Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032463 (polycythemia vera)
 3,374 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ionizing radiation used for diagnosis or therapy has been associated with an increased incidence of malignancies of blood-forming organs. The increased incidence of hematopoietic malignancies following exposure to ionizing radiation obtained in the course of occupation, diagnosis and therapy of disease, or as a weapon of war is documented. The natural occurrence and the induced progression to acute leukemia of polycythemia rubra vera, Hodgkin's disease, multiple myeloma, Di Guglielmo's disease, and reticuloendothelial malignancies are discussed. The status of transplantation and immunodeficiency states and their relationship to acute leukemia is reviewed. Finally, drugs, toxins, and the use of cytotoxic radiomimetic agents for nonmalignant purposes are shown to lead to the development of acute leukemia. Background information relevant to the proper use of future diagnostic and therapeutic modalities is provided.
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PMID:Malignancies in blood-forming organs following diagnostic and therapeutic procedures: a review. 106 32

Erythropoietin is a glycoprotein hormone that plays a vital role in erythropoiesis. It is mainly produced in the fetal liver till the third trimester of pregnancy. At that point, the kidney interstitium takes over this function and becomes the main source of erythropoietin. Hypoxia stimulates erythropoietin production by a mechanism that may require a heme protein as a second messenger. Erythropoietin stimulates the maturation of erythroid precursors (colony-forming unit-erythroid and burst-forming unit-erythroid) via at least two types of cell surface receptors. The higher-affinity receptors appear to be more important in modulating the effects of erythropoietin in vivo. Changes in intracellular calcium may ultimately mediate the action of erythropoietin on erythroid precursors. A specific and sensitive radioimmunoassay is now available for accurately measuring erythropoietin levels. All forms of erythrocytosis except polycythemia vera are associated with elevated erythropoietin levels. Levels are also high in cord blood obtained following fetal asphyxia. Reduced levels are seen in patients with anemia due to renal diseases. The response of erythropoietin to the degree of anemia appears to be attenuated in patients with cancer, chronic diseases, and human immunodeficiency virus (HIV) infection. Erythropoietin has been successfully used for treating patients with anemia due to renal failure. Its use has also been approved for the treatment of anemia patients receiving zidovudine for HIV infection. Encouraging results have been observed when erythropoietin was used to treat anemia due to rheumatoid arthritis, hematological malignancies, and prematurity. It has also been used to increase the yield of autologous blood collected prior to an elective surgical procedure. However, it has not proved to be useful in sickle cell anemia and myelodysplastic syndromes.
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PMID:Erythropoietin. Biology and clinical applications. 178 66

The long terminal repeat (LTR) region of the human immunodeficiency virus (HIV-1), which regulates viral gene expression, is modulated by viral trans-acting proteins of HIV and DNA viruses and by biologically active chemical agents that induce cellular proliferation and/or differentiation. The pseudorabies virus immediate early gene (PIE) shares similar transcriptional trans-activating properties with the gene products of several other DNA viruses. The transient expression chloramphenicol acetyl transferase (CAT) assays in HeLa cells transfected with HIV long terminal repeat (LTR)-CAT and PIE plasmids demonstrated trans-activation of the HIV LTR by PIE. Analyses of 5' deletion mutants and site-directed Sp1 and transactivation responsive (TAR) region mutants of the LTR indicated PIE-responsive sequences located between -65 and -17. Synergistic cooperativity between PIE and the HIV-1 tat protein was demonstrated. PIE exhibited a marked stimulatory effect upon HIV replication in HeLa cells transfected with a biologically active HIV proviral DNA. These data provide evidence that, like a number of other DNA containing viruses, PRV can trans-activate HIV gene expression.
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PMID:Activation of HIV LTR-directed expression: analysis with pseudorabies virus immediate early gene. 254 25

