Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.2.1.17 (lysozyme)
 21,489 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Foamy alveolar macrophages (FAM) are observed in lungs injured by Bleomycin (BLM), but their relation to pulmonary fibrosis is not clearly understood. We purified FAM from BLM-instilled rat lungs by density gradient centrifugation on Percoll, and studied the effect of FAM on pulmonary fibrosis. The cells lavaged from the rat lungs 14 days after the administration of BLM (B) or saline (S), were applied on Percoll. After centrifugation, the cells layered on each interface were collected and named as SI, SII, SIII, and BI, BII, BIII in order of gravity. The BI layer included 8.5% of unfractionated cells (U). These BI cells were viable (88%), significantly larger than the others, nonspecific esterase positive cells, and included much ferritin and lysozyme, and were morphologically identified as alveolar macrophages (AM). Therefore, we called the BI cells FAM. We estimated the capacity of FAM (2.5 X 10(5] to synthesize DNA (3H-thymidine uptake) and RNA (3H-uridine uptake), and the activities of silica-stimulated FAM to cause proliferation of mouse thymocytes (IL-1 activity) and rat lung fibroblasts (FP activity), and to produce PGE2. FAM has a lower mitogenic activity but did not have been protein synthetic activity as compared with the others. Silica-stimulated FAM released less IL-1 than BII or BIII, and induced less fibroblast growth than BII, but induced as much as BIII, possibly because of the increased capacity of BIII cells to produce PGE2, which is known to inhibit fibroblast growth. In this way, FAM were considered to be "already activated" rather than "highly activated" cells, but the presence of FAM suggested that smaller or denser AM might receive bleomycin stimulation and release fibrogenic mediators (IL-1 or MDGF) into the alveolar spaces during FAM formation, and that AM might participate in the fibrogenic responses.
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PMID:[The effect of foamy alveolar macrophages presented in bleomycin-injured rat lungs in pulmonary fibrosis]. 247 35

During coronary angioplasty, inflation of the balloon within the coronary artery produces transient arterial occlusion and frequently results in myocardial ischemia. Delivery of oxygenated autologous blood to the myocardium at risk during inflation may help mitigate this ischemia. Accordingly, we investigated the feasibility and safety of infusing blood through the central lumen of a dilatation catheter around the guidewire using both a model in vitro and clinical trials. In the tests in vitro, fresh blood was infused at flow rates up to 120 ml/min. Hemolysis was minimal at flow rates of 60 ml/min or less (less than or equal to 0.92 +/- 0.18%), but increased exponentially at higher rates (13.64 +/- 2.37% at 120 ml/min, p less than .002). A similar pattern was observed for potassium release. Platelet and leukocyte counts did not vary significantly, and beta-thromboglobulin and muramidase remained at control levels. Although mean erythrocyte volume did not change, erythrocyte histograms and light microscopy demonstrated a subpopulation of red cell fragments averaging 25 to 40 fl in size at higher rates. A randomized, crossover clinical trial was next performed by delivery of blood perfusion at 60 ml/min to 15 patients undergoing coronary angioplasty. Levels of plasma hemoglobin, beta-thromboglobulin, lactate dehydrogenase, and potassium remained constant before and after the perfusion and the control inflations. The maximum pain score was significantly lower with the perfusion inflation (4.1 +/- 0.8 vs 6.0 +/- 0.9, p less than .003). Relative to baseline, the maximum ST segment elevation during the perfusion inflation (0.5 +/- 0.3 mm) was nearly one-fourth that during the control inflation (1.9 +/- 0.6 mm, p less than .02). Thus, myocardial protection with oxygenated autologous blood perfusion at rates of 60 ml/min appears to be a safe and effective technique that may permit increased inflation time and extend the range of coronary angioplasty to include individuals at high risk for the procedure.
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PMID:Autologous blood perfusion for myocardial protection during coronary angioplasty: a feasibility study. 295 55

A paired prospective study was performed to compare the in vitro storage characteristics and in vivo kinetics of platelets stored in granulocyte-platelet concentrates prepared by apheresis with platelets prepared from whole blood. Platelet and granulocyte-platelet concentrates were collected from five healthy volunteer autologous donors and stored for 16 to 18 hours at 20 to 24 degrees C with and without agitation, respectively. After storage, pH, platelet count, percent release of beta-thromboglobulin, morphologic score, and percent osmotic recovery were measured. In addition, the granulocyte-platelet concentrates were assayed for total leukocyte count, release of lysozyme, and by several in vitro tests of granulocyte function. The platelets in both products were labeled with 111In oxine and infused into the donors. The pH of both products was above 6.0 at the end of storage. The units stored as platelet concentrates compared with those stored as granulocyte-platelet concentrates showed a higher percent release of beta-thromboglobulin, 18.4 +/- 4.0 percent versus 5.9 +/- 3.2 percent (mean +/- SD), but significantly better morphologic scores, 676 +/- 21 versus 525 +/- 56, and better osmotic recovery scores, 72 +/- 10 percent versus 40 +/- 7 percent, respectively (all p less than 0.05). The platelet concentrates (compared with the granulocyte-platelet product) had significantly better in vivo recovery, 49.5 +/- 15.8 percent versus 38.9 +/- 11.5 percent, and survival, 6.1 +/- 1.3 days versus 2.4 +/- 0.4 days, respectively (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:In vitro characteristics and in vivo viability of platelets contained in granulocyte-platelet apheresis concentrate. 381 Aug 9

Activated platelets release substances which potentially can contribute to joint lesions in inflammatory arthritides. To elucidate a possible participation of platelets in inflammatory joint reactions, the concentrations of the platelet protein beta-thromboglobulin (beta-TG) were measured in 90 inflammatory synovial fluids. Seven percent of the patients with rheumatoid arthritis and none of the patients with other inflammatory joint diseases (e.g., Reiter's disease, reactive or crystal arthritides) had beta-TG concentrations in synovial fluid exceeding the upper normal range of plasma beta-TG. The absent or very modest signs of local platelet activation were contrasted by the pronounced neutrophilic and monocytic activation, as assessed by the measurements of some granule proteins: lactoferrin, myeloperoxidase, lysozyme, and ferritin. No correlation was found between these inflammatory cell markers and beta-TG. A positive correlation (p less than 0.001) was noted between beta-TG and beta 2-microglobulin, which appeared in particularly high amounts in rheumatoid arthritis. This correlation may reflect a disturbed permeability of synovial membrane for LMW proteins or a related activation of platelets and lymphocytes. The present results do not give any evidence of platelet activation playing a major role in proliferative or destructive processes in arthritis.
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PMID:Beta-thromboglobulin in inflammatory synovial fluid. 619 77