Biomedical subjects

Ping Zou

Publications and source records attributed to Ping Zou.

At least 37 records · Page 2Linked to original sources

PubMed2006

Comparison of immunophenotype and clinical manifestations between patients with M5a and M5b of acute monocytic leukemia.

Acute monocytic leukemia is a distinct subtype of acute myeloid leukemia (AML) with characteristic biology and clinical features. This study was designed to compare the immunophenotypical features and clinical manifestations of the patients with AML-M(5a) to that of patients with AML-M(5b), and to identify differences between M(5a) and M(5b) and to explore their relations. A total of 58 cases of de novo adult patients with AML M(5) were investigated. Immunofluorescence analysis by flow cytometry was performed to determine the immunophenotype of the leukemic cells in all cases. Meanwhile, clinical data of these cases were studied retrospectively. The results showed that the immunophenotypes of monocytic leukemic cells in patients with AML M(5) were heterogeneous, and CD68 and CD11b were expressed higher in patients with AML M(5a), compared with that in patients with AML M(5b) (P < 0.01). The significant differences in sex, extramedullary infiltration, WBC counts of peripheral blood, complete remission rate and disease-free survival (DFS > 300 days) between the patients with AML M(5a) and M(5b) did not exist (P > 0.05). It is concluded that the special individual immunophenotype features can be detected in patients with either of AML M(5a) or M(5b), and that expressions of CD68 and CD11b were much higher in M(5a). It seems that the complete remission rate and disease-free survival of patients with M(5a) and M(5b) are not different from that of currently available therapy.

Adolescent↗

PubMed2006

[Mechanism of G2/M blockage triggered by activated-Chk1 in regulation of drug-resistance in K562/A02 cell line].

The study was purposed to investigate the effect of phosphorylated-chk1 on cell cycle and apoptosis of human erythroleukemic cell line K562 and K562/A02, and to explore the mechanism of chk1 in regulation of drug-resistance of leukemia cells. After treatment with adrimycin for six hours, the cell cycle distribution was detected by flow cytometry; the Chk1mRNA expression was detected by RT-PCR and the Chk1 phosphorylation level was detected by Western blot. Under the condition of down-regulation of Chk1mRNA expression in cells transfected with Chk1 short hairpin RNA, the cell apoptosis rates were detected by flow-cytometry following adrimycin. The results indicated that the proportion of K562/A02 cell line in G2/M phase was (54.12 +/- 0.57)% at 6 hours after drug treatment, significantly higher than that of K562 cell line (36.99 +/- 1.28)%. No evident difference of the Chk1mRNA expression was observed between K562 and K562/A02 cell lines, while elevated Chk1 phosphorylation following DNA damage induced by adriamycin was observed in the K562/A02 cell line (0.79 +/- 0.56), significantly higher than that in K562 cell line (0.27 +/- 1.47). The cell apoptosis rate of the Chk1 shRNA group in K562/A02 cell line was 3.84-fold of blank vector group, but that in K562 cell line was 1.30-fold of blank vector group. It is concluded that the increased chk1 activity that delay the progress of cell cycle are associated with cellular resistance to adrimycin in the K562/A02 cell line.

Apoptosis↗

PubMed2005

[Blocking the escape of leukemic cells from killing of T cell by combining anti-Fas ribozyme and CD80-IgG fusion protein].

