Background: Peripheral blood stem cells are today the mains source of cells for transplantation. The number of CD34 in peripheral blood of adult healthy volunteers is very low, so we have to mobilize. Objectives: To apply a protocol to collect CD4 cells in peripheral blood of normal donors mobilized by using G-CSF. Subjects and method: G-CSF (Leukokin) at a dose 10 mcg/kg/day was injected subcutaneously in 5 consecutive days for mobilization CD34 from 5 healthy donors. Count the number of CD34 everyday and collect CD34 cells in 5th \ufffd?6th day by automated blood cell separator (COBE-Spectra), observed clinical and hematilogy, biochemistry symtoms spontaneously. Results: The number of CD34 harvested is 215,5 \ufffd?570,2 x 106 CD34/donor. Almost other of parameters of hematology and biochemistry of donors were normal after one week from the last separation. Conclusion: Mobilization with G-CSF and aphaeresis of periphral blood stem cell from normal donors is feasibility and safety. The number of CD34 can be to allograft for an adult patient.
Hematopoietic Stem Cells ; Granulocyte Colony-Stimulating Factor ;

No abstract available.
Granulocyte Colony-Stimulating Factor* ; Humans ; Recurrence*

No abstract available.
Agranulocytosis* ; Granulocyte Colony-Stimulating Factor* ; Granulocytes* ; Humans*

PURPOSE: Granulocyte-colony stimulating factor(G-CSF) and granulocyte macrophage-colony stimulating factor(GM-CSF) are principal cytokines in granulopoiesis and their physiologic effects are mediated through binding to specific cell surface receptors. Although it is known that the level of serum G-CSF and GM-CSF, and presentation of the receptors are increased in infectious diseases, there have been no studies to find the correlation between the granulopoiesis and leukocytosis. This study was designed to measure G-CSF and GM-CSF in leukocytosis and in control and to demonstrate the possible pathogenesis of granulopoiesis in leukocytosis using quantitative analysis of G- CSF, GM-CSF and their CSFr. METHODS: The plasma levels of G-CSF, GM-CSF of 13 children without leukocytosis and 14 children with leukocytosis were measured. Counts of cell surface G-CSFr and GM-CSFr were measured by combining anti G-CSFr and anti GM-CSFr monoclonal antibodies to their respective receptors by using quantitative flow cytometric assay. RESULTS: There was no significant difference betweeen the plasma concentration of G-CSF and GM-CSF in acute leukocytosis and in the control group. However, levels of G-CSFr in acute leukocytosis decreased significantly compared to the control(P=0.012) and the levels of GM-CSFr in both groups revealed no significant difference. CONCLUSION: Increase in the number of leukocyte in leukocytosis was mediated by increasing the number of neutrophil, and increased plasma concentration of G-CSF may be the cause of neutrophilia. But GM-CSF did not have any influence on leukocytosis.
Antibodies, Monoclonal ; Child* ; Communicable Diseases ; Cytokines ; Granulocyte Colony-Stimulating Factor* ; Granulocyte-Macrophage Colony-Stimulating Factor* ; Granulocytes* ; Humans ; Leukocytes ; Leukocytosis* ; Neutrophils ; Plasma* ; Receptors, Cell Surface ; Receptors, Granulocyte Colony-Stimulating Factor ; Receptors, Granulocyte-Macrophage Colony-Stimulating Factor

No abstract available.
Granulocyte-Macrophage Colony-Stimulating Factor* ; Granulocytes* ; Humans* ; Macrophages* ; Methotrexate*

PURPOSE: This study aimed to demonstrate the possible pathogenesis of granulopoiesis in patients of Kawasaki disease(KD) using quantitative analysis of G-CSF, GM-CSF and their CSFr. METHODS: The plasma levels of G-CSF, GM-CSF, G-CSFr and GM-CSFr were studied in 14 patients in the acute phase of KD; 13 children with normal peripheral white blood cell counts were used as the normal control group. The plasma concentration of G-CSF, GM-CSF were analyzed by ELISA. The G-CSFr and GM-CSFr on the peripheral granulocytes were analyzed by a quantitative flow cytometric assay and QuantiBRITE, and the quantitative changes of receptors which did not combine with G-CSF and GM-CSF were measured. RESULTS: The total number of leukocytes in KD was similar to normal control group, but the leukocytes increased according to the number of neutrophils. The plasma concentration of G-CSF were decreased similar to normal control group(P=0.133), but that of GM-CSF decreased more than the normal control group(P=0.227). The quantity of G-CSFr, GM-CSFr were revealed to be no less than the normal control(P=0.721, P=0.912). After incubation with excessive G-CSF, the expressed G-CSFr on the neutrophils were decreased in both groups(P=0.554). The quantities of expressions of GM- CSFr on the neutrophil after incubation with the excessive GM-CSF were always increased in both groups(P=0.255). The amount of GM-CSFr of neutrophils are in proportion to total white blood cells (r=0.788, P=0.035), but it wasn't in the case of KD(P=0.644). CONCLUSION: The leukocytosis in KD that mediated by increasing neutrophil was not correlated with the plasma concentrations of G-CSF and GM-CSF, and the amount of expression of G-CSFr and GM-CSFr on granulocyte. It is possible that the reduction of concentration of GM-CSF results by increasing the active GM-CSFr.
Child ; Enzyme-Linked Immunosorbent Assay ; Granulocyte Colony-Stimulating Factor* ; Granulocyte-Macrophage Colony-Stimulating Factor* ; Granulocytes* ; Humans ; Leukocyte Count ; Leukocytes ; Leukocytosis ; Mucocutaneous Lymph Node Syndrome* ; Neutrophils ; Plasma* ; Receptors, Granulocyte Colony-Stimulating Factor ; Receptors, Granulocyte-Macrophage Colony-Stimulating Factor

