[Progress in the study of CD34+ cells in myelodysplastic syndrome].
Explore the source record for details and available documents.
Antigens, CD34↗
Biomedical subjects
Z Shao
Publications and source records attributed to Z Shao.
[Clinical study of aplastic anemia].
Explore the source record for details and available documents.
Anemia, Aplastic↗
[Treatment of chronic aplastic anemia with triolandren and cyclosporin A].
OBJECTIVE: To explore more effective regimen for chronic aplastic anemia (CAA). METHODS: Forty-five cases of CAA were treated with triolandren (TLD) (15 cases) or TLD and cyclosporin A (CsA) (30 cases). RESULTS: The response rate of TLD-CsA group (83.3%) was higher than that of TLD group (60.0%), furthermore, the recovery of bone marrow colony-forming cell (CFC) number of the responding patients was more complete and rapid in TLD-CsA group than in TLD group. Bone marrow CFC number had no significant change of all nonresponding patients in both groups. CONCLUSION: The response rate of TLD-CsA was higher than that of TLD alone, and the recovery of bone marrow CFC number of the responding patients was more complete and rapid in TLD-CsA group.
Adolescent↗
[Serum level of granulocyte colony stimulating factor in severe aplastic anemia patients].
OBJECTIVE: To investigate the relationship between serum level of granulocyte colony stimulating factor (G-CSF) and clinical status, treatment outcome and prognosis in severe aplastic anemia (SAA-I) patients. METHODS: Serum G-CSF level was detected by ELISA assay in 36 SAA-I patients. RESULTS: Pre-treatment serum G-CSF levels of 27/36 (75%) SAA-I patients were above normal. These patients achieved better curative outcomes in a shorter period of treatment. CONCLUSION: Detection of serum G-CSF level in SAA-I patients is helpful for judging the clinical status and prognosis.
Adolescent↗
[Efficacy of cyclosporin A in the treatment of aplastic anemia and its mechanism].
Explore the source record for details and available documents.
Anemia, Aplastic↗
Potentiation and inhibition of nicotinic acetylcholine receptors by spermine in the TE671 human muscle cell line.
Nicotinic acetylcholine receptors (nAChR) of the TE671 cell line were investigated using whole-cell and membrane patch recording techniques. At negative holding potentials (VH), pulses of acetylcholine (ACh) elicited whole-cell inward currents that rapidly desensitized. The EC50 value for ACh at VH = -60 mV was 7.8 microM. The ACh-induced current reversed at approximately 0 mV. Desensitization of nAChR by ACh was biphasic and reversible within approximately 20 sec. Spermine (1-100 microM) potentiated responses to ACh (10 microM - 1 mM) by reducing the rate of onset of desensitization; potentiation was inhibited by arcaine (10-100 microM). Spermine (1 mM) noncompetitively antagonized the AChinduced current. Antagonism by 1 to 5 mM spermine was voltage-dependent, increasing with negative VH. In 100 microM arcaine, this antagonism was shown to contain a voltage-independent component. Spermine (10 mM) increased the EC50 values for ACh, suggesting that at this concentration the polyamine is also a competitive antagonist. Single channel openings elicited during application of ACh to outside-out patches had a conductance of 47 pS at VH = -60 mV. At 10 and 100 microM, spermine increased channel open probability (po), but at 1 mM spermine, po was not significantly different from controls. The single channel conductance for ACh was unaffected by 10 and 100 microM spermine, but was decreased by 1 mM spermine. Spermine promoted the occurrence of approximately 27 pS openings. It is proposed that spermine acts at an excitatory modulatory site similar to that present on N-methyl-D-aspartate receptors and at least three inhibitory sites on nAChR of TE671 cells.
Acetylcholine↗
Rb interacts with TAF(II)250/TFIID through multiple domains.
The retinoblastoma tumor suppressor gene product (Rb) binds directly to the largest TFIID subunit, TATA-binding protein associated factor TAF(II)250, first identified as the cell cycle regulatory protein CCG1. Here we map the domains in Rb and TAF(II)250 important for their interaction in vitro and in vivo. Both the amino terminus and the large pocket of Rb are able to associate independently with TAF(II)250. The binding domain(s) within the large pocket are distinct from the viral oncoprotein and E2F binding region since certain pocket mutations, which abolish E1A binding, do not abolish TAF(II)250 binding. Consistent with the large pocket of Rb binding to TAF(II)250, the large pocket domains of both p107 and p130 are able to bind to TAF(II)250 in vivo. We also demonstrate that at least two regions of TAF(II)250 are able to bind to the large pocket of Rb independently whereas the amino terminus of Rb binds to a distinct domain in TAF(II)250. We further demonstrate that Rb can bind to TFIID in vitro, presumably in part through an interaction with TAF(II)250. Our results suggest a complex interaction between Rb and TAF(II)250 and imply that TAF(II)250, TFIID, and potentially other basal transcription factors are targets for regulation by Rb and Rb-related proteins.
