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Biomedical subjects

E C Lawrence

Publications and source records attributed to E C Lawrence.

68 records · Page 4Linked to original sources
PubMed1980

Asbestos body phagocytosis by human free alveolar macrophages.

Phagocytosis of asbestos bodies by human free alveolar macrophages (FAMs) was documented employing light microscopy. This process was more carefully studied utilizing scanning electron microscopy (SEM) which demonstrated morphological and surface membrane changes in FAMs following phagocytosis of asbestos bodies. FAM viability was also evaluated following 24--72-h incubation of cells with asbestos bodies at a final concentration of 250 micrograms/ml. Slight, but significant, cytotoxicity was observed following the initial 24-h culture period (P = 0.032, paired, 2-tailed t-test). No further cytotoxicity was observed, however, when cells were further incubated for 48-h and 72-h intervals (P greater than 0.05 in all instances). These studies demonstrate asbestos bodies are readily phagocytized by cultured FAMs, and are only slightly cytotoxic to these human lung cells.

Adult↗
PubMed1979

Tissue distribution of immunoglobulin-secreting cells in normal and IgA-deficient chickens.

A reverse hemolytic plaque assay was employed to enumerate lymphoid cells actively secreting either immunoglobulin (Ig)G, IgA, or IgM in the small intestine, lungs, and lymphoid organs of normal and IgA-deficient chickens. In normal birds, intestinal lamina propria lymphocytes were proportionately richest in cells secreting IgG and IgA whereas the bone marrow was richest in IgM-secreting cells. The highest ratio of IgA to IgG secreting cells was also found in the lamina propria lymphocytes of the intestine (0.9), followed by the IgA to IgG ratios in the intestinal epithelium (0.31), and the lungs (0.19). The IgA to IgG ratios in the bone marrow (0.08) and the spleen (0.02) were considerably lower. Thus, both the intestine and the lungs were relatively enriched in cells actively secreting IgA. These IgA-secreting cells are the likely source of the IgA found in such quantities in intestinal and respiratory secretions. The tissue distribution of Ig-secreting cells was also studied in two generations of birds with experimentally induced IgA deficiency. There was a striking diminution of IgA-secreting cells in all tissues, including the intestine and lungs, whereas cells secreting IgG and IgM were normal or increased. The lack of IgA-secreting cells in these birds represents the effects of donor suppressor T cells having specificity for IgA.

Agammaglobulinemia↗
PubMed1978

Immunoglobulin secreting cells in normal human bronchial lavage fluids.

Immunoglobulin secreting cells were quantitated in the bronchial lavage fluids of 12 normal volunteers and compared with immunoglobulin secreting cells in peripheral blood, by a reverse hemolytic plaque assay. The mean number of cells secreting immunoglobulin (Ig)G in bronchial lavage fluids was 489 per million lymphocytes vs. a mean of 175 IgG secreting cells per million lymphocytes in peripheral blood (P < 0.02). The mean number of IgA secreting cells in bronchial lavage fluids was 633 per million lymphocytes as compared to 100 per million lymphocytes in peripheral blood (P < 0.005). Thus, compared to peripheral blood, cells from the lavage fluids were relatively enriched for both IgG and IgA secreting cells. However, IgA secreting cells were the major class of immunoglobulin secreting cells in bronchial lavage fluids, whereas IgG secreting cells predominated in peripheral blood. The prominence of IgA secreting cells in bronchial lavage fluids was further demonstrated by a mean ratio of IgA/IgG secreting cells in bronchial lavage fluids of 1.26 compared to a ratio in peripheral blood of 0.57 (P < 0.02). Cells secreting IgM were identified in only four of seven bronchial lavage fluid samples studied but in all peripheral blood samples. IgE secreting cells were not present in normal peripheral blood but could be demonstrated in 5 of 11 lavage fluid specimens. Thus, cells actively secreting immunoglobulins can be identified in the lower bronchial-alveolar tree of normal human subjects. Cells secreting IgG, IgA, or IgM may function in local lung defenses against infection; cells secreting IgE may contribute to hypersensitivity reactions in the lung.

