No abstract available.
Anemia* ; Diagnosis*

Anemia is defined as an insufficient amount of RBC mass to adequately deliver oxygen to peripheral tissues. For practical purposes, however, the measurements of three parameters that can be obtained from the complete blood count (CBC) are enough to establish the presence of anemia; hemoglobin (Hb) concentration, hematocrit, and RBC number. Among these, the Hb level is the most convenient parameter to establish the diagnosis of anemia. Anemia is not a disease by itself but mostly a consequence of the underlying acquired or genetic abnormality. Although the clues to the cause of anemia may be found from the history and physical examination, three parameters from CBC provide most critical information for the differential diagnosis of anemia; mean corpuscular volume (MCV), red cell distribution width (RDW), and the reticulocyte count. MCV provides information on the size of the red cell. Values greater than 100 fL usually signify a nuclear maturation defect resulting in macrocytic anemias, while values less than 80 fL are diagnostic of hemoglobin synthesis defect causing microcytic anemias. Meticulous evaluation of the serum iron status and body iron storage is essential to the differential diagnosis of microcytic anemias. RDW is a measure of the red cell size variation. It is increased by the appearance of microcytic or macrocytic cells, or both. The reticulocyte count is a useful laboratory measurement of effective red cell production. Hemolytic anemia or acute bleeding can increase the reticulocyte count. There are four clinically useful laboratory measurements indicating the presence of hemolytic process; the reticulocyte count, the serum bilirubin, the serum lactate dehydrogenase (LDH), and the serum haptoglobin concentration. Once the presence of hemolytic anemia is established, laboratory assessment to differentiate between intravascular and extravascular hemolysis is important because clinical conditions producing intravascular hemolysis may be anticipated in certain clinical situations, which may be complicated by acute renal failure or disseminated intravascular coagulation that needs immediate interventions. If the definitive cause of anemia cannot be established by examining the peripheral blood, a bone marrow study may be helpful.
Acute Kidney Injury ; Anemia* ; Anemia, Hemolytic ; Anemia, Macrocytic ; Bilirubin ; Blood Cell Count ; Bone Marrow ; Cell Size ; Diagnosis ; Diagnosis, Differential ; Disseminated Intravascular Coagulation ; Erythrocyte Indices ; Haptoglobins ; Hematocrit ; Hemolysis ; Hemorrhage ; Humans ; Iron ; L-Lactate Dehydrogenase ; Oxygen ; Physical Examination ; Reticulocyte Count

No abstract available.
Blood Platelets* ; Humans* ; Membranes* ; Plasminogen*

No abstract available.
Leukemia*

No abstract available.
Disseminated Intravascular Coagulation* ; Plasma* ; Scrub Typhus*

No abstract available.
Bone Marrow Transplantation* ; Bone Marrow* ; Erythroid Precursor Cells* ; Pathology*

In thirty patients with acute leukemia and severe aplastic anemia receiving random single donor platelet transfusions, the development of refractoriness by consecutive platelet transfusions with cytapheresis and its relationship to the appearance of anti-platelet antibodies were investigated. The median number of platelet transfusions inducing refractoriness was 13 times, and 20% of the patients remained unrefractory despite of the repeated multiple platelet transfusions up to 20 to 25 times. The results of anti-platelet antibody tasts by the enzyme-linked immunosorbent assay(ELISA) and immunofluorescent techniques(IFT) showed no statistically significant relationship with the refractoriness (p greater than 0.1). Although there was significant correlation between the results of ELISA and IFT, both tests were insufficient to find out refractoriness even with the use of pooled platelets from multiple donors as target cells. This study shows that 13 single donor platelet transfusions result in refractoriness, that both ELISA and IFT are insufficient to detect refractoriness despite of their significant correlation, and that other methods than these are needed in order to detect alloimmunization.
Adolescent ; Adult ; Aged ; Anemia, Aplastic/therapy ; Anemia, Refractory/*etiology ; Antibodies/metabolism ; *Blood Platelets/immunology ; *Blood Transfusion ; Female ; Humans ; Leukemia/therapy ; Male ; Middle Aged