Binding Sites↗
Mitochondrial electron transport can become a significant source of oxidative injury in cardiomyocytes.
Ischemia/reperfusion causes oxidant injury in isolated cardiomyocytes without neutrophils or xanthine oxidase. Since these cells contain mitochondria, we hypothesized that the mitochondrial electron transport chain (ETC) causes this injury. To test this, we altered two conditions known to change within the mitochondria during ischemia/reperfusion-the extent of ETC redox-reduction and oxygen levels-and measured the resulting oxidant generation and injury. Specifically, we exposed cardiomyocytes for 1 h to the mitochondrial ETC inhibitors cyanide, antimycin, and rotenone and measured oxidant generation, using the intracellular fluorescent probe 2',7'-dichlorofluorescin (DCFH, sensitive to H2O2 and hydroxyl radicals). Inhibitors causing more extensive redox-reduction of the ETC (cyanide or antimycin) generated more oxidants than did partial ETC reduction with the inhibitor rotenone (10-fold v five-fold increases in DCFH oxidation). In addition, the DCFH oxidation caused by cyanide could be completely attenuated by the antioxidants 2-mercaptopropionylglycine (MPG) and 1,10 phenanthroline (PHEN). Finally, we tested the relevance of this oxidant generation on cell survival and contraction, with and without antioxidant interventions. Cell viability and contraction after 3-h recovery from cyanide exposure was significantly improved by either the addition of antioxidants, or by the "antioxidant" strategy of lowering O2 levels (i.e. from 150 to 3 tau) during the cyanide exposure (13.8% death with hypoxic cyanide v 48.6% cell death with normoxic cyanide). Collectively, these findings demonstrate that mitochondrial ETC carriers can cause significant oxidant injury, greatest when fully redox-reduced and exposed to oxygen, conditions known to occur in the transition from ischemia to reperfusion.
Animals↗
Significant levels of oxidants are generated by isolated cardiomyocytes during ischemia prior to reperfusion.
Oxidants such as reactive oxygen species (ROS) have been shown to participate in myocardial ischemia/reperfusion injury. While many studies report a burst of ROS at reperfusion, few reports have presented evidence of significant ROS generation during ischemia. Our previous studies of cultured cardiomyocytes indicated that antioxidants are most effective when given prior to reperfusion during ischemia. Therefore, we hypothesized that significant ROS generation may occur during ischemia prior to reperfusion. We tested this in a perfused isolated cardiomyocyte system (i.e. without neutrophils, endothelial cells, or xanthine/xanthine oxidase) during simulated ischemia/reperfusion while measuring oxidant generation using intracellular fluorescent probes. During ischemia, the ROS probes dihydroethidium and 2',7'-dichlorofluorescin were significantly oxidized, suggesting superoxide and H2O2 generation. At reperfusion following 1 h ischemia, these probes suggested a further burst of H2O2 and hydroxyl radicals. The antioxidants 2-mercaptopropionyl glycine and 1,10-phenanthroline used during ischemia attenuated oxidant generation, increased cell viability, and improved return of contraction after ischemia. To further evaluate the relationship between residual O2 and ROS generation, we administered O2 scavengers during ischemia and measured corresponding changes in oxidant generation, cell viability and contraction during reperfusion. Enzymatic scavenging of residual O2 during ischemia (reducing PO2 from 3.5 to 2.5 tau) paradoxically improved subsequent viability and contraction. These results indicate that cultured cardiomyocytes generate significant ROS during ischemia. This ROS generation is related to residual O2 present during ischemia and contributes significantly to the cellular injury seen at reperfusion.
Animals↗
Cryo-atomic force microscopy of smooth muscle myosin.