OBJECTIVE: To study Fas expression regulation of cytotoxic T lymphocyte(CTL)via anti-Fas ribozyme, increasing of CD80 epitope on the surface of acute myelomonocytic leukemia cells by CD80-IgG fusion protein and their effects on the apoptosis and killing ability against acute myelomonocytic leukemia cells of CTL. METHODS: A hammerhead ribozyme gene targeting the Fas mRNA was synthesized and its expression vector pEGFP-RZ596 was constructed and transfected into the mouse spleen T cells via electroporation. The Fas expression on T cells was detected by RT-PCR and Western bloting. In the meantime the eukaryotic expression vector pcDNA/CD80-IgG was constructed by gene recombinant technique and transfected into ovarian cells of hamster of the line CHO. The CD80-IgG fusion protein was purified from the supernatant of G418-selected CHO cells by Protein G affinity chromatography method. Then allogeneic mixed lymphocytes culture between the mouse spleen T cells transfected with pEGFP-RZ596 and WEHI-3 cells (mouse acute myelomonocyte leukemia cell line) incubated with CD80-IgG fusion protein was performed. The apoptosis rate of the T cells was detected with annexin V-FITC. The proliferation and killing ability in vitro against WEHI-3 cells of the T cells were detected by MTT colorimetry. RESULTS: The luminance of Fas Western bloting results from the mouse spleen T cells negative control, transfected with pEGFPC1 and transfected with pEGFP-RZ596 were separately 1, 0.98 and 0.45 (P < 0.01). After being cocultured with WEHI-3 cells, which has higher expression of Fas ligand (64% +/- 3%), the apoptosis rate and the killing ability against WEHI-3 cells of the mouse spleen T cells transfected with pEGFP-RZ596 were separately 37% and 67%. Whereas that of the mouse spleen T cells negative control and transfected with pEGFPC1 were separately 88%, 84% (P < 0.01) and 32%, 31% (P <0.01). The CD80 positive expression rate of WEHI-3 cells was upregulated from 5.1% +/- 0.4% to 27.4% +/- 2.2% after these cells were preincubated with CD80-IgG fusion protein (P < 0.01). The killing ability of the mouse spleen T cells against WEHI-3 cells preincubated and not preincubated with CD80-IgG fusion protein were separately 64% and 49% (P <0.01), but that of the mouse spleen T cells, which were transfected with pEGFP-RZ596, was further promoted to 82% (P < 0.01) CONCLUSION: The apoptosis of mouse CTL inducing by FasL-Fas pathway could be avoided and the killing ability of mouse CTL against WEHI-3 cells can be significantly promoted at the same time by combining anti-Fas ribozyme and CD80-IgG fusion protein.

Animals↗

PubMed2005

[Isolation and identification of chronic myelogenous leukemia bone marrow mesenchymal stem cells and their functional characteristics].

OBJECTIVE: To isolate and culture bone marrow mesenchymal stem cells (MSCs) from chronic myelogenous leukemia (CML) patients and examine their functional characteristics. METHODS: Bone marrow was extracted from the anterior superior iliac spines of 21 patients with CML. MSCs were isolated and cultured. Single colony derived MSCs were harvested by limiting dilution. The cell cycle and immunophenotype of the expanded clonal MSCs were detected by fluorescence-activated cell sorter (FACS). Different agents were used to induce the MSCs to differentiate into osteocyte, adipocyte and neural cells. Von Kossa staining, oil-red staining, and Western blotting was used to examine the ability of differentiation. PCR was used to detect the expression of BCR/ABL gene. The ultrastructure of the CML derived MSCs was observed with electron microscopy. Sixteen BALB/c nude mice were randomly divided into 2 equal groups to be inoculated with HL60 cancer cells and CML derived MSCs to observe the tumorigenicity. MSCs were cultured in soft agar for 2 weeks to observe the clone growth. RESULTS: Fibroblast-like, positive in CD29, CD44, and CD105, and negative in CD116, CD34, CD48, and HLA-DR, the CML derived MSCs could differentiate into osteocyte, adipocyte and neural cells. CML derived MSCs showed normal karyotype and ultrastructure, they did not express BCR/ABL gene. After 2 weeks' culture no clone was formed from the MSCs. Four weeks after tumors were shown in 6 of the 8 mice inoculated with HL60 cells, and no tumor was seen in the mice inoculated with MSCs. CONCLUSION: Able to differentiate into different types of cell and without tumorigenicity, MSCs from the bone marrow of CML patients have the potentiality in clinical application.

Animals↗

PubMed2005

Effects of EPI readout bandwidth on measured activation map and BOLD response in fMRI experiments.

