Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The histogenesis of alveolar soft part sarcoma (ASPS) has been investigated since its description. Twenty ASPS cases were analyzed for immunohistochemical content, with emphasis directed toward the paraganglial, Schwann cell, and muscle theories of histogenesis. In addition, the cases were examined for possible prognostic clinical features. The clinical characteristics of the patients were similar to those reported previously concerning average age (23 years); male:female ratio (1:1); and predominant primary site (lower extremity, nine cases). Despite a local recurrence rate of 20% and a metastatic rate of 68% (including four at presentation), the natural history was often indolent and relapse commonly occurred very late. The average follow-up period was 10.1 years. While the overall 5-year survival was 67%, only seven of 18 patients were alive without disease at last follow-up (1.7-32 years), and one patient died of tumor after a 28-year disease-free interval. Neither tumor size nor site appeared to affect prognosis. The tumors were analyzed immunohistochemically for neurofilament, S-100 protein, met-enkephalin, leu-enkephalin, acetylcholinesterase, alpha 1-antichymotrypsin, Factor VIII-related antigen, serotonin, lysozyme, neuron-specific enolase, myoglobin, cytokeratins, desmin, and vimentin. Except for weak vimentin immunoreactivity, no other antigenic expression was detected despite multiple repeated experiments with several antibodies. S-100 protein which is present in virtually all granular cell tumors was absent in the cases of ASPS. The lack of detectable expression of neurofilament, met-enkephalin and leu-enkephalin, and neuron-specific enolase is interpreted as evidence against the paraganglial theory of histogenesis. Similarly, the repeated absence of the muscle proteins, desmin and myoglobin, in contrast to a previous report, is interpreted as evidence against a myogenic origin.
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PMID:Alveolar soft part sarcoma. A clinicopathologic and immunohistochemical study. 243 29

Neuroendocrine (NE) neoplasms of the human bronchopulmonary tract were examined by electron microscopy, immunocytochemistry, and gel electrophoresis of cytoskeletal proteins from microdissected tissue samples. All samples (carcinoids, well-differentiated NE carcinoma, NE carcinomas of intermediate type, NE carcinomas of the small cell type) contained significant numbers of cells that immunostained for one or more of the following neuroendocrine markers tested: bombesin, calcitonin, ACTH, leu-enkephalin, gastrin, serotonin, somatostatin, alpha-melanocyte-stimulating hormone, vasoactive intestinal peptide, glucagon, insulin, substance P, and neuron-specific enolase. Electron microscopy revealed typical NE cell features, including variable abundant and frequently heterogeneous neurosecretory granules. Tumor cells contained filaments specifically stained with different conventional and monoclonal antibodies to cytokeratins and displayed punctate plasma membrane staining with antibodies to desmoplakins, in agreement with the electron microscopic demonstration of tonofilament bundles and desmosomes. Immunocytochemistry for NE markers and cytoskeletal proteins on consecutive sections revealed both cytokeratins and neuroendocrine substances in single cells. Using gel electrophoresis of cytoskeletal proteins of tissue regions extracted with high salt buffer and detergent, we could detect, in the tumors tested, appreciable amounts of cytokeratin polypeptides 8, 18, and 19, i.e., major cytokeratins also found in certain other lung carcinomas such as adenocarcinomas. Tumor cells were not significantly stained with antibodies to other intermediate filament proteins such as vimentin, desmin, glial filament protein, and neurofilament protein. The results show that NE substances can be synthesized in cells containing a typical epithelial cytoskeleton, i.e., cytokeratin filaments and desmosomes. These findings support the notion of an epithelial character of these tumors and appear in contrast with recent reports that neurofilaments are the only type of intermediate filaments present in carcinoids and other pulmonary NE tumors. These observations may have important implications for the histogenesis of NE carcinomas and for diagnostic pathology.
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PMID:Coexpression of neuroendocrine markers and epithelial cytoskeletal proteins in bronchopulmonary neuroendocrine neoplasms. 298 72

A case of a parotid mass in a 2-year-old boy, postoperatively diagnosed as neuroblastoma, a rare tumour not previously reported in the parotid gland is presented. The neoplasm developed within the parotid gland as a painless mass without regional lymphadenopathy. Histopathologically, the tumour showed primitive nerve cells-neuroblasts-with round or oval dark basophilic nuclei and scanty cytoplasm. The cells were arranged in circular rosettes around an eosinophilic mass consisting of very fine filaments originating in the tumour cells or papillary configuration and sometimes scattered in the poorly developed stroma. Immunohistochemical evaluation of the tumour showed a positive immunoreactivity for vimentin, alpha and beta subunits of S-100 protein, neurone-specific enolase (NSE), substance P, met-enkephalin and chromogranin but cytokeratins, desmin, actin, myosin, glial fibrillary acidic protein (GFAP) and calcitonin gene related peptide (CGRP) were negative. The histopathological and immunohistochemical findings conclude a diagnosis of neuroblastoma of the parotid gland.
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PMID:Neuroblastoma of parotid gland: report of a case and immunohistochemical characteristics. 770 7

