Immunolocalization of intercellular adhesion molecule-1 and leukocyte functional associated antigen-1 in schistosomal soluble egg antigen-induced granulomatous hyporesponsiveness.

In this work, the changes in expression of the adhesion molecules ICAM-1/LFA-1 on inflammatory cells of the liver were studied by immunohistochemistry. Mice sensitized with SEA and infected with S. mansoni and S. mansoni-infected controls were examined from day 35 to day 56 postinfection. A significant upregulation of ICAM-1 and LFA-1 in both the SEA group and the infected control group started shortly after egg deposition at day 35 and persisted up to day 56 p.i. Notably, both ICAM-1 and LFA-1 expression peaks were shifted earlier to day 38 p.i. in the SEA group compared to day 40 in the infected control group. The distribution of ICAM-1 and LFA-1 in both groups was comparable. At the early phase of infection before granuloma formation, both ICAM-1 and LFA-1 were detected along the sinusoidal wall of small blood vessels. At the acute cellular granuloma phase, they were homogeneously distributed all over the inflammatory cells, while at the chronic fibrocellular stage a non-homogeneous staining of granuloma cells at the periphery of the granuloma was apparent. The present data suggest that adhesion molecules play a role in the initiation and maintenance of granuloma formation. Thus, the granulomatous hyporesponsiveness induced by sensitization with SEA was associated with reduced expression of adhesion molecules.

Immunolocalization of macrophage adhesion molecule-1 and macrophage inflammatory protein-1 in schistosomal soluble egg antigen-induced granulomatous hyporesponsiveness.

This work studied the histopathological changes and the changes in the expression of macrophage adhesion molecule-1 (Mac-1) and macrophage inflammatory protein-1alpha (MIP-1alpha) in a murine model of soluble egg antigen (SEA) - induced granulomatous hyporesponsiveness. Histopathological results of hepatic sections in an SEA group showed early acceleration of ova destruction and markedly diminished granuloma cellularity with eosinophils and macrophages still being the predominant cells. Later, giant cells and pigmented macrophages that were scattered among granuloma cells and in intimate contact with the deposited eggs were more predominant in the SEA group than in the infected control group. Concurrently, the counts of Mac-1 positive cells were significantly increased in liver sections of the SEA group than the infected control group during the course of infection. MIP-1alpha showed early higher counts followed by lower counts in the later stages of infection on granuloma cells in the SEA group than the infected control group. During the course of infection, similar distribution of Mac-1 and MIP-1alpha was present in both groups. This study suggests that sensitization with SEA probably leads to enhancement of phagocytic activity of macrophages via increasing expression of Mac-1 and hence engulfment of ic3b coated schistosomal products such as ova. It leads to rapid destruction of ova and hence decreases the host inflammatory response to infection and amelioration of hepatic pathology which would be a promising approach in reduction of host morbidity and mortality.

Continuous ST-segment monitoring during coronary angioplasty using orthogonal ECG leads.

In order to characterize ST-segment shifts during transient coronary artery occlusion, 24 patients with single-vessel disease were continuously monitored during percutaneous transluminal coronary angioplasty by use of a computerized orthogonal lead system. Changes of ST-segment (J + 60 ms) in leads X, Y, and Z and of the ST vector magnitude were analyzed by using 20 microV as a threshold for significant ST-segment shift. The sensitivity and magnitude of this shift were compared among the left anterior descending, right coronary, and circumflex artery groups (11, 8, and 5 patients, respectively) during balloon inflation. Significant ST-segment shifts were seen in 22 patients (92%) in ST-VM, Y, and Z leads and all patients in lead X (100%). There was no significant difference in sensitivity of either the ST vector magnitude or the most sensitive lead for occlusion detection among the three groups. There was a significantly greater magnitude of ST shift during left anterior descending artery occlusion than during right coronary artery and circumflex artery occlusions in ST-VM. Analysis of the direction of ST shifts in the X, Y, and Z leads showed a characteristic pattern, which could distinguish among the three coronary groups in 21 patients (88%). The presence of collaterals was significantly associated with ST-segment depression in leads oriented toward ischemia (3 of 6 patients) as compared with ST-segment elevation in the absence of collaterals (all of 15 patients), P > .01. It is concluded that ST-segment shift in the orthogonal leads is a reliable marker for myocardial ischemia. It is equally sensitive to occlusion of each of the three major coronary arteries and can thus identify the occluded coronary. An ST-segment depression instead of an elevation was related to the presence of collaterals, which may reflect a lesser degree of ischemia.

Continuous ST segment recording during thrombolysis in acute myocardial infarction: a report on orthogonal ECG monitoring.

BACKGROUND: A noninvasive, real time method is needed to identify failures of thrombolysis and evaluate new treatments in acute myocardial infarction (MI). OBJECTIVE: To study XYZ monitored ST segment evolution during thrombolysis in acute MI and to examine the correlation of ST parameters to outcome. DESIGN: Thirty-five patients receiving tissue plasminogen activator (tPA) (n = 18) or streptokinase (SK) (n = 17) for acute MI were monitored by vector-cardiography during the first 12 h of thrombolytic therapy. Computer constructed ST vector magnitude (ST-VM) trends were analyzed for 0.5 or greater decline from the initial ST amplitude (IA) lasting for 10 mins or longer (ST response) and for ST re-elevation 0.75 IA or more following ST decline. The degree of ST response, time from treatment onset and ST-VM re-elevation were correlated to peak creatine phosphokinase (CPK), left ventricular ejection fraction (EF) and final ST-VM. RESULTS: The presence of an ST response correlated with a lower peak CPK (2691 +/- 1625 versus 4057 +/- 1622 U/L, P = 0.043) and tended to higher EF (0.48 +/- 0.11 versus 0.36 +/- 0.09, P = 0.057). The ST responder group had fewer patients with ST re-elevation than the group of nonresponders (13 of 30 versus five of five patients, P = 0.041). Moreover, ST response before 120 mins was associated with lower peak CPK (2089 +/- 1299 versus 3367 +/- 177 U/L, P = 0.02) and better EF (0.54 +/- 0.06 versus 0.41 +/- 0.12, P = 0.02) compared with later or no ST response. The degree of ST response correlated significantly with a lower ST-VM during the last hour (r = -0.744, P = 0.001). ST trends showed no significant differences between treatment groups (tPA versus SK). The tPA group, however, tended to an overall earlier ST response (117 +/- 75 versus 163 +/- 64 mins, P = 0.13). CONCLUSIONS: Early ST-VM trends are closely associated with electrocardiographic and clinical outcome and may provide a basis for clinical management, therapeutic comparisons and better insight into thrombolysis in MI.

Fluorescence microscopy in the detection of early myocardial infarction.

Fluorescent microscopy is amongst the many techniques devised for the post-mortem detection of early myocardial infarction. The method has the advantage of sensitivity, speed and simplicity, compared with more complex techniques such as enzyme histochemistry and electron microscopy. Disadvantages include the difficulty of permanent preservation of the sections and lack of sharp differentiation between normal and very early infarction--though the latter problem is common to most other methods, except enzyme histochemistry. There are two main techniques in fluorescent microscopy: The examination of sections specifically stained by fluorochrome dyes; The re-examination of haematoxylin-eosin sections for 'autofluorescence'.