Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.3.1 (alkaline phosphatase)
47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Five Thoroughbred and Quarter Horse cross foals were given 20 micrograms canine recombinant granulocyte-colony stimulating factor (rcG-CSF) per kg bwt intramuscularly (i.m.) on the day of birth and 10 micrograms rcG-CSF/kg for 13 additional days. During this time and for an additional 21 days haematology, bone marrow and clinical chemical analyses were performed. After one day of rcG-CSF administration leucocyte and neutrophil counts increased from 9.16 x 10(9)/l to 23.44 x 10(9)/l and from 6.45 x 10(9)/l to 19.61 x 10(9)/l, respectively. The counts continued to increase for the next 3-4 days and then there was a slight decrease. A second increase followed and the leucocyte and neutrophil counts increased to 52.84 x 10(9)/l and 45.16 x 10(9)/l on the day after the last rcG-CSF administration (Day 15). The counts decreased rapidly immediately after the administration of rcG-CSF was stopped and then at a slower rate. The cell counts were still higher than in the controls at the end of the study period (Day 35). Bone marrow cellularity increased from 10-25% before rcG-CSF was given to 60-80% after 5 days. The increase in cellularity was due to increased myeloid activity because the myeloid to erythroid ratio increased from 2.7 to 8.8. Serum chemistry changes were minimal although foals given rcG-CSF at various times had lower glucose concentrations and increased alkaline phosphatase and gamma glutamyl transferase activities.
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PMID:Haematological, bone marrow and clinical chemical changes in neonatal foals given canine recombinant granulocyte-colony stimulating factor. 857 99

Human parvovirus B19, which infects and lyses erythroid precursors, can cause severe anemia in patients with immunodeficiency. The incidence of parvovirus infection in adult acquired immunodeficiency syndrome (AIDS) patients is unknown. Eighty-one archival formalin-fixed, paraffin-embedded (FFPE) bone marrow biopsies from 73 AIDS adults were immunostained with monoclonal R92F6 against B19 VP1 and VP2 capsid proteins using streptavidin peroxidase and streptavidin alkaline phosphatase techniques. In addition, the same tissues were hybridized in situ with a digoxigenin-labeled parvovirus B19 DNA probe. Five FFPE bone marrows, from 3 HIV-negative patients with positive immunoglobulin M (IgM) serology for parvovirus B19, and 1 parvovirus B19-infected fetal liver were positive controls. By immunoperoxidase, all tissues were negative with R92F6 except the fetal liver, which exhibited strong positivity predominantly in viral inclusions. With immunoalkaline phosphatase, all positive controls were immunoreactive with R92F6; however, the AIDS marrows were negative. With in situ hybridization (ISH), all positive controls and 7 of 81 (8.6%) of AIDS marrows were positive for B19 parvovirus DNA. We conclude that ISH is more sensitive than R92F6 immunohistochemistry in parvovirus B19 detection. A small but significant number of bone marrows from AIDS adults shows evidence of human parvovirus B19 infection.
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PMID:Human parvovirus B19 in bone marrows from adults with acquired immunodeficiency syndrome: a comparative study using in situ hybridization and immunohistochemistry. 922 41

