PubMed Health⌕ Search

Biomedical subjects

Z H Li

Publications and source records attributed to Z H Li.

At least 55 records · Page 3Linked to original sources
PubMed1998

Inversion and transposition of Tc1 transposon of C. elegans in mammalian cells.

Tc1/mariner transposons are widespread in the eukaryotes. In vitro transposition test indicated that the transposase is the only protein that is needed in transpositions. It was shown later that the reconstructed Tc1-like transposon, "sleeping beauty" in fish, and the Tc1 transposon in C. elegans jumps in human cells. This discovery indicates that the Tc1/mariner transposon may be engineered as a somatic gene therapy vector if coupled with an efficient gene delivery system. We introduced the Tc1 transposon from C. elegans into different mammalian cell lines and detected the transposition events, indicating that Tc1 transposon functions in different mammalian cells. Interestingly, a high inversion frequency of the transposon was also detected, suggesting that this type of transposon may add variations to host genome when it is horizontally transferred into a new species.

Animals↗
PubMed1997

Wild-type p53 gene increases MDR1 gene expression but decreases drug resistance in an MDR cell line KBV200.

Inactivation of p53 gene and overexpression of MDR1 gene are both associated with drug resistance. Previous studies have suggested that p53 gene can modulate the expression activity of MDR1 gene promoter in a promoter-CAT system. In the present study, wild-type p53 gene cDNA was introduced into a multidrug-resistant cell line, KBv200, in which endogenous p53 gene is aberrant. In wt-p53 transfected cells, the expression of MDRI gene was significantly increased, accumulation of adriamycin (ADM) was decreased, and the sensitivity to vincristine (VCR), ADM and 5-fluorouracil (5-FU) was increased compared with the parent KBv200 cells. After treatment with ADM and VCR, the p53-transfectants were more susceptible to apoptosis. The results suggest that the increase in drug sensitivity of the cells may be, at least in part, due to p53-dependent apoptosis induced by anticancer agents.

Drug Resistance, Multiple↗
PubMed1997

Up-regulation of Tie gene expression by leukemia inhibitory factor and steel factor in CD34+ cells from human umbilical cord blood.

Tie, a new receptor tyrosine kinase, is expressed in vascular endothelial and hematopoietic cells. To determine whether Tie might be involved in early hematopoiesis, we asked whether the Tie gene is expressed in normal human hematopoietic stem/progenitor cells and if the expression of this gene could be regulated. Using a single-cell reverse-transcriptase polymerase chain reaction (RT-PCR) assay to study expression of the Tie gene in the subset of human umbilical cord blood (UCB) CD34+++ primitive stem/ progenitor cells with extensive replating capacity, we demonstrated at the single isolated cell level that Tie was expressed in these cells. The expression of Tie gene in CD34+ cells was at a low level but was enhanced up to two- to fourfold by steel factor (SLF) or leukemia inhibitory factor (LIF), two cytokines that regulate production of stem/progenitor cells, as assessed using competitive PCR and semi-quantitative RT-PCR assays. The fold increases were observed as early as 2 h for SLF and 4 h for LIF and remained elevated for 24 h. These results demonstrate modulation of gene regulation in the rare populations of CD34+ cells and suggest the possibility that Tie may play a role in the proliferation and differentiation of immature hematopoietic cells.

Antigens, CD34↗
PubMed1997

Functions of purified gB, gE:gI, and gH:gL, and their sialyl residues in varicella-zoster virus infection.

Varicella-zoster virus glycoproteins were purified by using monoclonal antibodies and analyzed for their effects on cell-free virus infection. Preinfection treatment of cells with gH:gL reduced the infection efficiency and increased the number of unadsorbed virus. Postinfection treatment of cells with gB increased the infection efficiency, but that with gE:gI reduced it. Treatment of gE:gI and gH:gL with neuraminidase (NA) abolished their inhibitory activity and the plaque formation was enhanced by NA treatment of glycoproteins and cells. Glycoproteins exhibited their diverse activities despite their common role in viral penetration, and sialyl residues were responsible for their function in cell-free virus infection.

Animals↗
PubMed1997

[Effect of chaihu guizhi decoction on the immunoglobulin and IgG subgroup in children with recurrent respiratory tract infection].