Adult↗
PubMed1974

The hypercalciurias. Causes, parathyroid functions, and diagnostic criteria.

The causes for the hypercalciuria and diagnostic criteria for the various forms of hypercalciuria were sought in 56 patients with hypercalcemia or nephrolithiasis (Ca stones), by a careful assessment of parathyroid function and calcium metabolism. A study protocol for the evaluation of hypercalciuria, based on a constant liquid synthetic diet, was developed. In 26 cases of primary hyperparathyroidism, characteristic features were: hypercalcemia, high urinary cyclic AMP (cAMP, 8.58+/-3.63 SD mumol/g creatinine; normal, 4.02+/-0.70 mumol/g creatinine), high immunoreactive serum parathyroid hormone (PTH), hypercalciuria, the urinary Ca exceeding absorbed Ca from intestinal tract (Ca(A)), high fasting urinary Ca (0.2 mg/mg creatinine or greater), and low bone density by (125)I photon absorption. The results suggest that hypercalciuria is partly secondary to an excessive skeletal resorption (resorptive hypercalciuria). The 22 cases with renal stones had normocalcemia, hypercalciuria, intestinal hyperabsorption of calcium, normal or low serum PTH and urinary cAMP, normal fasting urinary Ca, and normal bone density. Since their Ca(A) exceeded urinary Ca, the hypercalciuria probably resulted from an intestinal hyperabsorption of Ca (absorptive hypercalciuria). The primacy of intestinal Ca hyperabsorption was confirmed by responses to Ca load and deprivation under a metabolic dietary regimen. During a Ca load of 1,700 mg/day, there was an exaggerated increase in the renal excretion of Ca and a suppression of cAMP excretion. The urinary Ca of 453+/-154 SD mg/day was significantly higher than the control group's 211+/-42 mg/day. The urinary cAMP of 2.26+/-0.56 mumol/g creatinine was significantly lower than in the control group. In contrast, when the intestinal absorption of calcium was limited by cellulose phosphate, the hypercalciuria was corrected and the suppressed renal excretion of cAMP returned towards normal. Two cases with renal stones had normocalcemia, hypercalciuria, and high urinary cAMP or serum PTH. Since Ca(A) was less than urinary Ca, the hypercalciuria may have been secondary to an impaired renal tubular reabsorption of Ca (renal hypercalciuria). Six cases with renal stones had normal values of serum Ca, urinary Ca, urinary cAMP, and serum PTH (normocalciuric nephrolithiasis). Their Ca(A) exceeded urinary Ca, and fasting urinary Ca and bone density were normal. The results support the proposed mechanisms for the hypercalciuria and provide reliable diagnostic criteria for the various forms of hypercalciuria.

Adult↗
PubMedDate not supplied

The relationship of soluble interleukin-2 receptor levels to allograft arteriopathy after heart transplantation.

Certain dynamics of rejection after heart transplantation can be characterized by measuring soluble interleukin-2 receptor levels. To determine whether elevated levels could predict development of coronary artery disease, the mean of three weekly determinations the first month after heart transplantation, as well as values obtained at 6 months, 12 months, 18 months, and 24 months after the procedure, were evaluated. Comparison was made between the groups in whom allograft arteriopathy did or did not develop. Concomitant endomyocardial biopsy scores also were evaluated. Fifty-five patients surviving the initial 30 days after heart transplantation were prospectively followed up. Eighty-five percent were male, and the median age was 51 years. Coronary arteriopathy developed in 15 patients (27%) during a mean follow-up period of 26 months (range, 1 to 54 months). For the early follow-up point, mean (+/- standard deviation) receptor levels for those patients without allograft arteriopathy were 880 +/- 846 U/ml and for those with arteriopathy, 1410 +/- 590 U/ml (p = 0.001). At each follow-up point thereafter, soluble interleukin-2 receptor levels were greater in the group with allograft arteriopathy. Indeed, at all observation points, the group in whom disease developed had levels greater than 1000 U/ml, and these values were, from a statistical standpoint, always greater than the group without detectable arteriopathy. In contradistinction, endomyocardial biopsy scores were no different at either early or late follow-up periods. Allograft arteriopathy after heart transplantation seems predicted by early elevation of plasma soluble interleukin-2 receptor levels, and patients with this difficulty generally have elevated levels during long-term follow-up.

