Polarization of high-intensity high-harmonic generation.
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Biomedical subjects
Publications and source records attributed to D Du.
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OBJECTIVE: To observe the relationship between the filtration-index of erythrocytes and concentration of erythrocytic superoxide dismutase (SOD), plasma malonyldialdehyde (MDA) in cases of pregnancy induced hypertension (PIH). METHODS: We have measured the level of MDA and filtration-index, SOD content of erythrocytes in maternal and cord blood of 31 cases with PIH (group A) and 25 cases of normal pregnancy (group B) using TBA method, nucleopore membraned cell deformability meter and pyrogallol self-oxidizing method. RESULTS: The mean filtration-index level and erythrocytic SOD were significantly higher in group A than those of group B (P < 0.01 and P < 0.05). The mean content of plasmatic MDA in group A increased markedly (P < 0.01) compared to that of group B. There was no difference of these parameters in cord blood between group A and group B. CONCLUSION: The decrease of red cell deformability due to the increase of plasma MDA level may be the underlying mechanism of PIH.
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An expression vector encoding the human recombinant fusion protein interleukin 6/interleukin 2 (IL-6/IL-2) was constructed. When a flexible linker had been synthesized and ligated with the IL-2 gene fragment by polymerase chain reaction (PCR) amplification, the IL-6 gene fragment was unidirectionally inserted into the upstream of the linker-IL-2 sequence. The molecule of the IL-6-linker-IL-2 fusion gene named E. coli DH5 alpha/pfIL-6/2 was cloned and identified by DNA sequencing. The expressed protein named as CH925 showed a strong band on SDS-PAGE and amounted to 32% of total cell protein, and its estimated molecular weight was about 37 kDa. The fusion protein purified by gel filtration and reversed-phase HPLC showed as almost homogeneous. CH925 possesses both IL-2 and IL-6 activities when assayed by CTLL2- and 7TD1-dependent cell lines, respectively. The specific activity of IL-2 was 2.1 x 10(6) U/mg while that of IL-6 was 2.3 x 10(8) U/mg. Our studies exhibited that CH925 exerted a significant augmentative effect on the growth of erythroid colony forming units (CFU-E), and synergized with erythropoietin (EPO) and/or IL-3 in a dose-dependent way. Our experimental results also showed CH925 at a low dose causing active lymphokine-activated killer (LAK) cell proliferation more vigorous than IL-2 and/or IL-6 (p < 0.001). CH925 is a novel fusion protein, being neither IL-6 nor IL-2, more potent than IL-2 and/or IL-6 and causing non-IL-2 and non-IL-6 functions of strong EPO-like and mild IL-3-like effects on erythroid progenitor cell growth. There is a potential for efficacious clinical application of CH925.
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OBJECTIVE: The aim was to determine the beat to beat variability in local activation time during sustained monomorphic ventricular tachycardia in a canine model of experimental myocardial infarction. METHODS: A digital template matching algorithm was developed for detecting subtle beat to beat variability in local activation timing at each of multiple ventricular sites. Ten electrically induced sustained ventricular tachycardia episodes, mean cycle length 211 (SD 40) ms, were endocardially and epicardially mapped in mongrel dogs weighing 15-20 kg. Digitised data were analysed for beat to beat local activation time variability. Similar data recorded during ventricular pacing at comparable rates and during sinus rhythm served as controls. RESULTS: The overall mean variability of local activation time for all 10 ventricular tachycardias was 3.2(1.6) ms, range 1.8(1.1) ms to 4.7(2.8) ms, in contrast to the overall mean variability of 0.2(0.4) ms (p = 0.0001) for ventricular pacing and 0.7(0.6) ms (p = 0.0001) for sinus rhythm. Oscillations in local activation time manifested alternans type periodicity during seven of 10 ventricular tachycardias independent of any alternans in local electrogram morphology. CONCLUSIONS: During sustained, monomorphic ventricular tachycardia, beat to beat variability and alternans type oscillations in local activation time are common and may be an intrinsic property of re-entry since they are negligibly small during ventricular pacing.
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BACKGROUND: The precision and limitations of ventricular pacemapping as a method to localize the site of earliest breakthrough of ventricular tachycardia (VT) were investigated in a canine model of experimental myocardial infarction. METHODS AND RESULTS: Forty-one episodes of VT induced in 10 animals were mapped using a standard grid of 64 endocardial and epicardial bipolar electrodes to determine the site of earliest endocardial or epicardial breakthrough of activation during VT. Each of these 64 recording sites was also used for ventricular pacing during sinus rhythm at cycle lengths comparable to those of the VTs. Orthogonal X, Y, and Z Frank electrocardiographic (ECG) leads were recorded during all episodes of VT and ventricular pacing from all sites after the chest was closed in all animals. Surface ECG waveforms corresponding to each VT and each ventricular pacing were compared pairwise by measuring the Euclidean metric difference between the VT and ventricular pacing vectors with the orthogonal ECG leads as their X, Y, and Z components. The pacing site that generated the vector most similar to VT vector (smallest vectorial difference) was defined as the predicted breakthrough site. This predicted site of breakthrough was identical to the actual site of breakthrough determined by activation sequence mapping during VT for only nine VTs (22%). However, for an additional 27 VTs (66%), the observed and predicted breakthrough locations were at adjacent (1 cm or less apart) recording sites. For five VTs (12%), the two sites were remote, the distance between them exceeding 1 cm. CONCLUSIONS: In this model, locating the breakthrough site by pacemapping is exact in only a small minority of VTs. However, when orthogonal surface ECG leads are used for comparison, pacemapping can predict the site of earliest breakthrough during VT with a 1-cm resolution in the majority of VTs.
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