The populations of lymphocytes and serum immunoglobulins were explored in 20 patients with erythremia, 26 patients with sub-leukemic myelosis, 38 patients with pronounced chronic myeloid leukemia, and 33 patients with the blastic phase of the illness. The patients with chronic myeloproliferative diseases manifested cellular immunodeficiency that was aggravated as the disease progressed. In the pronounced stage, the patients showed relative preservation of humoral immunity whereas in the terminal stage they developed humoral deficiency. Study of the time-course of changes in the immunological characteristics has demonstrated that deterioration of the characteristics starts during blast transformation of myeloproliferative diseases. This may serve as a criterion for predicting exacerbations and early diagnosis of the blastic phase.
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PMID:[Indices of cellular and humoral immunity in chronic myeloproliferative diseases]. 349 38

The authors describe 4 families whose members showed myeloproliferative diseases. In one of the families, polycythemia vera (PV) was seen in twin brother and sister, in the other one, chronic myeloleukemia (CML) afflicted both daughter and mother, and in the two remaining families PV and CML afflicted two brothers and mother and daughter, respectively. It was established that neutrophil phosphatase activity was lowered not only in the afflicted brother but also in healthy members of the third family. Based on the reported and their own data the authors arrive at the conclusion that familial myeloproliferative diseases occur in rare cases. In all the cases of familial myeloproliferative diseases, the transmission of the illness by heredity was discovered to be impossible. It was also ascertained that transmitted by heredity are only those cell deficiencies of the tissues that later on will be afflicted by leukemia or will develop immunodeficiency manifested by increased mutation of the myelopoietic cells (DNA repair deficiencies) or by inability to eliminate the leukemic cells.
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PMID:[Familial myeloproliferative syndrome (study of 4 families and review of the literature)]. 386 57

In view of the possibility that immunological dysfunctions may be involved in initiating or contributing to the pathogenesis of myeloproliferative disease, we investigated quantitative and functional activity of natural killer (NK) cells in patients with polycythemia vera, essential thrombocythemia and myelofibrosis, and have demonstrated, especially in myelofibrosis, a measurable cytotoxic defect in the ability of their peripheral blood mononuclear cells to efficiently kill the standard NK target, K-562. Furthermore, highly purified, FACS-sorted CD16+ lymphoid cells from patients with myelofibrosis were consistently defective in their ability to lyse K-562 targets, and could not be augmented substantially with recombinant interleukin (IL)-2. Only patients with myelofibrosis had significantly lower percentages and absolute numbers of CD16+ cells as compared to patients with essential thrombocythemia and polycythemia vera. Further experiments demonstrated that patients with myelofibrosis, although having fewer CD16+ NK cells, had a significantly increased proportion of CD16+ cells with detectable platelet-derived growth factor (PDGF) on their surface. In contrast, surface PDGF was barely detectable on CD16+ cells from patients with polycythemia vera and essential thrombocythemia, as well as from normal controls. Having previously reported that physiologic quantities of PDGF significantly inhibit human NK cell cytotoxicity, and that patients with myelofibrosis and essential thrombocythemia have significantly elevated circulating levels of plasma PDGF, we now have demonstrated that pretreatment of normal NK cells with concentrated, PDGF-containing, platelet-poor plasma from patients with these diseases significantly inhibits NK cytotoxicity. This inhibitory effect was reversed by neutralization of plasma PDGF with anti-PDGF (coupled to Sepharose resin). Both the NK defects demonstrated in this study, and the abnormal plasma PDGF results reported earlier, are most striking in myelofibrosis and least abnormal in polycythemia vera, with an intermediate degree of abnormality in essential thrombocythemia. Our new findings suggest a causal correlation between abnormal platelet release, plasma accumulation of PDGF, and the observed NK immunodeficiency in these myeloproliferative patients.
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PMID:Quantitative and functional studies of impaired natural killer (NK) cells in patients with myelofibrosis, essential thrombocythemia, and polycythemia vera. I. A potential role for platelet-derived growth factor in defective NK cytotoxicity. 832 37

The nosoparasitic form of salmonellosis occurs not only in cases of the association of salmonellosis with infectious diseases, but also in noninfectious patients, mostly in oncological and hematological cases. The appearance of the nosoparasitic form of salmonellosis was observed in 9 patients; of these, 5 with leukosis, 2 with malignant tumors, 1 with erythremia and 1 with cytostatic disease. Concomitant Salmonella infection contributed to the aggravation of the main disease. In 6 out of 9 cases patients with the nosoparasitic form of salmonellosis remained in oncological and hematological hospitals, and no cases of hospital infection were registered. Immunodeficiency played an important role in the development of the nosoparasitic form of salmonellosis in these patients.
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PMID:[The nosoparasitic form of salmonellosis]. 882 Jun 86

