Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clinicopathological findings of six cases of Hairy cell leukaemia are presented. All the patients were males, the age ranged between 32-57 years. Complications of anaemia and neutropenia were common modes of presentation. Hepatomegaly and splenomegaly were present in all the cases whereas only 2 patients had lymphadenopathy. Severe pancytopenia was detected in 3 cases and circulating hairy cells were present in all the cases. Trephine biopsy done in all six patients was found to be diagnostic. Tartrate resistant acid phosphatase was detected in the hairy cells of 2 cases.
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PMID:A clinico-pathological study of six cases of hairy cell leukaemia. 179 14

Cytochemical studies were performed on peripheral blood from 30 patients with type 1 Gaucher disease. In 29 of the patients, peripheral blood monocytes stained positively for tartrate-resistant acid phosphatase, whereas monocytes from 18 normal individuals and 14 patients with monocytosis did not. In the Gaucher patients, the percentage of monocyte positivity for tartrate-resistant acid phosphatase ranged from 2 to 97. There was no correlation between the percent monocyte staining and the degree of disease severity, as measured by hepatosplenomegaly, pancytopenia, or extent of bone disease, for the group as a whole. In Gaucher patients who had not undergone splenectomy, however, there was a significant correlation between percent monocyte staining and the degree of hepatosplenomegaly, anemia, and thrombocytopenia. The presence of tartrate-resistant acid phosphatase may be secondary to the lysosomal accumulation of glucosyl ceramide within these monocytes, although this remains to be confirmed. If so, these circulating cells may represent precursors of the Gaucher cells in tissues. Tartrate-resistant acid phosphatase staining of peripheral blood monocytes may be useful as a diagnostic marker for Gaucher type 1 disease and for further studies on the pathogenesis of the disease.
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PMID:Tartrate-resistant acid phosphatase staining of monocytes in Gaucher disease. 401 24

Infants with platelet counts below 100,000/mm3 should be evaluated for the cause of the thrombocytopenia. A maternal history to determine previous illnesses and particularly thrombocytopenia, drugs taken, and perinatal complications is important, and a maternal platelet count must be obtained. Physical examination of the infant is revealing in the TAR and giant cavernous hemangioma syndromes and may suggest intrauterine infection. A complete blood cell count (CBC) should be done to look for associated anemia and neutropenia or for polycythemia. Red cell morphology may be helpful. A bone marrow examination may be necessary if the etiology is unclear after the initial studies are done. Investigation of the well child will usually find an etiology for the thrombocytopenia. It is important to consider and test for isoimmune thrombocytopenia and intrauterine infection. In the ill infant multiple factors may contribute to a low platelet count, and a single, precise etiology often cannot be established. Thrombocytopenia with or without DIC may be an important indicator of sepsis. Platelet transfusions are helpful if the thrombocytopenia is due to decreased production or intrinsic platelet defects. In disorders with increased platelet destruction, donor platelets may survive long enough to be of some benefit. In ill infants treatment of the underlying problem often results in resolution of the thrombocytopenia. Transfusions should be used for the bleeding child and for the infant with severe thrombocytopenia who is the product of a vaginal delivery. In addition to being therapeutic, platelet transfusions may also assist in diagnosis.
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PMID:Thrombocytopenia in the newborn. 635 31

Transcription of lentiviral DNA in the host cell is regulated by an interaction between the viral TAR RNA stem-loop and the viral Tat protein. Here we present a model of the three-dimensional structure of the TAR RNA stem-loop of the equine infectious anemia virus (EIAV), derived from two- and three-dimensional NMR data. This 25 nucleotide RNA consists of an A-form helical stem capped by two U-G base pairs and a four-nucleotide loop. Two loop cytidines are stacked into the loop interior and likely form a non-Watson-Crick C-C base-pair. The two nucleotides at the top of the loop, U13 and G14, appear to be excluded from the interior of the loop and solvent exposed. It is significant that now for the EIAV TAR-Tat system, three-dimensional structures are now known for both the RNA and protein components.
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PMID:NMR analysis of the trans-activation response (TAR) RNA element of equine infectious anemia virus. 747 65