The purpose of this study was to evaluate the effects of echo planar imaging (EPI) readout bandwidth and its interaction with data processing procedures on the measured blood oxygenation level dependent (BOLD) response and activation in fMRI experiments. Seventeen healthy subjects were scanned during a brief visual stimulation paradigm with two EPI pulse sequences having 'high' (1953 Hz/pixel) and 'low' (780 Hz/pixel) readout bandwidth. Functional data were analyzed with a general linear model including temporal filtering and a basic correlation model following (1) no preprocessing, (2) realignment, or (3) realignment and spatial smoothing. A range of statistical thresholds were used to generate activation maps. Despite slightly higher BOLD signal detected with the high bandwidth sequence from matched ROIs in the primary visual cortex, results showed that the low bandwidth pulse sequence was more sensitive under most conditions evaluated. That is, the low bandwidth sequence detected greater numbers of activated voxels with lower cluster average BOLD signal (e.g., low bandwidth detected 1.4 times more voxels, with average BOLD signal 30% lower compared to high bandwidth for P = 0.05 (corrected) with the 3rd preprocessing procedure using the general linear model). However, there was significant interaction between bandwidth and data preprocessing procedures. Of particular interest, the sensitivity advantage of the low bandwidth pulse sequence decreased for the smoothed data as the activation threshold became less conservative. For the frequently used threshold of P = 0.001 (uncorrected) and cluster size of at least 5 voxels, the bandwidth advantage became insignificant. These findings demonstrate that the effects of bandwidth should be considered carefully in the design, analysis, and interpretation of BOLD fMRI studies.

Adult↗

PubMed2005

Effects of adenovirus mediated vascular endothelial growth factor gene transfer on reconstitution of hematopoiesis in post-bone marrow transplantation mice.

BACKGROUND: Bone marrow transplantation (BMT) conditioning procedure is considered as the cause of damage to bone marrow microvasculature and the delay of hematopoiesis recovery. However, hematopoiesis regulation post BMT by vascular endothelial growth factor (VEGF) has not yet been studied. In this study, adenovirus were used to investigate the effects of VEGF gene transfer on preventing damages to bone marrow microenvironment and its promotion of hematopoiesis in post-BMT mice. METHODS: Recombinant adenovirus (Ad)-enhanced green fluorescent protein (EGFP)/hVEGF165 was injected via tail vein into BALB/c mice undergoing syngeneic BMT. During the different phases post BMT, the distribution of adenovirus and the plasma levels of hVEGF were measured as well as the numbers of white blood cells (WBC), platelet (PLT) and red blood cells (RBC) in peripheral blood. At the same time, the mice were injected with Chinese ink via tail vein, following which the tibias were separated and were used for analysis of bone marrow microvasculature surface area and cellularity. RESULTS: Significant expression of EGFP and hVEGF was observed in multiple organs at different phases post BMT, and the plasma level of hVEGF was up to (866.67 +/- 97.13) pg/ml. The recovery of WBC, PLT and RBC of the group treated with recombinant adenovirus Ad-EGFP/hVEGF165 were significantly more rapid than those of other BMT groups (P < 0.05, respectively). At the 20th day post BMT, the percentage of bone marrow microvasculature surface area in group treated with VEGF [(61.2 +/- 4.0)%] returned to normal level [(62.0 +/- 5.0)%, P > 0.05]. The restoration of hematopoiesis was retarded more than that of microvasculature. The cellularity of bone marrow in each group was still lower than that of normal control [(62.3 +/- 4.0)%, P < 0.05] at the 30th day post BMT, but the percentage in group treated with VEGF at the 20th and 30th days post BMT [(46.5 +/- 5.0)% and (55.1 +/- 4.5)%] exceeded those of other BMT groups (P < 0.05, respectively). CONCLUSION: VEGF gene transfer mediated by adenovirus may protect the hematopoietic microenvironment to promote the restoration of hematopoiesis in post-BMT mice.

Adenoviridae↗

PubMed2005

Experimental quantum cloning with prior partial information.

When prior partial information about a state to be cloned is available, it can be cloned with a fidelity higher than that of universal quantum cloning. We experimentally verify this intriguing relationship between the cloning fidelity and the prior information by reporting the first experimental optimal quantum state-dependent cloner, using nuclear magnetic resonance techniques. Our experiments may further cast important implications into many quantum information processing protocols.

Journal Article↗

PubMed2005

BOLD responses to visual stimulation in survivors of childhood cancer.