OBJECTIVE: To observe the effect of Chaihu Guizhi Decoction (CGD) on Immunoglobulin (Ig) and IgG subgroup in children with recurrent respiratory tract infection (RRTI). METHODS: Levels of Ig and IgG subgroup were measured in 23 cases of children with RRTI before and after treating with CGD, and compared with those in the control group. RESULTS: In RRTI group, the levels of IgG, IgA, IgM and IgG1 were lower than those of the control groups respectively (P < 0.01). The rate of IgG subgroup deficiency (ISD) was 60.9%. The effective rate of the CGD group was 95.6%. The IgG and IgG1 levels were increased after treatment as compared with before treatment (P < 0.05), and the ISD correcting rate being 71.4%. CONCLUSIONS: The hypoimmunofunction and IgG subgroup deficiency were important factors in RRTI pathogenesis. The CGD could improve the immunofunction and correct the IgG subgroup deficiency, and this effect might be one of the mechanism of CGD in treating RRTI.

Child↗
PubMed1997

[Clinical study on treatment of arteriosclerosis obliterans using huangqi tongmai decoction].

OBJECTIVE: To test and verify the effects of Huangqi Tongmai Decoction (HQTMI) regulating blood lipid in treating arteriosclerosis obliterans (ASO). METHODS: Thirty-two cases of ASO was treated with HQTMD for two months. The drug was in water decoction, oral taken. RESULTS: Compared with the blood lipid level before treatment, the high density lipoprotein of cholesterol (HDL-C) was increased, the low density lipoprotein of cholesterol (LDL-C), atherogenic index (AI) was decreased (P < 0.01). The serum total cholesterol (TC), triglyceride (TG), very low density lipoprotein of cholesterol (VLDL), apolipoprotein A1 (apoA1), apolipoprotein B100 (apoB100) were all changed (P < 0.05). apoA1/apoB100 ratio increased. CONCLUSION: HQTMD could regulate blood lipid. This method was effective in treating ASO.

Adult↗
PubMed1997

[Endoscopic papillosphincterotomy for the treatment of pancreaticobiliary disease].

From July 1987 to March 1996, endoscopic papillosphincterotomy (EST) was performed in 346 patients of 2,700 cases undergoing ERCP. Maj or indications for EST were choledocholithiasis, constrictive papillitis, chronic pancreatitis, biliary ascariasis and dysfunction of Oddi's sphincter. The EST was successful in 331 cases, ang the overall success rate was 95.7%. The stone discharge rate was 96%. The stricturotomy rate was 93.8%. The failure rate was 4.3% (15 cases). Clinical application and prevention of complications for EST were discussed.

Adult↗
PubMed1997

[Wild-type p53 stimulates vincristine-induced apoptosis].

Recent studies indicate that wild-type p53 can trigger cell apoptosis induced by many chemotherapeutic agents which induce DNA damage or cause disruptions of DNA metabolism, such as ADM, 5-FU, VP-16 and radiation. We introduced the wild-type p53 gene into a MDR cell line KBV200 in which the endogenous p53 was found to be rearranged. By G418 selection and Northern blot analysis, a G418-resistant clone named KBV200-p53 was obtained which continuously expressed the exogenous wild-type p53 mRNA. After treatment with Vincristine(VCR), the wild type p53-expression cells presented typical morphology characteristic of apoptosis analysed under electron and fluorescence microscopes. Flow cytometer analysis showed that the KBV200-p53 cells were more readily undergo apoptosis than their parental cells KBV200. After treatment with VCR 600 nmol.L-1 for 24 h, the apoptotic percentage of KBV200-p53 and KBV200 cells was about 42.4% and 8.4%, respectively. This result indicates that wild-type p53 stimulates VCR-induced apoptosis in KBV200 cells.

Antineoplastic Agents, Phytogenic↗
PubMed1996

Retroviral transfer of the recombinant human erythropoietin receptor gene into single hematopoietic stem/progenitor cells from human cord blood increases the number of erythropoietin-dependent erythroid colonies.