Tat (trans-activator) proteins are early RNA binding proteins regulating lentiviral transcription. These proteins are necessary components in the life cycle of all known lentiviruses, such as the human immunodeficiency viruses (HIV) or the equine infectious anemia virus (EIAV). Tat proteins are thus ideal targets for drugs intervening with lentiviral growth. The consensus RNA binding motif (TAR, trans-activation responsive element) of HIV-1 is well characterized. Structural features of the 86 amino acid HIV-1, Zaire 2 isolate (HV1Z2) Tat protein in solution were determined by two dimensional (2D) nuclear magnetic resonance (NMR) methods and molecular dynamics (MD) calculations. In general, sequence regions corresponded to structural domains of the protein. It exhibited a hydrophobic core of 16 amino acids and a glutamine-rich domain of 17 amino acids. Part of the NH2 terminus, Val4 to Pro14, was sandwiched between these domains. Two highly flexible domains corresponded to a cysteine-rich and a basic sequence region. The 16 amino acid sequence of the core region is strictly conserved among the known Tat proteins, and the three-dimensional fold of these amino acids of HV1Z2 Tat protein was highly similar to the structure of the corresponding EIAV Tat domain. HV1Z2 Tat protein contained a well defined COOH-terminal Arg-Gly-Asp (RGD) loop similar to the recently determined decorsin RGD loop.
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PMID:Structural studies of HIV-1 Tat protein. 772 10

The protein coding regions of all retroviral pre-mRNAs are flanked by a direct repeat of R-U5 sequences. In many retroviruses, the R-U5 repeat contains a complete core poly(A) site-composed of a highly conserved AAUAAA hexamer and a GU-rich downstream element. A mechanism that allows for the bypass of the 5' core poly(A) site and the exclusive use of the 3' core poly(A) site must therefore exist. In human immunodeficiency virus type 1 (HIV-1), sequences within the U3 region appear to play a key role in poly(A) site selection. U3 sequences are required for efficient 3' processing at the HIV-1 poly(A) site both in vivo and in vitro. These sequences serve to promote the interaction of cleavage and polyadenylation specificity factor (CPSF) with the core poly(A) site. We have now demonstrated the presence of a functionally analogous 3' processing enhancer within the U3 region of a distantly related lentivirus, equine infectious anemia virus (EIAV). U3 sequences enhanced the processing of the EIAV core poly(A) site sevenfold in vitro. The U3 sequences also enhanced the stability of CPSF binding at the core poly(A) site. Optimal processing required the TAR RNA secondary structure that resides within the R region 28 nucleotides upstream of the AAUAAA hexamer. Disruption of TAR reduced processing, while compensatory changes that restored the RNA structure also restored processing to the wild-type level, suggesting a position dependence of the U3-encoded enhancer sequences. Finally, the reciprocal exchange of the EIAV and HIV U3 regions demonstrated the ability of each of these sequences to enhance both 3' processing and the binding of CPSF in the context of the heterologous core poly(A) site. The impact of U3 sequences upon the interaction of CPSF at the core poly(A) site may therefore represent a common strategy for retroviral poly(A) site selection.
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PMID:A common mechanism for the enhancement of mRNA 3' processing by U3 sequences in two distantly related lentiviruses. 862 81

Human immunodeficiency virus, type 1, (HIV-1) encodes a transactivating regulatory protein, called Tat, which is required for efficient transcription of the viral genome. Tat acts by binding to a specific RNA stem-loop element, called TAR, on nascent viral transcripts. The specificity of binding is principally determined by residues in a short, highly basic domain of Tat. The structure in aqueous solution of a biologically active peptide, comprised of the ten-amino acid HIV-1 Tat basic domain linked to a 15-amino acid segment of the core regulatory domain of another lentiviral Tat, i.e., that from equine infectious anemia virus (EIAV), has been determined. The restraint data set includes interproton distance bounds determined from two-dimensional nuclear Overhauser effect (2D NOE) spectra via a complete relaxation matrix analysis. Thirty structures consistent with the experimental data were generated via the distance geometry program DIANA. Subsequent restrained molecular mechanics calculations were used to define the conformational space subtended by the peptide. A large fraction of the 25-mer peptide assumes a structure in aqueous solution with the lysine- and arginine-rich HIV-1 basic domain being separated from the basic domain by a turn and characterized by a nascent helix as well. The Tat peptide/TAR complex could be modeled with the basic alpha-helix lying in the major groove of TAR such that important interactions of a putative specificity-endowing arginine are maintained and very slight widening of the major groove is entailed.
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PMID:Aqueous solution structure of a hybrid lentiviral Tat peptide and a model of its interaction with HIV-1 TAR RNA. 890 85

