Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0268596 (EMA)
 2,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study reports six non-Hodgkin's lymphoma cases that we called histiocyte-rich B-cell lymphoma (BCL) because of the prominent reactive histiocytic infiltrate obscuring the malignant B-cell population. The involved lymph nodes are characterized by a mixed nodular and diffuse infiltrate and occasionally feature prominent sinuses. The infiltrate is composed of reactive lymphocytes and numerous histiocytes obscuring a tumor population composed of variably sized scattered cells with irregular or multilobar vesicular nuclei. Immunostaining of paraffin sections for the B-cell marker recognized by L26 helps in the identification of these neoplastic cells. The clonal nature and further evidence of the B-cell lineage of this condition is shown by immunoglobulin gene rearrangements detected in three cases. The six cases of histiocyte-rich BCL are remarkably similar clinically: all presented with stage IVB disease with splenomegaly and follow an aggressive clinical course. Except for these features, our series show striking similarities to paragranuloma lymphocyte-predominant Hodgkin's disease, including male preponderance (all patients are male), age distribution (mean age, 41 years), propensity to progress to a diffuse, large B-cell lymphoma (two cases), as well as morphology of the neoplastic B-cell population and expression of Hodgkin's cell markers (Leu-M1 positivity after neuraminidase digestion in three cases, Leu-M1 positivity without neuraminidase digestion in one case, and additional epithelial membrane antigen [EMA] positivity in two cases). Both morphologically and clinically, the present series can be differentiated from other types of infiltrate-rich BCL, such as T-cell-rich BCL. Although additional cases will have to be recognized, histiocyte-rich B-cell lymphoma most likely represents a distinct clinicopathological entity. We speculate that it develops from a subset of B cells that also gives rise to the lymphocytic-histiocytic (L/H) cell, the Hodgkin's cell variant of lymphocyte-predominant Hodgkin's disease, paragranuloma subtype.
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PMID:Histiocyte-rich B-cell lymphoma. A distinct clinicopathologic entity possibly related to lymphocyte predominant Hodgkin's disease, paragranuloma subtype. 172 95

Apocrine and eccrine sweat glands are distinct in function, although they are closely related to each other developmentally and morphologically. In certain sweat gland tumors, it is difficult to differentiate between eccrine or apocrine sweat glands. Therefore, this paper reviews histochemical and immunohistochemical markers to differentiate apocrine and eccrine sweat glands with the aim of better understanding the structural and functional characteristics of these sweat glands. Specific markers for apocrine sweat glands are as follows: neuraminidase sensitive anionic sites detected by cationic colloidal gold at pH 2.0, and mitochondrion-like secretory granules that have epidermal growth factor-like antigenicity. The following antibodies react with apocrine sweat glands but not with eccrine sweat glands; the antibodies raised against 70 kDa glycoprotein purified from human milk fat globule membranes, and HMFG-1 (1.10.F3) monoclonal antibody produced by immunizing mice with defatted human milk fat globule membranes. Markers for eccrine sweat glands are as follows: dark cell granules that have chondroitinase ABC sensitive anionic sites detected by cationic gold at pH 2.0 after pretreatment with EGTA, and intercellular canaliculi with high activity of alkaline phosphatase. CEA and GCDFP-15 are expressed in both eccrine and apocrine sweat glands. Anti-EMA monoclonal antibody (E29) stains both eccrine and apocrine sweat glands.
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PMID:Histochemical and immunohistochemical markers for human eccrine and apocrine sweat glands: an aid for histopathologic differentiation of sweat gland tumors. 1176 85

In spring 2006, highly pathogenic avian influenza virus (HPAIV) of subtype H5N1 was detected in Austria in 119 dead wild birds. The hemagglutinin cleavage site showed that the amino acid sequence motif was identical to that of the Qinghai lineage. For detailed analysis, the hemagglutinin (HA) and neuraminidase (NA) genes of 27 selected Austrian H5N1 viruses originating from different regions and wild bird species were analyzed phylogenetically, which revealed two clearly separated Austrian subclusters, both belonging to European cluster EMA-1. Subcluster South (SCS) contains virus isolates from the south of Austria as well as from Slovenia, Turkey, Egypt, and Nigeria. The second subcluster, Northwest (SCN), covered a larger group of viruses originating from different locations and wild bird species in the northern and very western parts of Austria, as well as from Bavaria and Switzerland. Surprisingly, virus isolates originating from two mute swans and one wild duck found on the north side of the Alps did not cluster with SCN but with SCS. Together with isolates from Bavarian, the Czech Republic, Italy, and Slovakia, they form a genuine subgroup, named subgroup Bavaria (SGB). This subgroup forms a link to SCN, indicating a spread of the virus from south to north. There has been a general assumption that the generic HPAI introduction route into Europe was from Russia to north Germany, introducing cluster EMA-2 into Europe. Interestingly, our findings support the assumption of an alternative introduction of the HPAI H5N1 virus from Turkey to central Europe, where it spread as cluster EMA-1 during the outbreak of 2006.
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PMID:Geographical spread of highly pathogenic avian influenza virus H5N1 during the 2006 outbreak in Austria. 2033 51