Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

The monoclonal antibody KP-1 that recognizes the lysosome-associated glycoprotein CD68 was used together with antibodies to other antigens (actin, glial fibrillary acidic protein, keratin, neurofilaments, chromogranin, synaptophysin, S-100 protein, HMB-45, lysozyme, and HLA-DR) in a labeled streptavidin biotin immunoperoxidase method to phenotypically characterize 27 granular cell tumors, five schwannomas, five neurofibromas, two ganglioneuromas, three ganglioneuroblastomas, five carcinoid tumors, five malignant melanomas, and five examples of histiocytosis X. The neoplastic cells in all 27 of the granular cell tumors and four of the five schwannomas strongly stained for CD68, whereas none of the neurofibromas, ganglioneuromas, ganglioneuroblastomas, or carcinoid tumors contained CD68-positive tumor cells. These findings further strengthen previous observations, suggesting a histogenetic relationship between granular cell tumors and Schwann cells. KP-1 reactivity also was demonstrated in cells of histiocytosis X and malignant melanoma, complementing other studies that extend the tumor types positive in immunoperoxidase stains using this antibody.
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PMID:Immunohistochemical demonstration of the lysosome-associated glycoprotein CD68 (KP-1) in granular cell tumors and schwannomas. 854 22

In an effort to shed light upon the nature of the colloid cyst, the immunohistochemical properties of 21 examples of this lesion were compared with those of other neuraxial cysts and choroid plexus epithelium. The neuraxial cysts included the following: eight Rathke's cleft cysts, 25 pituitaries containing follicular cysts of the pars intermedia, and four enterogenous cysts. Fifteen examples of normal choroid plexus and 12 choroid plexus papillomas were studied as well. These lesions were examined for localization of the following antigens: cytokeratins, epithelial membrane antigen, secretory component, carcinoembryonic antigen, prealbumin, vimentin, glial fibrillary acidic protein (GFAP), S-100 protein, neuron-specific enolase, 68-kD neurofilament protein, chromogranin, serotonin, and lysozyme, and with Leu-7 monoclonal antibodies. Five colloid cysts were immunostained with monoclonal antibodies that were specific for Clara-cell antigens and surfactant, respectively. Sugar moieties were localized using Ulex europaeus I, and Ricinus communis agglutinin I lectins. All Rathke's cleft cysts and follicular cysts of the pars intermedia as well as three selected colloid cysts were examined for pituitary hormones. The epithelial cells of colloid and enterogenous cysts, as well as those lining follicular and Rathke's cleft cyst, showed uniformly strong reactivity for cytokeratins, epithelial membrane antigen, secretory component, and vimentin, and bound Ulex europaeus lectin. Occasional cells in colloid cysts were positive for Clara cell-specific antigens. Reaction for carcinoembryonic antigen was present on the apical surface of scattered cells of colloid, follicular, and Rathke's cleft cysts. Many cells of follicles in the pars intermedia as well as individual cells of five Rathke's cleft cysts were also immunoreactive for chromogranin, S-100 protein, GFAP, and pituitary hormones. Colloid and enterogenous cysts were negative for prealbumin, S-100 protein, GFAP, and neuron-specific enolase; in all but a few instances, they failed to bind Ricinus communis agglutinin. In contrast, normal choroid plexus and choroid plexus papillomas were positive for prealbumin, S-100 protein, neuron-specific enolase, cytokeratin, vimentin, and Ricinus communis agglutinin receptors; they lacked Ulex europaeus lectin, 56/66-kD cytokeratins, and epithelial membrane antigen. Unlike normal choroid plexus, choroid plexus papillomas were often GFAP-positive. All tissues studied were nonreactive for lysosome, serotonin, and neurofilament, and with Leu-7 antibodies. This study indicates that the immunophenotype of epithelium lining colloid cysts is similar to that of other cysts showing endodermal or ectodermal differentiation and to respiratory tract mucosa. Epithelium of colloid cysts is immunohistochemically different from that of normal or neoplastic choroid plexus. These findings indicate an endodermal rather than neuroepithelial nature for colloid cysts.
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PMID:Colloid cyst of the third ventricle. A comparative immunohistochemical study of neuraxis cysts and choroid plexus epithelium. 841 24

