasonable values for fusion can be obtained in the weak friction case, but scattering angular distributions are not consistent with available experimental data. In the strong friction case it is more difficult to fit all the fusion cross sections with a single friction parameter. But the predicted angular distributions and energy losses are in better agreement with experiment than for the weak friction case.     

Analysis on heat stress-induced hyperphosphorylation of stathmin at serine 37 in Jurkat cells by means of two-dimensional gel electrophoresis and tandem mass spectrometry

Two-dimensional gel electrophoresis (2-DE) and tandem mass spectrometry were successfully used for determination of a phosphorylation site of stathmin induced by heat stress to Jurkat cells of a human T lymphoblastic cell line. The cells were incubated for 30 min at 41 degrees C up to 45 degrees C in a serum free 4-(2-hydroxyethyl)-1-piperazineethanesulfonic acid (HEPES) buffered culture medium. The intracellular soluble proteins were separated by 2-DE, and some of the proteins increased their abundance by heat stress. Those proteins were identified to be calmodulin, protein kinase C substrate, thymosin beta-4 and F-actin capping protein beta-subunit by peptide mass fingerprinting (PMF) with matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF-MS). On the contrary, protein phosphatase 2C gamma-isoform, nucleophosmin, translationally controlled tumor protein, Rho GDP-dissociation inhibitor-1, eukaryotic translation initiation factors 5A and 3A subunit 2, ubiquitin-like protein SMT 3B and chloride intracellular channel protein-1 were decreased their abundance. A protein spot of M(r) 18,000 and pI 5.9 was markedly increased at temperatures higher than 43 degrees C at which the cells were led to apoptosis. The spot was identified to be stathmin of a signal relay protein which has a function of sequestering microtubule. MALDI-quadrupole ion trap (QIT)-TOF-MS/MS and immunoblotting with a monoclonal antibody specific for a phosphorylation site of stathmin showed that the spot was a phosphorylated stathmin at serine 37 (Ser 37). The phosphorylation was suppressed by treatment of cells with olomoucine of an inhibitor specific for cyclin dependent kinase (Cdk-1). These results strongly suggest that heat stress activates Cdk-1 which phosphorylates Ser 37 on the stathmin molecule. The phosphorylation may cause the functional loss of stathmin for dynamic microtubule assembly and leads Jurkat cells to cell cycle arrest and apoptosis.     

Contraction-related variation in frequency dependence of acoustic properties of canine myocardium

Results of experiments performed in several laboratories indicate that contracting myocardium exhibits a cyclic variation of the magnitude of ultrasonic backscatter, with maxima occurring at end-diastole and minima at end-systole. The mechanisms responsible for this variation are not well understood. The purpose of the present study was to determine whether the frequency dependence of backscatter exhibits systematic variation throughout the cardiac cycle, analysis of which may facilitate improved understanding of biologic factors responsible for the cyclic variation of the magnitude of backscatter. In this study, the myocardial backscatter coefficient, as a function of frequency, was measured throughout the cardiac cycle in nine open-chest dogs. The frequency dependence of the backscatter coefficient was computed from a least-squares linear fit to log backscatter coefficient versus log frequency data. A cyclic variation of frequency dependence of backscatter was found with maximum near end-diastole (f2.6 +/- 0.1) and minimum near end-systole (f2.2 +/- 0.1), a significant variation (p less than 0.01). These results suggest that mechanisms responsible for the cyclic variation of backscatter may include changes in the effective size of the dominant scatterers throughout the cardiac cycle. An alternative explanation for the observed variation is an increase in the myocardial attenuation coefficient during systole followed by a decrease in diastole.