Objective To observe the effect of gait training under the analyzing with computer-aided gait analysis system on the hemiplegia after stroke.Methods 100 stroke patients with walk disturbance were randomly divided into observe group (n=50) and control group (n=50).All patients' gaits in two groups were analyzed with computer-aided gait analysis system before and after training.Both groups were treated with common drugs.The cases in observe group were trained under the result of computer-aided gait analysis system.The control group was trained without the instruction of computer-aided gait analysis.ResultsAfter 3-month training,the gaits of observe group improved better than that of the control group (P<0.05).ConclusionThe gait training guided with the computer-aided gait analysis system is more effective on the recovery of hemiplegic gait.

Many tumorigenesis in human are closely linked to the functional loss of P53. The tumor-suppressive functions of P53 are abrogated by mutations,but in 50% of all tumors it remains wild type. In these cases,loss of P53 tumor-suppressive function mainly results from the abnormal methylation of 5' CpG islands of tumor suppressor genes such as INK4a,ARF and ASPP. Restoring to normal methylation state of these genes might provide a new strategy for tumor therapy.

Many tumorigenesis in human are closely linked to the functional loss of P53. The tumor-suppressive functions of P53 are abrogated by mutations, but in 50% of all tumors it remains wild type. In these cases, loss of P53 tumor-suppressive function mainly results from the abnormal methylation of 5' CpG islands of tumor suppressor genes such as INK4a, ARF and ASPP. Restoring to normal methylation state of these genes might provide a new strategy for tumor therapy.

Objective To summarize the experimence of nonmyeloablative allogeneic peripheral blood cell transplantation in the treatment of chronic leukemia. Methods Seven patients, including 6 cases of chronic myeloid leukemia (in chronic phase), one of chronic lymphoid leukemia (in third stage), with HLA-identical siblings donor received allogeneic peripheral blood stem cell transplantation after a nonmyeloablative conditioning. Results All of them were engrafted with donor cells (4 with full of donor cells grafted, 3 with mixed chimerism) and recovered hematopoiesis (WBC recovered to more than 0.5 ?10 9/L during postoperative 9 day to 21 day and platelet recovered to more than 30?10 9/L during postoperative 11 day to 28 day). One of them developed a GVHD of degree IV. One of them developed aGVHD of degree I. Conclusion This procedure is much safe, effective and of less complications than the myeloablative condioning regimens and may represent another new approach in the management of patients with chronic leukemia.

Objective To investigate the effects of ZEB1 (Zinc finger E-box binding homeobox 1) gene knockdown on proliferation, cell cycle and apoptosis of human adipose-derived mesenchymal stem cells (hADSCs).Methods Primary mesenchymal stem cells were obtained from human adipose tissue by collagenase digestion and identified by immunological phenotype and differentiation potential of osteogenic and adipogenic lineages .The siRNA was trans-fected into hADSCs by lipofectamine 2000 .The expression of ZEB 1 and key proliferation , cell cycle and apoptosis-related genes were detected by real-time PCR and Western blot at mRNA and protein level respectively .The cell proliferation capacity was assessed by MTS .The apoptosis and cell cycle of hADSCs were evaluated by flow cytome-try.Results The ZEB1 expression at mRNA and protein level was significantly decreased in si-ZEB1 transfection cells as compared to transfection with si-NC.Inhibition of ZEB1 decreased the cell proliferation ability , and signifi-cantly inhibited the expression of cell proliferation related genes, including CCND1, MKI67, MYC and PCNA.After transfection with si-ZEB1 , the percentage of cells in G1 phase increased from 50.17% to 58.94%, and S phase and G2 phase decreased by 6.16% and 2.07% separately.Meanwhile, the apoptosis rate increased by 10.2%, the expression of apoptosis related genes TP53 and BAX was up-regulated , and the expression of anti-ap-optotic genes MCL1 and BCL2 was down-regulated in si-ZEB1 transfection cells as compared to transfection with si-NC.Conclusions ZEB1 may play an important role in promoting hADSCs proliferation , cell cycle progression and inhibit their apoptosis .