Lentiviral transactivator (Tat) proteins are essential for viral replication. Tat proteins of human immunodeficiency virus type 1 and bovine immunodeficiency virus form complexes with their respective RNA targets (Tat responsive element, TAR), and specific binding of the equine anemia virus (EIAV) Tat protein to a target TAR RNA is suggested by mutational analysis of the TAR RNA. Structural data on equine infectious anemia virus Tat protein reveal a helix-loop-helix-turn-helix limit structure very similar to homeobox domains that are known to bind specifically to DNA. Here we report results of gel-shift and footprinting analysis as well as fluorescence and nuclear magnetic resonance spectroscopy experiments that clearly show that EIAV Tat protein binds to DNA specifically at the long terminal repeat Pu.1 (GTTCCTGTTTT) and AP-1 (TGACGCG) sites, and thus suggest a common mechanism for the action of some of the known lentiviral Tat proteins via the AP-1 initiator site. Complex formation with DNA induces specific shifts of the proton NMR resonances originating from amino acids in the core and basic domains of the protein.
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PMID:Equine infectious anemia virus transactivator is a homeodomain-type protein. 954 68

A 49-year-old man was admitted to our hospital for investigation of splenomegaly and lymphocytosis. He had no significant past history and was not a smoker. Physical examination revealed massive splenomegaly and no palpable superficial lymph nodes. Hematological examination showed a hemoglobin concentration of 10.5g/dl, a platelet count of 9.8 x 10(4)/microliter, and a leukocyte count of 21.2 x 10(3)/microliter with 70% abnormal lymphocytes. In May-Giemsa stained blood films, the abnormal lymphocytes had round nuclei, abundant, pale cytoplasm, and slightly serrated edges. Phase-contrast microscopic and scanning electron microscopic examinations revealed many long surface villi. Tartrate-resistant acid phosphatase activity in these cells was negative. The abnormal lymphocytes had a CD5-, CD10-, CD11a+, CD11c+, CD19+, CD20+, CD22+ phenotype. These features were similar to those described for a variant form of hairy cell leukemia (HCL-Japanese variant). However, studies of Ig gene rearrangement and expression of sIg revealed a polyclonal proliferation of B cells. On the basis of these findings, this case was diagnosed as hairy B-cell lymphoproliferative disorder, a recently described condition characterized by polyclonal B-cell lymphocytosis and features resembling HCL-Japanese variant. Serological assays for antibodies against Epstein-Barr virus suggested a past infection. Splenectomy alleviated the anemia and thrombocytopenia, but not the lymphocytosis.
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PMID:[Polyclonal B-cell lymphocytosis with clinical and hematological features resembling hairy cell leukemia]. 975 Apr 56

The Tat protein of equine infectious anemia virus, EIAV, was shown to augment viral gene expression, presumably through interaction with the Tat responsive element, TAR. Recently, cell-free polyadenylation assays suggested that perturbation of the EIAV TAR secondary structure diminished polyadenylation efficiency. The present study indicates that the EIAV TAR regulates the efficiency of the 3'-end processing of viral RNA also in transfected cells. Moreover, our data suggest that the provision of the EIAV Tat protein in trans potentiates read-through transcription through the 3' viral long terminal repeat (3' LTR), thus suggesting activation of downstream-located cellular genes.
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PMID:The Tat protein of equine infectious anemia virus (EIAV) activates cellular gene expression by read-through transcription. 975 88


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