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)

A 6-year-old male Pointer dog was presented with a 4-week history of progressive hind-limb stiffness. Magnetic resonance imaging demonstrated a focal intramedullary lesion at T1 level with a pattern of ring contrast enhancement. At necropsy, a circumscribed intramedullary reddish-gray tumor was observed. Microscopically, the tumor was composed of thin-walled capillaries lined by endothelial cells and separated by pleomorphic cells (stromal cells) with a moderate degree of anisokaryosis. Immunohistochemically, the endothelial cells were positive for factor VIII-related antigen and the stromal cells were positive for neuron-specific enolase and vimentin. GFAP-positive astrocytes were occasionally observed within the tumor. Both endothelial and stromal cells were negative for synaptophysin, S-100 protein, pankeratin, smooth muscle actin, CD34, CD68, alpha1-antichymotrypsin, and lysozyme. The tumor showed considerable morphologic and immunohistochemical similarities with human hemangioblastoma, and hence the inclusion of this tumor type within the primary neoplasms of the canine central nervous system is suggested.
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PMID:Intramedullary hemangioblastoma in a dog. 1262 18

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

Intracerebral granular cell tumors (GCTs) are a rare finding. We report here on a case of cerebral GCT in a 47-year-old man who suffered with severe headache. The tumor appeared as a relatively well-defined, enhancing mass at the periventricular white matter of the left occipital lobe of the brain. Histologically, the tumor was entirely composed of granular cells. Some of the tumor cells showed peripherally accentuated cytoplasmic granules with central clearing, which produced a unique "targetoid" appearance. The granular cells of the current case were positive for neuron-specific enolase (NSE), S-100 protein, GFAP, vimentin, CD 68, lysozyme, and alpha-1-antitrypsin. These wide immunoexpressions were not observed for the previously reported cerebral GCTs. Interestingly, this case showed "targetoid" or "reversed targetoid" immunoreactive patterns in NSE, CD68, GFAP, and vimentin. Despite these wide immunoexpressions and the lack of any association with astrocytoma, the histogenesis of cerebral GCTs is still suggested to be of a glial origin, based on the tumor location, the GFAP positivity and the ultrastructural findings, of which the latter showed intermediate filaments, and these are reminiscent of neoplastic astrocytes.
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PMID:Cerebral granular cell tumor. 1846 22

A primary intracerebral plasmacytoma was identified in a 7-year-old spayed female Boston Terrier. Grossly, a well-demarcated, 2 cm in diameter, roughly spherical tumor was in the rostral aspect of the left cerebral hemisphere. Histologically, the neoplasm was composed of sheets of round cells with distinct plasmacytoid features and marked anisocytosis and anisokaryosis. Cells were positive for vimentin, CD18, CD79a, and lambda light-chain, and negative for kappa light chain, cytokeratin, lysozyme, glial fibrillary acidic protein, and S100 protein. Clonally rearranged B-cell antigen receptor genes were detected by PARR (polymerase chain reaction for antigen receptor rearrangements), confirming clonal proliferation of B lymphocytes. Although primary solitary intracerebral plasmacytoma is rare in dogs and other species, it should be included in the differential diagnosis for central nervous system round-cell neoplasms. Clonality testing can be utilized to support the histological diagnosis of this neoplasm type.
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PMID:Solitary intracerebral plasmacytoma in a dog: microscopic, immunohistochemical, and molecular features. 1942 98

We used DNA microarrays to identify panels of transcriptional markers of aging that are differentially expressed in young (5 month) and old (25 month) mice of multiple inbred strains (129sv, BALB/c, CBA, DBA, B6, C3H and B6C3F(1)). In the heart, age-related changes of five genes were studied throughout the mouse lifespan: complement component 4, chemokine ligand 14, component of Sp100-rs, phenylalanine hydroxylase and src family associated phosphoprotein 2. A similar analysis in the brain (cerebellum) involved complement component 1q (alpha polypeptide), complement component 4, P lysozyme structural, glial fibrillary acidic protein and cathepsin S. Caloric restriction (CR) inhibited age-related expression of these genes in both tissues. Parametric analysis of gene set enrichment identified several biological processes that are induced with aging in multiple mouse strains. We also tested the ability of dietary antioxidants to oppose these transcriptional markers of aging. Lycopene, resveratrol, acetyl-l-carnitine and tempol were as effective as CR in the heart, and alpha-lipoic acid and coenzyme Q(10) were as effective as CR in the cerebellum. These findings suggest that transcriptional biomarkers of aging in mice can be used to estimate the efficacy of aging interventions on a tissue-specific basis.
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PMID:Gene expression profiling of aging in multiple mouse strains: identification of aging biomarkers and impact of dietary antioxidants. 1955 70