To test whether an enforced expression of a lineage-specific cytokine receptor would influence the proliferation/differentiation of hematopoietic stem/progenitor cells, retroviral vectors containing the human erythropoietin receptor (hEpoR) gene were used to transduce the hEpoR gene into phenotypically sorted subsets of cells. CD34 , CD34++CD33-, and CD34++CD33+ populations of human cord blood, highly enriched for hematopoietic stem/progenitor cells, were sorted and plated as single cells per well in methylcellulose culture medium containing early acting growth factors in the presence or absence of Epo. The hEpoR gene was efficiently transduced into single high proliferative potential colony-forming cells (HPP-CFC) and multipotential (colony-forming unit granulocyte, erythroid, monocyte, megakaryocyte [CFU-GEMM]), erythroid (burst-forming unit-erythroid [BFU-E]), and granulocyte-macrophage (colony-forming unit-granulocyte-macrophage [CFU-GM]) progenitor cells. As expected in cultures grown in the absence of Epo, no BFU-E or CFU-GEMM colonies grew. In the presence of Epo, the hEpoR-gene transduced cells formed significantly more CFU-GEMM and BFU-E colonies than did the controls. A significant decrease in HPP-CFC colonies was also observed under these conditions. Little or no effect of hEpoR gene transduction was apparent in the numbers of CFU-GM colonies formed in the presence or absence of Epo. All of the above results were similar whether the cell populations assessed were CD34 or their CD33- or CD33+ subsets plated in the presence of growth factors at 200 cells/mL or after limiting dilution at 2 cells/well. These results suggest that the profile of detectable stem/progenitors can be altered by retrovirus-mediated expression of the hEpoR gene.

Antigens, CD↗
PubMed1996

Cloning and characterization of a maize cDNA encoding phytoene desaturase, an enzyme of the carotenoid biosynthetic pathway.

To study regulation of the plastid-localized maize carotenoid biosynthetic pathway, a cDNA encoding phytoene desaturase (PDS) was isolated and characterized. The DNA sequence of the maize Pds cDNA was determined and compared with available dicot Pds genes. The deduced PDS protein, estimated at 64.1 kDa (unprocessed), had a dinucleotide binding domain and conserved regions characteristic of other carotene desaturases. Alignment of available PDS sequences from distantly related organisms suggests that Pds has potential as a phylogenetic tool. By use of heterologous complementation in Escherichia coli, maize PDS was shown to catalyze two desaturation steps converting phytoene to zeta-carotene. RFLP (restriction fragment length polymorphism) mapping was used to place Pds on chromosome 1S near viviparous5 (vp5), and RT-PCR (reverse-transcriptase polymerase chain reaction) analysis indicated reduced Pds transcript in vp5 mutant relative to normal endosperm. Other phytoene-accumulating mutant endosperms, vp2 and white3 (w3), showed no difference in Pds transcript accumulation as compared with normal endosperm counterparts. RT-PCR analysis of Pds transcript accumulation in developing endosperm showed Pds was constitutively expressed. Therefore, endosperm carotenogensis is not regulated by increasing the level of Pds transcripts.

Amino Acid Sequence↗
PubMed1996

Macrophage-stimulating protein, a ligand for the RON receptor protein tyrosine kinase, suppresses myeloid progenitor cell proliferation and synergizes with vascular endothelial cell growth factor and members of the chemokine family.

Macrophage-stimulating protein (MSP), originally identified as an inducer of murine resident macrophage responsiveness to chemoattractants, is a ligand for human RON/murine STK receptor protein tyrosine kinases. Since STK was cloned from populations enriched for hematopoietic stem cells, we initiated studies on the effects of MSP on colony formation by granulocyte-macrophage (CFU-GM), erythroid (BFU-E), and multipotential (CFU-GEMM) myeloid progenitor cells. MSP alone had no colony stimulating activity. However, MSP caused about a 50% suppression of CFU-GM colony formation induced by synergistic combinations of SLF or Flt-L plus GM-CSF, G-CSF, or IL-3 and of BFU-E and CFU-GEMM colonies induced by SLF or Flt3-L plus Epo or Epo and IL-3. In contrast, MSP had no effect on progenitors stimulated by one growth factor. MSP also suppressed colony formation by stimulated cord blood progenitors, but only after preinduction to a rapidly cycling state. It was previously reported that several members of the chemokine family synergistically suppress myeloid progenitor proliferation. Likewise, synergistic suppression was observed when MSP was paired with VEGF, MIP-1 alpha, IL-8, PF4, MCP-1, IP-10, or ENA-78, or when VEGF was paired with the chemokines; and the required MSP concentration was more than 100-fold less than for MSP alone. Additionally, MSP or VEGF inhibited proliferation of the human myeloid growth factor-dependent cell line, M07e, but a sustained effect required multiple additions over time. At the least, some of the MSP suppressive effects on myeloid progenitors, as assessed on single isolated CD34 marrow cells, appeared to be directly on the progenitors; sustained additions of MSP were required to see this effect. The suppressive action of MSP and its synergism with proteins of the chemokine family may be of relevance to regulation of blood cell production.