The immunohistochemical expression of muscle actin has been studied in 45 canine hemangiopericytomas (CHP) using a monoclonal antibody (HHF35) and formalin-fixed, paraffin-embedded specimens. The distribution of vimentin, desmin, cytokeratins, lysozyme, factor VIII-related antigen, S-100 protein, and glial fibrillary acidic protein was studied both in CHP and in some canine soft-tissue neoplasms (seven fibrosarcomas, seven benign schwannomas, seven benign fibrous histiocytomas, and six leiomyosarcomas) used as controls for differential diagnosis. All CHP and control tumors expressed vimentin. Twenty-three CHP expressed muscle actin, whereas all control tumors analyzed were muscle actin-negative, with the exception of leiomyosarcomas. Among muscle actin- and vimentin-positive CHP, one case could be reclassified as leiomyosarcoma because it was desmin-positive, two cases expressed lysozyme, and nine cases expressed S-100 protein. Among muscle actin-negative and vimentin-positive CHP, seven expressed S-100 protein. In addition, S-100 protein was detected in five schwannomas. All CHP and control tumors analyzed were negative for cytokeratins, factor VIII-related antigen, and glial fibrillary acidic protein. Our results support the hypothesis of a pericytic origin of CHP, and suggest that muscle actin, desmin, vimentin, and lysozyme could be useful for the differential diagnosis of canine spindle cell tumors, but not all these neoplasms can be identified with these tumor tissue markers.
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PMID:Immunohistochemical characterization of hemangiopericytomas and other spindle cell tumors in the dog. 881 36

Rat optic nerves were subjected to crush injury to study the local tissue reactions leading to wound healing and tissue repair. We used antibodies against glial fibrillary acidic protein (GFAP), vimentin, the S1OO protein (S1OOP), lysozyme, and ED1 as markers for astroglial cells and microglia/macrophages at the light and electron microscopic level during the 3 weeks following the crush. The crush injury produced a vast area of tissue damage including the disruption of the blood-brain barrier (BBB). In the first days after crushing, astrocytes were absent from the lesion site. S1OOP-positive astrocytes reappeared in the lesion center as early as 6 days after crushing. These astrocytes reestablished former topological structures such as perivascular and subpial glia limitans. At the edges of the lesion site reactive astrocytes enclosed and embedded axonal and myelin debris. Preceding the astroglial repopulation, a massive infiltration of microglia/macrophages (phagocytes) into the lesion center took place. ED1-positive/lysozyme- positive cells of round shape were seen in the lesion center at 2 days after crushing, and their number peaked around 1 week after crushing. They efficiently cleared the debris from the lesion site and mostly disappeared after 3 weeks. With immuno-electron microscopy we found the ED1 antigen related to the membranes of phagosomes. The microglia/macrophages observed in the nerve segments distal of the lesion (Wallerian degeneration site) were different from those in the lesion center: 1) they appeared later, about 6 days after crushing; 2) they were ED1 positive, but lysozyme negative and showed a branched morphology; and 3) they persisted in the distal nerve segment but showed little phagocytosis. We suggest that these cells are mostly activated microglia.
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PMID:Cellular reactions at the lesion site after crushing of the rat optic nerve. 883 93

The canine transmissible venereal tumour is a naturally occurring contagious round-cell neoplasia which is primarily located in the mucous membrane of the external genitalia in dogs of either sex. In order to specify the controversial cytogenetic origin of this round-cell tumour, 14 cases of canine transmissible venereal tumour, formalin- or Bouin-fixed and paraffin-embedded, were subjected to extensive immunophenotypic analysis using reagents specific to a variety of cytoplasmic or surface antigens: lysozyme, ACM1 antigen, vimentin, neuron-specific enolase, glial fibrillary acidic protein, desmin, alpha smooth muscle actin, CD3, IgG, kappa and lambda light chains, and keratin. Lysozyme immunoreactivity was detected in all cases, ACM1 antigen in 11 of 14, neuron-specific enolase in 11 of 14, vimentin in 10 of 14, glial fibrillary acidic protein in 4 of 14 and desmin in 1 of 14. All the sections were negative to keratins, alpha smooth muscle actin and CD3, whereas in five cases, perivascular tumour cells contained Ig G, kappa and lambda light chains. The immunoreactivity to lysozyme and ACM1 antigen supports the hypothesis of a histiocytic immunophenotype for the canine transmissible venereal tumour.
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PMID:Immunophenotype of the canine transmissible venereal tumour. 923 33

