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)

Lysozyme activity was measured in cerebrospinal fluid (CSF) from 114 patients with inflammatory (bacterial and serous meningitis, polyradiculitis, encephalitis) and non-inflammatory (multiple sclerosis, CNS tumors, cerebral vascular diseases) CNS diseases. Highly elevated values were found consistently in patients with bacterial meningitis. Elevated values were found also in patients with encephalitis, polyradiculitis, multiple sclerosis and CNS tumors, but a considerable overlapping between these groups and normal controls precludes the use of CSF lysozyme measurements as a diagnostic aid in the latter disease groups. Simultaneous measurements of lysozyme, albumin and IgG in CSF and serum suggested that the mechanism for increased CSF lysozyme values in bacterial meningitis is mainly a breakdown of the blood/brain barrier, whereas the increased CSF lysozyme values in the remaining groups of patients are more likely caused by production of lysozyme by cells within the meninges (neutrophilic granulocytes, monocytes?).
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PMID:Lysozyme activity in cerebrospinal fluid. Studies in inflammatory and non-inflammatory CNS disorders. 85 79

A subcutaneously transplantable meningeal tumour (MM-KMY) was derived from a spontaneous malignant meningioma which developed in the cerebellar meninges of a female F344 rat. MM-KMY was subjected to 25 serial passages in syngeneic male and female rats. The transplants grew in 8 weeks into a nodule with an average diameter of 5.7 cm and average weight of 125.2 g. MM-KMY possessed large cysts containing fluid and necrotic tissue. Metastases frequently occurred in the lungs of MM-KMY-bearing rats. Histologically, both the original tumour and MM-KMY consisted of round to fusiform neoplastic cells of varying size, with nuclear pleomorphism. Mitotic figures occurred frequently. MM-KMY cells were positive for vimentin. Ultrastructurally, the cells showed desmosome-like structures, interdigitating processes and cytoplasmic intermediate filaments, suggesting an arachnoid cell origin. Abnormal accumulations of hyaline droplets in renal tubular epithelial cells were frequently observed in MM-KMY-bearing rats, suggesting overload of low molecular proteins in the renal tubules. The droplets gave a faint immunoreaction for lysozyme. The relation between the appearance of renal tubular hyaline droplets and the growth of MM-KMY remains to be determined. MM-KMY may prove useful for studying the biological behaviour and morphogenesis of meningeal tumours.
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PMID:Biological behaviour and morphological characteristics of a transplantable tumour (MM-KMY) derived from a malignant meningioma in an F344 rat. 753 Jul 32

Malignant histiocytosis is a well-recognized canine tumour, occurring primarily in Bernese mountain dogs and characterized by disseminated histiocytic infiltration of multiple visceral organs. This report describes the light microscopical and ultrastructural features of a neoplasm composed of malignant histiocytes and confined to the brain. A poorly demarcated mass in the right parieto-occipital lobe of a miniature schnauzer was composed of loosely aggregated, pleomorphic cells with abundant eosinophilic cytoplasm, expanding the meninges. Many binucleated and multinucleated giant cells and mitotic figures were seen. Immunohistochemically, the tumour cells reacted intensely for lysozyme. Ultrastructurally, the neoplastic cells had features of histiocytic cells with abundant lysosomes. The findings in this case were strikingly similar to those of disseminated malignant histiocytosis described in other dog breeds.
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PMID:Primary malignant histiocytosis of the brain in a dog. 1037 96

A cerebrospinal fluid sample collected from the cerebellomedullary cistern of a 10-year-old Shetland Sheepdog with a recent history of seizures was submitted for fluid analysis and cytologic examination. Key findings included a total nucleated cell count of 520/microL (reference interval 0-5 cells/microL), with a predominance of mononuclear cells, a protein concentration of 51.8 mg/dL (reference interval 0-35 mg/dL), and a glucose concentration of 44.7 mg/dL (reference interval 52-105 mg/dL). There was marked atypia of the mononuclear cells, with abundant eosinophilic cytoplasm, marked anisocytosis and anisokaryosis, occasional binucleated cells, mitotic figures, and rare erythrophagia. The cytologic interpretation was marked, monocytoid-rich, mixed cell pleocytosis with cellular atypia worrisome for neoplasia. In addition to histiocytic neoplasia, differentials included granulomatous meningoencephalomyelitis, necrotizing meningoencephalitis, and granulomatous inflammation. The dog did not respond to anti-inflammatory and anticonvulsive therapy. At necropsy, a mass involving the meninges and subtending the neuropil of the right temporal lobe of the cerebrum was found. Histologically, the mass was composed of large, bizarre histiocytic cells with multinucleated forms and numerous mitotic figures. Using immunochemistry on cytologic and histologic samples, the pleomorphic histiocytic cells were positive for CD1c, CD11ad, CD45, lysozyme, and vimentin, and were negative for CD3, CD4, CD79a, CD90, and pancytokeratin. These findings supported a diagnosis of primary CNS malignant histiocytosis of dendritic antigen-presenting cell (CD1c+) origin. To our knowledge, this is only the third reported case of primary CNS histiocytic sarcoma in dogs, and the first to demonstrate strong immunochemical evidence for dendritic antigen-presenting cell origin.
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PMID:Cerebrospinal fluid from a 10-year-old dog with a single seizure episode. 1651 5