The cloning of a G protein-coupled, extracellular calcium (Ca2+e)-sensing receptor (CaR) from bovine parathyroid provided direct evidence that Ca2+e-sensing can occur through receptor-mediated activation of G proteins and their associated downstream regulators of cellular function. CaR transcripts and protein are present in various tissues of humans and other mammals that are involved in Ca2+e homeostasis, including parathyroid, kidney, and thyroidal C-cells. The present study was performed to determine whether bone marrow cells express the CaR, since cells within the marrow space could be exposed to substantial changes in Ca2+e related to bone turnover. Using DNA and RNA probes from the human parathyroid CaR cDNA, we identified CaR transcripts of 5.2 and approximately 4.0 kilobases by Northern analysis of poly(A+) RNA from low-density mononuclear cells isolated from whole human bone marrow that are putatively enriched in marrow progenitor cells, including bone cell precursors. In situ hybridization also identified CaR transcripts in the same cell preparations. Reverse transcription-polymerase chain reaction demonstrated > 99% nucleotide identity between transcripts from human bone marrow cells and the corresponding regions of the human CaR cDNA. Antisera specific for several different regions within the extracellular domain of the CaR were reactive with low-density human marrow cells that were either adherent or nonadherent to plastic. About one-third of the adherent, CaR-immunoreactive cells were also positive for alkaline phosphatase, a nonspecific marker of preosteoblasts, osteoblasts, and assorted cells of the colony-forming unit-fibroblast lineage. In addition, a substantial fraction (approximately 60%) of low density murine marrow cells cultured for 1 week at 4.8 mM Ca2+e expressed both CaR immunoreactivity and nonspecific esterase, an enzyme expressed by monocyte/macrophages and fibroblasts. Finally, erythroid precursors and megakaryocytes from murine marrow as well as blood platelets expressed abundant CaR immunoreactivity, while peripheral blood erythrocytes and most polymorphonuclear leukocytes did not. These studies indicate that the CaR is present in low-density mononuclear bone marrow cells as well as in cells of several hematopoietic lineages and could potentially play a role in controlling the function of various cell types within the marrow space.
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PMID:Expression of an extracellular calcium-sensing receptor in human and mouse bone marrow cells. 942 Dec 29

In the present study, we investigated the effects of stem cell factor (SCF) and/or thrombopoietin (TPO) on the cell production by cord blood CD34(+) cells using a serum-deprived liquid culture system. Although SCF alone supported a modest production of neutrophilic cells and a remarkable generation of mast cells, the addition of TPO to the culture containing SCF caused an apparent generation of neutrophilic cells, identified by immunocytochemical staining and flow cytometric analysis. The significant production of neutrophilic cells by SCF and TPO was persistently observed from 2 weeks to 2 to 3 months of culture. The interaction between SCF and TPO on the neutrophilic cell generation was greater than the combined effects of SCF with granulocyte colony-stimulating factor (G-CSF) or granulocyte-macrophage colony-stimulating factor (GM-CSF). The addition of neutralizing antibody against G-CSF or GM-CSF did not influence the SCF + TPO-dependent neutrophilic cell production. A single-cell culture study showed that not only CD34(+)CD38(+) c-kit+ cells but also CD34(+)CD38(-)c-kit+ cells were responsible for the neutrophilic cell generation. In clonal cell cultures, GM progenitors as well as erythroid progenitors and multipotential progenitors expanded in the cultures supplemented with SCF and TPO. The neutrophilic cells grown by SCF + TPO were at myeloblast to band cell stages, and scarcely matured to segmented neutrophils. In addition, the cells generated by SCF + TPO were stained with monoclonal antibodies against myeloperoxidase, elastase, lactoferrin, and CD11b, but they had negligible levels of alkaline phosphatase (ALP) and CD35. The replating of the CD34(-)c-kit-/low CD15(+) cells grown by SCF + TPO into a culture containing SCF + G-CSF permitted both the terminal maturation into segmented cells and the appearance of ALP and CD35. These results indicate the existence of a G-CSF/GM-CSF-independent system of neutrophilic cell production.
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PMID:Neutrophilic cell production by combination of stem cell factor and thrombopoietin from CD34(+) cord blood cells in long-term serum-deprived liquid culture. 988 12