Children surviving certain cancers have a high incidence of cognitive deficits caused by central nervous system (CNS) disease or treatments directed at the CNS. To establish the feasibility of using blood oxygen level-dependent (BOLD) functional magnetic resonance imaging (fMRI) to study cognitive deficits in survivors of childhood cancer, we tested the hypothesis that this population has the same BOLD response to visual stimulation as healthy subjects. We used BOLD fMRI to measure spatial and temporal patterns of brain activity after brief visual stimulation in 16 survivors of childhood cancer, 11 age-similar healthy siblings of survivors, and 16 healthy adults. Functional data for the survivors were analyzed with two general linear models, one used a canonical hemodynamic response function (HRF) and the other used a Fourier set as basis functions. The measured BOLD signal and brain activation patterns were similar in the survivors with both models. The BOLD signal for survivors was qualitatively similar in timing and shape, but there were significant quantitative differences as compared with healthy subjects. The activation was normally located in the primary visual cortex in 13 survivors, but the activation volume was significantly smaller in brain tumor survivors than in other groups. These findings demonstrate the feasibility of using BOLD fMRI to investigate brain function in survivors of childhood cancer. However, fMRI studies in this population must take into account effects of quantitative differences in their BOLD responses as compared to healthy subjects.

Adolescent↗

PubMed2005

Effect of angiotensin II on cord blood CD34+ cells expansion in vitro.

In order to investigate the influence of angiotensin II on hematopoietic system, CD34+ cells in cord blood were purified, and the effects of angiotensin II in combination with various cytokines on their growth and differentiation were studied by cell culture in vitro. It was found that angiotensin II in suspending medium could stimulate both BFU-E and CFU-GM expansion. The number of BFU-E and CFU-GM was increased with the increases of angiotensin II concentrations during a certain range. In addition, the expansion fold of CFU-GM was increased from 2.3 +/- 0.8 times to 7.8 +/- 2.3 times when angiotensin II was added in the presence of SCF+G-CSF+GM-CSF+IL3 cytokines mixture. Similarly, the expansion fold of BFU-E was increased from 3.1 +/- 1.8 times to 9. 2 +/- 2.3 times with angiotensin II in the presence of SCF+EPO+TPO+IL-3. In the semi-solid medium, angiotensin II could stimulate CFU-GM expansion but had no effect on the growth of BFU-E. In conclusion, angiotensin II had some stimulating effects on cord blood hematopoietic progenitors expansion in vitro in the presence of other cytokines.

Angiotensin II↗

PubMed2005

Diffusion tensor imaging of intraaxial tumors at the cervicomedullary and pontomedullary junctions. Report of two cases.

Brainstem gliomas are a heterogeneous group of lesions that account for 15% of all pediatric tumors of the central nervous system. Diagnosis and treatment planning for these tumors is based on the observation of Epstein and Farmer that the growth of lesions with low malignant potential is limited by the anatomical structures of the brainstem. Surgery is offered only to those patients with a high probability of harboring a low-grade tumor, because the attendant risk for significant morbidity outweighs the therapeutic benefit of debulking the tumor in cases of high-grade tumors. The authors report two cases that highlight the potential of diffusion tensor (DT) imaging to identify local white matter tracts in the pons, medulla, and cervical cord and to improve the preoperative assessment of low-grade gliomas. Preoperative DT imaging in both cases demonstrated that the white matter tracts were displaced by the bulk of the low-grade tumors but were structurally preserved. Intraoperative and neurological findings were consistent with the preoperative interpretation of the DT images. These cases demonstrate that DT imaging is a useful method for visualizing the relationship between tumor and normal brainstem white matter architecture, as well as for improving the surgical evaluation and management of pediatric brainstem tumors.

Adolescent↗

PubMed2005

[Effect of vascular endothelial growth factor antisense oligodeoxynucleotides on angiogenesis in lymphoma of nude mice].

