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

Serial determinations of beta 2-microglobulin, lactoferrin and lysozyme in CSF were performed in 14 patients with acute cerebrovascular lesions. Marked elevations were noted in patients with cerebral bleeding or hemorrhagic infarction. Patients with infarction without signs of bleeding or with cerebrovascular lesions undetectable by computed tomography also had an increase in these proteins. The increases in CSF of beta 2-microglobulin, lactoferrin and lysozyme could not be explained by a damaged blood-brain barrier but was believed to be a local product of the central nervous system. Peak levels of lactoferrin and lysozyme were noted on day 2-3 after onset of symptoms. Lactoferrin then declined while lysozyme remained elevated for another few days. beta 2-microglobulin gradually increased reaching peak levels on day 4-5 and remained elevated even 2 weeks after the onset of symptoms. We suggest that the increases of lactoferrin, lysozyme and beta 2-microglobulin reflect various inflammatory reactions mediated by granulocytes, macrophages and lymphocytes, respectively.
Stroke
PMID:Lactoferrin, lysozyme, and beta 2-microglobulin in cerebrospinal fluid. Elevated levels in patients with acute cerebrovascular lesions as indices of inflammation. 616 35

A 75-year-old woman with sarcoidosis developed sudden weakness of the left upper and lower limbs. Neurological examination revealed left-sided hemiplegia, hyperreflexia with pathological reflexes and hypesthesia. She was disoriented and euphoric. Diffusion-weighted brain MRI showed high intensity lesions in the right parietooccipital lobes. Electroencephalogram showed diffuse slowing of the background activity. Serum lysozyme increased to 18.4 mg/ml, CSF protein to 51 mg/dl. After admission, she presented psychotic manifestation followed by a progressive disturbance of consciousness. Epithelioid granulomas without caseous necrosis were present in the biopsied lymph node and specimens from the occipital cortex, indicating neurosarcoidosis. Necrosis was also present in the sampled brain tissue. The psychotic symptoms and consciousness disturbance rapidly ameliorated after the treatment with oral prednisolone, 40 mg/day. Neurosarcoidosis should be considered even in an elder case of sarcoidosis complicated with a stroke.
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PMID:[An elder case of neurosarcoidosis associated with brain infarction]. 1519 54

Cardiovascular dysfunction in septic shock (SS) is ascribed to the release of inflammatory mediators. Norepinephrine (NE) is often administered to treat low MAP in SS. We recently found that lysozyme c (Lzm-S) released from leukocytes was a mediator of myocardial depression in an Escherichia coil model of SS in dogs. This effect can be blocked in an in vitro preparation by chitobiose, a competitive inhibitor of Lzm-S. In the present study, we examined whether chitobiose treatment can reverse myocardial depression and obviate NE requirements in two respective canine E. coli preparations. In a 6-h study, we administered chitobiose after 3.5 h of E. coli bacteremia and compared stroke work (SW) and MAP at 6 h with a sepsis control group. In a 12-h study, we determined whether chitobiose treatment can reduce the need for NE requirements during 12 h of bacteremia. In the latter study, either chitobiose or NE was given when MAP decreased approximately 20% from the presepsis value in respective groups. In anesthetized, mechanically ventilated dogs, we monitored hemodynamic parameters during continuous E. coli infusion. In the 6-h study, chitobiose improved SW and MAP at the 6-h period as compared with the nontreated sepsis group. In the 12-h study, SW and MAP increased after chitobiose without the necessity of NE administration. These results suggest that inhibitors of Lzm-S such as chitobiose may improve myocardial depression and reduce the need for NE requirements in SS.
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PMID:N,N'-diacetylchitobiose, an inhibitor of lysozyme, reverses myocardial depression and lessens norepinephrine requirements in Escherichia coli sepsis in dogs. 1788 42

Langevin mode theory and the coarse-grained elastic network model (ENM) for proteins are combined to yield the Langevin network model (LNM). Hydrodynamic radii of 6 A were assigned to each alpha-carbon on the basis of matching experimental translational and rotational diffusion constants of lysozyme, myoglobin, and hemoglobin with those calculated using a rigid body bead model with hydrodynamic interactions described by the Rotne-Prager tensor. LNM analysis of myosin II indicates that all ENM-like modes are overdamped at water viscosities. The low-frequency LNM modes in the pre-power stroke structure (PDB code: 1VOM) are substantially less mixed than the corresponding modes of the post-power stroke structure (1Q5G). Results from a four-bead model of the myosin "lever arm" indicate that coupling between modes increases as the array departs from linearity and are consistent with the results for 1VOM and 1Q5G. The decay times for all overdamped Langevin modes are shorter than the calculated rotational tumbling times found for lysozyme and myosin.
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PMID:Langevin network model of myosin. 1831 63