Refractory thrombocytopenia (RTC) is a counter-concept to refractory anemia, which is characterized by isolated thrombocytopenia associated with clonal chromosomal abnormality. The diagnosis of RTC is difficult to establish based on morphologic features alone. And steroid therapy for RTC is often ineffective. We examined 3 patients with RTC to identify its characteristics and measured serum thrombopoietin levels. The mean platelet count was 5.1 x 10(4)/microl and the mean age was 64 years. None of our patients had clinical nor laboratory evidence of liver dysfunction, renal disease or disseminated intravascular coagulation. All patients were negative for antiplatelet antibody, PA-IgG and anticardiolipin-beta2GPI antibody. Leukocyte alkaline phosphatase level was low in two patients. Clonal chromosomal abnormalities of different types were detected in all patients. Bone marrow smears showed micromegakaryocytes. But there were no apparent morphological abnormalities of erythroid and granuloid series. Thrombopoietin levels, as determined by enzyme-linked immunosorbent assay, varied from <0.2 to 1.40 fmol/ml. We could not find the screening tool of RTC. In conclusion, there is a need to identify RTC from isolated thrombocytopenia because the patients with RTC don't have good prognosis as patients with isolated thrombocytopenia. Cytogenetic analysis is necessary to establish the diagnosis of RTC. We recommend that a patient above 50 years of age presenting with isolated thrombocytopenia and a low leukocyte alkaline phosphatase score should be suspected of having RTC.
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PMID:Clinical analysis and TPO levels in three patients with refractory thrombocytopenia. 1050 5

The aim of this work is to describe the techniques that have been used for preparation and analysis of whole fetal liver extracts destined for in utero transplantation. Nine fetal livers between 12 and 17 weeks of gestation were prepared: cell counts and assessment of the hematopoietic cell viability were performed on cell suspensions. Hepatocytes represented 40 to 80% of the whole cell population. The remaining cells were constituted by hematopoietic cells (mainly erythroblasts), as well as by endothelial cells. The latter expressed CD34 on their surface, interfering with the assessment of CD34+ hematopoietic cells by flow cytometry. Direct visual morphologic control using alkaline phosphatase anti-alkaline phosphatase techniques was needed to differentiate hematopoietic from extra-hematopoietic CD34+ cells. Between 3.0 and 34.6 x 10(6) CD34+ viable hematopoietic cells were collected per fetal liver. Adequate differentiation of these cells into burst-forming units erythroid (BFU-E), colony-forming units granulocyte-macrophage (CFU-GM), and colony-forming units granulocyte erythroid macrophage megakaryocyte (CFU-GEMM) has been shown for each sample in clonogeneic cultures. In conclusion, fetal liver is a potential source of hematopoietic stem cells. Their numeration, based on the presence of CD34, is hampered by the expression of this antigen on other cells contained in the liver cell extract, in particular endothelial cells.
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PMID:Preparation and analysis of fetal liver extracts. 1103 73

There is no single diagnostic marker for the only known type of primary acquired erythrocytosis, polycythemia vera (PV). The Polycythemia Vera Study Group (PVSG) used a combination of major and minor diagnostic criteria. However, these guidelines have some limitations and in the presence of newer diagnostic tools, have been re-evaluated. The recommendations of the Radionuclide Panel of the International Council for Standardization Hematology based on surface area are recommended over red blood cell mass (RCM) mL/kg expressions. Absolute erythrocytosis can be assumed in males and females with packed cell volume (PCV) values greater than 0.60 and greater than 0.56, respectively. A satisfactory strategy of investigation for a secondary erythrocytosis must be used. Hypoxemia, as well as renal and hepatic pathology, must be excluded. In unexplained absolute erythrocytoses, pO(2)(50) values and serum erythropoietin (EPO) levels should be examined. The latter can be disappointing in the confirmation of a secondary erythrocytosis, but elevated values contraindicate a diagnosis of a primary erythrocytosis. Establishment of a clonal marrow population supports a diagnosis of PV. Thus an acquired karyotypic abnormality is a major criterion. Palpable splenomegaly remains an important diagnostic marker. Scanning techniques to demonstrate splenic enlargement should be used with caution. Allowance must be made for interobserver and intraobserver differences and variation in normal spleen size with age and size of the subject. Splenomegaly demonstrated in this way should be taken as a minor criterion. An increased neutrophil count (>10 x 10(9)/L and >12.5 x 10(9)/L in smokers) is readily measurable and should replace total white blood cell count. The error in measurement of neutrophil alkaline phosphatase (NAP) score is large, making it an unsuitable diagnostic criterion. Neutrophil and platelet counts (>400 x 10(9)/L) should be taken as separate minor criteria. Endogenous erythroid colonies (EEC) grown from the peripheral blood have been used as a marker of PV, but it is an expensive technique that is not standardized and not totally specific for PV. Low serum EPO values found in the majority of patients with PV should hold a linked minor criterion position with EEC. Expert opinions should be obtained if bone marrow histology is to be used in the diagnosis of PV, but histology holds an important role in confirming the diagnosis. Semin Hematol 38(suppl 2):21-24.
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PMID:Evaluation of diagnostic criteria in polycythemia vera. 1124 98