A 40-year-old Black man presenting with increasing nasal discharge of bloody, mucoid pus as well as nasal obstruction over a 2-month period is described. Magnetic resonance imaging of the skull showed a tumor eroding through the skull base into the clivus and extending into the sphenoid sinus. Endoscopy of the sphenoid sinus demonstrated a polypoid mass extending into the posterior choanae. The lesion was partially resected. Histologic evaluation showed a cellular small blue cell tumor punctuated by bland, epithelial-lined microcysts. Electron microscopy revealed epithelial cells with abundant rough endoplasmic reticulum and electron-dense membrane-bound endocrine granules, some undergoing misplaced exocytosis. Immunohistochemical evaluation demonstrated cytoplasmic reactivity for neuron-specific enolase, synaptophysin, and prolactin. Stains for leukocyte common antigen, HMB-45, desmin, cytokeratin, chromogranin, and the remaining spectrum of pituitary hormones including growth hormone, corticotropin, luteinizing hormone, follicle-stimulating hormone, and thyrotrophic hormone were negative. In contrast, the epithelium lining the cysts was cytokeratin positive and synaptophysin negative. This ostensibly small cell tumor therefore represented a remarkably extensive and aggressive prolactin cell adenoma with unusual light microscopic features. Characterization of the lesion required electron microscopy and further confirmation by immunocytology. The distinction of pituitary adenomas and particularly of prolactin cell tumors from other adenoma types and from other small cell lesions markedly affects therapy and patient prognosis.
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PMID:Aggressive small cell tumor of the skull base. 819 26

Two experiments were conducted with laying hens (Lohmann Brown) in an individual cage system and with single feeding conditions. Experiment 1 (n = 24) was a performance trial (22 to 61 wk) to evaluate phytase effects on performance and nutrient utilization in corn-soybean meal (CSM1) and wheat-soybean meal (WSM1) basal diets (0.12% NPP; 3.1% Ca) supplemented (300 U/kg) with an experimental microbial phytase (CSM2 and WSM2) or 1.5 g/kg inorganic P (CSM3 and WSM3). Experiment 2 (n = 16) was also conducted as a performance trial (22 to 61 wk) only using CSM diets with dietary treatments similar to those in experiment 1. In addition, parallel N and P balance experiments in 2 age periods (26 and 33 wk, respectively) were conducted. In experiment 1, no significant (P < 0.05) differences in mortality, feed intake, egg production, egg weight, or body weight were observed. Tibia bone mineral composition was significantly affected by microbial phytase. Microbial phytase in the low-P CSM diet significantly (P < 0.05) improved the feed conversion ratio. In experiment 2, only feed conversion ratio was significantly improved by microbial phytase. The phytase supplementation had no significant effect on P excretion, P balance, P utilization, N balance, N utilization, or AMEn in the balance experiments.
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PMID:Performance and nutrient utilization of laying hens fed low-phosphorus corn-soybean and wheat-soybean diets supplemented with microbial phytase. 1633 27

The clinical effectiveness of adrenocorticotropin in inducing remission of steroid-resistant nephrotic syndrome points to a steroidogenic-independent anti-proteinuric activity of melanocortins. However, which melanocortin receptors (MCR) convey this beneficial effect and if systemic or podocyte-specific mechanisms are involved remain uncertain. In vivo, wild-type (WT) mice developed heavy proteinuria and kidney dysfunction following Adriamycin insult, concomitant with focal segmental glomerulosclerosis (FSGS) and podocytopathy, marked by loss of podocin and synaptopodin, podocytopenia and extensive foot process effacement on electron microscopy. All these pathologic findings were prominently attenuated by NDP-MSH, a potent non-steroidogenic pan-MCR agonist. Surprisingly, MC1R deficiency in MC1R-null mice barely affected the severity of Adriamycin-elicited injury. Moreover, the beneficial effect of NDP-MSH was completely preserved in MC1R-null mice, suggesting that MC1R is likely non-essential for the protective action. A direct podocyte effect seems to contribute to the beneficial effect of NDP-MSH, because Adriamycin-inflicted cytopathic signs in primary podocytes prepared from WT mice were all mitigated by NDP-MSH, including apoptosis, loss of podocyte markers, de novo expression of the podocyte injury marker desmin, actin cytoskeleton derangement and podocyte hypermotility. Consistent with in vivo findings, the podoprotective activity of NDP-MSH was fully preserved in MC1R-null podocytes. Mechanistically, MC1R expression was predominantly distributed to glomerular endothelial cells in glomeruli but negligibly noted in podocytes in vivo and in vitro, suggesting that MC1R signaling is unlikely involved in direct podocyte protection. Ergo, melanocortin therapy protects against podocyte injury and ameliorates proteinuria and glomerulopathy in experimental FSGS, at least in part, via a podocyte-specific non-MC1R-mediated melanocortinergic signaling.
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PMID:Melanocortin therapy ameliorates podocytopathy and proteinuria in experimental focal segmental glomerulosclerosis involving a podocyte specific non-MC1R-mediated melanocortinergic signaling. 3216 44