26 research outputs found
Elimination of metal interference in the determination of fluoride ion by non-suppressor type ion chromatography
A simple method has been developed to eliminate metal interferences in the ion-chromatographic determination of fluoride ion in aqueous solutions. Negative interferences become appreciable on 0.2-mM F at 0.01 to 0.02 mM of Al(III), Ce(IV), La(III), Y(III), Ce(III) and Pb(II); and at 0.25 mM of Ca(II). The interference from Cd(II), Co(II), Fe(II) and Ni(II) is insignificant at ≤ 5.0-mM metal for 5.0-mM F-. By alkalifying F- solutions at pH 12.3, the metal interference can be eliminated up to the concentrations of 0.25-mM Al(III), La(III) and Y(III); 1.0-mM Ce(IV); 2.5-mM Ce(III); and 5.0-mM Pb(II), Cd(II), Co(II), Fe(II) and Ni(II). The Ca(II) interference cannot be eliminated. The pretreatment enables determination of 0.2- to 5.0-mM F- in presence of 0.25-mM Al(III) or La(III) with coefficient-of-variations of 1.99 to 6.20%
Acute Myeloid Leukemia Presenting as Subcutaneous and Epidural Granulocytic Sarcoma Inside and Outside of the Frontal Bone
An 18 year-old male was admitted to our hospital suffering from a large tumor which was located
at the right frontal bone. He was diagnosed to have acute myeloid leukemia (AML) with granulocytic
sarcoma (GS). A chromosomal analysis showed t(8; 21), and a flow cytometric analysis demonstrated
the leukemic cells to be positive for CD56.
Systemic chemotherapy and radiation therapy to the GS, but the patient experienced a relapse in the
lumbar vertebrae. He underwent an umbilical-cord blood stem cell transplantation, however, he died 7
months thereafter. GS is a localized tumor consisting of leukemic myelolasts, which is generally
observed as a complication of either AML, myelodysplastic syndrome, or myelobproliferative disorders.
We herein report this case due to its rarity, even though various sites of GS have been reported
Acute Myeloid Leukemia Presenting as Subcutaneous and Epidural Granulocytic Sarcoma Inside and Outside of the Frontal Bone
Polycythemia Vera Terminating in Refractory Ascites
A 64-year-old woman,with more than a 20 year history of polycythemia vera(PV),developed portal
hypertension,myelofibrosis and extramedullary hematopoiesis accompanied by massive ascites. Portal
hypertension resulted not only from infiltration of the liver sinusoids by hematopoietic cells but also from
nodular regenerative hyperplasia of the liver. Wright-stained smears of ascites samples consisted of
mesothelial cells and macrophages. However,cultures of mononuclear cells from the ascites showed the
presence of hematopoietic progenitor cells including megakaryocyte colony formation and burst forming
units. The JAK2-V617F mutation was positive in granulocytes. Contrary to other reports, radiation
therapy was not effective and severe myelosuppression continued for more than one month. We present
the unusual clinical course for this case of PV and discuss the pathophysiology of refractory ascites
Der(2)t(2;11)(p21;q23), a Variant form of t(2;11), in Biphenotypic Acute Leukemia with T Lymphoid Lineage and M yeloid Lineage Differentiation
We describe a patient with biphenotypic acute leukemia (BAL) with T-lymphoid lineage and
myeloid lineage differentiation[BAL (T/M)]. Cytogenetic analysis revealed complex chromosomal
abnormalities, including der(2)t(2;11)(p21;q23). Neither leukemia cells nor T-cell receptor gene
rearrangements were detected in the bone marrow samples after four courses of high dose cytosine
arabinoside regimen. However, der(2)t(2;11)(p21;q23) anomaly persisted in most of metaphases.
Fluorescence in situ hybridization (FISH)analysis with a probe for MLL did not detect the split signal.
Forty-five cases of hematological disorder with t(2;11)(p21;q23) abnormality have been previously
reported. The majority of such cases have been classified as myelodysplastic syndrome(MDS) or acute
myeloid leukemia (AML). This is the first case BAL (T/M) associated with a t(2;11)(p21;q23)
anomaly