Bone Marrow Cells↗
PubMed1996

Somatic microsatellite mutations as molecular tumor clocks.

Microsatellite (MS) mutations can potentially unravel the past of mutator phenotype tumors, with greater genetic diversity expected in older regions. Rapid clonal expansions of xenografts were characterized by relatively homogenous MS alleles, whereas greater diversity was observed in a colorectal cancer with the greatest variation in its adjacent adenoma. A subcutaneous lung cancer metastasis demonstrated diversity consistent with its one-month clinical duration and evidence of active mitosis during dormancy. The genetic legacy inherent to multistep tumorigenesis provides direct estimates of tumor ages, with up to thousands of cell divisions and high death rates necessary to yield the observed diversities. MS molecular tumor clocks have the unique potential to systematically reconstruct the early and occult evolution of individual human mutator phenotype tumors.

Adenocarcinoma↗
PubMed1996

Inhibitory effects of interleukin 12 on retroviral gene transduction into CD34 cord blood myeloid progenitors mediated by induction of tumor necrosis factor-alpha.

Interleukin 12 (IL-12), a heterodimeric cytokine with potent biologic activity, was evaluated for effects on retroviral-mediated gene transduction into human myeloid progenitor cells in vitro. Cord blood CD34 cells were prestimulated with Steel factor (SLF), IL-3, GM-CSF, and erythropoietin (Epo) in the presence and absence of 5-80 ng/ml IL-12 for 40 hr in suspension culture prior to gene transduction using viral supernatant collected from a packaging cell line containing the pLNL6 vector encoding Neo sequences. After gene transduction, cells were assayed for colony formation stimulated by Epo, GM-CSF, IL-3, and SLF, and gene transduction efficiency was determined by the percentage of G418 resistant (R) colonies and confirmed by PCR analysis. IL-12 dose-dependently inhibited retroviral-mediated gene transduction into human cord blood CD34 granulocyte-macrophage (CFU-GM) and erythroid (BFU-E) progenitors. These suppressive effects could be neutralized by incubation of IL-12 with polyclonal antihuman IL-12. IL-12 had no inhibitory effects directly on colony formation. To understand the possible mechanisms for this suppression, ELISA assays were used to detect the release of interferon (IFN)-gamma and tumor necrosis factor (TNF)-alpha, which could potentially have been induced by IL-12 from CD34 cells. TNF-alpha protein release was significantly increased in CD34 cells incubated with IL-12. No detectable levels of IFN-gamma were noted. Anti-TNF-alpha, but not anti-IFN-gamma, blocked the inhibitory effects of IL-12 on gene transduction. Moreover, TNF-alpha, but not IFN-gamma, suppressed gene transfer to the same degree as IL-12. No change of amphotropic receptor mRNA expression was noted by Northern blot analysis in cells treated with or without IL-12. The results suggest that the suppressive effects of IL-12 on retroviral gene transduction are, at least in part, mediated by IL-12 induction of the release of TNF-alpha.

Antigens, CD↗
PubMed1996

Influence of retroviral-mediated gene transduction of both the recombinant human erythropoietin receptor and interleukin-9 receptor genes into single CD34++CD33-or low cord blood cells on cytokine-stimulated erythroid colony formation.

