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)

N-acetyl-beta-glucosaminidase (EC 3.2.1.30, recommended name beta-N-Acetylglucosaminidase) was found to be a constituent of human cardiac lysosomes. beta-glucuronidase was also found in this tissue, while lysozyme, an enzyme present in leucocyte lysosomes, was not detectable in the heart. The activities of both N-acetyl-beta-glucosaminidase and beta-glucuronidase were elevated in plasma during the first 24 h after the onset of chest pain in patients with acute myocardial infarction and the peak levels of N-acetyl-beta-glucosaminidase correlated well with those of creatine kinase. N-acetyl-beta-glucosaminidase showed a further rise in plasma activity which gave a peak at 72 h after the onset of chest pain and this was accompanied by a rise in lysozyme activity. It is suggested that lysosome disruption caused by myocardial cell necrosis was responsible for the initial rise in plasma lysosomal enzyme activity and that the subsequent inflammatory reaction gave rise to the second peak.
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PMID:Plasma lysosomal enzyme activity in acute myocardial infarction. 64 16

We report a case of latent cardiac sarcoidosis in reference to differential diagnosis from giant cell myocarditis. A 68-year-old woman succumbed to subarachnoid hemorrhage and acute myocardial infarction within a period of 3 days. Autopsy revealed white fibrotic lesions in the lateral wall of the left ventricle and interventricular septum of the heart in addition to acute myocardial infarction of the anterior wall. Histology showed fibrotic granulomatous lesions with infiltration of lymphocytes and epithelioid cells. Many multinucleated giant cells of Langhans and foreign body types were scattered among these lesions. There was no lesion in the bilateral hilar lymph nodes, but typical epithelioid granuloma was noticed in the lymph node of the carina, liver, and spleen. So we concluded that the heart lesion was a case of cardiac sarcoidosis. Striation could not be seen in the multinucleated giant cells of the cardiac sarcoid lesion, and, using light microscopy, it seemed to us that these cells had no relation to the cardiac muscles. However, by immunohistochemistry (PAP method) some giant cells tested positive for myoglobin, and others tested positive for lysozyme. The fact that giant cells are not always derived from the cardiac muscle can't be used, as a criterion for the diagnosis of cardiac sarcoidosis. Giant cells in the lung and lymph nodes tested positive only for lysozyme. Hence, using only cardiac histology, it is difficult to make a differential diagnosis between cardiac sarcoidosis and giant cell myocarditis, especially in cases where there is multiple organ involvement.
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PMID:[A case of latent cardiac sarcoidosis in reference to differential diagnosis from giant cell myocarditis]. 230 29

Lidocaine is used extensively in coronary care units, yet the effect of lidocaine infusions on neutrophil function has not been known. Lidocaine and other local anesthetics impair leukocyte antibacterial functions when added in vitro. We found that lidocaine added to human neutrophils in vitro markedly impaired the release of superoxide anion (O2-) and the granule enzymes lysozyme and myeloperoxidase after stimulation by phorbol myristate acetate or opsonized zymosan. We then measured production of O2- during stimulation of neutrophils from eight normal subjects, five coronary artery disease patients not receiving lidocaine and 13 coronary artery disease patients receiving lidocaine infusions for at least 12 hr. Release of O2- by cells from lidocaine-treated patients (14.2 +/- 3.8 nmol/2.5 X 10(6) neutrophils per 15 min) was significantly lower than from cells of the normal subjects (78.4 +/- 7.2 nmol; P less than .001) and the coronary patients not receiving lidocaine (70.6 +/- 4.0 nmol; P less than .001). Bactericidal assays at a high concentration (2 mg/ml) of lidocaine demonstrated slight reductions in 2 hr killing rates for Escherichia coli (70% with lidocaine vs. 95% control). Inhibition by lidocaine of the release of toxic oxygen metabolites from neutrophils could potentially reduce infarct size in patients with acute myocardial infarction; but as there is only a slightly reduced ability to kill bacteria, increased susceptibility to infections is unlikely although it cannot be excluded.
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PMID:Reduced neutrophil superoxide anion release after prolonged infusions of lidocaine. 299 33