Coronary Disease↗
PubMedDate not supplied

Elevated soluble interleukin-2 receptor levels early after heart transplantation and long-term survival and development of coronary arteriopathy.

Rejection dynamics after heart transplantation might be characterized by soluble interleukin-2 receptor levels. To determine whether elevated levels early (measured by enzyme-linked immunosorbent assay once weekly the first 3 weeks at time of heart biopsy) after transplantation predict mortality and development of coronary disease, the means of these three determinations and the endomyocardial biopsy scores (McAllister scale 0-10) were compared for survivors and nonsurvivors and patients who had coronary arteriopathy develop and those who did not. Fifty-five patients alive 30 days after heart transplantation were prospectively followed up. Overall, 47 patients were male (85%), and the median age was 51 years. Mean +/- SD follow-up was 26 +/- 15 months (range, 1 to 54 months). There were 38 survivors (69%), and coronary arteriopathy developed in 15 patients (27%). Whereas mean +/- SD heart biopsy scores for the early weeks were similar between survivors and nonsurvivors (3.6 +/- 1.4 vs 4.4 +/- 1.6; p greater than 0.05), the difference in soluble interleukin-2 receptor levels was significant (703 +/- 362 U/ml vs 1793 +/- 1070 U/ml; p less than 0.001). A mean level less than 1000 U/ml in any given patient predicted long-term survival with a 76% sensitivity, 79% specificity, and 88% negative predictive value. Mean receptor levels for those patients in whom coronary arteriopathy did not develop were 880 +/- 846 U/ml and for those with this difficulty, 1410 +/- 590 U/ml (p = 0.001). Late morbidity and mortality after heart transplantation seem predicted by early elevation of plasma soluble interleukin-2 receptor levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Biopsy↗
PubMedDate not supplied

Differential perfusion: potential complication of femoral-femoral bypass during single lung transplantation.

Single lung transplantation may be performed without pump oxygenation in the majority of patients. From April 1987 to August 1989, 3 of 12 patients undergoing single lung transplantation required pump oxygenation. One patient required pump oxygenation because of a marked drop in oxygen saturation during test clamping of the pulmonary artery; one patient was brought to the operating room while receiving extracorporeal membrane oxygenation; and one patient had such markedly elevated pulmonary artery pressures that pump oxygenation was used to lower pressure in the pulmonary circuit, allowing safe pulmonary artery clamping. These three patients had cannulas placed in the femoral vein and femoral artery. The latter two patients manifested marked upper body oxygen desaturation while maintaining excellent lower body oxygen saturation during their transplant procedures. Ventricular fibrillation, induced by alternating current, was used as a means to correct this differential perfusion. Should pump oxygenation be necessary during single lung transplantation, the region of the body adjacent to the arterial cannula may be perfused with oxygenated blood, and the remainder of the patient may be perfused with deoxygenated blood. Induced ventricular fibrillation is one method to correct this potentially fatal problem.

Cardiopulmonary Bypass↗
PubMedDate not supplied

Evolution of hemodynamics after orthotopic heart and heart-lung transplantation: early restrictive patterns persisting in occult fashion.