Introduction of genes for cytokine receptors into hematopoietic stem/progenitor cells (HSC/HPC) may be of clinical use in the future. We recently reported that retroviral-mediated transduction of either the human erythropoietin receptor (hEpoR) or interleukin-9 receptor (hIL-9R) genes into highly purified HSC/HPC from cord blood (CB) resulted in increased numbers of detectable cytokine-responsive erythroid progenitors (burst-forming units-erythroid [BFU-E]). In the present study, we evaluated if this increase could be further enhanced by cotransducing both these genes into single isolated HSC/HPC. Single CD34++CD33-or low-expressing cells from CB were transduced with viral supernatant containing the hEpoR or hIL-9R genes or cotransduced with both genes. In the presence of Steel factor (SLF), interleukin-3 (IL-3), granulocyte-macrophage colony-stimulating factor (GM-CSF), erythropoietin (Epo), and IL-9, the numbers of erythroid colonies formed were significantly increased after transduction of cells with either the hIL-9R or hEpoR gene compared to mock-transduced cells. This increase was significantly enhanced in cells cotransduced with both genes compared with either gene alone. Integration and expression of both genes was confirmed by polymerase chain reaction (PCR) and reverse-transcriptase (RT)-PCR analysis, respectively. The data demonstrate that myeloid progenitors can be transduced at the single-cell level with both hEpoR and hIL-9R genes with resultant enhanced proliferation of these progenitors in the erythroid lineage by combinations of cytokines including Epo and IL-9.

Antigens, CD34↗
PubMed1996

Telomerase activity is commonly detected in hereditary nonpolyposis colorectal cancers.

Telomerase activity can be detected in most human cancers. These findings are consistent with the telomere hypothesis, which predicts telomerase expression after a number of mitotic divisions to prevent the progressive and catastrophic loss of telomeres. However, telomerase is not detected in a minority of colorectal cancers suggesting either alternative mechanisms of immortalization or that their telomeres have not yet shortened sufficiently to require telomerase activity. Colorectal cancers arising in patients with hereditary nonpolyposis colorectal cancer (HNPCC) were examined for telomerase activity because compared to sporadic tumors, HNPCC tumors are less likely to pass a telomere threshold as they occur in younger patients and exhibit "accelerated" progression, perhaps because of their characteristic mutator phenotypes and losses of mismatch repair. Primary, colorectal cancers, 13 in HNPCC patients, and 37 sporadic tumors (17 with mutator phenotypes) were examined for telomerase activity by the TRAP (telomeric repeat amplification protocol) assay. The majority of colorectal cancers contained detectable telomerase activity regardless of underlying phenotype (77 percent of HNPCC; 81 percent of sporadic tumors, 88 percent with mutator phenotypes and 75 percent without mutator phenotypes). Therefore, telomerase expression appears to be commonly acquired in the progression of both mutator phenotype and sporadic colorectal cancers.

Aged↗
PubMed1996

Effects of mutation and growth rates on patterns of microsatellite instability.

The detection of somatic microsatellite (MS) alterations in tumors is often interpreted as a sign of underlying genomic instability. However, it is unclear why the proportions of altered MS loci vary between different mutator phenotype tumors. We present a simple mathematical analysis that can account for some of these differences, recognizing that the mutations accumulated in a tumor reflect both its mutation rate and number of cell divisions. Only a small proportion of mutated MS loci are expected in tumors with normal or low mutation rates. In contrast, tumors with high mutation rates may or may not acquire mutations depending on the numbers of divisions that proceed the onset of the mutator phenotype. The majority of MS loci should accumulate mutations if high mutation rates are acquired early in tumor progression. Somatic MS mutations provide clues to both the mode and tempo of tumori-genesis.

Adult↗
PubMed1996

A novel method for studying preadipocyte differentiation in vitro.

In vitro differentiation of rat preadipocytes has typically been induced in medium supplemented with pharmacological concentrations of hormonal mixtures. These conditions probably do not reflect the milieu within adipose tissue in vivo. We have developed a new method for inducing differentiation of preadipocytes using culture medium which has been conditioned by isolated adipocytes (ACM). In the presence of ACM, 70%-80% of test preadipocytes contained lipid inclusions compared to < 5% of control. When differentiation was assessed by assay of glycerol-3-phosphate dehydrogenase activity, ACM activity was shown to be reproducible and the consistency of response to ACM by different pools of preadipocytes was comparable to that induced by standard differentiation procedures. We have also demonstrated that the adipogenic activity of ACM may not depend on prostaglandin secretion by adipocytes. We propose that use of paracrine factors produced by components of adipose tissue provides a new approach to preadipocyte differentiation induction which may more closely reproduce the adipose tissue environment.

Adenosine↗