Free radicals play an important role in the pathogenesis of tissue damage in many clinical disorders, including atherosclerosis. Antioxidants protect the body from damage caused by free radicals. In this study we investigated oxidative stress, antioxidants and inflammatory molecules in patients with acute myocardial infarction. This study has been carried out on 106 patients with acute myocardial infarction, (89 men and 17 females). The control group consisted of 50 healthy, age-matched subjects (40 men and 10 females). Levels of Glucose, lipid profile, glutathione reduced, glutathione peroxidase, Superoxide dismutase, Glycosylated hemoglobin, fibrinogen, vitamin C, vitamin E, malondialdehyde, ceruloplasmin, adenosine deaminase, lysozyme and sialic acid were measured. Malondialdehyde and ceruloplasmin levels were significantly high and antioxidants such as vitamin C, vitamin E, glutathione reduced, glutathione peroxidase and superoxide dismutase were significantly decreased in diabetic and non-diabetic AMI patients as compared with control (p<0.001). Inflammatory markers showed significant rise in diabetic patients as compared with controls. Our results clearly show increased inflammation and oxidative stress in patients with acute myocardial infarction. Depression of antioxidant system in these patients confirms this conclusion.
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PMID:Antioxidant status in patients with acute myocardial infarction. 2310 51

In this study, we prepared surface plasmon resonance (SPR) sensor using the molecular imprinting technique for myoglobin detection in human serum. For this purpose, we synthesized myoglobin imprinted poly(hydroxyethyl methacrylate-N-methacryloyl-l-tryptophan methyl ester) [poly(HEMA-MATrp)] nanofilm on the surface of SPR sensor. We also synthesized non-imprinted poly(HEMA-MATrp) nanofilm without myoglobin for the control experiments. The SPR sensor was characterized with contact angle measurements, atomic force microscopy, X-ray photoelectron spectroscopy, and ellipsometry. We investigated the effectiveness of the sensor using the SPR system. We evaluated the ability of SPR sensor to sense myoglobin with myoglobin solutions (pH7.4, phosphate buffer) in different concentration range and in the serum taken from a patient with acute myocardial infarction. We found that the Langmuir adsorption model was the most suitable for the sensor system. The detection limit was 87.6 ng/mL. In order to show the selectivity of the SPR sensor, we investigated the competitive detection of myoglobin, lysozyme, cytochrome c and bovine serum albumin. The results showed that the SPR sensor has high selectivity and sensitivity for myoglobin.
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PMID:Microcontact imprinted surface plasmon resonance sensor for myoglobin detection. 2391 Feb 56

CodY, a nutritional regulator highly conserved in low G+C Gram-positive bacteria, is essential in Streptococcus pneumoniae (the pneumococcus). A published codY mutant possessed suppressing mutations inactivating the fatC and amiC genes, respectively belonging to iron (Fat/Fec) and oligopeptide (Ami) ABC permease operons, which are directly repressed by CodY. Here we analyzed two additional published codY mutants to further explore the essentiality of CodY. We show that one, in which the regulator of glutamine/glutamate metabolism glnR had been inactivated by design, had only a suppressor in fecE (a gene in the fat/fec operon), while the other possessed both fecE and amiC mutations. Independent isolation of three different fat/fec suppressors thus establishes that reduction of iron import is crucial for survival without CodY. We refer to these as primary suppressors, while inactivation of ami, which is not essential for survival of codY mutants and acquired after initial fat/fec inactivation, can be regarded as a secondary suppressor. The availability of codY- ami+ cells allowed us to establish that CodY activates competence for genetic transformation indirectly, presumably by repressing ami which is known to antagonize competence. The glnR codY fecE mutant was then found to be only partially viable on solid medium and hypersensitive to peptidoglycan (PG) targeting agents such as the antibiotic cefotaxime and the muramidase lysozyme. While analysis of PG and teichoic acid composition uncovered no alteration in the glnR codY fecE mutant compared to wildtype, electron microscopy revealed altered ultrastructure of the cell wall in the mutant, establishing that co-inactivation of GlnR and CodY regulators impacts pneumococcal cell wall physiology. In light of rising levels of resistance to PG-targeting antibiotics of natural pneumococcal isolates, GlnR and CodY constitute potential alternative therapeutic targets to combat this debilitating pathogen, as co-inactivation of these regulators renders pneumococci sensitive to iron and PG-targeting agents.
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PMID:Co-Inactivation of GlnR and CodY Regulators Impacts Pneumococcal Cell Wall Physiology. 2590 69