AIM: To investigate the chemotaxis mechanisms of polymerphonuclear leukocytes (PMNs) under the stimulation of LPS and its regulation by polydatin (PD). METHODS: Chemotactic chamber assay was used to investigate the regulatory role of formyl peptide receptor like-1 (FPRL1) in the chemotaxis of PMNs in response to LPS and PD. RESULTS: LPS increased the secretion of PMN chemotactic factor and up-regulated the function of formyl peptide receptor like-1. PD did not obviously affect the chemotactic factor secretion in normal PMN and the function of formyl peptide receptor like-1, but it significantly reduced the rise of chemotactic factor excretion in PMNs caused by LPS stimulation and PMNs transfected with formyl peptide receptor like-1. CONCLUSION: FPRL1 may mediate LPS-induced PMN chemotaxis, and PD regulates PMN chemotaxis by down-regulating the secretion of chemokine and the function of FPRL1 and may play a crucial role in the treatment of inflammation.

Phosphatidylinositol-3-kinase(PI3K),AKT,TSC1/2,and the mammalian target of rapamycin(mTOR) signaling cascade involves many cellular processes including apoptosis,growth,proliferation and differentiation,This pathway has been found to be the most variable one in human tumors.As tumor is a poorly differentiated disease,this review examines the role of the PI3K-AKT signal pathway in cell differentiation and tumor development.

Objective To identify the function and mechanism of MR1 in proliferation of BEL-7402 cells.Methods siRNA targeting MR1 and negative control siRNA were synthesized and transfected into BEL-7402 cells using Lipofectamine 2000.The silencing effect of MR1 siRNA was determined by semi-RT-PCR.SRB assay,colony formation assay and growth curve assay were used to investigate whether MR1 siRNA regulated cellular proliferation.Cell cycles were assessed by flow cytometry.G2 arrest reagent nocodazole was used to show the potential effect of MR1 siRNA on G1 arrest.The expression of Cyclin D1 was determined by Western blotting.Results(1)MR1 mRNA significantly decreased in BEL-7402 cells 24 h after MR1 siRNA transfection.(2)MR1 siRNA induced the down-regulation of cell growth.The expression of Cyclin D1 in MR1 siRNA tranfected BEL-7402 cells decreased significantly.(3)Flow cytometry results showed that MR1 siRNA markedly decreased G2 phase population with nocodazole treatment,and distinctly increased G1 phase population.Conclusion The gene MR1 is involved in the proliferation of BEL-7402 cells.MR1 siRNA causes inhibition of the proliferation of BEL-7402 cells.One of the mechanisms ofMR1 siRNA on the proliferation of BEL-7402 cells is the induction of G1 arrest.

Objective To study the effect of Sca1+ cells on the HSCs`(hemopoietic stem cells) differentiation to dendritic cells(DCs),and identify the morphology,function and surface markers of the cells.Methods CD117+ HSCs were isolated and purified from the bone marrow of healthy Balb/c mice by magnetic affinity cell sorting.After cell expansion by treatment with the support of Sca1+ cells,the HSCs were induced for directional differentiation into DC-like cells.Studied the surface markers by FACS and function via LSCM and animal experiments. Results After 10 days of culture,we demonstrated that Sca1+ cells induced HSCs to differentiate into a distinct regulatory DC subset with high expression of CD11b but low expression of Ia.They had phagocytotic activity,and suppressed the GVHD(graft versus host disease) reaction.Conclusion HSCs can differente into dendritic cells with the support of Sca1+ cells.

Aim To observe the effect of polydatin(PD) on the activities of ?-AR in cardiomyocytes under the stimulation of LPS. Methods Cardiac myocytes were isolated and cultured from neonatal rats. Radioligand binding assay and flow cytometry were used to detect the function of ?-AR. Results In control group, the density of ?-AR (B max) was 4.14?1.41 fmol?(1?105 cells) -1 and ?-AR affinity (K d) was (4.02?0.59) nmol?L -1. In LPS group, ?-AR density was down-regulated 〔B max=1.78?0.12 fmol?(1?105 cells) -1〕 and the affinity decreased (K d=23.88?2.34 nmol?L -1). In LPS+PD group, ?-AR B max was recovered to 3.37?0.36 fmol?(1?105 cells) -1 and the affinity increased (K d=3.44?0.44 nmol?L -1). In PD group, ?-AR functions had no significant difference with normal group 〔B max=2.76?0.32 fmol?(1?105 cells) -1 and K d=4.63?1.54 nmol?L -1〕. The ?-AR amount measured by flow cytometry showed the same change tendency as the radioligand binding assay. Conclusion ?-AR activities may be down-regulated during the pathological process of LPS treatment. PD could reverse the effects of LPS by up-regulating ?-adrenoreceptors.