A cerebral granular cell tumor is described in a 6-year-old, short-haired, female cat. The tumor was observed above the corpus callosum and completely infiltrating the third ventricle. Histologic examination revealed that the tumor was characterized by large cells containing densely packed intracytoplasmic granules and expressed psammoma body-like patterns and cholesterinic degeneration. Immunohistochemical analysis revealed granular neoplastic cells that were diffusely and strongly vimentin-positive, while they did not express cytokeratins, lysozyme, and synaptophysin. Based on morphologic and immunohistochemical findings, the tumor under study was considered to be of meningeal origin arising directly from the meninges or from meningeal elements scattered in the tela choroidea of the third ventricle roof.
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PMID:A cerebral granular cell tumor in a cat. 1696 66

We have studied the initial innate immune response to focal necrotic injury on different sides of the mouse blood-brain barrier by two-photon intravital microscopy. Transgenic mice in which the promoter of the myeloid isoform of lysozyme drives GFP were used to track granulocytes and monocytes. Necrotic injury in the meninges, but not the brain parenchyma, recruited GFP+ cells within minutes that fully surrounded the necrotic site within a day. Recently, it has been suggested that microglial cells and astrocytes cooperate to mount a distinct response to laser injury behind the blood-brain barrier. We followed the microglial response in heterozygous knockin mice in which GFP replaces CX3CR1 coding sequence. Prior to injury, microglial cell bodies were immobile over days, but moved to the laser injury site within 1 day. We followed astrocytes, which have been proposed to cooperate with microglial cells in response to focal injury, using transgenic mice in which glial fibrillary acidic protein promoter drives GFP expression. Before injury fine astrocyte processes permeate the parenchyma. Astrocytes polarized toward the injury in an ATP, connexin hemichannels, and intracellular Ca2+ -dependent process. The astrocytes network established a cytoplasmic Ca2+ gradient that preceded the microglial response. This is consistent with astrocyte-microglial collaboration to mount this innate response that excludes blood leukocytes.
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PMID:Innate response to focal necrotic injury inside the blood-brain barrier. 1701 12

Sixteen isolates of gram-positive, coccoid bacteria were obtained from clinical cases of diverse conditions in cattle and identified as Streptococcus suis using 16S ribosomal DNA gene sequencing and other bacterial identification methods. None of the isolates could be assigned to any of the known S. suis capsular types. Virulence-associated gene profiling that targeted muramidase-released protein, extracellular protein factor, suilysin, 89-kb pathogenicity island, and arginine deiminase ( arcA) genes were negative except for 1 isolate that was arcA positive. The arcA-positive isolate caused severe widespread lesions, including multiorgan suppurative and hemorrhagic inflammation in the meninges, lung, liver, spleen, lymph nodes, and serosae of heart and intestines. The other isolates were primarily associated with meningitis, bronchopneumonia, and multifocal acute necrotizing hepatitis. The isolates differed from each other by 4-6 fragments when examined by pulsed-field gel electrophoresis, indicating they are possibly related. The isolates were susceptible to ampicillin, penicillin, and tiamulin. Resistance was noted to sulfadimethoxine (93%), oxytetracycline (86%), chlortetracycline (86%), neomycin (67%), tilmicosin (47%), clindamycin (47%), enrofloxacin (33%), gentamicin (13%), florfenicol (7%), trimethoprim-sulfamethoxazole (7%), and spectinomycin (53%). Multi-drug resistance (defined as resistance to at least 1 agent in 3 or more antimicrobial classes) was detected in 67% of the isolates. The pathology observations provide evidence that S. suis may be an important pathogen of bovine calves. S. suis is an agent that clinical bacteriology laboratories should consider when dealing with cases involving cattle.
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PMID:Isolation and partial characterization of Streptococcus suis from clinical cases in cattle. 2816 7