We have successfully established highly enriched astrocyte cultures upon passaging of primary cultures derived from various regions of postmortem human adult brain and spinal cord. Tissues were collected at autopsies with relatively short postmortem times (3-9 hr) from multiple sclerosis (MS) and (normal) control cases. Immunocytochemical analysis showed that primary cultures were composed of colonies of oligoclonal cells that expressed the intermediate filament proteins glial fibrillary acidic protein (GFAP), vimentin, as well as glutamine synthetase (GS). Passaging the astrocytes did not affect their proliferating capacity as monitored by bromodeoxyuridine (BrdU) incorporation. Astrocyte-specific markers were stably expressed for at least 12 passages per individual tissue sample. Large numbers of GFAP-positive astrocytes were obtained from each sample and could be stored frozen and recultured. Very few macrophages/microglial cells (1-3%) were present in the human adult astrocyte cultures, using a panel of macrophage-specific markers. However, the monoclonal antibodies (mAbs KP1, EBM1, 25F9) and lysozyme antiserum directed against lysosomal antigens strongly immunostained cultured astrocytes derived from MS and control cases, implicating that expression of these lysosomal antigens is not restricted to macrophages/ microglial cells in human glial cell cultures. Interestingly, astrocytes derived from active demyelinated MS lesions showed an increased proliferating capacity compared to astrocytes derived from non-lesioned and normal brain and spinal cord regions, as shown with a microculture tetrazolium assay (MTT assay).
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PMID:Establishment of human adult astrocyte cultures derived from postmortem multiple sclerosis and control brain and spinal cord regions: immunophenotypical and functional characterization. 926 Jul 45

Crystalloid inclusions or "pole bodies" observed in brain macrophages in human demyelinating disease represent a morphological enigma. Similar inclusions were detected in brain macrophages from the GFAP-IL3 mouse, a transgenic murine model for macrophage mediated demyelination. Mice also showed inclusions in hematopoietic tissue. They appear to be related to phagocytosis and secretion, respectively, as evidenced by the fact that in phagocytosing cells they often merged with lysozomes and that affected cells showed empty channels open to the interstitium. Based on ultrastructural and immunolocalization studies using chaperonin-10, lysozyme, and cathepsin the authors suggest that these inclusions are consistent with phagocytosis-related secretory products. This study may provide insight into the nature and significance of similar macrophage inclusions recently identified in multiple sclerosis.
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PMID:Crystalloid inclusions in brain macrophages and hemopoietic tissue in GFAP-IL3 mice resemble inclusions identified in multiple sclerosis. 1058 66

Niemann-Pick disease type C (NPC) is a progressive neurodegenerative disorder with characteristic storage of glycolipids in the brain. This study investigated cellular origin and temporal changes of monosialoganglioside storage in the Balb/c npc(nih) mouse brain by immunohistochemistry. Anti-GM1 gave positive staining of the hippocampus, thalamus, cerebellar molecular and Purkinje cell layers in the 3-week old NPC mouse brain and in general, the staining progressively diminished in an age-dependent manner. Anti-GM2 gave positive staining of the hippocampus, thalamus, cerebellar granule cell layer and brainstem nuclei in the 3-week old NPC mouse brain. In contrast to GM1, GM2 staining in these regions, except for the hippocampus, progressively augmented in an age-dependent manner. Double labeling experiments with antibodies against glial fibrillary acidic protein and lysozyme showed localization of GM1 and GM2 in reactive astrocytes and macrophages, respectively. Thus in the NPC mouse brain, GM1 accumulated primarily in neurons and astrocytes whereas GM2 accumulated primarily in neurons and macrophages. Temporal profiles of storage were different from each other and depended on the cell type, presumably reflecting both developmental changes and progression of the disease process. We also investigated subcellular sites of storage in primary-cultured Purkinje cells from the neonatal NPC mouse by immunocytochemistry. In NPC Purkinje cells, GM1 accumulated both in the cytoplasm and dendrites whereas GM2 showed punctuate accumulation in perinuclear vesicles. Thus, subcellular sites of storage were also different between GM1 and GM2 in NPC neurons.
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PMID:Sites and temporal changes of gangliosides GM1/GM2 storage in the Niemann-Pick disease type C mouse brain. 1157 53