A mass lesion in the subependymal region of the lateral ventricle in a 13-year-old neutered male mongrel cat with a complaint of somnolence, right circling movement and posture abnormality was examined. The magnetic resonance image examination revealed a relatively large T1-hypointense and T2-hyperintense mass lesion in the left interventricular foramen region, and there were no abnormalities in the chest and abdominal x-ray radiographic, funduscopic, and electric retinogram findings. The cat was died 43 days after the initial referral, and the post-mortem examinations revealed a poorly demarcated subependymal mass. Histologically, the brain lesion consisted of complex proliferation of highly pleomorphic cells resembling histiocytes with atypia and abundant mitotic figures. Moderate infiltrates of small reactive lymphocytes were admixed with the pleomorphic cell population. Gemistcytic astrocytes were also intermingled with the periphery of neoplastic foci. Immunohistochemically, most of the pleomorphic cells were positive for HLA-DR alpha-chain and ionized calcium binding adaptor molecule 1, and few were positive for lysozyme and alpha-1 antichymotrypsin. The atypical pleomorphic cells were negative for CD3, IgG (H and L), glial fibrillary acidic protein and neurofilament, suggesting monocytic/histiocytic-origin of the cells. The number of Ki-67-positive cell nuclei was extremely large, reflecting the high growth activity of these cells. Based on the findings, the lesion was considered as histiocytic sarcoma.
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PMID:Histiocytic sarcoma in the brain of a cat. 1991 32

The present paper describes an astrocytic thalamic hamartoma associated with tectal meningoangiomatosis in a 3-month-old female German shepherd dog showing strabismus, opistotonus, circling, and fore limb hypermetria. MR images of the brain showed a well-defined intra-axial mass in the tectal region. The mass was hypointense to gray matter on T2-weighted images and hyperintense to gray matter on precontrast T1-weighted images. Histologically, glial cells arranged in a multinodular pattern characterized the mass. More caudally the lesion merged with subpial abnormal newly formed plaque-like shaped tissue characterized by thick branching bundles of spindle-shaped cells surrounding a central vessel. In the nodules, GFAP and vimentin were diffusely expressed. In the vascular proliferation Factor VIII-positive reaction was limited to endothelial cells while the remaining spindle-shaped cells were diffusely SMA-positive. The glial nodules did not express lysozyme and MAC387, nor neurofilaments and nestin.
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PMID:Thalamic astrocytic hamartoma and associated meningoangiomatosis in a German shepherd dog. 2326 Nov 50

Epithelioid glioblastoma (E-GBM) was recently designated as a subtype of glioblastoma (GBM) by the World Health Organization (2016). E-GBM is an aggressive and rare variant of GBM that primarily occurs in children and young adults. Although most characterized cases of E-GBM harbor a mutation of the BRAF gene in which valine (V) is substituted by glutamic acid (E) at amino acid 600 (BRAF-V600E), in addition to telomerase reverse transcriptase promoter mutations and homozygous CDKN2A/B deletions, the origins and cellular nature of E-GBM remain uncertain. Here, we present a case of E-GBM that exhibits antigenic and functional traits suggestive of microglia. Although no epithelial [e.g., CKAE1/3, epithelial membrane antigen (EMA)] or glial (e.g., GFAP, Olig2) markers were detected by immunohistochemical staining, the microglial markers CD68 and Iba1 were readily apparent. Furthermore, isolated E-GBM-derived tumor cells expressed microglial/macrophage-related genes including cytokines, chemokines, MHC class II antigens, lysozyme and the critical functional receptor, CSF-1R. Isolated E-GBM-derived tumor cells were also capable of phagocytosis and cytokine production. Treating E-GBM-derived tumor cells with the BRAF-V600E inhibitor, PLX4032 (vemurafenib), resulted in a dose-dependent reduction in cell viability that was amplified by addition of the CSF-1R inhibitor, BLZ945. The present case provides insight into the cellular nature of E-GBM and introduces several possibilities for effective targeted therapy for these patients.
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PMID:Epithelioid glioblastoma with microglia features: potential for novel therapy. 3268 79


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