The motor and regulatory domains of the head and the 14-nm pitch of the alpha-helical coiled-coil of the tail of extended (6S) smooth-muscle myosin molecules were imaged with cryo atomic force microscopy at 80-85 K, and the effects of thiophosphorylation of the regulatory light chain were examined. The tail was 4 nm shorter in thiophosphorylated than in nonphosphorylated myosin. The first major bend was invariant, at approximately 51 nm from the head-tail junction (H-T), coincident with low probability in the paircoil score. The second major bend was 100 nm from the H-T junction in nonphosphorylated and closer to a skip residue than the bend (at 95 nm) in thiophosphorylated molecules. The shorter tail and distance between the two major bends induced by thiophosphorylation are interpreted to result from melting of the coiled-coil. An additional bend not previously reported occurred, with a lower frequency, approximately 24 nm from the H-T. The range of separation between the two heads was greater in thiophosphorylated molecules. Occasional high-resolution images showed slight unwinding of the coiled-coil of the base of the heads. We suggest that phosphorylation of MLC20 can affect the structure of extended, 6S myosin.
Adenosine Triphosphate↗
[Study on p53, mdm-2 and p21WAF1 protein expression in ER-positive and ER-negative human breast cancer cell lines and its relation to biological features].
OBJECTIVE: To study p53, mdm-2 and p21WAF1 protein expression levels in ER-positive and ER-negative human breast cancer cell lines and their relations to biological features. METHODS: Using cell culture, DNA stable transfection and immunohistochemical methods, the protein expression levels of p53, mdm-2 and WAF1 genes in ER-positive expressing wtp53 MCF-7 cells, ER-negative expressing mtp53 MDA-MB-231 cells and ER-transfected MDA-MB-231 cells were determined, and then, their relation to biological features were compared. RESULTS: (1) The function and expression of p53 protein of MCF-7 and MDA-MB-231 cells were obviously different. The expression levels of mdm-2 and p21WAF1 proteins in MCF-7 cells were higher than those of MDA-MB-231 cells (P < 0.05), The biological features of the former were more favorable than those of the latter. (2) The ER-transfected MDA-MB-231 cells showed lower expression of mtp53 and higher expression of mdm-2 protein (P < 0.05), but no significant difference from that of p21WAF1 protein (P > 0.05). Meanwhile, biological features leading to favorable prognosis were manifested. CONCLUSION: The ER status of breast cancer cell lines is related to the expression level of p53 and mdm-2 proteins and the biological features.
Breast Neoplasms↗
[Male breast cancer: experience with 42 cases].
Data were collected on 42 men with breast cancer treated at department of surgery, cancer hospital in Shanghai between 1960 to 1996. We studied several clinical features and the importance of established prognostic factors. Observation for 76 months showed the 5 year survival rate was 57.1%, and the total survival was 64.3%. Prognostic indicator analysis showed that only axillary lymph node status proved to have a prognostic impact. Tumor size, age did not show any prognostic influence. Because of less cases, we can not use Cox's regression model to do multivariate analysis.
Adult↗
[In situ DNA labeling apoptosis in breast cancer as related to prognosis].
OBJECTIVE: This study was undertaken to determine the expression of apoptosis in breast cancer and to evaluate it's significance as a prognostic marker. METHODS: A series of 91 invasive breast cancer was analysed for the expression of apoptosis by using the 3-end-labeling method of DNA in tissue sections. The apoptotic indexes were the percentages of apoptotic cells among tumor cells. RESULTS: The end-labeling method allowed a precise evaluation of the expression of apoptosis. Apoptosis occurred in 91.2% of breast cancer patients, and apoptotic indexes were divided into two groups, 0-0.21 and 0.28-0.62. Low apoptotic index was related to axillary lymph node metastasis (P < 0.01). In survival analysis, higher apoptotic index was related to disease free survival (P = 0.0095) and overall survival (P = 0.0348) in the entire cohort. Cox's analysis showed apoptotic index had no independent prognostic value. CONCLUSION: The apoptosis was a spontaneous phenomenon in breast cancer tissue, and the expression was different from each other. Further analysis was needed to clarify the relationship between apoptosis and prognosis, especially the response to adjuvent therapy.
Adult↗
[Inhibition of estrogen receptor-positive human breast carcinoma cell growth by retinoic acid].