Idiopathic myelofibrosis (IMF) is generally characterized by bone marrow (BM) fibrosis, anemia, splenomegaly and a leuko-erythroblastic blood picture. Although, histopathology is in keeping with the assumption of a stepwise evolution of the disease, little hematological data are available for patients with prefibrotic and early stages of disease. Therefore a clinicopathological study was performed that included firstly an exploratory sample of 68 patients with minor supportive therapy in whom BM biopsies during follow-up (41 +/- 32 months) revealed an evolution of a prefibrotic or very early fibrotic lesion into overt IMF. The validation sample consisted of 556 patients with pretreatment marrow specimens on admission. Diagnostic features and BM lesions were identical compared with the patients of the exploratory sample at their first examination. BM biopsies were processed by routine stainings including silver impregnation (reticulin fibers) and frequently also by immunohistochemistry to identify megakaryocytes and erythroid precursor cells more properly. Apart from minor hemorrhage and peripheral thrombosis patients with early stage IMF presented with non-specific symptoms including varying degrees of leukocytosis (51%), anemia (38%), a platelet count exceeding 600 x 10(9)/l (86%), splenomegaly (15%) and increase in leukocyte alkaline phosphatase (LAP) (24%) and serum lactate dehydrogenase (LDH) (20%). BM histology confirmed a moderate increase in hematopoiesis with a mixed granulocytic and megakaryocytic myeloproliferation, a reduction of erythroid precursors and significant megakaryocytic abnormalities. In keeping with the first BM examination of the exploratory sample no or only a borderline to slight increase in reticulin fibers was detectable, however, in 68 of 134 patients follow-up biopsies revealed a transition into overt IMF (intervals about three years). Median survival of this cohort with early-stage IMF was 129 months thus contrasting manifest IMF with an usually more unfavorable prognosis. Recognition of early stage IMF certainly alters the generally applied diagnostic criteria of this disorder. Regarding patients with associated thrombocytosis, differentiation from essential thrombocythemia is recommended. Moreover, characterization of early stage IMF probably exerts an impact on survival and may influence the decision to perform a BM transplantation.
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PMID:Early-stage idiopathic (primary) myelofibrosis--current issues of diagnostic features. 1214 83

The study of the human hematopoietic system would be facilitated by availability of a relevant animal model. Because the medullar microenvironment is made of different types of cells, interactions between hematopoietic cells and stromal cells are difficult to analyze in detail. As an approach for establishing an in vivo model to dissect these interactions, we grafted murine bone marrow fibroblastic cells (MS-5 cell line) with hematopoietic cells into the kidney capsule of syngenic mice. To identify the origin of cells present in the graft, we used green fluorescent protein-stable transfected MS-5 cells for the transplantation. To analyze the evolution of stromal cells and identify hematopoietic cells able to develop in these conditions, we performed morphology, histochemistry, and immunohistology on tissue sections at different times after transplantation. When injected alone, MS-5 cells differentiate into adipocytes. When injected with a bone marrow suspension or with isolated CD45+ cells (leukocytes), the stromal cells keep their fibroblastic morphology and their alkaline phosphatase expression and sustain granulopoiesis. When injected with hematopoietic stem cells called c-kit+ Sca-1+ Lin- suspension, clusters of hematopoietic cells are also observed: They do not present any granulopoietic activity and do not belong to B or T population nor to erythroid lineage. They are quiescent, induce bone marrow recovery and survival of lethally irradiated recipients, are able to form macroscopic colonies in the spleen, and are able to form very few colonies in vitro, suggesting that they are hematopoietic stem cells. In conclusion, our results show that reticular fibroblastic stromal cells MS-5 sustain the survival of stem cells and are not able to induce their differentiation. However, they can control differentiation, proliferation, and/or survival of hematopoietic cells engaged in myeloid lineage.
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PMID:Murine bone marrow stromal cells sustain in vivo the survival of hematopoietic stem cells and the granulopoietic differentiation of more mature progenitors. 1629 84