Though successfully transplanted hearts respond in such a way that individuals remain remarkably asymptomatic, they do not function normally. Characterization of early hemodynamic patterns and their evolvement has not been done. The evolution of hemodynamic indices in 20 patients receiving orthotopic heart (n = 17) or combined heart-lung (n = 3) transplants is therefore documented. In 15 isolated heart recipients, right heart catheterization was performed at 24 to 48 hours, 1 to 2 weeks, 4 to 8 weeks, and greater than 3 months after surgery at the time of routine endomyocardial biopsy. Early, patients had elevated mean blood pressure (96 +/- 14 mm Hg, mean +/- standard deviation), mean right atrial pressure (15 +/- 6 mm Hg), right ventricular end-diastolic pressure (16 +/- 7 mm Hg), mean pulmonary artery pressure (30 +/- 7 mm Hg), and mean pulmonary capillary wedge pressure (19 +/- 6 mm Hg), but normal resting heart rate (96 +/- 14 beats/min) and cardiac output (5.6 +/- 1.6 L/min). Heart rate, blood pressure, and output did not change during follow-up, but right atrial pressure decreased dramatically (4 +/- 2 mm Hg at 3 months), as did right ventricular end-diastolic pressure (4 +/- 4 mm Hg), mean pulmonary artery pressure (21 +/- 8 mm Hg), and pulmonary capillary wedge pressure (11 +/- 4 mm Hg). Analysis of right heart filling dynamics revealed an abnormal inspiratory rise in mean right atrial pressure (15 +/- 6 and 27 +/- 7 mm Hg at 24 to 48 hours) that subsequently resolved. In eight patients whose resting follow-up right heart pressures normalized, rapid volume challenge uncovered occult restrictive right atrial pressure patterns that increased from 4 +/- 4 to 9 +/- 4 mm Hg after infusion of saline solution. Kussmaul's response was not apparent with prevolume infusion, but volume expansion caused appearance of this hemodynamic pattern. All patients had early evidence of tricuspid insufficiency, but in two patients, the Doppler regurgitant fraction was over 50%. These two individuals had hemodynamics similar to the other 15 patients initially, but in contrast, their right heart filling pressures did not change during follow-up. Other significant echocardiographic findings included enlarged atria and increased left ventricular mass in all patients. In two of three combined heart-lung transplant patients, similar hemodynamic patterns were evident. Rejection indices did not correlate with hemodynamic observations. Thus a characteristic evolvement of hemodynamics in heart and heart-lung transplants that mimic dynamics associated with restrictive myocardial disease is documented.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMedDate not supplied

Relationship of increased levels of circulating intercellular adhesion molecule 1 after heart transplantation to rejection: human leukocyte antigen mismatch and survival.

Noninvasive methods to assess immune activation would be helpful in optimizing therapy after heart transplantation to reduce rejection (acute and chronic) and complications caused by excessive immunosuppressive therapy. Intercellular adhesion molecule 1 has been shown to play an important role in T-cell activation and allograft rejection. A soluble form of intercellular adhesion molecule 1 has been discovered to be circulating in plasma. To test the hypothesis that increased levels of circulating intercellular adhesion molecule 1 may have prognostic value as a marker of immune activation, we examined whether levels of circulating intercellular adhesion molecule 1 during the early postoperative period correlated with endomyocardial biopsy scores, soluble interleukin-2 receptor levels, human leukocyte antigen mismatch, and survival. For the first 3 weeks after surgery, serum was obtained once weekly on the same day as endomyocardial biopsy samples from 52 patients who survived more than 30 days after heart transplantation. A sandwich enzyme-linked immunosorbent assay was used to measure circulating intercellular adhesion molecule 1 and soluble interleukin-2 receptor. Increased circulating intercellular adhesion molecule 1 levels did not correlate with endomyocardial biopsy scores but were associated with greater mismatch at the human leukocyte antigen-B and -DR loci (p = 0.02). A significant correlation was found (p = 0.002) between circulating intercellular adhesion molecule 1 levels and soluble interleukin-2 receptor, albeit with a low r value of 0.27. Survival was reduced in patients with high levels of circulating intercellular adhesion molecule 1 (p = 0.006) or soluble interleukin-2 receptor (p = 0.001) with the greatest reduction in survival when both were elevated.(ABSTRACT TRUNCATED AT 250 WORDS)

Biopsy↗