Histone deacetylation and demethylation are epigenetic mechanisms implicated in cancer. Studies regarding the role of modulation of gene expression utilizing the histone deacetylase inhibitor scriptaid and the demethylating agent 5-azacytidine in HL-60 leukemia cells have been limited. We studied the possibility of recovering epigenetically silenced genes by scriptaid and 5-azacytidine in human leukemia cells by DNA microarray analysis. The first group was leukemia cells that were cultured with 5-azacytidine. The second group was cultured with scriptaid. The other group was cultured with both agents. Two hundred seventy newly developed genes were expressed after the combination of 5-azacytidine and scriptaid. Twenty-nine genes were unchanged after the combination treatment of 5-azacytidine and scriptaid. Among the 270 genes, 13 genes were differed significantly from the control. HPGD , CPA3, CEACAM6, LOC653907, ETS1, RAB37, PMP22, FST, FOXC1, and CCL2 were up-regulated, and IGLL3, IGLL1, and ASS1 were down-regulated. Eleven genes associated with oncogenesis were found among the differentially expressed genes: ETS1, ASCL2, BTG2, BTG1, SLAMF6, CDKN2D, RRAS, RET, GIPC1, MAGEB, and RGL4. We report the results of our leukemia cell microarray profiles after epigenetic combination therapy with the hope that they are the starting point of selectively targeted epigenetic therapy.
Azacitidine ; Cell Transformation, Neoplastic ; Epigenomics ; Gene Expression ; Histone Deacetylase Inhibitors ; Histone Deacetylases ; Histones ; Humans ; Hydroxylamines ; Leukemia ; Oligonucleotide Array Sequence Analysis ; Quinolines

BACKGROUND: In acute leukemia patients, several successful methods of expression profiling have been used for various purposes, i.e., to identify new disease class, to select a therapeutic target, or to predict chemo-sensitivity and clinical outcome. In the present study, we tested the peripheral blood of 47 acute leukemia patients in an attempt to identify differentially expressed genes in AML and ALL using a Korean-made 10K oligo-nucleotide microarray. METHODS: Total RNA was prepared from peripheral blood and amplified for microarray experimentation. SAM (significant analysis of microarray) and PAM (prediction analysis of microarray) were used to select significant genes. The selected genes were tested for in a test group, independently of the training group. RESULTS: We identified 345 differentially expressed genes that differentiated AML and ALL patients (FWER < 0.05). Genes were selected using the training group (n=35) and tested for in the test group (n=12). Both training group and test group discriminated AML and ALL patients accurately. Genes that showed relatively high expression in AML patients were deoxynucleotidyl transferase, pre-B lymphocyte gene 3, B-cell linker, CD9 antigen, lymphoid enhancer-binding factor 1, CD79B antigen, and early B-cell factor. Genes highly expressed in ALL patients were annexin A 1, amyloid beta (A4) precursor protein, amyloid beta (A4) precursor-like protein 2, cathepsin C, lysozyme (renal amyloidosis), myeloperoxidase, and hematopoietic prostaglandin D2 synthase. CONCLUSION: This study provided genome wide molecular signatures of Korean acute leukemia patients, which clearly identify AML and ALL. Given with other reported signatures, these molecular signatures provide a means of achieving a molecular diagnosis in Korean acute leukemia patents.
Amyloid ; Antigens, CD79 ; Antigens, CD9 ; B-Lymphocytes ; Cathepsin C ; Diagnosis ; DNA Nucleotidylexotransferase ; Gene Expression* ; Genome ; Humans ; Leukemia* ; Leukemia, Myeloid, Acute ; Lymphoid Enhancer-Binding Factor 1 ; Muramidase ; Peroxidase ; Precursor Cell Lymphoblastic Leukemia-Lymphoma ; Precursor Cells, B-Lymphoid ; Prostaglandin D2 ; RNA ; Transcriptome*

No abstract available.
Korea* ; Lymphoma*