Agranulocytosis as a side effect of clozapine has been reported to be associated with initial phases of treatment, i.e., first six months. Agranulocytosis with clozapine during the initial phases of treatment has been linked to genetic vulnerability in the form of variations in the human leukocyte-antigen haplotypes. However, there is limited literature on late onset agranulocytosis with clozapine and this has very rarely been linked to human leukocyte-antigen haplotypes vulnerability. In this report we review the existing data on late onset agranulocytosis with clozapine and describe the case of a young man, who developed agranulocytosis with clozapine after 35 months of treatment and was found to have genetic vulnerability in form of being positive for HLA DR4. This case highlights underlying autoimmune immune mechanism in clozapine-induced agranulocytosis and the need for frequent blood count monitoring on clozapine even after the initial 6 months of starting treatment especially in patients with genetic vulnerability to develop this condition.
Agranulocytosis* ; Clozapine* ; Granulocyte Colony-Stimulating Factor* ; Granulocytes* ; Haplotypes ; Humans ; Neutropenia

No abstract available.
Drug Therapy* ; Granulocyte Colony-Stimulating Factor* ; Granulocytes* ; Leukemia, Myeloid, Acute*

OBJECTIVE: To investigate the influence of granulocyte colony stimulating factor (G-CSF) and granulocyte macrophage colony stimulating factor (GM-CSF) on preimplantation development and implantation in mouse embryos. MATERIAL AND METHODS: Eight-cell stage mouse embryos were cultured for 96 hours with G-CSF or GM-CSF at concentrations of 10 pg/ml, 100 pg/ml, 1 ng/ml and 10 ng/ml. Embryos not treated with G-CSF or GM-CSF were served as control. The percentages of embryos which developed to expanded, hatched blastocyst stage and in vitro implantation at 96 hours were determined. Results were analyzed with Kolmogorov-Smirnov test and analysis of variance (ANOVA). The statistical significance was defined as p<0.05. RESULTS: The percentages of fully expanded blastocysts in all G-CSF and GM-CSF treatment groups were not significantly different from the control. The percentages of hatched blastocysts were significantly higher in 100 pg/ml and 10 ng/ml of G-CSF treatment group compared to the control (p<0.05, p<0.05, respectively). The percentages of hatched blastocysts were significantly lower in 1 ng/ml of GM-CSF treatment group compared to the control, 10 pg/ml, and 100 pg/ml of GM-CSF treatment group (p<0.05, p<0.05, p<0.05, respectively), and the percentages of hatched blastocysts were also significantly lower in 10 ng/ml of GM-CSF treatment group compared to the control and 100 pg/ml of GM-CSF treatment group (p<0.05, p<0.05, respectively). The percentages of implanted blastocysts in vitro were significantly higher following incubation with all concentrations of G-CSF compared to the control and, especially in 100 pg/ml and 10 ng/ml of G-CSF treatment groups compared to the control and other treatment groups. The percentages of implanted blastocysts in vitro were significantly higher in 10 pg/ml of GM-CSF treatment group than the control and 100 pg/ml of GM-CSF treatment groups (p<0.05, p<0.05, respectively). CONCLUSION: G-CSF and GM-CSF might influence on embryonic development and implantation in mouse embryos.
Animals ; Blastocyst ; Colony-Stimulating Factors* ; Embryonic Development ; Embryonic Structures* ; Female ; Granulocyte Colony-Stimulating Factor ; Granulocyte-Macrophage Colony-Stimulating Factor* ; Granulocytes* ; Mice* ; Pregnancy

PURPOSE: Cryopreservation has been the standard method of storing hematopoietic cells for the past 20 years, but this prdegrees Cedure is laborious and expensive. So, we evaluated the hematopoietic recovery of stored PBSCs at 4degrees C for a variable storage period MATERIALS AND METHODS: Eight leukapheresis products were kept unprdegrees Cessed at 4degrees C for 96 hours. To evaluate the effect of storage period on the hematopoietic recovery of PBSCs, assays for viability of mononuclear cells (MNCs), CFU-GM colony counts and CD34 cell counts were performed every 24 hours after PBSC collection. We tried to compare hematopoetic recovery of stored PBSCs at 4degrees C with that of cryopreserved PBSCs by using repeated measures ANOVA. RESULTS: Viability of MNCs, CFU-GM colony counts and CD34 cell counts were monitored at 24 hour, 48 hour, 72 hour and 96 hour after PBSC collection. Data are expressed as percentage of baseline value and shown as mean s.d.; MNCs viability (96+/-2%, 94+/-2%, 92+/-2%, 88+/- 3%), CFU-GM colony counts (87+/-10%, 79+/-11%, 65+/-13%, 56+/-15%), and CD34 cell counts (93+/-13%, 93+/-12%, 88+/-14%, 85+/-19%). After storing PBSCs at 4degrees C for 96 hours, viability of MNCs and CFU-GM colony counts were significantly reduced (p<0.05) except CD34 cell concentration (p>0.05). Prdegrees Cedures of controlled-rate freezing and thawing resulted in a notable loss of viability (77+/-9%) and CFU-GM colony count (71+/-29%). CFU-GM colony counts of 72 hour-stored PBSCs at 4degrees C was similar to those of cryopreserved PBSCs. CONCLUSION: If G-CSF mobilized PBSCs are stored at 4degrees C in less than 72 hours after collection, those hematopoietic recovery would be comparable to that of cryopreserved stem cells which are achieved by the rate-control freezer.
Bezafibrate ; Cell Count ; Cryopreservation ; Freezing ; Granulocyte Colony-Stimulating Factor ; Granulocyte-Macrophage Progenitor Cells ; Leukapheresis ; Stem Cells*