BACKGROUND & OBJECTIVE: It has been reported that vascular endothelial growth factor (VEGF) plays an important role in progression of lymphoma, and lymphoma with high level of VEGF is likely to metastasise at early stage. This study was to explore effects of antisense oligodeoxynucleotides (ASODN) targeting VEGF on angiogenesis of lymphoma through in vitro, and in vivo experiments. METHODS: Human lymphoma cell line Namalwa cells were incubated with VEGF ASODN (final concentrations were 10, 20, and 30 micromol/L, respectively), or scrambled sequence for 24 h or 48 h. VEGF mRNA expression in treated cells was detected by reverse transcriptase-polymerase chain reaction (RT-PCR), and its protein expression was detected by SP immunohistochemistry. After incubation of 30 micromol/L of VEGF ASODN, 30 micromol/L of scrambled sequence, and PBS as negative control, Namalwa cells were injected into nude mice. Diameters of tumors in ASODN group (6 mice), scrambled sequence group (6 mice), and PBS group (4 mice) were measured, microvessel density (MVD) was detected via immunohistochemistry. RESULTS: Expression of VEGF mRNA in cells treated with 10, 20, and 30 micromol/L of ASODN were 1.28, 0.86, and 0.47, respectively; those of PBS-treated cells, and scrambled sequence-treated cells were 1.79, and 1.84. Positive rate of VEGF protein in ASODN-treated cells was significantly lower than those in scrambled sequence-treated cells, and PBS-treated cells (23.3% vs. 46.9%, and 47.8%, P<0.05). MVDs of ASODN group, scrambled sequence group, and PBS group were 12.26+/-0.78, 23.92+/-1.14, and 24.13+/-1.21, respectively. CONCLUSION: VEGF ASODN can down-regulate expression of VEGF, and suppress angiogenesis in lymphoma.

Animals↗

PubMed2005

[Expression and its significance of TRAIL and its receptors in cells of patients with acute myeloid leukemia].

This study was aimed to detect the expression of TNF related apoptosis-inducing ligand (TRAIL) and its receptors on acute myeloid leukemic (AML) cells, and explore its possible role in leukemia therapy. RT-PCR and flow cytometry were used to detect the expression of TRAIL and its receptors on AML cells of 39 cases (patient group), AML cells of 18 cases with complete remission (CR group) and BMMNC or PBMNC of 21 normal persons (control group). The results showed that (1) TRAIL, DR4 and DR5 were highly expressed in both patient group and CR group, while the DcR1 and DcR2 were poorly expressed. (2) The level of DR5 expression in CR group was higher than that in patient group. (3) The level of DR5 was higher than DR4 in both patient group and CR group. (4) TRAIL and its receptors were expressed similarly in different subtypes of AML. In conclusion, there are differences between the expressions of TRAIL and its receptors in AML cells. DR5 may play an important role in TRAIL-inducing apoptosis of AML cells.

Adult↗

PubMed2005

[Protein kinase C inhibitor Gö6976 sensitizes arsenic trioxide-induced cell apoptosis in chronic myeloid leukemic cells].

To investigate the As(2)O(3)-chemosensitization of Gö6976 in K562 cells by its abrogation of As(2)O(3)-induced G(2)/M cell cycle arrest, K562 cells were treated with As(2)O(3) (5 micromol/L) and Gö6976 with various concentrations, the distributions of cell cycles were detected by flow cytometry, the cell viability was observed by trypan blue exclusion test and cell proliferation was tested by MTT assay. The results indicated that having treated by As(2)O(3) for 24 h and 48 h, the proportion of K562 cells in G(2)/M phase were (38.02 +/- 7.70)% and (32.58 +/- 7.43)% respectively, and no obvious cell apoptosis appeared. 50 nmol/L Gö6976 combined with As(2)O(3) decrease the proportion of cells in G(2)/M phase to (23.24 +/- 2.93)% and (16.18 +/- 1.60)% respectively and increase the proportion of cells in subG(1) phase to (11.82 +/- 2.31)% and (27.80 +/- 2.89)% respectively. Gö6976 abrogated G(2)/M cell cycle arrest induced by As(2)O(3) and increased cell apoptosis in a concentration- and time-dependent manner. Additionally, comparing to the control group, Gö6976 combined with As(2)O(3) decreased the cell viability and depressed the cell proliferation, but Gö6976 alone showed no same effect on them. In conclusion, the effects of AS(2)O(3)-chemosensitization of Gö6976 on K562 cells is associated with its abrogation of As(2)O(3)-induced G(2)/M cell cycle arrest.

Antineoplastic Agents↗

PubMed2005

Inhibitory effect of anti-fas ribozyme on apoptosis of mouse T cells.

