To investigate the possibility that skeletal muscle satellite cells implanted into injured myocardium in different time after myocardial infarction differntiate into cardiac-like muscle fibers, thus repairing the damaged heart muscle.

To establish a human/goat hematopoietic stem cell (HSC) xenogeneic transplant model and to probe the engraftment, expansion and differentiation of human HSC in vivo.

To investigate the development potential of blastomeres isolated from 4-cell human embryos.

To observe the role of calcitonin (CT) during the implantation.

Mesenchymal stem cells (MSC) are thought to be multi-potent cells that have the potential to differentiate into lineages of mesenchymal tissues, including bone, cartilage, tendon, fat, muscle, and marrow stroma during embryo morphogenesis. In recent years, cells that have the characteristics of mesenchymal stem cells were isolated from marrow aspirates of human and a few animals. It was found that these cells retain the characteristics of stem cells in vitro and could be induced to differentiate exclusively into the osteocytic, chondrocytic, myoblastic and adipocytic lineages. It was demonstrated that MSC could heal clinically significant bone and cartilage defects in animal models. The role of MSC in repairing tendon defect was also testified. In addition, for its multi-potential to differentiate into lineages of mesenchymal tissues, MSC could be used as gene vehicle for gene therapy of trauma care.

The aim of this study was to determine the expression of heat shock protein 70 (HSP70) as molecular chaperones, following traumatic brain stem injury(TBSI). The expression of HSP70 was detected in respective brain regions of rats 1 h, 3 h, 6 h, 12 h, 24 h after brain stem stabbing wound. Numerous HSP70 immunoreactivity positive blood vessel endothelioid and glia cells were found in cerebral, cerebellar cortex and hippocampus after 1 h, with H.E stain unchanged. In the area near the focal of brain stem injury, HSP70 immunoreactivity positive neurons increased significantly after 1 h of injury, reaching the highest level after 3 h, much higher than in other areas. HSP70 immunoreactivity positive cells still existed after 24 h of injury. It was suggested that TBSI cause the defectiveness of protein structure in brain, and induce HSP70 proteolysis of denature protein including misfolding or aggregate. TBSI can be diagnosed regionally by the increasing of HSP70 immunoreactivity positive neurons in the focal of brain stems.

The bone marrow cells of CML(chronic myelogenous leukemia) transgenic mice carrying metallothionein(MT) promoter/enhancer, bcr-abl(p210) cDNA and SV40 splicing/poly(A) signal sequences were cultured in liquid and soft agar with hydroxyurea (Hu), 5-fluorouracil(5-Fu), mouse stem cell factor (mSCF) and mouse interleukin-3(mIL-3) independently or combinatively. The cell or colony counting and transgene RT-PCR analysis showed that the proliferation, colony formation and transgene expression of the bone marrow cells were advanced in the combinative culture of mSCF with mIL-3, but they were significantly inhibited in the culture without any growth factors, or with mSCF, mIL-3 and Hu or 5-Fu. These findings suggest that the combinative utilization of chemotherapeutants and cytokines is a potentially effective strategy of the clinical treatment for CML.

To explore the effects of reducing the incidence of severe acute graft-versus-host disease (GVHD) and improving the disease free survival(DFS) in haploidentical donor transplantation by granlocyte colony-stimulating factor (G-CSF) administration to donor before harvesting and a number of immunosuppresants added to host.

To investigate the effect of stem cells derived from autogenous skeletal muscle, namely satellite cells, and implanted into ischemic myocardium on inhibition of myocardium fibroatrophy.

To study the effects of allogeneic peripheral blood stem cell transplantation (allo-PBSCT) in high-risk leukemia.

To investigate the relationship between the stroma of bome marrow and the abnormality of hematopoiesis in patients with paroxysmal nocturnal hematoglobinuria (PNH).

In the present study, the effects of murine bone marrow endothelial cell conditioned medium (ECM) combined with flt3 ligand (FL) or/and thrombopoietin (TPO) on the proliferation of HPP-CFC and CFU-GM were investigated. Both ECM and the concentrated retentate of ECM (MW>10 kD) promoted the growth of CFU-GM and HPP-CFC, and this promoting effect was further enhanced by addition of FL or TPO. Using reverse transcriptase-polymerase chain reaction (RT-PCR) technique, the expression of FL and TPO mRNA was not found in murine bone marrow endothelial cells.

In order to elucidate the intrinsic mechanism underlying proliferation and differentiation of megakaryocytes during ontogenesis, CD34(+) cells were isolated from human fetal liver (FL) with a high-gradient magnetic sorting system (MACS) and were incubated in liquid suspension with 50 and 100 ng/ml of thrombopoietin (TPO) and in MegaCult(Tm) -C semi-solid culture system with 0, 12.5, 25, 50, 100, and 200 ng/ml of TPO. The cell number, colony number of CFU-Mk, platelet-associated antigen phenotype, and DNA ploidy of CD41(+) cells were examined from d 0 to d 12 in culture. The expression patterns of cyclins B1, D1, and D3 were also analyzed by using immunoblot and flow cytometry. TPO stimulated proliferation of CD34(+) cells of FL from 1 x 10(5)/ml to 13.12 +/-4.06 10(5)/ml with 95% of CD41a(+) cells and 3% of CD34(+) cells after 12 d of culture. Most of the megakaryocytes (MKs) derived from FL were in 2 N ploidy class, and few in 4 N ploidy class, but no megakaryocytes ploidy class was higher than 4 N. The effect of TPO on the formation of CFU-Mk colonies from FL derived CD34(+) cells is shown in a dose-response curve. The expression of cyclin B1 increased progressively and the high level of cyclin B1 was maintained in FL CD34(+) cells induced by TPO during 12 d of culture. A high level of cyclin B1 appeared on FL derived MKs of G1 phase at d 12. The expression of cy-of cyclins D1 and D3 gradually increased in FL CD34(+) cells, which was induced by TPO during the initial 6-day incubation. Afterwards, the level of cyclins D1 and D3 decreased progressively, particularly in MKs which were in G2+M phases. These data suggest that (1) TPO induced proliferation and differentiation of FL derived CD34(+) cells through upregulation of cyclin B1 in G2+M phases and cyclins D1 and D3 in all phases of cell cycle, and (2) Continuing high level of cyclin B1 and decreases of cyclins D1 and cyclin D3 on MKs in G2+M phases may contribute to a retardation of MK endoreduplication.

To investigate the clinical impact of CD(34)(+) cell selected autologous peripheral blood stem cell transplantation (APBSCT) in multiple myeloma (MM).

To study the patterns of transformation from myelodysplastic syndromes (MDS) into acute leukemias (AL).

To observe the influence of chemotherapy on hematopoietic progenitor cells (HPC) and hematopoietic microenvironment (HME). To observe whether intravenous infusion of autologous bone marrow stromal cells (ABMSC) expanded in vitro can improve the hematopoietic function.

To establish a highly efficient expression system of recombinant human Flt3 ligand (rhFL) in E. coli and a suitable purification method of the expressed products.

To investigate in vitro autonomous growth of megakaryocytic progenitors and the role of Tpo in essential thrombocythemia (ET).