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

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