BACKGROUND & OBJECTIVE: Tumor cells can express FasL, and induce apoptosis of activated T cells expressing Fas, which is so called "Fas counterattack". This study was to investigate inhibitory effect of anti-Fas ribozyme on apoptosis of mouse T cells, and explore a new way to enhance antitumor ability of T cells. METHODS: A hammerhead ribozyme targeting Fas mRNA was synthesized, its in vitro cleavage reaction was performed. Anti-Fas ribozyme was transfected into mouse spleen T cells by electroperation (ribozyme-transfected group), empty control and mock-transfected groups were set up. Fas expression on T cells was detected by reverse transcription-polymerase chain reaction (RT-PCR) and Western blot. After treatment of anti-Fas antibody (JO(2)), cell apoptosis was measured by flow cytometry, proliferation of T cells was measured by MTT assay. In vitro killing activity of cytotoxic T lymphocytes (CTLs) was detected by lactate dehydrogenase (LDH) releasing assay. RESULTS: Anti-Fas ribozyme cleaved Fas mRNA efficiently with a rate of 60%. mRNA level of Fas was significantly lower on ribozyme-transfected cells than on control and mock-transfected cells (0.4 vs. 1.1, and 1.0, P < 0.01)u its protein level was according to this result. After treatment of JO(2), cell apoptosis rate was significantly lower in ribozyme-transfected group than in the rest 2 groups (35% vs. 86%, and 87%, P < 0.01), but cell proliferation rate was significantly higher in ribozyme-transfected group than in the rest 2 groups (208% vs. 100%, and 98%, P < 0.01). In vitro killing activity of CTLs was significantly stronger in ribozyme-transfected group than in the rest 2 groups (67% vs. 32%, and 31%, P < 0.01). CONCLUSION: Anti-Fas ribozyme can remarkably suppress Fas expression on mouse activated spleen T cells, and protect T cells from Fas-mediated apoptosis, which may enhance antitumor ability of T cells.

Animals↗

PubMed2005

[Hematopoietic reconstitution of recipient mice after mFasL-cDNA transfected hematopoietic cell transplantation].

OBJECTIVE: The study was designed to explore the influence of transfected bone marrow mononuclear cells (BMMNC) transplantation on the hematopoietic cells activity and the recipient mice hematopoietic reconstitution. METHODS: The exogenous mFasL-cDNA gene was transferred to Balb/C mouse BMMNC by liposomes. Then the transferred BMMNC was co-cultured with BMMNC from BAC mouse (H-2d x b, male) at a ratio of 0.625 to 1 for 6 days. In the experimental group (the 3rd group), 1 x 10(7) (0.5 ml) mixed viable cells were injected into whole bodily irradiated ((60)Co-r) mice (6 to 8 week old female Balb/C) via the tail vein. The following grafted mice were simultaneously used in the study, the mice transplanted with 0.5 ml of culture medium, the mice transplanted with the mixture of untransferred Balb/C mouse BMMNC and BAC mouse BMMNC, the mice transplanted with the mixture of transferred Balb/C mouse BMMNC and BAC mouse BMMNC and the mice transplanted with Balb/C mouse BMMNC. The hematopoietic reconstitution, the origin of bone marrow cells responsible for the reconstitution, the graft versus host disease (GVHD), the survival rate for the recipient mice were observed after bone marrow transplantation (BMT). RESULTS: The counts of leukocytes and platelets in recipient blood of group four on +10 d and +20 d after BMT were higher than those in group three and group two (P < 0.01), but on +30 d after BMT the counts of leukocytes and platelets in recipient blood of group two, group three and group four were at their normal levels. The Y chromosome from donor mice was discovered in BMMNC of recipient mice having survived for over two months after BMT in group two and group three. The survival rate of the recipient mice two mouths after BMT in all groups were 0% for group one, 30% for group two, 80% for group three, and 100% for group four, respectively. The total survival rate of recipient mice in the experimental group was obviously higher than that of group two (P < 0.01). Grade II to III GVHD signs were found on the histology from dead mice after BMT in group three and group two, and the mice having survived for over two months in the group two. Grade I GVHD signs were found on histology from 7 out of 8 mice which survived for over two months after BMT in group three. CONCLUSIONS: The transplantation of mixed cells into recipient mice made the recipient mice achieve hematopoietic reconstitution from donor BMMNC.