True histiocytic lymphoma, as defined by strict criteria, is a very rare neoplasm. We describe three cases occurring as primary tumors in the central nervous system. The patients, two females and one male, ranged in age from 11 to 69 years. The tumors involved the brain in two cases and spinal cord in one, with a size ranging from 7 to 17 mm. Two patients died at 4 months and 8 months, respectively, and one was alive with disease at 5 months. Pathologically, the tumors comprised groups and sheets of noncohesive large cells with pleomorphic vesicular nuclei, distinct nucleoli, and abundant eosinophilic cytoplasm. A dense inflammatory infiltrate consisting of neutrophils, lymphocytes, plasma cells, and histiocytes was present, with multiple foci of necrosis and abscess formation. All three cases demonstrated an identical immunophenotype: positive for CD68 and lysozyme; focally positive for S-100 protein, CD45RB, and CD4; and negative for CD3, CD20, CD21/CD35, CD1a, CD30, ALK1, myeloperoxidase, glial fibrillary acidic protein, and cytokeratin. The proliferative index ranged from 20% to 35%. Ultrastructural examination further confirmed the histiocytic nature of the tumor cells, characterized by irregularly folded or multisegmented nuclei and abundant cytoplasm containing lysosomes; Birbeck granules, interdigitating cell processes, and cell junctions were not found. Although the presence of abundant inflammatory cells could obscure the neoplastic histiocytes, making the distinction from inflammatory conditions difficult, awareness of this unusual histologic feature and the invariable finding of pleomorphic cells in some areas of the lesion permit the correct diagnosis to be made.
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PMID:Primary histiocytic lymphoma of the central nervous system: a neoplasm frequently overshadowed by a prominent inflammatory component. 1168 53

We present 12 patients with 20 plexiform xanthomatous tumors (PXTs). All patients were male. Patient ages ranged from 20 to 59 years (mean 45 years). Clinical information was available for 11 (92%) patients. Only one patient with markedly elevated cholesterol levels had a family history of hypercholesterolemia; none of the others had a family or personal history of diabetes mellitus, hypercholesterolemia, or hyperlipoproteinemia. Three patients had markedly elevated serum triglyceride levels. The tumors were solitary in seven patients and multiple in five patients: three patients had two tumors, one presented had three, and one had four. PXTs were located on the knee (n = 8), elbow (n = 5), foot or hand (n = 3), and one each on the Achilles tendon, buttock, toe, and back. PXT was white to yellow in color and ranged in size from 0.7 to 5 cm (mean 2.7 cm). The tumors were located in the dermis and subcutis, had a distinctive plexiform arrangement, and were composed of various admixtures of uniform epithelioid and xanthomatous cells. All tumors in patients with solitary or multiple lesions had a plexiform architecture. Most of the nodules of the plexiform pattern of PXTs measured 0.5-2 mm. Rarely cholesterol clefts, necrosis, sparse inflammation, and multinucleated Touton giant cells were present. In two patients with multiple tumors, the PXT completely lacked the xanthoma cells and thus resembled an epithelioid lesion. Immunohistochemically, all lesions were KP1 (CD68) and vimentin positive and lysozyme, S-100 protein, HMB-45, epithelial membrane antigen, cytokeratins, factor VIIIrag, CD34, muscle-specific actin, alpha-smooth muscle actin, desmin (D33), desmin (Der-11), chromogranin, synaptophysin, neurofilament protein, and glial fibrillary acidic protein negative. Two patients with multiple lesions noted recurrences over 10 years. With the exception of one patient who died of an unknown cause, all 10 patients with follow-up were alive, some with residual disease, over a mean of 9 years (range 1-25 years). Some PXTs may represent a morphologic variant of tuberous or tendinous xanthoma, yet its exclusive occurrence in men, absence of personal/familial hyperlipemia/hypercholesterolemia in some patients, and relative paucity of inflammation and cholesterol clefts may make this a distinctive entity.
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PMID:Plexiform xanthomatous tumor: a report of 20 cases in 12 patients. 1236 45


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