Tuberculous splenic abscess is an exceptional disease with silent presentation in disseminated tuberculosis infection. Imaging procedures allow to suspect this diagnosis in case of multilocular nodules of the spleen, or unilocular pseudotumoral macronodule. We report three cases of tuberculous splenic abscesses in two patients with acquired immunodeficiency syndromes and one with polycythemia vera. Under antituberculous treatment, clinical evolution was good with regression of the radiological features.
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PMID:[Clinical and radiological aspects of tuberculous splenic abscesses. Presentation of 3 cases]. 888 75

To determine the efficacy of a clean-in-place system for the inactivation of viruses present in human plasma, the effect of 0.1 M sodium hydroxide at 60 degrees C on viral infectivity was investigated. Inactivation of the following model and relevant viruses were followed as a function of time: human hepatitis A virus (HAV), canine parvovirus (CPV; a model for human parvovirus B-19) pseudorabies virus (PRV, a model for hepatitis B virus), and bovine viral diarrhoea virus (BVDV, a model for hepatitis C virus and human immunodeficiency virus). Infectivity of CPV was determined by a novel in situ EIA method which will prove useful for studies to validate parvovirus inactivation or removal. Infectivity of BVDV, PRV and CPV were shown to be reproducibly inactivated below the limit of detection by 0.1 M NaOH at 60 degrees C within 30 s. HAV was inactivated to below the limit of detection within 2 min. Treatment with heat alone also resulted in some log reduction for all viruses tested except for CPV which remained unaffected after heating at 60 degrees C for 16 min. Treatment of HAV with hydroxide alone (up to 1.0 m) at 15 degrees C did not lead to rapid inactivation. Collectively, these data suggest that 0.1 M NaOH at 60 degrees C for two min should be sufficient to inactivate viruses present in process residues.
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PMID:Inactivation kinetics of model and relevant blood-borne viruses by treatment with sodium hydroxide and heat. 1020 25

The recognition of naturally occurring rhadinoviruses in macaque monkeys has spurred interest in their use as models for human infection with Kaposi sarcoma-associated herpesvirus (human herpesvirus 8). Rhesus macaques (Macaca mulatta) and pig-tailed macaques (Macaca nemestrina) were inoculated intravenously with rhadinovirus isolates derived from these species (rhesus rhadinovirus [RRV] and pig-tailed rhadinovirus [PRV]). Nine rhadinovirus antibody-negative and two rhadinovirus antibody-positive monkeys were used for these experimental inoculations. Antibody-negative animals clearly became infected following virus inoculation since they developed persisting antibody responses to virus and virus was isolated from peripheral blood on repeated occasions following inoculation. Viral sequences were also detected by PCR in lymph node, oral mucosa, skin, and peripheral blood mononuclear cells following inoculation. Experimentally infected animals developed peripheral lymphadenopathy which resolved by 12 weeks following inoculation, and these animals have subsequently remained free of disease. No increased pathogenicity was apparent from cross-species infection, i.e., inoculation of rhesus macaques with PRV or of pig-tailed macaques with RRV, whether the animals were antibody positive or negative at the time of virus inoculation. Coinoculation of additional rhesus monkeys with simian immunodeficiency virus (SIV) isolate SIVmac251 and macaque-derived rhadinovirus resulted in an attenuated antibody response to both agents and shorter mean survival compared to SIVmac251-inoculated controls (155.5 days versus 560.1 days; P < 0.019). Coinfected and immunodeficient macaques died of a variety of opportunistic infections characteristic of simian AIDS. PCR analysis of sorted peripheral blood mononuclear cells indicated a preferential tropism of RRV for CD20(+) B lymphocytes. Our results demonstrate persistent infection of macaque monkeys with RRV and PRV following experimental inoculation, but no specific disease was readily apparent from these infections even in the context of concurrent SIV infection.
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PMID:Experimental infection of rhesus and pig-tailed macaques with macaque rhadinoviruses. 1055 50


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