Animals↗

PubMed2005

Impact of trisomy 8 on cytobiological and clinical features of acute myelomonocytic and monocytic leukemia.

To evaluate the impact of trisomy 8 on cytobiological and clinical features of acute myelomonocytic and monocytic leukemia (M(4), M(5)), a total of 56 cases of acute myelomonocytic and monocytic leukemia were investigated. Karyotypes were analyzed by G-banding or R-banding. The immunotypes in all cases were detected by flow cytometry. And the clinical characteristics at the first visit were analyzed retrospectively. The results showed that thirty-four of 56 (60.7%) patients had normal cytogenetics; 10 (17.9%) patients had trisomy 8 in their karyotypes, including 3 (5.4%) patients with trisomy 8 as the sole aberration; and 12 (21.4%) patents had other cytogenetic abnormalities (except trisomy 8). All trisomy 8 cases demonstrated a increased expression frequency of surface markers of myeloid progenitor cells CD34 (P < 0.01) and CD117 (P < 0.05) and a decreased expression frequency of surface markers of mature monocytes CD11c (P < 0.01) and CD14 (P < 0.05), compared with normal cytogenetics cases. Patients with trisomy 8 were slightly older (P < 0.05), which had lower percentages of peripheral blasts (P < 0.05) and lower WBC (P < 0.05) than the patients without trisomy 8. Patients with trisomy 8 had a shorter disease-free survival time than that of patients with normal cytogenetics (P < 0.05). It is concluded that trisomy 8 may play an important role in the pathogenesis and progression of acute myelomonocytic/monocytic leukemia (M(4)/M(5)), whic seems to be related with a block in differentiation of monocytes. Therefore, trisomy 8 may be an adverse prognostic factor for patients with M(4) or M(5).

Adolescent↗

PubMed2005

[Experimental study on apoptosis in leukemia cells induced by econazole].

To investigate apoptosis of mouse leukemia cell (WEHI-3) induced by econazole and its mechanism, apoptosis induced by econazole was examined by flow cytometry, while free calcium ([Ca(2+)]i) was determined by Fura-2 fluorescein load technique. The protein was isolated from endoplasmic reticulum of WEHI-3 cells, and then the expression of caspase-12 and caspase-7 was evaluated by Western blot. The results showed that WEHI-3 exhibited typical change of apoptosis when it was treated by econazole, [Ca(2+)]i was significantly higher in comparison with the control. The expression of caspase-12 and caspase-7 enhanced as the econazole concentration increased. In conclusion, econazole can induce WEHI-3 cell apoptosis and the caspase-12 plays a key role in this process.

Animals↗

PubMed2005

[Recombinant adenovirus mediated hVEGF165 gene transfer promotes recovery of hematopoiesis in post-BMT mice].

To investigate the effects of vascular endothelial growth factor (VEGF) on the recovery of hematopoiesis in post-BMT mice, the recombinant adenovirus Ad-EGFP/hVEGF(165) was injected into syngeneic BMT BALB/c mice via the tail vein. At day 10, 20, 30 after BMT, the in vivo expression of hVEGF(165) was measured. At the same different time points, the numbers of WBC, Plt, RBC in peripheral blood and MNC in bone marrow were counted. By the way, the bone marrow MNCs at day 30 post-BMT were used for further CFU-S assay. The results indicated that a long-term expression of hVEGF(165) in plasma and different organs was successfully mediated by recombinant adenovirus. At each time point of post-BMT, the numbers of WBC, Plt, RBC as well as bone marrow MNC observed in the group treated with recombinant adenovirus Ad-EGFP/hVEGF(165) were lower than those of the normal control group, but were higher than those in other testing groups (P < 0.05). The number of CFU-S (21.4 +/- 2.67) formed by bone marrow MNC at day 30 after BMT reached to the normal level (19.50 +/- 2.46) (P > 0.05), which was much higher than that in other groups (P < 0.05). It is concluded that hVEGF(165) gene transfer mediated by recombinant adenovirus plays a role of promoting the recovery of hematopoiesis in post-BMT mice.

Adenoviridae↗