The clinical criteria according to the Polycythemia Vera Study Group (PVSG) do not distinguish between essential thrombocythemia (ET), thrombocythemia associated with early-stage polycythemia vera (PV) and prefibrotic chronic idiopathic myelofibrosis (CIMF). The criteria only classify the advanced stage of PV with increased red cell mass. The classification of myeloproliferative disorders (MPDs), proposed by the World Health Organization (WHO) in 2001, is a compromise of the clinical PVSG and WHO bone marrow criteria, and excludes early stages of ET and PV. The updated European clinical and pathological criteria combine the WHO bone marrow criteria with established and new clinical, laboratory, biological, and molecular MPD markers. This allows clinicians and pathologists to diagnose early-stage MPD and to differentiate ET, PV, and prefibrotic chronic idiopathic myelofibrosis (CIMF). Depending on laboratory tests and diagnostic criteria used, the population of the MPD patients defined as ET, PV, and CIMF are heterogeneous at the clinical, laboratory, and biological and pathological levels. The recent discovery of the JAK2 V617F mutation, which is the cause of a distinct trilinear MPD in its manifold clinical manifestations during long-term follow-up, increases the specificity of a positive JAK2 V617F polymerase chain reaction (PCR) test for the diagnosis of MPD (near 100%), but only half of the ET and CIMF patients according to the PVSG (sensitivity 50%) and the majority of PV patients (sensitivity 95%) are JAK2 V617F positive. A comparison of the laboratory features of JAK2 V617-positive and JAK2 wild-type ET patients clearly showed that JAK2 V617-positive ET is characterized by higher values for hemoglobin, hematocrit, and neutrophil counts; lower values for serum erythropoietin (EPO) levels, serum ferritin, and mean corpuscular volume; and by increased cellularity of the bone marrow in biopsy material. This indicates that JAK2 V617-positive ET patients, diagnosed according to the PVSG criteria, represent a "forme fruste of PV" consistent with early PV mimicking ET (JAK2 V617F trilinear MPD). In contrast, the JAK2 wild-type ET patients had significantly higher platelet counts and usually had a clinical picture of ET with normal serum EPO levels, PRV-1 expression, and leukocyte alkaline phosphatase score, and a typical WHO ET bone marrow picture. The clinical and pathological data on JAK2 V617F-positive MPD patients suggest that the JAK2 V617F mutation defines one disease entity with several sequential steps of ET, PV, and secondary myelofibrosis during long-term follow-up, and that the wild-type JAK2 MPDs may represent another distinct entity with a related but different molecular etiology. MPD-specific markers such as serum EPO, endogenous erythroid colony formation (EEC), and JAK2 V617F have high specificities, but the sensitivities are not high enough to detect the early stages of the MPDs, ET, PV, and prefibrotic CIMF. Bone marrow histopathology in addition to clinical, laboratory, biological, and molecular markers, including the JAK2 V617 PCR test, serum EPO, PRV-1, EEC, LAP score, peripheral blood parameters, and spleen size on echogram will detect the early stages of MPD and allows diagnostic differentiation of the three primary MPDs (ET, PV, and CIMF) in both JAK2 V617F-positive and JAK2 wild-type MPD patients.
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PMID:The 2001 World Health Organization and updated European clinical and pathological criteria for the diagnosis, classification, and staging of the Philadelphia chromosome-negative chronic myeloproliferative disorders. 1681 Jun 9


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