OBJECTIVE: To evaluate whether the growth inhibition by retinoic acid and RAR alpha mRNA expression levels were affected by the change of ER expression. METHODS: The ER-negative breast cancer cell line MDA-MB-231 was transfected with the ER gene by stable transfection. RESULTS: In ER-transfected cells not only was the RAR alpha mRNA expression increased, but their growth was inhibited by retinoic acid as well. Estrogen could greatly stimulate the RAR alpha gene expression not only in established ER-positive cell lines but also in ER-transfected MDA-MB-231 cells. CONCLUSION: Our data strongly suggest that ER-mediated enhancement of RAR alpha levels play an important role in RA inhibition of human breast cancer cell growth.
Antineoplastic Agents↗
Estrogen receptor-negative breast cancer cells transfected with estrogen receptor exhibit decreased tumour progression and sensitivity to growth inhibition by estrogen.
Breast cancer containing estrogen receptors (ER) are responsive to antiestrogen treatment and have a better prognosis compared with ER-negative tumors. The loss of estrogen receptors appears to be associated with a progression to less-differentiated cells. We transfected the human ER into the ER-negative breast cancer cell line MDA-MB-231 cells. We found that expression of adequate ER is strong associated with the ability of human breast cancer cell growth inhibition and progression. Compared with nontransfected or mock-transfected cells, ER-transfected cells exhibited growth slower, forming smaller colonies in soft agar and growth inhibited by estrogen and tamoxifen. Therefore reactivation or transfection of the estrogen receptor gene can be considered as therapeutic approaches to hormone-independent breast cancer.
Breast Neoplasms↗
p53 independent G1 arrest and apoptosis induced by adriamycin.
The biological activity of adriamycin was investigated in human breast carcinoma (HBC) cells, Adriamycin inhibited the growth of a number of HBC cell lines and induced G1 arrest followed by apoptosis. In MCF-7 cells that harbor wild-type p53, adriamycin-induced G1 arrest and apoptosis was accompanied by p53-independent regulation of WAF1/CIP1 as well as bax mRNA levels. In MDA-MB-231 cells which possess a mutant p53, adriamycin-induced G1 arrest and apoptosis was also associated with a concomitant up-regulation of WAF1/CIP1 mRNA while these cells did not express bax or bcl-2 messages. Thus, adriamycin induces G1 arrest and apoptosis via a unique pathway which appears to involve activation of downstream effectors of p53-independent manner.
Antineoplastic Agents↗
[Colony-stimulating activities of serum from patients with severe aplastic anemia].
OBJECTIVE: To investigate the correlation between colony-stimulating activities of serum from patients with severe aplastic anemia (SAA) and their responses to immunosuppressive therapy (IST). METHODS: In vitro effects of sera from SAA patients before and after IST and from normal subjects on human marrow colony growth were examined in a semisolid methylcellulose culture system for burst promoting activity (BPA) and granulocyte/macrophage colony-stimulating activity (GM-CSA). Serum erythropoietin (Epo) level was also measured by ELISA method before and after IST in SAA patients. RESULTS: Serum BPAs in SAA patients at diagnosis were significantly higher than that in normal controls (P<0.001), but serum GM-CSAs in 13 of 22 SAA patients were normal,and in 9 of 22 extremely low as compared with normal values. After IST, serum BPA and GM-CSA in SAA patients had no changes. Serum Epo levels in SAA patients at diagnosis were significantly higher than that in normal controls (P<0.001). After IST,serum Epo levels declined in responded patients, while further increased in nonresponded. CONCLUSION: Serum GM-CSA of SAA patients was a predictive factor for responsiveness to IST, and a normal value was associated with a good response.
Anemia, Aplastic↗
[Correlation between the serum levels of interleukin-2 and soluble interleukin-2 receptor and the response to immunosuppressive therapy in severe aplastic anemia patients].
OBJECTIVE: To explore factors influencing the effectiveness of immunosuppressive therapy in severe aplastic anemia (SAA). METHODS: The serum levels of interleukin-2 (IL-2) and soluble IL-2 receptor (sIL-2R) of 22 SAA patients and 15 normal controls were measured by immunoenzyme assay. RESULTS: Comparing with the normal controls, 40.9% and 63.6% of the SAA patients had higher serum levels of IL-2 (>840ng/L) and of sIL 2R (>320 x 10(3) U/L), respectively. Those who had higher IL-2 levels and higher sIL-2R levels got better responses to cyclosporin A(CsA) and CsA plus antilymphocyte globulin (ALG). CONCLUSION: The serum levels of IL-2 and sIL-2R were correlated with the responsiveness to immunosuppressive therapy in SAA patients and might be useful for directing treatment.
Adolescent↗